Pathology CVS Ischemic heart disease. Title : Done by ...

YSTEMICISTS

Pathology CVS

Title : Ischemic heart disease.

Done by: Farah Al-Fraihat .

A man may die, nations may rise and fall ..But an idea lives on

Ischemic heart disease

IHD is synonymous with coronary artery disease (CAD) ,

obstructive atherosclerotic more than 90% of cases due to

: , other vascular disease

- Increased demand (e.g., with increased heart rate or

hypertension)

- Diminished blood volume (e.g., with hypotension or shock)

- Diminished oxygenation (e.g., due to pneumonia or CHF)

- Diminished oxygen-carrying capacity (e.g., due to anemia

or carbon monoxide poisoning).

Clinically :

Ischemia induces pain but is insufficient to cause myocyte death .

Angina pectoris

Ischemia sufficient to cause cardiomyocyte death .

Acute MI

Progressive cardiac decompensation after acute MI , or secondary to accumulated small ischemic insults , precipitates mechanical pump failure .

Chronic IHD with CHF

Lethal arrhythmia , After MI Sudden cardiac death Catastrophic manifestations of unstable angina , acute MI and SCD .

Acute coronary syndrome

Pathogenesis : Inadequate coronary perfusion relative to

myocardial demand.

- If obstruction occludes more than 70% of a lumen: stable

angina.

- If occludes 90% or more of vascular lumen: unstable

angina.

- Slow rate atherosclerosis, over years : collateral perfusion

can subsequently protect against MI even if the vessel

eventually becomes completely occluded.

- Acute coronary blockage: no time for collateral flow to

develop and infarction results

* Angina Pectoris*

Intermittent chest pain , Ischemia-induced release of

adenosine, bradykinin, and other molecules that stimulate

the autonomic afferents.

IMPORTANTTYPES :

Episodic chest pain associated : Typical or Stable angina) 1

with particular levels of exertion , Crushing or squeezing

substernal sensation, that can radiate down the left arm or

to the left jaw (referred pain), Pain relieved by rest

(reducing demand) or by drugs such as nitroglycerin

(vasodilator) .

Unstable angina ( crescendo ) 2

Increasingly : angina )

frequent pain, precipitated by

progressively less exertion or even occurring at rest ,

Associated with plaque disruption and superimposed

thrombosis, and/or vasospasm .

Caused by , Occurs at rest: Prinzmetal or variant angina) 3

coronary artery spasm , Completely normal vessel can be

affected , Responds to vasodilators such as nitroglycerin and

calcium channel blockers.

* Myocardial infarction (MI )*

Heart attack , necrosis of heart muscle due to ischemia , any

age ( rises with increasing age and with increasing

atherosclerotic risk factors ) , Vast majority of MIs are

caused by acute coronary artery thrombosis , Preexisting

atherosclerotic plaque serves as the nidus for thrombus

generation , 10% of MIs : occurs in the absence of occlusive

atherosclerosis, Embolization from mural thrombi .

Myocardial response to Ischemia :

Within seconds of vascular obstruction : aerobic glycolysis

ceases --> Drop in ATP --> accumulation of lactic acid in

cardiac myocytes .

Within a minute of onset ischemia : RAPID loss of

contractility .

within few minutes : myofibrillar relaxation , glyogen

depletion , cell swelling .

all of above are reversible .

Severe ischemia lasting 20-40 minutes ( irreversible damage

and coagulative necrosis .

If myocardial blood flow is restored before irreversible

injury occurs, cell viability can be preserved , This is the

rationale for early diagnosis and prompt intervention by

thrombolysis or angioplasty to salvage myocardium .

Irreversible : occur in the

subendocardial zone ( last area

to receive blood delivered by the

epicardial vessels , Exposed to

relatively high intramural

pressures, which act to impede

the inflow of blood.

With more prolonged ischemia, a

wave front of cell death moves,

with the infarct usually achieving

its full extent within 3 to 6 hours.

Patterns :

The location, size, and morphologic features of an acute MI

depend:

- The size and distribution of the involved vessel

- The rate of development and the duration of the occlusion

- Metabolic demands of the myocardium

- Extent of collateral supply .

Involve the full Transmural infarctions :. 1

thickness of the ventricle , ST segment

elevations on ECG .

: limited to the Subendocardial infarctions . 2

inner third of myocardium , NON- ST elevation

infarcts .

Vessels involved in MI :

- 40% to 50% of all MI: proximal left anterior descending

(LAD) artery occlusion

Infarction of the anterior wall of the LV, the anterior two

thirds of the ventricular septum, and most of the heart apex

- 30% to 40%: Proximal right coronary artery (RCA)

Affects much of the RV

- 15% to 20% : proximal left circumflex (LCX) artery

Infarction of the lateral LV

Morphology : ( Depend on age of the injury )

Grossly : Infarcts more than 3 hours old can be visualized by

, a triphenyltetrazolium chlorideexposing myocardium to

substrate for lactate dehydrogenase , this enzyme is

depleted in the area of ischemic necrosis and the infracted

area is unstained ( pale ) .

12 - 24 hours after MI: red-blue discoloration caused by

stagnated, trapped blood , then infarcts become soft ,

yellow-tan areas .

10 - 14 days: infarcts are rimmed by hyperemic (highly

vascularized) granulation tissue.

Over the succeeding weeks: fibrous scar

Microscopic : - Coagulative necrosis : 4-12 hours of

infarction ( wavy fibers ) , - acute inflammation : 1-3 Days

after MI , - Macrophages : 4-7 Days after MI , - infracted

zone replaced by granulation tissue : 1-2 weeks after MI ,

- Scarring advanced by the end of sixth week , Once an MI

is completely healed, it is impossible to distinguish its age:

Whether present for 8 weeks or 10 years, fibrous scars look

the same.

Clinically : severe crushing substernal chest pain that can

radiate to the neck , jaw , epigastrium or left arm , typically

lasts several minutes to hours and not relieved by

nitroglycerin or rest .

( common in DM and elderly ) % of MIs15-silent infarcts : 10

The pulse generally is rapid and weak, and patients are

often diaphoretic (sweaty) and nauseous .

With massive MIs (involving more than 40% of the left

ventricle): cardiogenic shock develops.

Electrocardiographic abnormalities : Q waves, ST segment

changes, and T wave inversions , Arrhythmias .

: Complications

- hospital death of MI : 7%

- out of hospital mortality is worse : - A third of persons with

(STEMIs) will die, usually of an arrhythmia within an hour of

symptom onset, before they receive appropriate medical

attention .

1 ) Contractile dysfunction

2 ) Papillary muscle dysfunction

3 ) myocardial rupture :

- 1-5% of MIs

- Within 3- 7 days after infarction

- Left ventricular free wall rupture is most common

- Ventricular septal rupture creates a VSD with left-to-right

shunting

- Papillary muscle rupture leads to severe mitral

regurgitation .

4 ) Pericarditis : fibrinous or fibrinohemorrhagic ( Dressler

syndrome ) 2-3 days after MI .

5 ) Chamber dilation .

6 ) Mural thrombus .

7 ) Ventricular aneurysm .

8 ) Progressive late heart failure .

9 ) Arrhythmias : Heart block of variable degree (including

asystole) , Bradycardia , Supraventricular tachyarrhythmias ,

Ventricular premature contractions , Ventricular tachycardia

, Ventricular fibrillation .

(ischemic Chronic ischemic heart disease*

)*cardiomyopathy

Progressive heart failure secondary to ischemic

myocardial damage , history of previous MI .

appears when compensatory mechanisms (e.g.,

hypertrophy) of residual viable myocardium begin to fail.

left ventricular dilation and hypertrophy, often with

discrete areas of gray-white scarring from previous healed

infarcts.

* deathSudden cardiac *

Sudden death, typically due to sustained ventricular

arrhythmias in individuals who have underlying structural

heart disease which may or may not have been symptomatic

in the past.

Coronary artery disease is the leading cause of death,

responsible for 80% to 90% of cases

SCD often is the first manifestation of IHD.

The ultimate mechanism of SCD most often is a lethal

arrhythmia (e.g., asystole or ventricular fibrillation).

-Hereditary (channelo atherosclerotic causes of SCD :-Non

pathies) or acquired abnormalities of the cardiac conduction

system, Congenital coronary arterial abnormalities , Mitral

valve prolapse , Myocarditis or sarcoidosis , Dilated or

hypertrophic cardiomyopathy ,Pulmonary hypertension.

* Hypertensive heart disease*

Major cardiac complications of hypertension, result from

pressure overload .

Myocyte hypertrophy is an adaptive response, but there

are limits .

Persistent hypertension eventually can culminate in

dysfunction, cardiac dilation, CHF, and even sudden death.

Systemic hypertension: affects the left side of the heart .

((1) left ventricular hypertrophy in the absence of other

cardiovascular pathology (e.g., valvular stenosis)

(2) a history or pathologic evidence of hypertension .. )

morphology :

left ventricular hypertrophy .

- No ventricular dilation until very late in the process

- Heart weight can exceed 500 g (normal, 320 - 360 g)

- Left ventricular wall thickness can exceed 2.0 cm (normal,

1.2 - 1.4 cm).

Microscopically :

- Transverse diameter of myocytes is increased

- Prominent nuclear enlargement and hyperchromasia

- Intercellular fibrosis .

Clinically :

- Compensated hypertensive heart disease typically is

asymptomatic

- The disease can comes to attention with the onset of atrial

fibrillation and/or CHF .

Pulmonary hypertension : can cause right-sided

hypertensive changes called cor pulmonale.

- Right ventricular hypertrophy and dilation, frequently

accompanied by right heart failure

- Cause of chronic cor pulmonale:

1- Primary disorders of the lung parenchyma

2- Disorder of pulmonary vasculature

- Acute : pulmonary embolism

Morphology :

- Acute cor pulmonale:

Right ventricle usually shows only dilation

If an embolism causes sudden death, the heart may even be

of normal size.

- Chronic cor pulmonale:

Right ventricular hypertrophy

When ventricular failure develops, the right ventricle and

atrium are dilated

.. THE END