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Introduction to Hemodynamics ....................................................................................... 5
A. Role of Cardiac Catheterization in assessment of Cardiac hemodynamics .... 5
B. Cardiac Catheterization Assessment of Normal Hemodynamics..................... 5
a. Right Heart Catheterization............................................................................... 5
b. Left Heart Catheterization................................................................................. 8c. Cardiac output (CO) determination .................................................................. 9
d. Hemodynamic Equations................................................................................. 13
C. Principles of Fluid Dynamics ............................................................................. 14
D. Role of Echocardiography in Assessment of Cardiac Hemodynamics .......... 16
a. Valvular Stenosis.............................................................................................. 17
b. Cardiac output determination by echocardiography ...................................... 18
Indices of Left Ventricular Systolic Function .............................................................. 19
A. Cardiac catheterization ...................................................................................... 19
a. Assessment of LV volume and LVEF ............................................................. 19b. Measurement of LV mass ................................................................................ 20
B. Echocardiography ............................................................................................... 21a. LV mass ............................................................................................................ 21
b. Fractional Shortening ..................................................................................... 22
c. Left ventricular volume and ejection fraction ................................................ 23
d. Velocity of circumferential fiber shortening (Vcf) ......................................... 25
e. The rate of change of LV pressure (dP/dt)...................................................... 26
f. LV wall stress ( σ ).............................................................................................. 27
Diastolic Function and Dysfunction .............................................................................. 28
A. Introduction ......................................................................................................... 28
B. Assessment of LV diastolic function with Cardiac Catheterization............... 29
a. Time constant of ventricular relaxation ( τ ) .................................................... 29
b. Diastolic filling rate (DFR).............................................................................. 30C. Echocardiographic assessment of LV diastolic function ................................. 31
a. Doppler echocardiography .............................................................................. 31
b. Index of myocardial performance ................................................................... 34
c. Time constant of ventricular relaxation ( τ ) .................................................... 34
d. Tissue Doppler imaging (TDI) ........................................................................ 35
e. Color M-mode echocardiography (CMM) ...................................................... 36
A. Introduction ......................................................................................................... 38
B. Cardiac Catheterization ..................................................................................... 39
C. Echocardiography ............................................................................................... 40
a. RA collapse ........................................................................................................... 41b. RV Diastolic collapse ........................................................................................... 41
c. Respiratory variations in diastolic filling ............................................................ 41
d. IVC plethora......................................................................................................... 42
A. Introduction ......................................................................................................... 50B. Cardiac Catheterization ..................................................................................... 50
C. Echocardiography ............................................................................................... 53
a. Measurement of gradient ................................................................................. 53b. Valve area determination................................................................................. 54
A. Introduction ......................................................................................................... 57
B. Cardiac Catheterization ..................................................................................... 58
a. Acute aortic regurgitation................................................................................ 58
b. Chronic aortic regurgitation............................................................................ 58
C. Echocardiography ............................................................................................... 59
a. Assessment of jet area and jet length (Color flow mapping).......................... 60b. LV response to AR............................................................................................ 60
c. M-mode echocardiography .............................................................................. 61e. Flow reversal in descending aorta................................................................... 62
f. Regurgitant volume and fraction .................................................................... 63
A. Introduction ......................................................................................................... 76
B. Cardiac Catheterization ..................................................................................... 76
C. Echocardiography ............................................................................................... 78
a. Color flow mapping .......................................................................................... 78b. Vena Contracta ................................................................................................ 78
c. Continuous wave Doppler ................................................................................ 79
d. Volumetric method ........................................................................................... 79
e. Proximal isovelocity surface area method (PISA).......................................... 80
f. Pulmonary vein flow reversal .......................................................................... 81
g. Peak mitral inflow velocity .............................................................................. 81
A. Introduction ......................................................................................................... 92
B. Cardiac Catheterization ..................................................................................... 93
C. Echocardiography ............................................................................................... 94
a. Doppler derived gradients................................................................................ 94b. Other findings (M-mode and 2-D) .................................................................. 96
c. RV isovolumetric relaxation time.................................................................... 96
A. Role of Cardiac Catheterization in assessment of Cardiac hemodynamics
At the turn of the last century, only pulse, respiratory rate, and temperature were
monitored and recorded in patients regardless of severity of illness. It wasn’t untillate 1920s when blood pressure measurements became standard for assessment of
circulatory system. The onset of the electronic revolution in 1960s coincided withthe advent of intensive therapy. First cardiac catheterization by Werner Forssman
in 1929 (on himself), initiated interest in this technique by a small group of
investigators. It wasn’t until the 1950s when this technique gained wide
acceptance and with technological advancements over the years, cardiaccatheterization has a mainstay in both investigation and therapy of patients with
cardiovascular disease.
B. Cardiac Catheterization Assessment of Normal Hemodynamics
The pressure wave created by cardiac muscular contraction is transmitted along a
closed, fluid filled column (catheter) to a pressure transducer. This transducerconverts the mechanical pressure to an electrical signal that can be recorded anddisplayed number of different ways.
a. Right Heart Catheterization
Right heart catheterization allows for measurement and analysis of right atrial
Figure1. Pressuretracings recorded via
a Swan-Ganz catheter
during right heart
catheterization.
(RA) pressures, right ventricular (RV) pressures, pulmonary artery (PA)
pressures, pulmonary capillary wedge pressures (PCWP), cardiac output (CO)determination using thermodilution, assessment for intracardiac shunts,
temporary ventricular pacing, and pulmonary angiography.
i. Right Atrium
The normal RA pressure tracing (Figure 2) is characterized by an a wave (atrial systole), c wave (isovolumetric systole of RV during which thetricuspid valve (TV) is closed), and a v wave (RV systole and filling of RA
from systemic veins and coronary sinus). The x descent follows the a wave
(RA relaxation), following the c wave there is a second pressure declinereferred to as the x’ descent (fall in RA pressure as the RV ejects blood), and
the y descent follows the peak of v wave and begins immediately after the
i. Left ventricleThe pressure pulse (Figure 6) is characterized by a peak systolic
pressure nearly equal to the peak aortic pressure (there may be a small
mid-systolic or late-systolic pressure gradient). In the absence of anyobstruction to LV outflow, this peak pressure occurs at the end of the first
1/3rd
of systole. The peak positive rate of rise of LV pressure (dP/dt )
occurs before the opening of the AV; the peak negative dP/dt occurssimultaneously with closure of the AV and marks the beginning of
isovolumetric relaxation in the LV. Following AV closure, the LV
pressure declines until decreasing pressure differential between LV andLA causes the opening of MV. At end-diastole, the pressure rises quickly
in response to atrial systole. The LVEDP immediately precedes the
beginning of isovolumetric contraction in the LV pressure pulse. Ingeneral, the mean PCWP, mean LAP, and LVEDP are all near equivalent
in magnitude.
The LVEDP is elevated (>12 mmHg) in:
1) LV diastolic volume overload (e.g. MR, AR, a large left-to-
right shunt)2) Concentric hypertrophy (decreased compliance) e.g. AS or
long-standing HTN
3) Decreased myocardial contractility (dilated LV)4) Restrictive or infiltrative cardiomyopathy
5) Constrictive pericardial disease (or a high pressure pericardial effusion)
6)
Ischemic heart disease. (Acute or chronic secondary to non-
compliance, scar)
ii. Ascending aorta
During ejection normal pressure in the ascending aorta parallelsLV pressure (Figure 6). Once the AV closes the aortic pressure declines
somewhat slower than the LV pressure. This reflects the accumulated
pressure waves from thoracic aorta and its tributaries as well as thecapacitance of the aorta. Following the dicrotic notch, there is a brief
increase in pressure due to some retrograde flow from the periphery into
the ascending aorta and the elastic recoil of ascending aorta. Then as the blood runs off into the periphery, there is a gradual decline in the systolic
arterial pressure until the next cardiac cycle.
The rate and magnitude of decline of aortic pressure duringdiastole are dependent on:
3) Presence or absence of abnormal connection of aorta and the
pulmonary circulation or the right heart (e.g. PDA)4) Presence or the absence of a large arteriovenous fistula
Table 1. Hemodynamic values for normal adults
Figure 6. Normal Hemodynamics
c. Cardiac output (CO) determination
In the cardiac catheterization laboratory the cardiac output is usually
determined by one of two methods: (1) measurement of oxygen consumption,
and (2) indicator dilution technique. Each of these techniques will be reviewedfurther.
i. Measurement of Oxygen Consumption (Fick Method)Adolph Fick initially described this technique in 1870. The
principle used is that the uptake of a substance by any organ
system is the product of the arteriovenous concentration difference
of that substance and the blood flow to that organ. Hence if thelungs are used as the end organ, the pulmonary blood flow (whichis equal to the systemic blood flow in the absence of an
intracardiac shunt) can be determined by measuring the
arteriovenous difference in the oxygen across the lungs and theuptake of oxygen by the lungs.
The arteriovenous oxygen content difference (Ao – PA O2 content)
can be calculated (in ml oxygen) by the difference between the leftventricular oxygen content:
Where VEATP is the measured expired volume at atmospherictemperature and pressure, T is room temperature in °C, P is the
barometric pressure in the room (mmHg), and W is the water vapor
pressure at the current room temperature (mmHg) (Table 2). At
20°C this value is 17.54 mmHg.
Table 2. Water Vapor Pressure (W) at various temperatures (°C) (From Sutton,
1998)
T (°C) W (mmHg)18 15.48
19 16.48
20 17.54
21 18.65
22 19.83
23 21.07
24 22.38
25 23.76
2) The metabolic hood (or polarographic method) utilizes a polarographic oxygen sensor cell to measure the oxygen content of
expired air. Room air is withdrawn at a constant rate from a plastic
hood that is placed over the patient’s head. The polarographmeasures the contents of the hood and the rate meter readout on the
unit provides the oxygen consumption in liters per minute. This
value is then used to calculate cardiac output.
ii. Indicator Dilution MethodThis method uses the mean concentration and transit time of an artificial
substance that is added to the blood stream. The most commonly usedmethod is cold saline (thermodilution) injected into the RA and theresulting temperature change is detected in the PA. Another indicator not
commonly used these days, is the indocyanin green dye. The dye is
injected into the central circulation (preferably PA) and is then detected in
a systemic artery.a. Indocyanin green dye
A precise quantity of green dye is mixed in a measured volume of
normal saline solution, and then precise known concentrations of 1mg/L, 5 mg/L and 10 mg/L are made. These solutions are then
used to calibrate the densitometer. Subsequently a measured
quantity of the green dye solution (typically 5 mg) is injected intothe blood stream (usually PA or SVC) and blood is continuously
withdrawn from the sampling site (usually aorta or any systemic
artery) using a pump. This blood is then sampled continuously
with the densitometer set to measure the concentration of the dyeaccording to the previous calibration. 20 to 30 seconds of data are
May use CO instead of Qp in absence of intracardiac
shunting. Multiply by 80 to get in metric units(dynes.sec.cm
-5) (i.e. PVRI). Normal range for PVRI is
225-315 dynes.sec.cm-5
Mean PAP = PAD + PAS – PAD
3
Normal range for mean PAP is 11-18 mmHg.
vii. Total Pulmonary Resistance (Wood units)
TPR = mean PAP
CO
Multiply by 80 to get in metric units (dynes.sec.cm
-5
) (i.e.TPRI)
viii. Systemic Vascular Resistance (Wood units)
SVR = mean systemic arterial P – mean RAP
CO
Multiply by 80 to get in metric units (dynes.sec.cm-5
) (i.e.
get SVRI). Normal range for SVRI is 1970-2390 dynes.sec.cm
-5.
Mean AP = DBP + SBP – DBP3
Normal range for MAP is 80-100 mmHg
C. Principles of Fluid Dynamics
Blood flow is a complex phenomenon. Time, space, location, and rheological
properties of the fluid within the vasculature are a few things that affect the
characteristics of blood flow. Normal intracardiac flow patterns are characterized
by laminar flow. This is the movement of fluid along well-defined parallelstreams with uniform flow velocities. In three dimension this flow consists of
concentric layers of flow, each with predictable direction and velocity (Figure 9).The outermost layer, which is in contact with the wall, is fixed in place by the
high degree of friction encountered at the interface. Adjacent, axially positionedlayers, however, slip past one another, with the velocity of motion of each layer
increasing from the tube wall to the central axis. Particles in each layer move
parallel to the vessel wall with no effective interaction occurring between the
particles of individual layers. The slippage of fluid lamina over one another is
opposed by internal friction between fluid layers (viscosity).
Figure 9. Normal laminar flow can be represented as slippage of a series of thin concentric
cylindric shells over one another. The outermost shell is stationary, and the velocity increases to a
maximum at the central axis of the tube (From Weyman, 1994).
A fundamental property of all fluids is viscosity which opposes the slippage offluid lamina over one another. The amount of force required to overcome the
viscous resistance between layers is proportional to the area over which the layersare in contact and the velocity at which they are sliding past one another. The
stress (S) or force per unit area required to slide the layers over one another is
equal to the viscosity times the velocity gradient:
S = η dv/dx
Where dv/dx is the velocity gradient or the rate of shear across the tube, and η is
the viscosity. Viscosity therefore is equal to the ratio of stress to velocity gradientand is an inherent physical property of all fluid. This relationship implies that at
any given viscosity, the velocity gradient is a
function of the stress applied.
As mentioned earlier for laminar flow, the
particles in the flow stream move in a constant
direction, generally parallel to the vessel wall.This requires that sequential layers slip over one
another at an increasingly rapid rate as velocity
increases in the vessel. As the velocity reaches acritical threshold this orderly flow pattern begins
to breakdown and is replaced by an irregular,
seemingly random, particle motion known asturbulence. The progression from laminar to
turbulent flow follows a series of less well-
defined stages shown in figure 10.
Figure 10. Transition from laminar (A) to turbulent flow
Osbourne Reynolds in 1833 described in detail factors that influence transitionfrom laminar to turbulent flow. These variables were combined in a
dimensionless term known as the Reynolds number ( N r ) which is described as
follows (for a cylinder):
N r = 2rv ρ / η
Where r is the radius of the tube, v is the mean velocity of the flow, ρ is the
density of blood, and η is the viscosity. This number represents the ratio of inertial
to viscous forces. The higher theReynolds number, the greater the
tendency towards turbulence.
The critical threshold betweenlaminar and turbulent flow is
roughly 2300.
Figure 11. Parabolic flow pattern that
normally occurs during steady flow in a
rigid cylindric tube (From Weyman,
1994).
The speed at which individual lamina move and the pattern or profile assumed bythe blood column in different circumstances are the net result of the balance of the
inertial forces promoting forward motion and the viscous forces retarding thatmotion. For steady flow in a rigid tube the flow is parabolic (Figure 11). Such
parabolic profile assumes a velocity gradient that changes linearly across the tube
and is the most energy efficient form of fluid flow.
D. Role of Echocardiography in Assessment of Cardiac Hemodynamics
Since the first attempt to use ultrasound as a medical diagnostic tool in 1942 by
Dusik, the technology has undergone dramatic change. With the advent of highfrequency transducers, Doppler imaging, and tissue harmonic imaging (just to
mention a few), echocardiography has become an invaluable tool for assessmentof patients with cardiac disease. Doppler echocardiography has for the most partreplaced cardiac catheterization for assessment of cardiac hemodynamics.
However there are still a number of hemodynamic parameters that can only be
determined at cardiac catheterization (eg PVR) The obvious noninvasive nature
of echocardiography makes it an attractive tool for assessment of cardiachemodynamics. Data that can be obtained by echocardiography are listed below:
Cardiac catheterization has been used to assess the LV systolic and
diastolic function
a.
Assessment of LV volume and LVEFGeometric methods for estimation of LV volumes assume that the LV
shape is a prolate spheroid. Although this is not exactly the case, it can beused to calculate LV volume and EF. The 30° RAO projection is used.
Assuming an ellipsoid, volume is calculated as:
V = 4π x D x D x L = π x D2 x L
3 2 2 2 6
Where D is the length of the minor axis and L is the length of the major
axis. This equation is uncorrected for magnification; the magnificationfactor (f) is calculated from filming a marked catheter of known length.Hence the corrected volume equation becomes:
V = π x D2 x L x f
3 = 0.524 x D
2 x L x f
3
6The above formula can be simplified by measurement of area (A) in cm
2
and the major axis length (L) in cm and their relationship to the minor axis
length by the following formula:
D = 2A
2 π LSubstituting for D in the previous formula we get:
V = 0.849 x A2 x f
3
L
For measurements of EF, f 3 cancels out and one can use the following
formula for calculation of volumes:
V = 0.85 x A2
L
The LV volumes are then measured in end systole (ESV) and end diastole(EDV), ejection fraction is then calculated by:
the absence of wall motion abnormalities,there is a relatively good correlation between
FS and ejection fraction (EF).
Another important issue is the way thedistances are measured during M-mode
echocardiography. The American Society of
Echocardiography (ASE) has recommendedleading-edge-to-leading-edge M-mode
measurements. Leading-edge is the edge of the echo closest to the transducer,and the edge away from the transducer is the trailing edge. Another conventionis the measurement of M-mode distances using the trailing-edge-to-leading-edge
method. Although this method is attractive because it corresponds to visual space
between two objects it is highly variable. This variability is secondary to
instrument differences, and gain settings.
c. Left ventricular volume and ejection fraction
Usually end-diastolic (EDV) and end-systolic volumes (ESV) aremeasured for assessment of LVEF according to the formula:
EF (%) = SV_ X 100 EDV
SV = EDV – ESV
i. Modified Simpson’s (Apical Biplane method)One can imagine the left ventricle as a series of discs of equal height
(Figures 18 and 19). LV volume is the sum of the volumes of the
discs. The volume of each disc can be calculated from its thickness
and area. Recordings from the apical two and four-chambered viewsare used to calculate the volumes of discs in two views. The LV
volume is then calculated as the sum of the volumes of the discs as:
∑=
=20
1
4/i
iibaV π x (L/20)
Where V is the LV volume, ai and bi are the disc diameters in the
apical two- and four-chambered views respectively, and L is thelongest length of the left ventricle which is divided into 20 discs.
This method is highly dependent on the operator’s ability to identify
endocardial borders. This is a major source of error for this method.
Figure 18. Determination of LV
volume by modified Simpson’s
rule. Apical two chamber andfour chamber views are used. ai
and bi are disc diameters in
apical two chamber and four
chamber views respectively.
Figure 19. Use of biplane modified Simpson’s rule to calculate EF (From ECHO SAP III, ACC)
ii. Single plane area-length method
When only one apical plane is available for measurement thismethod is used for measurement of LV volume (Figure 20). Thesingle plane area-length method uses the length, L and the two-
dimensional area, A of a single long-axis view. The LV volume is
calculated assuming an ellipsoid shape of the LV as:
Where h is wall thickness and LVID is the left ventricular internaldimension
Non-invasive measure of σ m in end systole (es) can be done using the
following formula using systolic blood pressure (SBP):
σ m(es)=0.334(SBP)(LVIDs)
h(1+h/LVIDs)
Normal values for meridional wall stress have been reported between 65
to 73 x 103 dynes/cm
2.
Circumferential wall stress σ c can be calculated using the same variables plus the ventricular length L measured from the apical four-chamberedview as:
σ c = [(1.33P √ Ac )/( √(Am +Ac ) - √ Ac )] x [1- (4Ac√ Ac / π L2 )/( √(Am +Ac ) - √ Ac ) kdynes/cm2
Normal end-systolic circumferential wall stress has been reported as 213 ±
29 dynes/cm2.
Diastolic Function and DysfunctionA. Introduction
Some patients with heart failure and normal LV systolic function have predominantly diastolic dysfunction. More patients have a combination of
systolic and diastolic dysfunction. In these patients the LV is not dilatedand may contract normally, but the ventricular diastolic function is greatly
impaired. In this form of heart failure, the LV has reduced compliance
and is unable to fill adequately at normal diastolic pressures. This
condition results in reduced end-diastolic volumes, an elevated end-diastolic pressure, or both. Reduced LV filling volume leads to decreased
stroke volume and symptoms of low output, whereas increased filling
pressures lead to symptoms of pulmonary congestion.Several studies have shown that as many as 40% of all patients evaluated
for clinical diagnosis of heart failure have preserved LV systolic function.Several factors predispose to increased diastolic “stiffness” in a LV withnormal systolic performance. These include myocardial ischemia,
myocardial fibrosis, LVH, and LV pressure overload. One condition in
which many of these factors coexist is systemic hypertension. Due to high prevalence of HTN routine assessment of diastolic function in patients
presenting with symptoms of heart failure is important.
The normal value for the time constant ( τ ) of relaxation using the above
method is 41 ± 12 msec.
b. Diastolic filling rate (DFR)
Another measure of diastolic function is the diastolic filling rate (FR).
This value can be obtained angiographically from frame-by-frameanalyses at 20 msec intervals. Diastolic FR is calculated as:
FR = V(t + 0.02) – V (t – 0.02)
0.04
FR is the filling rate (ml/s), V is the LV volume (ml), and t is time (sec).
The greatest values occurring in the first and second halves of diastole are
termed early and late peaking filling rates, respectively (Figure 25).
The diastolic filling time interval from the beginning of diastolic filling toend-diastole can be divided into a first and second half, and the ratio of the
volume increase during the first (%V1) and second (%V2) halves of
diastole can be used as a measure of early and latediastolic filling. Normal values for peak filling rate
have been determined. These are 483 ± 111 ml/s during early diastole (PFR
1) and 321 ± 102 ml/s
during late diastole (PFR 2); %V1 amounted to 65%
and %V2 to 35%.
Figure 25. LV diastolic filling in a normal patient. LV
volumes (upper) were determined angiographically every 20
msec. Instantaneous LV filling rates (lower) and peak filling
rates during early diastole (PFR1) and during atrial contraction(PFR2) are shown. The volume increase from MV opening to
end-diastole (ED) are shown and divided into a first (t1) and
second (t2) halves. Percent volume increase during the first
(%V1) and second (%V2) halves of diastole are used as a
measure of early and late diastolic filling. ES, end-systole.(From Peterson, 1997)
Impaired LV relaxation results in the classic pattern of diastolic dysfunction
with impaired early diastolic filling and an increased contribution of theatrium to total LV filling. This results in a reduced E velocity, a longer IVRT,
a prolonged early diastolic deceleration time, and an E/A ratio of <1 (Figure
27). Abnormal ventricular compliance (restrictive pattern) results in a rapid
early diastolic filling with a shortIVRT. The atrial contribution to
filling is small due to an elevated
LVEDP (small pressure difference between LA and LV).
Figure 27. LV and LA pressure tracings
and the corresponding mitral inflow
velocities in three different diastolic
filling patterns (From Oh, 1999).
As diastolic function deteriorates, a transition from impaired relaxation to
restrictive filling occurs. During this transition, mitral inflow pattern goesthrough a phase resembling a normal pattern, with an E/A ratio of 1 to 1.5 and
a normal deceleration time (160 to 200 ms). This occurs because of a
moderately increased LA pressure superimpose on the relaxation abnormality.This is referred to as a pseudonormalized pattern, and represents moderate
diastolic dysfunction. This abnormality can be unmasked using the Valsalva
maneuver (Figure 28). The E/A ratio decreases to <1.0. In normal subjects
both the E and A velocities decrease proportionally keeping the same E/Aratio.
Figure 28. PW Doppler mitral inflowvelocities recorded during the
different phases of the Valsalva
maneuver. During Valsalvamaneuver, the reduction in preload
unmasks the underlying impaired
relaxation of the LV (End), with a
decrease in E velocity and an increase
in A velocity.
An indirect approach to evaluation of diastolic function is the measurements ofatrial filling patterns and pressures (Figure 29). RA filling is characterized by a
small reversal of flow following atrial contraction (a wave), a systolic phase, asmall reversal of flow at end-systole (v wave), and a diastolic filling phase.
Doppler evaluation of hepatic vein flow can be used to assess RA filling. For LA
filling the pulmonary vein (PV) Doppler flow is assessed. The PV Doppler flowis characterized by a small reversal of flow following atrial contraction (a wave),
The time constant of relaxation is relatively independent of preload but is
altered by afterload. A limitation of the use of this value is that theisovolumetric LV pressure decay is not always a perfectly simple exponential
decay function. Actual LV pressure tends to fall faster during the latter part of
isovolumetric relaxation than the one predicted from the monoexponential
decay. Normal value for τ derived from echocardiographic studies is 33 ± 6ms.
d. Tissue Doppler imaging (TDI)
Recently developed technique of tissue Doppler imaging (TDI) has been applied
to measurements of diastolic function and dysfunction. Instead of blood flow,
TDI measures the velocity of the myocardium during the cardiac cycle. Bloodflow is typically low amplitude and high velocity in nature, whereas myocardial
velocities are of high amplitude and low velocity. TDI velocities can be displayed
three ways, either as spectral PW signal (Figure 32), as a color velocity encodedM-mode, or as a 2D color map.
Figure 32. Characteristic
mitral annular motion
spectra compared to
normal and abnormal PWmitral inflow velocity
patterns. Sample volume
is placed either at theseptal wall or the lateral
wall at the mitral annulus.
Imaging from an apical window is performed, because from this view theaxial motion of the LV is parallel to the transducer axis and the velocities are
primarily related to the LV contraction and relaxation. A 3-7 mm PW sample
volume is placed in different segments of LV (e.g. septum, anterior, inferiorwalls) and regional quantification of segmental velocities are obtained. For
the purpose of recognition of pseudonormal mitral velocity patterns, the PWsample volume is usually placed within the septal or the lateral regions ofmitral annulus (Figure 33).
Color M-mode recordings (CMM) provide the spatial and temporal
velocity characteristics of flow along an entire echocardiographic scan line.
The obvious advantage of this modality is that it allows measurement of flowvelocities in many points along the heart with superior temporal, spatial, and
velocity resolutions. To obtain CMM recordings, the color Doppler function
is activated while imaging from the apical four-chamber window. The colorsector is placed to include the LV, MV, and about half of the LA. Aliasing
velocity is set to 55-60 cm/s, then M-mode cursor is aligned with mitral
inflow (from LV apex through the MV and into the LA) and a sweep rate of
100-200 mm/s is set. Similar to PW recordings patients in sinus rhythmdisplay two distinct waves (corresponding to E and A waves) in diastole. The
most commonly used variable of CMM is the propagation velocity of early
diastolic flow (E wave) into the LV (Vp). There is a significant negative
correlation between Vp and the time constant of LV relaxation (τ). Figures 34and 35 represent different profiles (and hence Vp) in diastolic dysfunction. It
must be noted that TDI and CMM currently are mainly investigational butshow great deal of promise and will soon be part of routine echocardiographic
evaluation of patients with diastolic dysfunction.
Figure 34. Transthoracic color M-mode image from patient with normal diastolic function.The slope of early diastolic (E wave) flow propagation (Vp) is identified (dashed line). A
steeper line is associated with faster relaxation and greater diastolic suction whereas a
shallower slope (Figure 32) is associated with impaired relaxation.
Figure 35. Transthoracic CMM image from a patient with severe diastolic dysfunction
secondary to dilated cardiomyopathy. Compare the slope of the early diastolic flow
propagation (Vp) in this patient with one from a patient with normal diastolic function in
normally contains 5 to 10 ml of fluid which may be detected by
echocardiography. This fluid serves as a lubricating material to allow normalrotation and translation of the heart during cardiac cycle.
A wide variety of disorders can result in pericardial effusion. Table 8 shows
some of the main causes of large effusion causing tamponade.When the intrapericardial pressures exceed the pressures in cardiac chambers,
impaired cardiac filling occurs, this is known as tamponade physiology. As the
pericardial pressures increase, filling of each cardiac chamber is affectedsequentially, starting with lower-pressure chambers (atria). The compressive
effect of the fluid is seen best in the phase of cardiac cycle when pressure is
lowest in that chamber (diastole for the ventricle and systole for atrium). Insevere tamponade, diastolic pressures in all cardiac chambers are equal and
elevated.
B. Cardiac Catheterization
Diastolic equilibration or pressures is the hallmark of cardiac tamponade. Hence,accurate measurement of pressures in right and left-sided chambers is mandatorywhen tamponade is suspected, although this is rarely necessary these days with
advent of echocardiography. The pressure tracings should be recorded
simultaneously, along with the
respiratory cycle (Figure 37).
Figure 37. Simultaneous recordings of
aortic (Ao) and the respiratory cycle in
a patient with cardiac tamponade.
During inspiration systemic venousreturn is increased and the aortic
pressure is decreased (pulsus paradoxus). This is an exaggeration of
the normal response.
Ideally both right and left heart catheterization should be done to show the
equalization of diastolic pressures in these chambers. However, if PCWP tracingsis of good quality, and if clinical, non-invasive, and hemodynamic data are
consistent with tamponade, left heart catheterization may be omitted.
When the intrapericardial pressure has increased to equal RA pressure cardiactamponade begins. With the rise in intrapericardial (IP) pressure, the venous
pressure rises to maintain intracardiac volume. In early cardiac tamponadewithout pre-existing heart disease, the intrapericardial and RA pressures are equal
but only slightly elevated. Furthermore PCWP (or LA pressure) remains higherthan the RA pressure. When cardiac tamponade becomes more severe, the RA
and IP pressures remain equal and rise progressively as the tamponade gets moresevere. The point at which the RA, and PCWP (or LA pressure) become equal
defines classic cardiac tamponade (this finding is not pathognomonic, other
conditions can cause this equalization such as constrictive pericarditis). RA andPCWP should be recorded simultaneously rather than sequentially (Figure 38).
The height to which the venous pressure is elevated depends on the severity of
tamponade. In milder cases, these pressures range from 7-10 mmHg. Inmoderate cases, pressures are 10-15 mmHg and are often accompanied by
reduction in cardiac output and arterial BP. Severe tamponade is characterized by
pressures in the range of 15-30 mmHg usually accompanied by profound
reduction in CO and arterial BP, which at this stage will demonstrate pulsus paradoxus. Often there is a narrow pulse pressure before the drop in peak systolic
pressure.
In establishing the diagnosis of cardiac tamponade, special attention should be paid to the waveform of RA and PCWP tracings. Inspiratory decrease in RA
pressure should be observed. Cardiac tamponade exerts its abnormal pressure on
heart chambers throughout the cardiac cycle. However, ventricular ejection isfaster than venous return, causing cardiac volume to decrease. With this event
there is a slight decline in IP pressure. For this reason, venous return is confined
to the period of ventricular systole that translates to prominence of x descent andabsence of y descent of venous pressure. Thus, in typical tamponade, RA
pressure is elevated and equal toPCWP and shows an inspiratory dropand absence of y descent. This is in
contrast to constrictive pericarditis
which demonstrates a sharp x and y
descents.
Figure 38. PCW and RA pressure tracings
simultaneously recorded in a patient with
cardiac tamponade. Note the equalization of
the pressure tracings throughout therespiratory cycle, with only a mild deviation
during expiration.
C. Echocardiography
Pericardial effusion is easily recognized on 2D echocardiography
as an echo lucent space next to cardiac structures (Figure 39).These effusions are usually diffuse and symmetric in absence of
previous pericardial disease or surgery. M-mode recordings may
be helpful in identifying small effusions. Fibrinous strandingwithin the pericardial fluid and on the epicardial surface may be
seen with recurrent or long-standing disease. Pericardial effusionis considered small when the separation between the two layers of
pericardium is <0.5 cm, moderate when it is 0.5 to 2 cm, and largewhen >2cm.
Figure 39. Parasternal long (A) and short axis (B) views of a large posterior
The effusion may be loculated as seen in postoperative patients and in those with
recurrent disease. It is important to note that hemodynamic compromise can
occur with even small loculated effusions. Drainage of loculated effusions maynot be feasible using percutaneous techniques. Care should be taken to
distinguish a pleural effusion from pericardial effusion. A left pleural effusion
will extend posterolateral to the descending aorta, whereas pericardial effusionwill track anterior to the descending aorta (best seen in parasternal long-axis). In
the apical four-chamber view, an isolated echo-free space superior to the RA
likely represents pleural fluid. The subcostal view is useful during echo-guided
pericardiocentesis. Echocardiographic signs of cardiac tamponade are discussedas follows:
a. RA collapse
When intrapericardial pressure rises above the RA
systolic pressure, inversion and collapse of the RA free
wall occurs. The longer the duration of this collapsewhen compared to the cycle length, the greater the
likelihood of cardiac tamponade. Inversion or collapse
greater than 1/3rd
of RA systole (this happens in
ventricular diastole) has a sensitivity of 94% andspecificity close to 100% for diagnosis of tamponade.
Careful frame-by-frame analysis of the 2D images is
necessary for this evaluation.
b. RV Diastolic collapse
This occurs when the intrapericardial pressure exceeds
RV diastolic pressure (Figure 40 & 41). The RV free
wall needs to be of normal thickness and compliancefor this event to take place. RV diastolic collapse is
best seen in parasternal long-axis or from subcostalview. M-mode can be used to assess this phenomenon
more carefully. In cases of tachycardia onset of
diastole is better timed with MV opening and is best
appreciated on M-mode view through MV leaflets andRV. Presence of this sign is 60 to 90% sensitive and 85
to 100% specific for diagnosis of cardiac tamponade.
Figure 40. Parasternal long-axis (A) and short axis (B) views showing RV diastolic collapse (arrows)
(Otto, 2000).
c. Respiratory variations in diastolic filling
With inspiration the LV diastolic filling velocity decreases and theRV early diastolic filling increases (Figure 41 & 42). A decrease in
mitral inflow E velocity greater than 25% has a high sensitivity and
of pericardium are joined, fibrous, andthickened. This results in an impairment
of ventricular diastolic filling. Maincauses of constrictive pericarditis are
listed in table 9. Constrictive pericarditis
occurs in approximately 0.2% of patientsafter cardiac surgery.
The typical hemodynamic picture is of
markedly elevated ventricular diastolic
pressures with characteristic pattern of rapid early diastolic filling that stopsabruptly as the limit of ventricular expansion is achieved. This results in an early
dip in the RV pressure tracing, followed quickly by an equally rapid rise in pressure followed by a plateau as the limitation to filling is reached (the so called square-root sign).
B. Cardiac Catheterization
Cardiac catheterization is used to assess patients suspected of having constrictive
pericarditis for (1) presence of elevation and equalization of diastolic filling
pressures, (2) effect of constrictive pericarditis on stroke volume and cardiacoutput, (3) evaluation of systolic function, (4) discrimination between constrictive
pericarditis and restrictive cardiomyopathy, and (5) regional outflow tract orcoronary compression by the fibrotic pericardium. Both RV and LV should be
catheterized to allow for simultaneous recording of filling pressures in right andleft heart. Typical findings include elevation and equalization (within 5 mmHg)
of RA, RV diastolic, LA (i.e. PCWP), and LV diastolic pressures before the a wave. The RA pressure recording (Figure 44) is characterized by preserved
systolic x descent, a prominent
early diastolic y descent, and a and v waves that are small and
equal in height (resulting in
typical M or W configuration).
Figure 44. RA pressure recording
from a patient with constrictive pericarditis. There is a prominent y
descent in the pressure waveform.
The prominent X and Y descents givethe waveform the characteristic M or
Both the RV and LV diastolic pressures show an early diastolic dip followed by a plateau (Figure 45). This is the so called square-root sign and may be obscured
by the presence of tachycardia. Another sign seen in constrictive pericarditis is
the reciprocal changes seen in the RV and LV pressures with respiration
(ventricular interdependence). Number of traditional hemodynamicmeasurements for diagnosis of constrictive pericarditis are shown in tables 10 and
11. Unfortunately these signs are not very specific for diagnosis of constrictive
pericarditis with the exception of ventricular interdependence.
Figure 45. LV and RV (A), and LV and PCW (B) tracings from a patient with constrictive Pericarditis. Note the discordant changes in LV and RV pressures (ventricular interdependence) and variability in the
early diastolic PCW-LV gradient with respiration; this represents dissociation of intrathoracic and
intracardiac pressures.
Table 10. Hemodynamic criteria comparison for diagnosing constrictive pericarditis
show abrupt posterior motion of the LV septum in early diastole and abrupt
anterior motion following atrial contraction. This is due to an initial rapid RVdiastolic filling, followed by equalization of RV and LV filling (plateau phase),
followed by an increase in RV filling after atrial contraction. On subcostal views
the IVC and hepatic veins are dilated, reflecting an elevated RA pressures.
Figure 46. M-mode in constrictive pericarditis showing
rapid anterior motion of the septum (arrow) with atrial
contraction before QRS (From Otto, 2000).
Doppler findings of constrictive pericarditis are
shown in Figure 47. Both RV and LV diastolic
filling show a high E velocity due to rapid earlydiastolic filling occurring simultaneously with the
initial high atrial to ventricular pressure difference
during the brief early diastolic dip in ventricular pressure. As LV pressure rises, filling ceases
abruptly causing a short deceleration time of E velocity. Due to the elevated LV
diastolic pressure, very little late diastolic filling occurs, giving rise to a verysmall A velocity following atrial contraction. Marked reciprocal respiratory
variations are seen in this condition. With inspiration, the intrapleural pressure
becomes more negative, augmenting the RV diastolic filling and inflow velocity.
LV filling velocity decreases with inspiration and increases with expiration.Another change with constrictive pericarditis is the
increase in the IVRT (measured from AV closure to
MV opening) by >20% with inspiration.
Figure 47. Doppler flow patterns in constrictive pericarditis.
LV inflow shows reduced early diastolic filling with
inspiration, while pulmonary vein (PV) shows a prominent a wave (atrial reversal) and blunting of systolic phase (From
Otto, 2000)
Table 12. Doppler findings in constrictive pericarditis and restrictive CM.
Comparison between constrictive pericarditis and restrictive cardiomyopathy
based on 2D echo and Doppler studies are shown in table 12.
Restrictive PhysiologyA. Introduction
Restrictive cardiomyopathy is characterized by a normal LV systolic functionwith an impaired diastolic function secondary to a stiff ventricle. In many
patients with restrictive disease right sided failure symptoms predominate. Table13 shows the common etiologies for restrictive cardiomyopathies. It is important
to remember that restrictive cardiomyopathies are rare when compared with other
causes of heart failure.
Table 13. Classification of Restrictive Cardiomyopathies.
Restrictive CM can be defined as a primary or secondary myocardial disorderwithout ventricular dilatation and without significant ventricular hypertrophy in
which abnormality in myocardial compliance produces diastolic dysfunction that
closely mimics constrictive pericarditis. The patient typically presents withdyspnea, elevated JVP with prominent x and y descents, and peripheral edema.
The RA pressure tracing is indistinguishable from that of constrictive pericarditis,
and ventricular pressure tracings show the typical dip-plateau configuration
(Figure 48). When a large diastolic pressure difference is found between LV andRV during cardiac catheterization, the diagnosis is more likely to be restrictive
CM than constrictive pericarditis. However, equalization of diastolic pressures in
the two ventricles are just as consistent with constrictive pericarditis or restrictiveCM. Patients with restrictive disease typically have LV filling pressures that
exceed RV filling pressures by more than 5 mmHg; this difference is accentuated
by exercise, fluid challenge, and Valsalva maneuver (not all patients demonstratethis). The PA systolic pressure is often greater than 55 mmHg in patients with
restrictive disease but is lower in patients with constrictive pericarditis.
Furthermore, the plateau of RV diastolic pressure is usually at least 1/3rd
of the peak of RV systolic pressure in patients with constrictive pericarditis, whereas it
is frequently less in patients with restrictive CM. It should be noted that in up to
25% of patients the difference (between constrictive pericarditis and restrictive
CM) can not be made on the basis of hemodynamic grounds, and further
information (endomyocardial biopsy or pericardial biopsy) is required fordifferentiation.
Figure 48. Tracings of LV, RV and PCW pressures from a patient with restrictive cardiomyopathy. Note
the concordant changes in LV and RV pressures, despite end-diastolic pressure equalization and dip plateaumorphology. There is also a lack of variability in the early diastolic PCW-LV gradient with respiration.
C. Echocardiography
Echocardiographic imaging in patients with restrictive cardiomyopathy, reveal anon-dilated, thick-walled LV with preserved systolic function and abnormal
diastolic function. Biatrial enlargement is often seen and secondary signs of
pulmonary HTN may be present including paradoxical motion of septum and TR(Figure 49 and 50). Doppler evaluation reveals moderate pulmonary HTN on the
basis of time to peak velocity in the pulmonary artery, and an elevated RVSP
(using TR jet and estimated RA pressures based on IVC plethora and respiratory
variation).
Figure 49. Echocardiographic features ofrestrictive cardiomyopathy (Thick walled, small
LV; impaired diastolic function; LA and RA
enlargement; and signs of secondary pulmonaryHTN including paradoxical septal motion and a
high velocity TR jet). (From Otto, 2000).
Early in course of the disease, impaired
diastolic relaxation of the LV results in impaired early diastolic filling, and theMitral inflow Doppler curve show a reduced E velocity, increased A velocity,
prolonged IVRT, and decreased deceleration slope. PV flow curve shows a
reduced diastolic filling phase and a normal systolic filling phase (resulting in adecreased ratio). As the disease progresses, LA pressure rises, resulting in an
increased pressure gradient between LA and LV. The mitral inflow curve shows
an increased E velocity and a rapid deceleration slope. The A velocity is
decreased. This pseudonormal pattern can be distinguished from normal by (1)
the rapid early diastolic deceleration slope, (2) Clinical data (age, presentation,symptoms, etc.), and (3) Pattern of pulmonary venous inflow. With
pseudonormal pattern there is an increase in atrial flow reversal, an increase in
diastolic phase, and a decrease in the systolic phase (Figure 50).
Figure 50. Apical four chamber view of patient with restrictive
CM due to amyloidosis. There is biventricular hypertrophy and
biatrial enlargement. (From Otto, 2000)
Examination of the RA filling by Doppler interrogation of the Hepatic vein
(Figure 51) can be helpful. This shows a prominent reverse flow with atrial
contraction (a wave) followed by a rapid filling curve in systole ( x descent). Thediastolic phase of RA filling is blunted corresponding to a diminished v wave and
y descent.
Figure 51. LV diastolic filling (A) in a patient with restrictive
cardiomyopathy shows an increased E velocity and reduced A
velocity consistent with pseudonormalization. This pattern can be distinguished from normal by the pulmonary venous inflow
Aortic stenosis results in progressive LVOT obstruction. The sequelae of this is
compensatory LVH, classic triad of symptoms (angina, syncope, CHF), and
sudden death.
Table 16. Causes of Aortic Stenosis
CongenitalBicuspid
Unicuspid
AcommissuralOther (e.g. quadracuspid)
Degenerative conditions
Rheumatic
Active infective endocarditisOther conditions
Homozygous type II hyperlipoproteinemiaMetabolic or enzymatic (e.g. Fabry’s disease)
SLE
Figure 53 shows the result from surgical series showing the different etiologies of
valvular AS in patients younger and older 70. Currently the commonest cause of
AS is degenerative (premature degeneration in bicuspid AV and the so calledsenile degeneration of tricuspid AV). If the cause of AS is rheumatic, a careful
search for mitral disease should be made.
> 70 years old
Bicuspid
27%Post inflammatory
23%
Degenerative
48% Unicommissural
0%
Indeterminate
0%
Hypoplastic
2%
Figure 53. Etiology of AS, shown for two age groups. Among patients younger than 70 (left),
calcification of congenitally bicuspid valves accounted for half of the surgical cases. In contrast,in those older than 70 (right), degenerative calcification accounted for almost half the cases. (From
An estimate of severity of aortic stenosis is obtained from the gradient across the
valve. However the pressure gradient does not take into account the cardiac outputwhich, if reduced, results in a smaller pressure gradient. This is seen clearly in
patients with severe left ventricular impairment secondary to AS or coronary disease
who may have no significant transaortic gradient. The gradient across the valve is
also dependent on the time available for the flow of blood to take place; this is thesystolic ejection period (SEP). R. Gorlin and his father G. Gorlin recognized that the
flow is dependent on the pressure gradient. They used a hydraulic model to calculate
the valve orifice size. The Gorlin formula is based on the following relationship:
Q = A x V x C c or A = Q ___
V x C c
Where A is the anatomic area of the valve, Q is the flow during the period that a
given valve is open (SEP for AV), V is the velocity of flow, and C c is a constant oforifice contraction relating functional to anatomical valve area. Velocity of flow (V)
is represented by the following formula,
ghC V v 2= or hC V v 1960=
Where V is the average velocity of transvalvular flow, Cv is a second constant for
viscous frictional losses, g is acceleration due to gravity (9.8 m/s2), and h is the mean
pressure gradient across the valve in cm of water. Then by substituting andcombining Cc, Cv, and 1.166 (the square root of the conversion factor from mmHg to
cm of water) into a comprehensive constant, K , a simplified Gorlin equation is
obtained as follows:
A = Q ______ K x 44.3√ MVG
Where, MVG is the integrated valve gradient. In addition to the above equation Q
(flow) refers to the cardiac output divided by the number of seconds per minute
occupied by the transvalvular flow. Thus,
Q = CO ( ml/min )_____ For aortic and Pulmonic valves
SEP (s) x HR (beats/min)
Q = CO ( ml/min )______ For mitral and tricuspid valves
DFP (s) x HR (beats/min)
Where SEP is systolic ejection period and DFP is the diastolic filling period. Note
that the cardiac output (CO) is in ml/min.
Once the empiric constants are substituted we get the following formula,
Where K is the combined constant and is 1.0 for aortic, Pulmonic and tricuspid valves
and 0.85 for mitral valve. Note that the CO is in ml/min [Hence must multiply CO(l/min) by 1000]
AVA (cm2 ) = CO ( ml/min )/SEP x HR
44.3√ MVG
Measurements of AVA (aortic valve area) using the above formula are inaccurate atlow and high heart rates, at low and high cardiac outputs, and in the presence of
irregular rhythms. The Gorlin formula is also invalid in presence of valvular
regurgitation. The MVG is measured by planimetry of the superimposed aortic andLV pressure tracings in systole (Figure 54). SEP is also measured from this tracing
and used to calculate the valve area. It should be noted that if femoral artery pressuretracing is used there will be a delay in pressure transmission and this artificiallyincreases the gradient. Modifications of the widely used Gorlin formula have been
made. To estimate aortic valve area, the Bache formula uses either the peak-to-peak
or the maximum systolic gradient, thus avoiding planimetry. Hakki omits the ejection
or filling period and the empirical constant. He uses the square root of either themitral mean, aortic mean, or aortic peak pressure gradients divided into the cardiac
output.
AVA (cm2 ) = CO (l/min)_____
√ peak-to-peak gradient
The quick formulas for valve area differ from the Gorlin formula by 18 ± 13% in
patients with bradycardia (<65 bpm) and tachycardia (>100 bpm). The Hakkisimplification of the Gorlin formula can be used to get a quick estimate of AVA.
AVA (cm2 ) = CO (l.min)
√ MVG
For HR >90 one can use the Angel modification of Hakki simplification can be used
Doppler derived pressure gradients are highly accurate, with an excellent
correlation with catheter-derived pressure gradients across the LVOT (Figure55). This figure shows simultaneous intracardiac pressure tracings (LV and
Ao) and Doppler measurements of a stenotic AV. The two techniques show
an excellent
correlation. However there is
no correlation
between theDoppler derived
gradients and
peak-to-peakgradient derived in
the catheterization
laboratory. Thereis a dependence of
pressure gradientson volume flowrate and this
dependence can
lead to erroneous
conclusions about severity of disease. Hence a patient with coexisting ARand AS will have a high transaortic pressure gradient with only a moderate
degree of valve narrowing. Conversely a patient with LV systolic dysfunction
or coexisting MR may have a low transaortic pressure gradient despite severeAS. Since these coexisting conditions are common in adults determination of
stenotic orifice area is necessary for complete evaluation of disease severity.In other words the estimated valve area is influenced by the flow across the
valve as well as the pressure gradient.
b. Valve area determination
AVA is calculated based on the principle of continuity of flow. Hence the
stroke volume (SV) just proximal to the aortic valve (SVLVOT) and that in thestenotic valve orifice (SVAo) are equal
SV LVOT = SV Ao
If the assumption is made that the flow is laminar with a flat velocity profile,
SV = CSA x VTI
Where, CSA is the cross-sectional area of flow (cm2), SV is the stroke volume
(cm3), and VTI is the velocity-time integral (cm). Since flow both proximal
and distal to the stenosis is laminar with flat velocity profile,
Aortic regurgitation may be caused by primary disease of either the aortic valve
leaflets or the wall of the aortic root, or both. Of patients with isolated ARrequiring valve replacement, close to 50% have aortic root disease as the cause.
Prolapse due to VSDAbnormal aorta and abnormal valve
Ankylosing spondylitis, RA, SLE
Marfan’s syndrome
Ehlers –DanlosOstegenesis imperfecta
Syphilis (i.e. aortitis with commissural separation)
Table 19 lists the causes of AR. Rheumatic fever is the commonest cause of
primary disease of valve leading to regurgitation. The cusps become infiltrated with
fibrous tissue and retract. This process prevents cusp apposition in diastole leading toregurgitation. The associated fusion of commissures will lead to combined AS and
AR. Associated mitral valve disease should be sought.
When aortic annulus becomes greatly dilated, the aortic leaflets separate, and AR
may ensue. Dissection of the diseased aortic wall may occur and will oftenexacerbate the associated aortic insufficiency. Regardless of the cause, AR produces
dilatation and hypertrophy of LV, dilatation of MV ring, and sometimes dilatationand hypertrophy of LA.
1. Asymptomatic patients with normal LV systolic function
Progression to symptoms and/or LV dysfunctionProgression to asymptomatic LV dysfunction
Sudden death
2. Asymptomatic patients with LV systolic dysfunction
Progression to cardiac symptoms3. Symptomatic patients
Mortality rate (with surgery)
<6% per year<3.5% per year
<0.2% pear year
>25% pear year
>10% per year
B. Cardiac Catheterization
a. Acute aortic regurgitation
Acute AR does not allow sufficient time for myocardial adaptation, andLV moves quickly up its diastolic pressure-volume curve, causing a
marked elevation of LVEDP and early closure of mitral valve (Figure 58).
There is minimal increase in LVED volume or fiber length, and the totalstroke volume cannot increase sufficiently to compensate for theregurgitant volume; thus forward SV and CO fall. The high LVEDP also
serve to minimize the run-off into LV, therefore the diastolic pressure in
the aorta may remain near normal and the arterial pulse pressure increasesvery little, if at all.
b. Chronic aortic regurgitation
In this case, the LV has time to adapt to the volume overload by using the
Frank-Starling mechanism (increase fiber stretch). The hemodynamic and
afterload conditions in chronic AR (Figure 57 and 58) resemble those of
chronic MR with two important differences: (1) the total SV is ejected intoa high-impedance circuit (the aorta and systemic arteries), and because the
total forward SV is augmented, the LV and aortic systolic pressures are
elevated (>160 mmHg); and (2) because the AV is incompetent, thediastolic pressure in the aorta falls to subnormal levels during diastole,
thereby reducing the diastolic perfusion pressure across the coronaryarterial bed. Because eccentric myocardial hypertrophy is associated with
a sizeable increase in total myocardial oxygen demand, patients with AR
are particularly prone to develop angina in absence of CAD.
volume or dimension provides arelatively load independent measure of ventricular performance. Severalstudies have shown that a LV end-systolic dimension of <55 mm is
predictive of preserved LV systolic function and an excellent prognosis
following AV replacement. There is also a good correlation between
severe AR and LVEDD ≥75 mm.
c. M-mode echocardiography
M-mode echocardiography is helpful in demonstrating premature MVclosure or diastolic opening of AV as a sign of severe, usually acute AR
and a marked increase in LV diastolic pressure. It also demonstrates thefluttering motion of the anterior MV leaflet caused by significant AR
(Figure 61). The regurgitant jet can also be directed against the
interventricular septum. Another M-mode sign is increased E-point septalseparation (EPSS) seen in cases of chronic AR. These signs are neither
sensitive nor specific for the presence of AR. In a large series the
sensitivity of anterior MV leaflet flutter was only 46%, with a specificityof 81%. Interventricular septal flutter was less
sensitive (9%) but had a higher specificity of
90%. The differential diagnosis of mitral leaflet
flutter includes severe MR (even with intactchordae), atrial flutter, and rarely high flow
The CW spectral recording of AR has its onset at the closure of AV(during isovolumetric relaxation) with a rapid increase in velocity to a
maximum of 3-5 m/s, followed by a gradual
decline in the velocity during diastole. The
velocity abruptly decelerates during isovolumetriccontraction, reaching baseline at AV opening. The
intensity of the signal, relative to the antegradevelocity, is an indicator of severity of AR.
The CW signal for AR (Figure 62) is best recorded
from an apical window to obtain a parallel
intercept angle between the jet and the blood flowdirection. The slope and pressure half-time (PHT)
of this CW signal have been used to assess the
severity of AR.
Figure 62. CW Doppler recording in two patients, one withchronic AR (A) and one with acute AR (B) showing the
differences in the deceleration slope in each situation. (From
Otto, 2000).
Based on a number of studies it has been suggested that a mean slope of<2m/s in patients with mild AR; a mean slope of 2-3 m/s in groups with
moderate AR; and a mean slope of >3m/s in those patients with severe
AR. A PHT of 400 msec has also been reported to separate mild (1 to 2+)from significant (3 to 4+) regurgitation with a specificity of 92% (a lower
PHT correlating with more severe AR). It should be noted that there are anumber of inconsistencies between these studies and the above numbers
can not be used to provide definitive group separation.
With acute AR, even if only moderate in severity, LV compliance has notyet adapted, as occurs in response to chronic volume overload, so a
significant increase in end-diastolic pressure is seen. This is reflected in a
more rapid decline in slope (Figure 59) when compared to chronic AR.
e. Flow reversal in descending aorta
With severe AR, a holodiastolic flow reversal can be seen in the
descending aorta. This observation is analogous to the Duroziez's sign seen on physical exam (diastolic reversal in femoral arteries). The finding
of diastolic flow reversal in proximal abdominal aorta (Figure 63), is both
sensitive (100%) and specific (97%) for the diagnosis of severe AR. False positive can result from presence of a patent ductus arteriosus. This is best
(SV) positioned in the descending aorta from asubcostal window (inset). The Doppler
velocity curve shows holodiastolic flow
reversal (arrows) consistent with severe AR.
(from Otto, 2000)
f.
Regurgitant volume and fractionAR volume and fraction can be calculated as the difference betweentransaortic and transmitral volume flow. If there is no significant MR, mitral
valve inflow can be used to represent systemic stroke volume.
MV flow = MV annulus area x MV VTI
MV annulus area = MV annulus diameter 2 x π /4
MV flow = MV annulus diameter 2 x 0.785 x MV VTI
Regurgitant volume is the difference between the SV across LVOT and
MV, therefore
AR volume = LVOT flow – MV flow
AR volume = (LVOT diameter 2 x 0.785 x LVOT VTI) – (MV annulus diameter 2 x 0.785 x MV VTI)
A regurgitant volume ≥60 mls indicates severe AR.
Regurgitant fraction (RF) can be calculated according to the following
equation:
RF = AR volume____ x 100%
LVOT stroke volume
A RF ≥55 % indicates severe AR. The AR orifice area can be calculated by dividing
An effective AR orifice area ≥0.3 cm2 indicates severe AR.
Table 22 shows the echocardiographic and Doppler signs associated with severe AR.
Table 22. Echocardiographic signs of severe and mild AR
Mitral Stenosis
A. Introduction
The primary pathophysiologic abnormality in patients with MS is mechanical
obstruction at the mitral valve level. Secondary upstream consequences of MVobstruction include the effects of an elevated transmitral pressure gradient on the
LA and pulmonary vasculature. In isolated MS, the downstream LV is relativelyspared and tends to be normal or small with normal contractile function unless
aortic or mitral regurgitation is also present.
Obstruction at the MV level increases the diastolic pressure gradient between the
LA and LV. As obstruction becomes more severe, the pressure gradientincreases, with mean transmitral gradients at rest of 10 to 25 mmHg in patients
with severe MS. In addition to the severity of the mitral obstruction, transmitral
pressure gradients also depend on the volume flow rate across the valve indiastole. For a given valve area, a higher transmitral gradient occurs with an
elevated transmitral flow rate, for example, with fever, anemia, during exercise, orwith coexistent MR.
Table 23 lists the causes of MS. The commonest cause by far is rheumatic
MS. The most characteristic finding for rheumatic MS is fusion of leaflet edges
along the commissures between the anterior and posterior leaflets. Additionalfeatures include fusion, thickening, and shortening of the chordae; fibrous
thickening of the valve leaflets; and superimposed calcific changes. Flow is
obstructed by a combination of reduced leaflet opening caused by commissural
fusion, and increased rigidity of the leaflets as well as by the obstruction at the
Severe AR
Regurgitant jet width/LVOT diameter ratio ≥60%Regurgitant jet area/LVOT area ratio ≥60%
AR PHT ≤250 msec
Restrictive mitral inflow pattern (usually seen in acute AR)
Holodiastolic flow reversal in the descending aorta
Dense CW signalRF ≥55%
AR volume ≥60 ml
LV diastolic dimension ≥75 mm (chronic AR)Effective AR orifice ≥0.3 cm2
With moderate to severe MS, the overall profile of diastolic flow into the LV is blunted so that distinct rapid-filling and slow-filling phases are no longer seen
before atrial systole. The pressure difference between LA and LV is relativelyhigh during early diastole, declines slowly throughout mid and late diastole
(delayed y descent), and then, if normal sinus rhythm persists, the gradient again
augments with atrial contraction (a wave). The height of the a wave depends onthe integrity of atrial contractility and severity of valvular obstruction (Figure 64).
The height of v wave during ventricular systole depends on the compliance of LA,
the rate and magnitude of LA filling, and the presence and magnitude ofcoincident MR.
Heart rate exerts an important influence on the pathophysiologic manifestations of
MS because diastolic flow per minute across MV depends not only on the valvearea and pressure gradient but also on the duration of diastole. As the heart rate
increases there is less time for the atrial and ventricular pressures to equilibrate,
and the mean LA pressures increase (Figure 65).
Figure 64. Simultaneous
recordings of PCW and LV
pressures in a patient with
MS. On the first beat the
atrial contribution is evident.Loss of atrial activity in beat
2 results in loss of the a
wave and a large v wave
with an increased mitralvalve gradient.
In the above figure simultaneous LV and PCW pressures are recorded demonstrating
a mitral valve gradient throughout diastole. The a wave in the first beat is associatedwith a normal v wave. In the following beat, atrial activity is delayed and follows the
QRS, contributing to a large v wave. The augmented filling increases the MV
contained between the two mitral leaflets, it isobtained by multiplying the hemispheric area by
the correction factor (α/180).
The MVA is calculated by the PISA method according to the
following equation:
MVA = 6.28r 2 x V aliasing x α˚ __
Peak Velocity MS 180˚
Angle correction factor may not be necessary if the bottom surface
of the hemispheric PISA is relatively flat (i.e. α = 180˚).
Balloon Mitral Commissurotomy
Several factors are important in selection of patients for catheter mitral
valvuloplasty. These are:
1) Does the severity of valve obstruction require intervention
2) Anatomy and morphology of the mitral valve
3) Degree of coexistent MR is considered4) Presence and severity of other valve lesions or CAD are assessed (since if surgery
is needed for these, the stenotic mitral valve can be dealt with at that time)
5) Comorbid conditions or technical considerations that may affect the procedure areevaluated
6)
The patient’s preference for a catheter based or surgical procedure is incorporatedin the decision making process.
The predictors of a poor initial result include older age, smaller baseline valve area,
higher pulmonary pressures, and a smaller area of the dilating balloon. However, theanatomy of the mitral valve appears to be the strongest predictor of both immediate and
long-term outcome. Patients with thin, flexible valve leaflets; little calcifications of theleaflets or the commissures; and minimal chordal involvement have the best
hemodynamic results and long-term outcome. Patients with heavily calcified and
deformed valves have a poor long-term outcome and are also at a higher risk for procedural death and major complications. The most widely used approach to evaluation
of mitral valve morphology is the composite Massachusetts General Hospital (MGH)
score (Table 25). This score predicts both immediate increase in valve area and restenosis
at 6 month follow-up after valvuloplasty. When the morphology score is considered tohave a cutoff score of 8, a greater valve area increase is seen in group with lower score
Other approaches to evaluation of mitral valve morphology that also predict immediate
hemodynamic result is the three group grading (Table 26). This system is primarily
based on the extent of subvalvular involvement and the extent of leaflet calcification.When this system was used for a series of 1512 patients, inadequate hemodynamic results
were seen in only 2.2% of Group 1 and 7.4% of Group 2 patients but in 22.3% of Group
3 patients.
Table 26. The three group grading of mitral valve anatomy Echocardiographic Group Mitral Valve Anatomy
1 Pliable, noncalcified anterior mitral leaflet and mild
subvalvular disease (ie thin chordae ≥10 mm long)
2 Pliable, nonclacified anterior mitral leaflet and
severe subvalvular disease (ie thickened chordae<10 mm long)
3 Calcification of mitral valve of any extent, as
assessed by fluoroscopy, whatever the state of the
Several of these criteria have been combined into an overall criteria forassessment of mitral valve morphology (Table 27). One problem with all these scoring
systems is that the continuous range of mitral valve anatomy is compressed into discrete
categories, so that borderline cases will be classified inconsistently. Further all the
scoring systems are subject to interobserver variability.
Table 27. Two-dimensional echocardiographic assessment of mitral valve morphology
Variable Predicted ResultsOptimal Suboptimal
Leaflet motion Highly mobile with
restriction only of leaflettips, and H/L ratio ≥0.45
Minimal forward motion
of the leaflets indiastole, or H/L ratio
≤0.25
Leaflet thickening Leaflets <4-5 mm or
MV/PWAo ratio of 1.5-2.0
Leaflets >8.0 mm thick
or a MV/PWAo ratio≥5.0
Subvalvular disease Thin, faintly visiblechordae tendinae with
only minimal thickening
below the valve
Thickening andshortening of chordae to
papillary muscle; areas
with echodensity greater
than endocardium
Commissural calcium Homogeneous density
of both commissures
Both commissures
heavily calcified
Finally the general accepted contraindications to mitral valvuloplasty are listed in
table 28.
Table 28. Contraindications to mitral valvuloplasty
Left atrial thrombus
MR >2/4
Massive or bicommissural calcification
Severe aortic valve disease, or severe tricuspid stenosis + regurgitation associated with MS
Severe concomitatnt CAD requiring bypass surgery
Both autopsy as well as echocardiographic data suggest that the splitting of fusedcommissures is the mechanism of the increase in valve area with catheter balloon
commissurotomy. The dilating balloon is advanced from the right femoral vein into the
RA and then, through a trans spetal approach, into the left atrium. This is a potential
source of complications and requires considerable expertise. Echocardiography has beenused for guidance during trans spetal puncture as well as balloon placement (Figure 74).
The balloon dilating catheter is then advanced across the mitral valve. After the correct
position is insured, the balloon is dilated briefly, with one to four inflation needed toachieve an adequate increase in valve area. Balloon sizes are often chosen empirically
based on patient’s size. With a single balloon technique (Inoue), balloon size is chosen
based on the patient’s height. Each balloon allows inflation to several different finaldiameters, allowing a stepwise approach to valve dilation. Figure 76 shows the use of the
Inoue balloon. After the balloon is positioned across the mitral valve, the distal segment
in the LV is dilated first, followed by the proximal segment in the LA. This approach
holds the balloon securely in position while the middle (dilating) balloon is brieflyinflated.
Complication of catheter balloon valvuloplasty (Table 29) include, development
of a small ASD (at the site of transspetal approach). This defect is found in over 60% of
patient by color flow Doppler. In most cases the defect closes spontaneously with adetectable shunt visualized in 20-30% of patients at 18 months follow-up evaluation. A
significant shunt across the iatrogenic ASD is uncommon, occurring in only 4-20% in
different series. The most serious complication is cardiac tamponade resulting from perforation by a guiding or dilating catheter. This has been reported in 0.8-4% of cases.
An increase in MR from none or mild at baseline to moderate or severe after the
procedure is seen in 13% of cases (1-8% developed severe MR). The numbers are lowerwith Inoue balloon. Urgent surgical intervention (for tamponade or MR) is needed in
between 0.4-4.8%. Systemic embolization occurs in 0.5-3.3% of patients. This is due to
dislodgement of LA thrombus during the procedure. This risk can be minimized by usingTEE evaluation prior to the procedure.
Univariate predictors of procedural death include older age, history of cardiacarrest, cerebrovascular disease, dementia, renal insufficiency, cachexia, CHF symptomsat rest, smaller valve area, and a higher echocardiographic morphology score.
Table 29. Major complications of balloon mitral valvuloplasty
Procedural mortality 0.1% to 4.5%
Systemic embolization 0.5% to 3.3%
Tamponade 0.8% to 4%
Shunt 4% to 14%
Severe MR 1% to 8%
Immediate surgery 0.4% to 4.8%
Figure 74. TEE guidance of Inoue
balloon mitral valvuloplasty. The
transspetal needle is seen indenting the
atrial septum (arrow) just before puncture(A), followed by positioning of balloon
catheter (arrow) in the left atrium (B).
After the balloon catheter is advancedacross the mitral valve, first the distal
segment of the balloon (arrow) is inflated
(C), followed by a brief inflation (arrow)of the proximal and dilating segments (D).
Normal MV closure, which prevents the systolic backflow of blood into the LA,
depends on the complex interaction of each of the components of the valve
apparatus (LA wall, the annulus, the MV leaflets, the chordae, the papillary
muscles, and the LV wall). Abnormalities in the anatomy and function of any ofthese components lead to valvular regurgitation. Table 30 shows the etiologies of
MR classified as those with abnormal valve and those with normal valve.
Pressure measurements either in the PCW or LA positions usually reveal an
elevated v wave (>20 mmHg peak value), followed by a relatively rapid y descentas the MV opens and an excessive inflow of blood traverses the MV (Figure 79).
There is not uncommonly a small pressure gradient across the MV during early
diastole, reflecting functional MS in the presence of increased flow. If the MR isrelatively acute and severe, a very large v wave is generated owing to the fact that
the LA remains relatively normal sized and noncompliant and LV shortening
remains normal to supranormal. Conversely in longstanding severe MR, the v wave may be extremely small owing to massive dilatation of LA and a significant
increase in its capacitance. When myocardial contractility becomes severelydiminished, depression of the total stroke volume may also contribute to the lackof generation of a significantly elevated v wave.
The effective CO depends on the severity of the regurgitation, the acuteness
versus chronicity of the process, the adaptation of the LV to the volume overload,
and the maintenance of normal myocardial contractility.
Combined MS and MR is often associated with a heavily calcified valve that haslimited leaflet mobility. Because systolic regurgitation augments antegrade flow
during the subsequent diastole, a transvalvular pressure gradient can develop in patients with a relatively mild compromise of the mitral orifice area(approximately 2.0 cm
2). Significant dilatation of LA is seen owing to the
combined pressure and volume overload of the chamber. In this setting, the
pressure recordings from the left heart reveal an early and mid-diastolic pressuregradient across the MV, but if the DFP is sufficiently long, the LA and LV
pressures equilibrate during the period of slow ventricular filling (Figure 80). The
v wave is often dominant, reflecting the augmented systolic expansion anddilatation of LA. The amount of regurgitation is calculated as the difference
between total LV stroke volume (measured on contrast LV angiogram) and thestroke volume calculated from a Fick or indicator-dilution CO and the resting HR.
Figure 80. LV and
LA pressure tracings
in combined MS and
MR in atrial
fibrillation.
As detailed in Table 31, semiquantitative criteria have been established that, when
combined with clinical and noninvasive diagnostic features, serve to categorize the
severity of a volume overload imposed by valve leakage.
e. Proximal isovelocity surface area method (PISA)
As the blood in the LV converges towards the mitral regurgitant orifice
(Figure 83), the velocity of blood
flow increases and forms a series
of hemispheric waves, whosesurface has the same velocity.
Based on the principle of volumeflow calculation by Doppler
techniques, the regurgitant flow
rate for this surface, when
averaged over temporal flow, is
Figure 83. Flow accelerates proximal to the orifice, resulting inconcentric proximal isovelocity surface areas. The color Doppler
aliasing velocity allows identification of one of these PISAs, whichthen can be used to calculate regurgitant volume (see text)
Regurgitant volume = PISA x Velocity
The PISA velocity can be determined from the color flow image as the aliasing
velocity where a distinct red blue interface is seen. At this interface the velocity isknown and is equal to the Nyquist limit on the velocity color scale. The size of the
PISA can be maximized for more accurate assessment of regurgitant orifice, by
decreasing the velocity range or shifting its baseline (< 30 cm/s). Given that the
shape of the isovelocity surface is hemispherical, PISA can be calculated from themeasurements of the distant from the aliasing velocity to the regurgitant orifice as
(area of a hemisphere):
PISA = 2π r 2
One can determine the effective regurgitant orifice (ERO) using the following
formula,
PISA flow = MR flow
2π r 2
x Velocity PISA = ERO x Peak Velocity MR Velocity PISA = V aliasing
Regurgitant volume (RV) can be then calculated from the ERO by:
RV = ERO x VTI MR
RV = 6.28r
2
x V aliasing x VTI MR Peak Velocity MR
f. Pulmonary vein flow reversal
In severe MR, there may be a systolic flow reversal in the pulmonary vein
(Figure 84); however, the absence of systolic flow reversal in pulmonary
vein does not exclude severe MR. False negative results occur when LAis severely enlarged and compliant so that all the excess volume is
contained in the LA without displacement into pulmonary veins. False
positive results occur when an eccentric jet is directed into a pulmonaryvein, causing flow reversal when MR is not severe.
Figure 84. Pulmonary vein CW Doppler
tracing in a patient with severe MR showing a
systolic flow reversal (SR), D is the diastolic
flow. (From Oh, 1999).
g. Peak mitral inflow velocity
Early diastolic mitral inflow velocity relates directly to the instantaneous
pressure gradient between the LA and the LV. The added regurgitantvolume increases the LA to LV pressure gradient, which in turn increasesthe early mitral inflow velocity (E wave). The peak E wave velocity >1.2
m/s identified patients with severe MR (isolated) with a sensitivity of 85%
and a specificity of 86% (Thomas et al, 1998). It must be mentioned thatincreased mitral inflow velocity has also been observed in patients with
severe AR. Moreover, the predictive value of this marker has not been
tested in patients with acute MR. Therefore, although peak E velocity
Infective endocarditis (IV drug users)Carcinoid syndrome
Floppy tricuspid valve
B. Cardiac Catheterization
The normal TV orifice area is 8 to 12 cm2; significant symptoms and signs of TS
may be seen when the valve area is compromised to ≤2cm2. As with MS the
gradient across the valve is dependent on the diastolic filling period and cardiac
output. Thus, exercise is associated with a significant increase in the gradientacross the valve.
The RA pressure pulse in TS is characterized by an exaggerated a wave (if insinus rhythm). As with MS, there is slowing of the y descent and the absence of
diastasis between the RA and RV pressure pulses (Figure 85). HR influences the
pressure gradient as it does in MS. These effects are subtle though since in mostcases the valve gradient is no more than 5 to 8 mmHg.
As with MV the TV area can be calculated from the planimetered area under the
RV and RV pressure curves using the Gorlin formula (see section on AS for
derivation of this formula):
TVA (cm2 ) = CO ( ml/min )/DFP x HR44.3√ MVG
This method is not always accurate due to low pressure system at the tricuspid
valve. TR is detected, at the time of right heart catheterization, by the presence of
large v waves in the RA pressure pulse; in severe cases of TR, the v wave mayfollow the contour of the RV pressure pulse, although the peak systolic pressure
in RA always remains less than that of RV (Figure 86).
Figure 86. RV
and RA
pressuretracings in a
patient withsevere TR.
In cases of combined TR and TS (Figure 87), there is a diastolic gradient along with the v
wave of the TR.
Figure 87. Simultaneous RV and RA pressure tracings in combined TS and
TR and atrial fibrillation. Note the early
diastolic delay in y descent and the c-v wave during systole. The shaded area
represents the diastolic gradient during
a single beat.
C. Echocardiography
a. Tricuspid stenosis
Echocardiography can be used to determine the cause of TS and the
associated abnormalities (MS in patients with rheumatic disease). 2D
echocardiographic images show thickening and shortening of TV leaflets.Commissural fusion and diastolic bowing indicate rheumatic disease. The
normal tricuspid inflow velocity is lower than 0.5 to 1 m/s, with a mean
gradient of <2 mmHg. There is a respiratory variation in TV inflowvelocity. The evaluation of TR by Doppler (Figure 88) is similar to the
method described for MS (use the constant of 190 for PHT method). TS is
considered severe when the mean gradient is ≥7 mmHg and PHT ≥190
ms.
TVA = 190
T 1/2
Figure 88. A. PW Doppler recording of TV inflow from a patient with mild TS. The
peak velocity is 1.7 m/s and rapidly falls to 0 by end diastole. B. CW Doppler recording
from a different patient with more severe TS. Note the increase in the rate of flowacceleration, increased peak velocity (2 m/s) and a slow rate of flow deceleration. (From
Wayman, 1994)
b. Tricuspid regurgitation
Hemodynamically significant TR results in progressive RV and RA
enlargement due to volume overload. RV volume overload is associated
with a pattern of abnormal septal motion seen on M-mode
echocardiography (paradoxical septal motion). On 2D short axis imaging,the interventricular septum appears flattened in diastole. The differential
diagnosis of paradoxical septal motion and RV dilatation includes other
causes of RV volume overload such as ASD, partialanomalous pulmonary venous return, pressure
overload due to Pulmonic valve disease, or pulmonary HTN (either due to left-sided heart
disease or intrinsic lung disease). TR can be
evaluated with Doppler flow techniques in a similarmanner to that described for assessment of MR.
Figure 89. Schematic diagram of color flow mapping for
semiquantitative evaluation of TR severity from the subcostal
window. Severe (4+) TR is associated with systolic reversal in
Color flow mapping allows for assessment of severity. Mild TR is
characterized by localized flow disturbance in systole with less than a 1/3rd
of atrial area. Moderate TR fills between 1/3rd
and 2/3rd
of the RA, whilesevere TR fills more than 2/3
rd of an enlarged RA (Figure 89).
Severe TR results in systolic flow reversal in the IVC and SVC, analogous
to the physical finding of a systolic pulsation in the neck veins. IVC flowis best recorded in the central hepatic vein, which provides a flow channel
parallel to the ultrasound beam from a subcostal approach with no venous
valves between the recording site and the RA (Figure 90).
Figure 90. A. Hepatic vein PW and
CW Doppler showing markedsystolic reversal (arrows) caused by
severe TR. B. Doppler spectrum of
TV in a patient with severe TR.Forward inflow velocity is increased
(E=1.4 m/s) and TR peak velocity isrelatively decreased because of a
small pressure gradient between theRV and the RA. A large v wave
makes the Doppler spectrum dented
during mid to late systole
(arrowheads). C. In comparison, CW
Doppler velocity spectrum from a patient with pulmonary HTN and
moderate TR shows increased peak
velocity but with a roundedconfiguration. (From Oh, 1999)
The absolute value maximum velocity in TR CW Doppler
recording reflects the maximum pressure difference acrossthe TV and not the severity of regurgitation. Severe
regurgitation with a normal RVSP (as seen with TV
endocarditis) has a low maximum velocity. Mild TR in the
presence of pulmonary HTN (as seen in PPHTN) has a highmaximum velocity. However, the intensity of CW signals,
relative to the antegrade flow signal intensity does not
relate to TR severity. In addition the shape of velocity-timecurves indicates the time course of instantaneous pressure
differences across the valve (Figure 91). A RA v waveseen in acute TR, results in a more rapid decline in velocityin late systole similar to that seen in acute MR. Table 35
lists the echocardiographic criteria for severe TR.
Figure 91. Continuous-wave Doppler recording of TR in a patient withchronic (above) and acute (below) TR. Note the late systolic velocity
decline (v wave) in the acute case (arrow). (From Otto, 2000)
Carcinoid syndromeInfective endocarditis, with perforation or retraction
Catheter trauma (Balloon dilatation)
External blunt trauma
RheumaticRheumatoid arthritis and syphilis
Pharmacologic agents (Fenfluramine-phentermine)
B. Cardiac Catheterization
a. Pulmonary stenosis
Moderate to severe obstruction of the PV places a pressure overload on the
RV that, in turn, leads to significant RVH. The pressure tracings from RVand PA (Figure 92) can be used to calculate the mean gradient similar tothe method used for AS. Pulmonic valve area can also be calculated by
the Gorlin formula as follows:
PVA (cm2 ) = CO ( ml/min )/SEP x HR
44.3√ MVG
Where MVG is the mean valve gradient calculated from the pressuretracings of RV and PA. This method however has not been validated
The basic cardiac defect in PR is retrograde leakage of blood from themain PA into RV during diastole (Figure 93). Unless the PADP is
severely elevated, the driving force between the PA and RV is not large,and the regurgitant fraction of the stroke volume remains relatively small.Moreover RV can tolerate a relatively large volume overload, and thus,
the patient with PR commonly exhibits no impairment of CO either at rest
or during exercise. Also, the RVEDP and RAP are not elevated unless
there is an associated pressure overload on RV, or PR is long-standing.
Figure 93. Simultaneous RVand PA pressure
recordings from a
patient with PR.
C. Echocardiography
a. Pulmonary stenosis
The echocardiographic study of valvular PS should include:(a) The morphology of the stenotic pulmonic valve
Morphologically the valve can be unicuspid (acommissural orunicommissural), bicuspid (usually seen in association with tetralogyof Fallot), tricuspid and quadracuspid.
(b) The diameter of pulmonary annulus
In isolated pulmonic valve stenosis, the pulmonary annulus is usuallynormal in size but can also be hypoplastic.
(c) The size of the RV
The RV is usually concentrically hypertrophied. Infundibular
hypertrophy can result in subvalvar obstruction (seen in close to 1/3rd
of valvular PS). Size of the RV can be assessed from parasternal long-
axis view tilted towards the RV inflow, from short-axis view, and fromapical four-chamber and subcostal four-chamber and short-axis view.
(d) The degree of dilatation of the PA
Isolated PS is almost always associated with Poststenotic dilatation of
the PA, which can extend to the proximal portion of the left branch.This is the result of high velocity flow across the stenotic valve
impacting on the arterial wall. The degree of Poststenotic dilatation is
not related to the severity of PS. The dilatation is best seen from parasternal long-axis view of the RVOT and also from short-axis view.
(e) The severity of the obstruction
Maximal velocities are recorded using CW-Doppler. Peak and meangradients are calculated from the velocities using the simplified
Bernoulli equation. Color flow Doppler mapping of the RVOT should
be done prior to CW interrogation to guide sample line positioning.The RVOT should be interrogated with PW Doppler to establish
presence of any infundibular stenosis. If the velocities proximal to thePV are >1 m/s, the expanded Bernoulli equation should be used tominimize the errors in predicting the peak gradient.
(f) Associated anomalies.
It is unusual to find other anomalies with PS and an intact ventricular
septum. However when present PFO and ASD (secundum) are themost common.
Echocardiographically, PS is characterized by (1) systolic doming of thestenotic leaflets into the pulmonary artery (Figure 89), (2) abnormal initial
systolic leaflet motion, (3) opening or doming following atrial systole but before ventricular systole in more severe cases, and (4) measurements of
peak flow velocity and pressure gradient using CW Doppler (Figure 95).
Poststenotic PA dilatation may be present and should be sought for.Differentiation of valvular PS from subvalvular or supravalvular
obstruction can be difficult by 2D echo. Careful interrogation with PW
Doppler should be used to better delineate the nature of the obstruction.In patients with relatively normal cardiac
output, classification of PS is routinely
based on measurements of RV pressure and
valve gradient. Mild stenosis ischaracterized by a RV pressure less than ½
of LV pressure or a valve gradient of <35-40
mm Hg.
Figure 94. Parasternal short-axis view of a stenotic pulmonic valve. Note the doming of the valve in
systole and the thickened, redundant tissue in
diastole. The annular size can also be measured from
ejection, paradoxical septal motion). Also vigorous pulsations of the main
PA and its branches are seen (especially in suprasternal views ifaccessible).
When PR is present (even mild), the velocity in PR Doppler profile
reflects the PA to RV diastolic pressure difference (Figure 97). The
instantaneous end-diastolic PA to RV gradient (calculated by modifiedBernoulli equation, 4v2) can be added to an estimate of RV diastolic
pressure (from IVC size and respiratory variation) to provide an estimate
of PA diastolic pressure.
PA diastolic pressure = 4v PR2 + RA pressure
Figure 97. Diagram of
CW Doppler interrogation
of PR from the left
parasternal window andthe PR Doppler spectrum.
For example if the end-
diastolic PR velocity is 3m/s, the end-diastolic PAP
= (4 x 32) + 20 = 56 mm
Hg, assuming an RAP of20 mm Hg (Oh, 2000).
Pulmonary Hypertension
A. Introduction
The normal PAP for a person living at sea level has a peak systolic value of 18 to 25
mmHg, a peak end-diastolic value of 6 to 10 mmHg, and a mean PAP value of 12 to 16
mmHg. The normal mean pulmonary venous pressure is 6 to 10 mmHg, therefore themean AV pressure difference, which moves the entire cardiac output across the
pulmonary vasculature, ranges from 2 to 10 mmHg (compared to a mean of 90 mmHg
required to move the same cardiac output across the systemic vascular bed). Thus, thenormal pulmonary vascular bed offers close to 1/10
th the resistance to flow offered by the
systemic bed. Vascular resistance is generally quantified, by analogy to Ohm’s law, as
the ratio of pressure drop (DP in mm Hg) to mean flow (Q in liters/min). The ratio iscommonly multiplied by 79.9 (or 80 for simplification) to express the results in dynes-
seconds-centimeters –5
. This conversion to metric units may be avoided, i.e., resistance
may be expressed in units of mm Hg/liter/min, which is referred to Wood units (after the
English cardiologist Paul Wood). The calculated pulmonary vascular resistance in normaladults is 67 ± 23 dynes-sec-cm
–5, or 1 Wood unit. Vascular resistance reflects a
composite of variables that includes (but is not limited to) the cross-sectional area of
small muscular arteries and arterioles, blood viscosity, the total mass of lung tissue (i.e.,resistance is higher in infants and children than in adults), proximal vascular obstruction
(e.g., pulmonary coarctation, pulmonary embolism, peripheral pulmonic stenosis), and
extramural compression of vessels (perivascular edema). Hemodynamically pulmonaryHTN is defined as systolic pulmonary pressures >35 mmHg, diastolic pressure >15
mmHg, and mean PAP >25 mmHg.
Table 37. Etiologic classification of pulmonary HTNPulmonary venous HTN
Thoracic Aorta (CoA, Supravalvular AS)
LV (AS or AI, HOCM, Constrictive pericarditis)
LA (Myxoma, MS, Cor triatriatum)Pulmonary veins (Congenital PV stenosis, Mediastinitis or fibrosis, neoplasms)
Chronic hypoxia
High altitudeInadequate respiratory excursion (Obesisty, kyphoscoliosis, neuromuscular disease)
Various causes of pulmonary HTN are listed in table 37 according to the pathophysiologic mechanism.
B. Cardiac Catheterization
Right heart catheterization is used to assess RVEDP, PAP, and PCWP in patients
with pulmonary HTN. Pulmonary angiography is usually undertaken at the same
time. Pulmonary angiography often represents the final step in assessing a patientwith pulmonary HTN. Delineation of precapillary causes of pulmonary HTN is
the primary goal of this procedure. Postcapillary causes, such as long-standing
pulmonary venous HTN (e.g. MS, LV failure), or other pulmonary vasculardisorders, such as those associated with venous occlusion, generally present
clinical and laboratory features that provide the diagnosis. However, left heartcatheterization, coronary angiography, regional PCWP determinations, andretrograde pulmonary venography may be required to confirm or exclude these
diagnoses. Consequently, the usual goal of pulmonary angiography in the patient
with pulmonary HTN is to define the prearteriolar anatomy to distinguish between
major vessel (main, lobar, and segmental) and small vessel disease.
Determination of PAP is routine part of echocardiographic examination. Severalapproaches have been suggested for non-invasive estimation of PAP including (1)
Doppler derived gradients, (2) changes in PV motion and PA flow profiles, and
(3) measurement of RV IVRT. At least one measure of PAP can be obtained in
up to 98% of patients.
a. Doppler derived gradients
PAP can be estimated from (1) RV-RA pressure gradient in patients withTR, (2) LV-RV pressure gradient in patients with VSD, (3) the aorta-PA
gradient in patients with aortopulmonary connections (e.g. PDA), and (4)
from the PA-RV gradient in patients with PR. The most commonapproach is to estimate PASP from RV pressure (assuming there is no PS)
determined as the sum of RV-RA pressure gradient and either an assumed
or clinically determined RAP (Figure 98).
Figure 98. A. Diagram demonstrating measurement of RV pressure from TR velocity. The peak RVSP is
estimated by adding RAP to the pressure gradient derived from TR velocity (4 x (peak TR velocity)2) B.
Simultaneous RA and RV pressure tracings and TR velocity recording by CW Doppler echocardiography
(Oh, 2000).
RAP is best estimated from evaluation of IVC during respiration. From asubcostal window this segment of IVC is imaged during quiet respiration
(M-mode can be used for accurate measurements). If the IVC diameter isnormal (1.2 to 2.3 cm) and the segment next to RA collapses at least 50%during respiration, then RAP is equal to normal intrathoracic pressure (i.e.
5-10 mmHg). Failure to collapse with respiration and/or dilatation of IVC
and hepatic veins is associated with higher RAP (Table 38).
IVC Changes with respiration or Sniff Estimated RAP
Small (<1.5 cm) Collapse 0-5 mmHg
Normal (1.5-2.5 cm) Decreased by >50% 5-10 mmHg
Normal Decreased by <50% 10-15 mmHg
Dilated (>2.5 cm) Decrease by <50% 15-20 mmHg
Dilated with dilated hepatic veins No change >20 mmHg
In patients with VSD, the RVSP can be determined as the peak aortic
pressure (measured by a sphygmomanometer), which is equal to the LV
systolic pressure minus the gradient across the defect.
RVSP = SBP – 4vVSD2
With associated PS, the PAP will equal the RV pressure minus the
transpulmonary gradient. When a VSD and PS coexist, the combined
calculated pressure differences may exceed the true gradient between the
LV and PA by 10-15 mmHg, because the velocity peaks can occur atdifferent points in systole.When there is a direct systemic to PA connection (e.g. PDA, BT shunt),
the PAP will equal the systemic cuff pressure minus the gradient.
RVSP = SBP – 4v shunt 2
Finally in a patient with PR, the maximal velocity in the regurgitant jet
approximates the diastolic pressure in the PA except when the RVdiastolic pressure is elevated.
PAP (end-diastolic) = 4v PRend-diastolic2
+ RAP
A characteristic pattern in hepatic venous flow is seen in patients with
pulmonary HTN (Figure 99). There is a prominent atrial flow reversal in
hepatic vein caused by increased diastolic pressure and decreasedcompliance of RV.
Doppler) showing measurements used to calculatemean PAP (MPAP). AcT, acceleration time; IVRT,
isovolumetric relaxation time.
Figure 102. Spectral Doppler velocity
waveform of the PA in PHTN. Note the rapid
acceleration time (45 msec) and the notching(arrow) of the systolic curve (W pattern) due to
decreased flow in mid systole (From Valdes-
Cruz, 1999).
The ratio of AcT and RV ejection time(ET) can also be used to assess severity
of PHTN. It is generally agreed that
patients without PHTN have a AcT/ETratio >0.36.
Intracardiac ShuntsA. Introduction
Normally, pulmonary blood flow and systemic blood flow are equal. Whenthere is an abnormal communication between intracardiac chambers or great
vessels, blood flow is shunted either from the systemic circulation to the
pulmonary circulation (left-to-right shunt), from the pulmonary circulation tothe systemic circulation (right-to-left shunt), or in both directions
(bidirectional shunt). Although many shunts are suspected before cardiaccatheterization, unexpected findings during catheterization should trigger athorough search for the cause. For example, an unexplained pulmonary artery
oxygen saturation exceeding 80% should raise suspicion of a left-to-right
shunt, whereas unexplained arterial desaturation (<95%) may indicate a right-to-left shunt. Arterial desaturation commonly results from alveolar
hypoventilation and associated physiological shunting, the causes of which
may include oversedation from premedication, pulmonary disease, pulmonary
venous congestion, pulmonary edema, and cardiogenic shock. Persistence of
arterial desaturation after administration of 100% oxygen should raise a
suspicion of a right-to-left shunt. Noninvasive methods for the detection ofintracardiac shunts include echocardiographic, radionuclide, and magnetic
resonance imaging techniques.
B.
Cardiac Catheterizationa. Oximetric method:
The oximetric method is based on blood sampling from various cardiac
chambers for oxygen saturation determination. A left-to-right shunt is detectedwhen there is a significant increase in blood oxygen saturation between two
right-sided vessels or chambers (step up). A screening oxygen saturation
measurement for any left-to-right shunt should be performed with every rightheart catheterization by sampling blood in the superior vena cava (SVC) and
the pulmonary artery (PA). If the difference in oxygen saturation between
these samples is ≥8%, a left-to-right shunt may be present, and a full oximetryrun should be performed. This includes obtaining blood samples from the
superior vena cava (SVC), inferior vena cava (IVC), right atrium, rightventricle, and pulmonary artery. In cases of ASD or VSD, it may be helpful toobtain multiple samples from the high, middle, and low right atrium or the
right ventricular inflow tract, apex, and outflow tract in order to localize the
level of the shunt. One may miss a small left-to-right shunt using the right
atrium for screening purposes rather than the SVC because of incompletemixing of blood in the right atrium, which receives blood from the IVC, SVC,
and coronary sinus. Oxygen saturation in the IVC is higher than in the SVC
because the kidneys use less oxygen relative to their blood flow than do otherorgans, while coronary sinus blood has very low oxygen saturation. Mixed
venous saturation is most accurately measured in the pulmonary artery aftercomplete mixing has occurred.
A full saturation run involves obtaining samples from the high and low IVC;
high and low SVC; high, mid, and low right atrium; right ventricular inflow,outflow tracts, and mid-cavity; main pulmonary artery; left or right pulmonary
artery; pulmonary vein and left atrium if possible; left ventricle; and distal
aorta. When a right-to-left shunt must be localized, oxygen saturation samplesmust be taken from the pulmonary veins, left atrium, left ventricle, and aorta.
Despite its lack of sensitivity, clinically significant shunts are generally
detected by this technique. Another method uses a balloon-tipped fiberoptic
catheter that allows for continuous registration of oxygen saturation as it iswithdrawn from the pulmonary artery through the right heart chambers into
the SVC and IVC.
The principles used to determine Fick cardiac output are also used to quantifyintracardiac shunts. To determine the size of a left-to-right shunt, pulmonary
blood flow and systemic blood flow determinations are required. Pulmonary
blood flow (PBF) is simply oxygen consumption divided by the difference inoxygen content across the pulmonary bed, while systemic blood flow (SBF) is
oxygen consumption divided by the difference in oxygen content across the
systemic bed. The effective blood flow (EBF) is the fraction of mixed venousreturn received by the lungs without contamination by the shunt flow. In the
absence of a shunt, PBF, SBF, and EBF are all equal. These equations are
shown below:
PBF = O2 consumption (ml/min)
(PVO2 – PAO2 )
SBF = O2 consumption (ml/min)(SAO2 – MVO2 )
EBF = O2 consumption (ml/min)(PVO2 – MVO2)
Where PVO2, PAO2, SAO2, and MVO2 are the oxygen contents (in millilitersof oxygen per liter of blood) of pulmonary venous, pulmonary arterial,
systemic arterial, and mixed venous bloods, respectively. The oxygen content
is determined as outlined in the section on Fick cardiac output and iscalculated by:
O2 conent = O2 saturation x O2 carrying capacity (1.36 ml/gm) x Hgb Concentartion (gm/L)
Systemic arterial oxygen content may be substituted, assuming systemic
arterial saturation is 95% or more. As discussed above, if systemic arterialsaturation is less than 95%, a right-to-left shunt may be present. If arterial
desaturation is present but not secondary to a right-to-left shunt, systemic
arterial oxygen content is used. If a right-to-left shunt is present, pulmonaryvenous oxygen content is calculated as 98% of the oxygen capacity.
The mixed venous oxygen content is the average oxygen content of the blood
in the chamber proximal to the shunt. When assessing a left-to-right shunt atthe level of the right atrium, one must calculate mixed venous oxygen content
on the basis of the contributing blood flow from the IVC, SVC, and coronary
sinus. The most common formula used is the Flamm formula:
MVO2 = 3(SVC O2 content) + (IVC O2 content)4
The difference between the SVC and the IVC O2 content is due to loweroxygen extraction of the kidneys. Assuming conservation of mass, the size of
a left-to-right shunt, when there is no associated right-to-left shunt, is simply:
L → R shunt = PBF – SBF (Or Q p – Q s )
When there is evidence of a right-to-left shunt in addition to a left-to-rightshunt, the approximate left to right shunt size is:
L → R shunt = PBF – EBF (or Q p – Q EP )
While the approximate right-to-left shunt size is:
The flow ratio PBF/SBF (or QP/QS) is used clinically to determine the
significance of the shunt. A ratio of less than 1.5 indicates a small left-to-right
shunt. A ratio of 2.0 or more indicates a large left-to-right shunt and generally
requires repair in order to prevent future pulmonary and/or right ventricularcomplications. A flow ratio of less than 1.0 indicates a net right-to-left shunt.
If oxygen consumption is not measured, the flow ratio may be calculated asfollows:
Qp = SAO2 – MVO2
Qs PVO2 – PAO2
Figure 103. Schematic diagram of blood oxygenation in the heart in presence of a relatively large ASD
with L to R shunting and a normal PVR. Numbers in the diagram indicate Oxygen content in differentchambers calculated from O2 saturations measured at the time of cardiac catheterization. (From Peterson,
1997)
Figure 104. Schematic diagram of blood oxygenation in the presence of a relatively large VSD and normal
Figure 105. Schematic diagram of blood oxygenation in the heart in the presence of PDA and normal
PVR. (From Peterson, 1997)
Figure 106. Schematic diagram of blood oxygenation in a heart with tetralogy of Fallot and bidirectionalshunting at the high ventricular septal level. L to R shunting is relatively small owing to obstruction to
pulmonary vascular bed by pulmonary stenosis. R to L shunting is facilitated by aortic override to
ventricular septum. (From Peterson, 1997)
Figures 103 to 106 are different examples of both intra and extra-cardiac
shunts and calculation of Q p/Qs.
b. Indicator dilution method
While the indicator-dilution method is more sensitive than the oximetric
method in detection of small shunts, it cannot be used to localize the level of a
left-to-right shunt (Figure 107). An indicator such as indocyanine green dye
is injected into a proximal chamber while a sample is taken from a distalchamber using a densitometer and the density of dye is displayed over time. In
order to detect a left-to-right shunt, dye is injected into the pulmonary arteryand sampling is performed in a systemic artery. Presence of a shunt is
indicated by early recirculation of the dye on the down slope of the curve. The
presence of aortic or mitral regurgitation may distort the downslope of the
curve, thereby yielding a false positive result. In adults, the indocyanine greenmethod provides estimates of shunt magnitude that are somewhat smaller than
those of the oximetric method, although they are in general agreement with
one another concerning the Q p/Qs. In order to detect a right-to-left shunt, dyeis injected into the right heart proximal to the presumed shunt and sampling is
performed in a systemic artery. If there is a right-to-left shunt, a distinctive
early peak is seen on the upslope of the curve. The level of the right-to-left
shunt may be localized by injecting more distally until the early peakdisappears. Shunts may also be quantified using this technique.
Figure 107. Indicator dilution curves for shunts. L→ R shunts (increased pulmonic flow). Indicator is notcleared rapidly but recirculates through central circulation via defect. Based on the magnitude of the shunt,
a constant fraction leaves the central pool with each circulation. R→ L shunt (decreased pulmonic flow). A
portion of the indicator passes directly to the arterial circulation via the defect without passing through thelungs and arrives at the arterial sampling site before the portion that did traverse the pulmonary circulation.
(From Kern, 1999)
C. Echocardiography
With PW Doppler or color flow imaging, a flow disturbance is found
downstream from the defect: on the right side of the IVS for the VSD, in the
RA for ASD, and in PA for a PDA. Similar to a stenotic or regurgitantorifice, the velocity of blood flow through the shunt orifice is related to the
pressure gradient across the defect.A L to R intracardiac shunt imposes a chronic volume overload on the
receiving chamber with consequent dilatation of the affected chamber. With
ASD both RA and RV dilate and paradoxical septal motion is seen. With a
PDA, the volume overload is imposed on LA and LV. Although it mightseem that a VSD would cause RV volume overload, in fact RV size usually is
normal since the LV effectively ejects the shunt flow across the defect directlyinto the PA in systole. Instead, LA and LV dilatation are seen, since these
chambers receive the increased pulmonary blood flow as it returns to the left
side via the pulmonary veins.The Q p/Qs can be calculated by Doppler echocardiographic measurements of
SV at two intracardiac sites (Figure 108). In the case of an ASD,
transpulmonic flow (Q p) is calculated from PA CSA and velocity-time integral
(VTI), while systemic flow (Qs) is calculated from measurements of LVOTCSA and VTI.
Figure 108. Schematic diagram of Doppler echo calculation of Q p/Qs ratio. Q p is calculatedfrom transpulmonic SV using PA diameter measured at the site of Doppler sample position
and the VTI of the PA flow. A circular CSA is assumed. Similarly Qs is calculated from
LVOT diameter and VTI. (From Otto, 2000)
Q p and Qs are calculated as follows:
Qp = CSA PA x VTI PA
Qs = CSA LVOT x VTI LVOT
Q p = ___CSA PA x VTI PA ___
Q s CSA LVOT x VTI LVOT
This approach is fairly accurate when high quality 2D images are obtained
for precise measurements of the diameters (LVOT and PA) and whenDoppler velocities are recorded at a parallel intercept angle to flow.
D.
Man-made shunts and palliative procedures
First surgical treatment for congenital heart disease was ligation of patent-
ductus arteriosus by Robert Gross in 1938. Subsequently in 1944 successfulrepair of coarctation of aorta was performed by Clarence Crafoord. First
palliative procedure was the creation of arterial to pulmonary shunt in patient
with tetralogy of Fallot by Alfred Blalock in 1944 (Blalock-Taussig shunt).
Since the early days of surgical treatment for congenital heart disease many
b. Percutaneous transluminal septal myocardial ablation (PTSMA)
PTSMA using alcohol induced septal branch occlusion aims to
directly reduce the hypertrophied interventricular septum with a
subsequent expansion of LVOT and a reduction in LVOT gradient.
This is achieved by infarction of the area supplied by the occludedseptal branch.
Current indications are presence of a dynamic LVOT gradient (>30mmHg at rest and >100 mmHg with provocation), and
symptomatic patients (NYHA >III) despite medical therapy.
Patients who have had a previous myectomy or DDD pacing but
continue to have symptomatic disease may also be treated withPTSMA.
After determination of gradients by conventional cardiac
catheterization techniques, coronary angiography is done. Leftcoronary angiography identifies the septal branches (best view is
LAO with caudocranial angulation). The first septal perforator isusually the target for PTSMA. Some centers use myocardialcontrast echocardiography (after selective contrast injections into
septal branches) to identify the target septal branch. After
identification of the target septal branch, up to 5 mls of alcohol is
administered selectively in 1 ml aliquots. After final angiographicdemonstration of septal branch occlusion (Figure 111),
hemodynamic measurements are repeated and new gradient
The degree of accompanying MR can also be assessed usingcolor and other Doppler modalities. The MR jet in this setting is
often directed posterolaterally, and occurs after the onset of
LVOT obstruction. Because of its position the MR jet may beconfused with the LVOT velocity during Doppler interrogation.
The duration of flow, color flow assessment, and configuration
of the Doppler spectral profile helps differentiate the two (Figure115). The rising slope of the MR jet in midsystole is usually
perpendicular to the baseline, compared to a curvilinear profile inthe LVOT jet.
Figure 115. CW Doppler
spectra from LVOT
obstruction and MR jetobtained from the apex.
MR in HCM usually
begins at midsystole when
there is SAM of anteriorMV leaflet, therefore the
Doppler spectrum of MR
may resemble that of
LVOT. However, the
rising slope in midsystoleis usually perpendicular to
the baseline in MR,
whereas it is curvilinear in LVOT signal. Furthermore, the MR velocity signal extends beyondejection. Also the MR velocity will always be higher than the LVOT jet velocity (From Oh,
During rest normal coronary blood flow is approximately 60-90 ml/min per 100 g of
myocardium. It can be affected metabolic, autonomic, and mechanical factors.
Metabolic factors include adenosine, NO, endothelin, and prostaglandins. Adenosine isthe most important factor and is produced by breakdown of high energy phosphates
(ATP), and accumulate during ischemia.Changes in the coronary blood flow with either sympathetic or parasympathetic
stimulation are due predominantly to the accompanying changes in the loading conditions
and contractility. On the other hand mechanical factors have a major effect on thecoronary blood flow. During myocardial contraction, intramyocardial pressure increases,
causing compression of small blood vessels and reduction of coronary blood flow. The
result is a predominant diastolic blood flow pattern (Figure 117). In the left coronary
artery, approximately 60% of blood flow occurs during diastole. In the proximal RCAthe situation is opposite. There is much less vessel compression during low-pressure RV
contraction, with the result that there is much less reduction in blood flow during systole.The blood flow in proximal RCA duringsystole is nearly equal to that during
diastole. In the distal RCA (beyond RV
marginal branch), diastolic flow predominates.
Figure 117. Flow-velocity measurements obtained
in the left main coronary artery (LM) and the
proximal segments of left anterior descending (LAD),left circumflex (CX), and right coronary arteries
(RCA) of a normal patient (From Topol, 1999)
Coronary blood flow is closely correlated with the diastolic pressure-time index (PTI).
PTI = (DBP ς – LVEDP ς ) x t D
Where DBP ς is the average diastolic blood pressure, LVEDP ς is the average LV end-
diastolic pressure, and t D is the average time duration in diastole. The PTI can be altered by changes in aortic diastolic pressure, LV diastolic pressure, and length in diastole (ie
HR). Hence systemic hypotension, increased LVEDP, and tachycardia decrease coronary
blood flow.
With physical or mental stress, the metabolic demands of the myocardium increase andcoronary blood flow must increase to increases MVO2. This increase occurs as a result of
dilatation of resistance vessels. When the resistance vessels are dilated maximally,
coronary blood flow can not be increased further without an increase in aortic pressure.
Table 43. Coronary flow reserves in angiographically normal arteries
LAD RCA CX
CFR 2.68 2.81 2.39
Table 43 shows the coronary flow reserves in normal subjects. The average CFR appears
to be 2.5 for normal arteries, and there does not seem to be a difference between the three
main coronary arteries.
The maximal myocardial blood flow in the presence of stenosis is reduced relative to theexpected normal flow in the absence of a stenosis and can be expressed as a fraction of its
normal expected value, if there was no lesion. This value called the fractional flowreserve (FFR MYO) can be derived from pressure data. The proposed equations have been
derived from theoretical models of coronary circulation and have been tested in
experimental models satisfactorily. During maximal hyperemia (with adenosine),coronary resistance is at the lowest level and remains constant, so that the flow is directly
related to the measured pressure gradient. The total myocardial blood flow (Q) in a n
area de-served by a coronary artery with a stenosis is the sum of the flow through thestenosis (Qs) and the collateral flow (Qc). The FFR MYO is the ratio of the measured flow
(Q) over the maximal flow that should be present without any stenosis (Q N
):
FFR MYO = Q/Q N
= (P D – P V )/R
(P A – P V )/R
PA = mean arterial pressure; PV = mean venous pressure; PD = mean pressure distal tothe stenosis, and R = the resistance of the myocardial vascular bed.
the proximal LAD artery. The diastolic tosystolic velocity ratio (DSVR) is
automatically calculated and displayed. The
comparison between diastolic and systoliccomponents (Bottom panel) can be based on
peak velocities in diastole and systole (PVd
and PVs) or, more correctly, on the flowintegrals (DVi/SVi). (from Topol, 1999)
Simplifying this equation further we get:
FFR MYO = (P D – P V ) = 1 – _ ∆ P ~ = P D Assuming a low and constant P V
(P A – P V ) (P A – P V ) P A
For a normal vessel FFR MYO = 100%. This is a lesion specific index independent of
microcirculation, HR, and other hemodynamic variables, and it can be applied tomultivessel disease. Fractional collateral flow reserve (FFR COLL) and fractional coronary
flow reserve (FFR COR ) are calculated with similar equations as follows:
FFRCOR = 1 – ∆ P_
(P A – P W )
FFRCOLL = FFR MYO – FFRCOR
With PW = the coronary wedge pressure measured distally when PTCA balloon is inflated