1 Heart Journal I r a n i a n IHJ According to the ruling of the Medical Sciences Publications Commission No. 14313-80/10/1 and 36914-85/2/10 signed by the Minister of Health and Medical Education and the Head of the Medical Sciences Publications Commission of the Islamic Republic of Iran, this journal has been granted accreditation as a scientific-research journal. This Journal is indexed in the Scientific Information Database (WWW.SID.IR ) and IMEMR and Index COPERNICUS, SCOPUS, CINAHL and Google Scholar. ISSN: 1735-7306
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ISSN: 1735-7306journal.iha.org.ir/Files/Journal/issue_6.pdf · 1 Department of Interventional Cardiology, Rajaie cardiovascular, Medical and Research center, Iran University of Medical
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1
Heart Jo
urn
al
I r
a n
i a n
IH
J
According to the ruling of the Medical Sciences Publications Commission No. 14313-80/10/1 and 36914-85/2/10 signed by the Minister of Health and Medical Education and the Head of the Medical Sciences Publications Commission of the Islamic Republic of Iran, this journal has been granted accreditation as a scientific-research journal. This Journal is indexed in the Scientific Information Database (WWW.SID.IR) and IMEMR and Index COPERNICUS, SCOPUS, CINAHL and Google Scholar.
1 Department of Interventional Cardiology, Rajaie cardiovascular, Medical and Research center, Iran University of Medical Sciences, Tehran, I.R.Iran. 2 Department of Education Rajaie cardiovascular, Medical and Research center, Iran University of Medical Sciences, Tehran, I.R.Iran.
Corresponding Author: Hamid Reza Sanati, MD; Rajaie cardiovascular, Medical and Research center, Iran University of Medical Sciences, Tehran, I.R.Iran.
Conclusions: None of the echocardiographic diastolic function parameters examined in this study
were found to be suitable for cardiac surveillance in transfusion-dependent patients affected
by thalassemia major. Longitudinal studies are needed to evaluate the utility of
echocardiographic and MRI parameters to predict cardiac events. At the moment, we cannot
recommend the replacement of cardiac MR and T2* measurements, indicating myocardial
iron loading, by Doppler echocardiography in patients with a normal systolic function.
(Iranian Heart Journal 2016; 17(3):12-17)
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Association between Diastolic Function Parameters and MRI T2* Measurements with Major Thalassemia Rajabipour F, et al.
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Keywords: Diastolic dysfunction Thalassemia major Hemoglobin disorders Iron overload
1 Pediatric Department of Baharlou Hospital, Tehran University of Medical Sciences, Tehran, I. R. Iran. 2 Department of Cardiology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, I.R. Iran.
*Corresponding Author: Atoosa Mostafavi, MD; Shariati Hospital, Tehran University of Medical Sciences, Tehran, I.R. Iran.
1 Department of Cardiology, Madani Hospital, Lorestan University of Medical Sciences, Khorramabad, I.R. Iran. 2 Razi Herbal Medicines Research Center and Department of Physiology and Pharmacology, Lorestan University of Medical Sciences, Khorramabad,
I.R. Iran.
Corresponding Author: Mehrdad Namdari, MD; Madani Hospital, Lorestan University of Medical Sciences, Khorramabad, I.R. Iran.
Oxygen pre-Exposure and Coronary Angioplasty Mohammadi A, et al.
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eart ischemia/reperfusion (I/R) not only
occurs after myocardial infarction but
also some degree of I/R may occur as a
result of elective procedures such as cardiac
surgery and coronary angioplasty.1 Ischemic
preconditioning (IPC) was originally
introduced by Murry et al.,2 who reported that
short periods of cardiac I/R in dogs increased
myocardial tolerance to more prolonged
subsequent ischemia and the consequent
reperfusion. Preconditioning consists of 2
windows of protection. The 1st window
begins immediately and the 2nd one
commences about 12 hours after ischemia.3
Many agents have been proven to induce
preconditioning or to be involved in IPC
mechanism; these include bradykinin,
adenosine, opioids, and reactive oxygen
species (ROS).4-7
Although excess amounts of
ROS produced during the reperfusion period
are involved in myocardial injury, a small
amount of ROS released during a short period
of ischemia or short term hyperoxic pre-
exposure can induce cardiac preconditioning,
while the cardioprotective effects of IPC are
canceled out by free radical scavengers.7-9
Additionally, many pharmacological agents
that generate ROS are able to reduce the
myocardial infarct size.8-10
Several animal
studies have shown that normobaric oxygen
pretreatment could reduce heart I/R injury.8-12
Moreover, it has been demonstrated in human
studies that hyperoxic pre-exposure improves
renal function in patients undergoing kidney
transplantation and that the administration of
hyperbaric oxygen improves myocardial
function after coronary artery bypass grafting
surgery (CABG).13,14
Percutaneous
transluminal coronary angioplasty (PTCA) is
a clinical setting with inevitable periods of I/R
and provides an excellent situation to assess
the effects of different possible protective
protocols in the human myocardium.15
Based
on previous animal studies on the effects of
oxygen pre-exposure on reducing cardiac I/R
injury and the role of ROS in the mechanism
of IPC, the present study for the 1st time
aimed to assess the effects of hyperoxic
preconditioning on heart injury biomarkers
and the chest pain score of patients
undergoing coronary angioplasty. It should be
noted that short-term hyperoxic pre-exposure
is a benign protocol, which leads only to a
sub-lethal increase in ROS production and
works as a possible inducer of cellular
endogenous defense mechanisms.
METHODS
Study Population
In this randomized clinical trial, 32 patients—
referred for elective PTCA—were randomly
divided into the oxygen group and the control
group. The study was carried out in Shahid
Madani Heart Hospital in Khorramabad, Iran,
between February 2013 and December 2014.
The study protocol was approved by the
Medical Ethics Research Committee of
Lorestan University of Medical Sciences.
First, the method of study was explained to
each patient and then a written informed
consent was obtained from each patient. All
the patients had stable angina when
undergoing coronary angioplasty. Patients
were included if they had isolated obstructive
lesions in at least 1 coronary artery branch
with ≥70% reductions in the luminal
diameter. Patients who had chronic
obstructive lung disease, exposure to oxygen
3 days prior to the commencement of PTCA,
episode(s) of chest pain 48 hours before
PTCA, Prinzmetal angina, or upper
respiratory infection were excluded from the
study. Both the control group and the oxygen
group consisted of 16 patients (10 men and 6
women, mean age =53±11 y and 53±9 y,
respectively). The mean ejection fraction
was 52±5% in the control group and
49±1% in the oxygen group. The last
episode of chest pain in all the patients
occurred 48 hours prior to PTCA.
Study Protocol
In this single-blinded randomized clinical
trial, each patient in the intervention (oxygen)
group was exposed to normobaric oxygen
twice (about 70% O2 in the inspired air) via a
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Oxygen pre-Exposure and Coronary Angioplasty Mohammadi A, et al.
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non-rebreathing mask at 12 and 2 hours
before PTCA. Each episode of oxygen
pretreatment lasted for 1 hour. One hour after
the last period of oxygen pre-exposure,
diagnostic angiography was performed and a
nonionic contrast agent (Visipaque GE,
Healthcare Ireland, osmolality: 320 mg/mL)
was administrated intravenously to each
patient. After diagnostic angiography, the
patients who had isolated obstructive lesions
in at least 1 coronary artery branch with ≥70%
reductions in the luminal diameter underwent
coronary angioplasty. The PTCA procedure
was performed via a routine technique using
the femoral approach. After prep and drape,
heparin (2000 IU) was administered
intravenously before coronary angioplasty.
Subsequently, the balloon was positioned
across the lesion and 1 session of balloon
inflation was done for 20 seconds. The stent
was thereafter inserted into the narrowed
coronary artery, and then there was a 2-
minute period of reperfusion. The balloon
inflation pressure ranged from 11 to 14 atm.
At the end of the procedure, the angioplasty
balloon was deflated and was withdrawn from
the stenotic site; and after 2 minutes, the
reperfusion study protocol was finished.
Similar procedures were carried out for the
control group patients, except that they were
not exposed to normobaric oxygen
pretreatment with oxygen masks. The
cardiologist who did the angiography and
angioplasty procedures was not aware of the
patients’ group and did not know whether the
patients had been subjected to oxygen
pretreatment or not.
Laboratory Measurements
Venous blood samples were obtained from
each patient before and 12 hours following
the PTCA procedure to measure troponin I
and CKMB levels and C-reactive protein
(CRP) as biomarkers of cardiac cell injury.
Troponin I and CKMB activities were
measured with standard kits (RAMP
Vancouver, Canada) using an auto-analyzer
and expressed as nanograms per milliliter
(ng/mL). Also, the level of highly sensitive C-
reactive protein (hs-CRP) was determined
with a standard kit (Enison, Iran) and
expressed as positive or negative. The normal
values of CKMB and cTnI were considered to
be ≤5 ng/mL and ≤0.1 ng/mL, respectively.
Assessment of Chest Pain At the end of balloon inflation, the severity of
chest pain was assessed with visual analog
scores by a nurse, who had no knowledge of
the patients’ group. The patients were asked
to indicate the severity of chest pain on a
scale of 0 (no pain) to 10 (severe pain).
Statistical Analysis
The biomarker data are expressed as means ±
SDs. All the chest pain score data are shown
in the relevant figure, and the median has also
been presented. The data were analyzed with
SPSS, version 21, and the comparisons
between the groups were analyzed with the
Mann–Whitney test and the changes within
the groups were analyzed with the Wilcoxon
t-test. The ratio of cases with positive CRP
results was compared between the 2 groups
using the Fisher exact test. A P value <0.05
was considered statistically significant.
RESULTS
The demographic characteristics of the
control and oxygen groups are summarized in
Table 1. There were no statistically significant
differences between the 2 groups in terms of
the determined parameters. Angioplasty was
successfully performed in all the patients.
Chest Pain
The average pain score during balloon
inflation in the oxygen group was lower than
that in the control group (2.8±1.2 vs.
4.11±1.21; P=0.008). The chest pain score
data are depicted in Figure 1.
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Figure 1. Chest pain score at the end of balloon inflation in the control and oxygen groups. The chest pain score was higher in the control group than in the oxygen group. The line shows the median in each group. **, P=0.008
Cardiac Biomarkers
Troponin level: The troponin level changed
from 0.001±0.0001 ng/mL to 0.039±0.062
ng/mL in the oxygen group and from
0.0055±0.012 ng/mL to 0.061±0.21 ng/mL in
the control group. The changes were not
significant in either group (P=0.068 and
P=0.28, respectively). There were no
significant differences in the values of
troponin I between the 2 groups before and
after angioplasty (P=0.23) (Table 2).
CKMB level: The CKMB level changed from
1.44±1.18 ng/mL to 3.04±2.56 ng/mL in the
oxygen group and from 1.8±1.16 ng/mL to
3.78±3.61 ng/mL in the control group. The
changes were significant in both groups
(P=0.034 and P=0.017, respectively). There
were no significant differences in the values
of CKMB between the 2 groups before and
also after angioplasty (P=0.47) (Table 3).
CRP value: According to the Fisher exact
test, there was no significant difference in
terms of positivity between the 2 groups
(P=0.57) (Table 4).
Table 1. Demographic and clinical characteristics of the patients in the 2 groups
Variable Control Group
(n=16) Oxygen Group
(n=16)
Age (y) (mean± SD) 53±11 53±9
Gender, M/F 10/6 10/6
Hypertension, n 3 5
Smoking, n 5 5
Diabetes mellitus, n 3 9
Previous CABG , n 0 2
Previous PTCA , n 4 0
Left ventricular ejection fraction, %, (mean± SD) 52%±5 49%±1
Use of Long-acting nitrates, n 5 10
Use of β-blocker agents, n 9 8
Glibenclamide usage, n 3 7
Opioid usage, n 3 2
CABG, Coronary artery bypass graft surgery; PTCA, Percutaneous transluminal coronary angioplasty There were no statistically significant differences between the 2 groups in terms of the determined parameters.
Table 2. Serum troponin values before and after PTCA in the 2 groups
1Department of Biomedical Engineering, Science and Research Branch, Islamic Azad University, Tehran, I.R. Iran. 2 Department of Biomedical Engineering and Physics, Shahid Beheshti University of Medical Sciences, Tehran, I.R. Iran. 3Modares Hospital, Institute of Cardiovascular Research, Shahid Beheshti University of Medical Sciences, Tehran, I.R. Iran.
Corresponding Author: Morteza Darjani; Science and Research Branch, Islamic Azad University, Tehran, I.R. Iran.
Background: We aimed to identify the clinical and echocardiographic factors related to false results
in the exercise tolerance test (ETT).
Methods: The present study included all patients who underwent transthoracic echocardiography
and the ETT, followed by coronary angiography, within 6 months prior to echocardiography
between March 2008 and March 2013. Clinical, 12-lead resting ECG, ETT, transthoracic
echocardiography, and coronary angiography data were extracted. The multivariable logistic
regression analysis was used to investigate the independent predictors of the false results of
the ETT.
Results: Totally, 4057 patients, who underwent transthoracic echocardiography, ETT, and
angiography, were enrolled. From 1132 patients with no significant coronary stenosis on
angiography, 979 (84%) had false-positive results in the ETT and 153 (14%) had true-
negative ETT results. In patients with significant coronary artery disease (CAD), there were
2728 (93%) true-positive and 197 (7%) false-negative ETT results. In our univariate
analysis, the patients with false ETT results were more likely to be female and younger than
the group with true ETT results. In our multivariable model, female gender increased and
right bundle branch block and dilated left ventricular diastolic internal dimension (LVID)
decreased the likelihood of a false-positive result in the ETT. The probability of a false-
negative result in the ETT was increased by resting ECG changes, hemiblocks, and dilated
LVID.
Conclusions: The diagnostic value of the ETT in patients with suspected CAD should be adjusted
according to sex, presence of resting ECG changes, CAD risk factors, and traditional
echocardiographic measurements. A dilated LV increases the risk of false-negative
results and decreases the likelihood of a false-positive result in the ETT. (Iranian Heart
Journal 2016; 17(3):36-45)
Keywords: Exercise tolerance test False positive False negative Echocardiography
1 Department of Cardiology, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, I.R. Iran. 2 Department of Cardiology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, I.R. Iran.
*Corresponding Author: Seyed Abdolhussein Tabatabaei, MD; Shariati Hospital, Tehran University of Medical Sciences, Tehran, I.R. Iran.
Echocardiographic and Clinical Factors Related to False Results of Exercise Tolerance Test Sadeghian H, et al.
37
he predictive power of normal as well
as abnormal exercise tolerance test
(ETT) results can provide us with a
very useful tool in the clinical management of
patients with coronary artery disease (CAD),
not least those with chest pain.1,2
As the ETT
results are considered a decisive factor in
performing angiography in patients with
suspected CAD,3 the false-positive results of
the ETT can impose invasive procedures on
patients with no obstruction in the coronary
artery and lead to inattention to patients with
false-negative ETT results. The
accompanying clinical and paraclinical factors
that increase the likelihood of false ETT
results require further evaluation with other
subsequent stress tests for a more precise
discrimination of patients in need of
angiography. In the previously published
studies, the accuracy of the ETT varies
broadly due to different factors such as
heterogeneity in the population
characteristics, methodological variations,
technical factors, data interpretation methods,
and drug consumption.4,5
The sensitivity, specificity, predictive value,
and accuracy of the ETT have been
accentuated in previous publications
abundantly.1,3,6,7
Nevertheless, to our
knowledge, there is no study to feed all
clinical and echocardiographic variations into
analysis as a whole. The purpose of the
present study was to identify the clinical and
echocardiographic factors that are strongly in
relation with false-positive ETT results on
normal angiograms and patients with CAD.
METHODS
From March 2008 up to March 2013, this
retrospective study recruited 4057 patients,
who underwent transthoracic
echocardiography, ETT, and angiography
within 6 months prior to echocardiography.
All the inclusion and exclusion criteria to
perform the ETT were in accordance with the
current guidelines.8
Patients with the Wolff–
Parkinson–White syndrome or a left
ventricular hypertrophy (LVH) pattern on
ECG or those using digoxin were excluded.
The study protocol was approved by our
institutional review board. All the patients
signed a consent form prior to angiography,
allowing the investigators of the hospital to
use their data for research purposes.
The ETT was performed in accordance with
the Bruce protocol—with continuous
monitoring of blood pressure, heart rate, and
12-lead ECG up to 5 minutes into recovery.
Drugs like β-blockers, calcium channel
blockers, and nitrates were discontinued 2
days before the test. From the ECG point of
view, ETTs with ≥1 mm horizontal or
downsloping ST-segment depression 0.08
seconds after the J point were interpreted as
positive. A nondiagnostic test result was
defined as an exercise ECG without ischemic
changes at a peak heart rate > 85% of the age-
predicted maximum rate.8 Patients with
nondiagnostic test results were excluded from
the present study.
Additionally, the patients’ clinical data—
comprising age, sex, symptoms, family
history of CAD (first-degree relatives with
CAD at age <55 y), current smoking (in the
past month), history of dyslipidemia (total
cholesterol >200 mg/dL or LDL ≥130 mg/dL
or HDL <30 mg/dL or TG >150 mg/dL or
taking lipid-lowering agents), hypertension
(repeated blood pressure >140/90 mm Hg or
under treatment with antihypertensive drugs),
and diabetes (repeated fasting glucose >126
mg/dL or controlled by diet, tablet, or
insulin)—were recorded systematically by
physicians at the time of clinic visit. In
sequence, paraclinical data such as 12-lead
resting ECG, ETT, and transthoracic
echocardiography were completed and
merged with the clinical data if any or all of
them were requested. 2D transthoracic
echocardiography was conducted using a
Vingmed-General Electric, Horten, Norway
machine. The patients were asked to lie in the
left lateral decubitus position, and
T
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echocardiography was conducted with a 3.5-
MHZ phased-array transducer. Measurements
were carried out in accordance with the
guidelines of the American Society of
Echocardiography.9 Finally, the databank was
completed with the results of coronary
angiography recorded by the treating
cardiologist. In the negative ETT cases,
eligibility for angiography was based on the
clinician’s assessment and the results of other
stress tests.
Within all the variables in the clinical
component of the database, we extracted age,
sex, family history of CAD, current smoking,
history of dyslipidemia, hypertension, and
diabetes. Additionally, we obtained ST-
segment or T-wave changes, existence of Q
wave, and conduction disorders such as right
bundle branch block, left bundle branch
block, and hemiblocks from the recorded
resting 12-lead ECG variables.
Statistical Analysis
The data are presented as means ± SDs for the
continuous variables and frequencies (%) for
the categorical variables. The Pearson χ2
test
was used to compare the categorical variables,
and the Student t-test or the Mann–Whitney
test was employed to compare the continuous
variables between the study groups, as
required. Multivariable logistic regression
models with the backward selection method
for the factors associated with false, false-
positive, and false-negative ETT results were
constructed, and the associations between the
independent predictors and false, false-
positive, and false-negative ETT results in the
final models were expressed as ORs with 95%
CIs. Model calibration was estimated using
the Hosmer–Lemeshow goodness-of-fit
statistic. (A higher P implies that the model
fits the observed data better.) The variables
were incorporated into the multivariable
model if there was a P ≤ 0.15 in the univariate
analysis. A P <0.05 was considered
statistically significant. The statistical
analyses were conducted using SPSS, version
15 for Windows.
RESULTS
Of 45330 consecutive patients referred for
coronary angiography between March 2008
and March 2013, a total of 4057 patients met
our inclusion criteria and were enrolled in our
study. The mean age of the patients was 57.39
± 9.36 years. Sex distribution was 72% male
and 28% female. Based on the angiographic
results, 1132 (28%) patients had no or <50%
stenosis in coronary arteries and 2925 (72%)
had ≥50% stenosis of any coronary artery.
From the 4057 patients, who underwent the
ETT, 979 (24.1%) had false-positive, 2728
(67.2%) had true-positive, 197 (4.9%) had
false-negative, and 153 (3.8%) had true-
negative results.
Of the 1132 patients, who had no significant
coronary stenosis on angiography, 979
(86.5%) patients had false-positive results in
the ETT and 153 (13.5%) had true-negative
ETT results. In the CAD group, there were
2728 (93%) true-positive and 197 (7%) false-
negative ETT results. In the entire
population—according to the angiographic
results—2881 patients had true results and
1176 had false results in the ETT.
Table 1 depicts the clinical characteristics and
echocardiographic findings of the patients
with false ETT results in comparison to those
of the patients with true ETT results. In the
unadjusted analysis, the patients with false
ETT results were more likely to be female and
younger than those with true ETT results. All
the traditional CAD risk factors—namely
diabetes mellitus, smoking, hypertension,
dyslipidemia, and family history of CAD—
had a higher prevalence in the patients with
true ETT results. Moreover, the patients with
true ETT results had a significantly higher
frequency of resting ECG changes than those
with false ETT results.
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Table 1. Baseline clinical characteristics and echocardiographic findings of the total study population according to the ETT results
True Results
(n=2881)
False Results
(n=1176) P
Female 636(22.1) 489(41.6) <0.001
Age, mean ± SD 58.4±9.19 54.93±9.32 <0.001
BMI 27.39±3.92 27.91±4.12 <0.001
BSA 1.84±0.177 1.84±0.181 0.988
Symptomatic 2739(95.4) 1119(95.5) 0.953
Risk Factors
Family history of CAD 663(23.3) 239(20.7) 0.075
Hypertension 1248(43.5) 473(40.3) 0.061
Dyslipidemia 2333(81.4) 899(76.9) 0.001
Current smoker 599(20.8) 197(16.8) 0.003
Diabetes mellitus 821(28.5) 218(18.6) <0.001
ECG
Resting ECG changes 1146(40) 356(30.5) <0.001
Right bundle branch block 37(1.3) 19(1.6) 0.409
Left bundle branch block 31(1.1) 7(0.6) 0.156
Hemiblock 82(2.9) 35(3) 0.816
Echocardiography
Abnormal LA sizea 708(24.7) 283(24.1) 0.722
Abnormal LVIDdb 141(4.9) 77(6.6) 0.035
Abnormal IVSTc 1489(52) 589(50.4) 0.344
Abnormal PWTd 1426(49.9) 577(49.4) 0.753
LVMI, g/m2
97.45±27.49 92.69±27.36 <0.001
Left ventricular hypertrophye 768(27.3) 263(22.9) 0.004
Moderate or severe MR 128(4.4) 48(4.1) 0.607
Moderate or severe AI 48(1.7) 19(1.6) 0.909
Moderate or severe TR 59(2) 34(2.9) 0.105
*Categorical variables are presented as frequencies (percentages) and the continuous variables as means ± SDs. ETT, Exercise tolerance test; BMI, Body mass index; BSA, Body surface area; CAD, Coronary artery disease; LA, Left atrium; LVIDd, Left ventricular internal diastolic diameter; IVST, Interventricular septal thickness; PWT, Posterior wall thickness; LVMI, Left ventricular mass index (0.8*[(LVIDd + PWT + IVST)
Aortic insufficiency; TR, Tricuspid regurgitation a: male >4 cm, female >3.8 cm; b: male >5.9 cm, female >5.3 cm; c: male >1 cm, female >0.9 cm; d: male >1 cm, female >0.9 cm; e: male LVMI >115, female LVMI >95
One important interaction was found between
female gender and diabetes mellitus in
decreasing the likelihood of a false result in
the ETT. Among the conventional
echocardiographic measurements, dilated left
ventricular diastolic internal dimension
(LVID) was significantly more common in
the patients with false ETT results. The mean
of the left ventricular mass index (LVMI) in
the group with true ETT results was
significantly higher than that of the group
with false ETT results. Accordingly, left
ventricular hypertrophy (LVH) by
echocardiography was also more prevalent in
the group with true ETT results. In the
multivariate model, the contribution of the
above variables remained statistically
significant in the same pattern (Table 4).
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Table 2. Baseline clinical characteristics and echocardiographic findings of the patients with <50% stenosis on angiography according to the ETT results
True Negative (n=153)
False Positive (n=979)
P
Female 55(35.9)* 450(46) 0.021
Age, y 52.22±10.1 54.66±9.17 0.012
Symptomatic 147(96.1) 926(95) 0.557
BMI, kg/m2
29.22±4.99 27.94±4.15 0.003
BSA, m2
1.91±0.20 1.83±0.18 <0.001
Risk Factors
Family history of CAD 34(23.4) 182(18.9) 0.201
Hypertension 57(37.3) 379(38.8) 0.723
Dyslipidemia 116(76.3) 736(75.6) 0.857
Current smoker 20(13.1) 144(14.7) 0.593
Diabetes mellitus 24(15.7) 161(16.5) 0.809
ECG
Resting ECG changes 48(31.4) 225(23.1) 0.028
Right bundle branch block 9(5.9) 14(1.4) 0.001
Left bundle branch block 2(1.3) 7(0.7) 0.455
Hemiblock 5(3.3) 24(2.5) 0.562
Echocardiography
Abnormal LA sizea 37(24.2) 237(24.3) 0.984
Abnormal LVIDdb 17(11.1) 52(5.3) 0.005
Abnormal IVSTc 76(49.7) 489(50.3) 0.893
Abnormal PWTd 69(45.4) 491(50.5) 0.24
LVMI, g/m2
94.79±34.1 90.95±26.35 0.279
Left ventricular hypertrophye 38(25.5) 212(22.1) 0.36
Moderate or severe MR 10(6.5) 37(3.8) 0.117
Moderate or severe AI 5(3.3) 15(1.5) 0.139
Moderate or severe TR 6(3.9) 30(3.1) 0.575
*Categorical variables are presented as frequencies (percentages) and the continuous variables as means ± SDs. ETT, Exercise tolerance test; BMI, Body mass index; BSA, Body surface area; LA, Left atrium; LVIDd, Left ventricular internal diastolic diameter; IVST, Interventricular septal thickness; PWT, Posterior wall thickness; LVMI, Left ventricular mass index (0.8*[(LVIDd + PWT + IVST)
a: male >4 cm, female >3.8 cm; b: male >5.9 cm, female >5.3 cm; c: male >1 cm, female >0.9 cm; d: male >1 cm, female >0.9cm; e: male LVMI >115 female LVMI >95
As the clinical and paraclinical conditions that
accompany a false ETT result may differ
between false-positive and false-negative ETT
results, we classified the patients into 2
groups based on their angiographic results:
patients with no stenosis or stenosis <50% on
the angiogram and patients with ≥50%
occlusion of any coronary artery. The results
of the univariate comparison between the
true-negative and false-positive ETT results
and true-positive and false-negative results of
the ETT in terms of clinical characteristics,
ECG findings, and echocardiographic
measurements are exhibited in Table 2 and
Table 3—respectively. There were
statistically significant differences between
the true-negative and false-positive ETT
results in female gender, resting ECG
changes, right bundle branch block, and
dilated LVID. After adjusting, female gender
increased and right bundle branch block and
dilated LVID decreased the likelihood of a
false-positive result in the ETT (Table 5). A
comparison of the true-positive and false-
negative ETT results indicated that the
probability of a false-negative result in the
ETT was increased by resting ECG changes,
hemiblocks, and dilated LVID (Table 6).
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stenosis on angiography according to the ETT results
True Positive
(n=2728)
False Negative
(n=197) P
Female 581(21.3)* 39(19.8) 0.619
Age, mean ± SD 58.74±9.02 56.23±9.98 0.001
Symptomatic 2592(95.4) 193(98) 0.090
BMI 27.30±3.83 27.75±4.00 0.108
BSA 1.84±0.18 1.90±0.18 <0.001
Risk Factors
Family history of coronary artery disease 629(23.3) 57(29.7) 0.045
Hypertension 1191(43.8) 94(47.7) 0.288
Dyslipidemia 2217(81.7) 163(83.2) 0.605
Current smoker 579(21.3) 53(27) 0.059
Diabetes mellitus 797(29.2) 57(28.9) 0.928
ECG
Resting ECG changes 1098(40.4) 131(66.8) 0.001
Right bundle branch block 28(1) 5(2.5) 0.062
Left bundle branch block 29(1.1) 0 0.998
Hemiblock 77(2.8) 11(5.6) 0.033
Echocardiography
Abnormal LA sizea 671(27.7) 46(23.6) 0.727
Abnormal LVIDdb 124(4.6) 25(12.7) <0.001
Abnormal IVSTc 1413(52.2) 100(51) 0.758
Abnormal PWTd 1357(50.2) 86(43.9) 0.087
LVMI, g/m2
97.6±27.08 101.44±30.57 0.276
LVHe 730(27.4) 51(26.7) 0.843
Moderate or severe MR 118(4.3) 11(5.6) 0.408
Moderate or severe AI 43(1.6) 4(2) 0.624
Moderate or severe TR 53(1.9) 4(2) 0.939
*Categorical variables are presented as frequencies (percentages) and the continuous variables as means ± SDs. ETT, Exercise tolerance test; BMI, Body mass index; BSA, Body surface area; LA, Left atrium; LVIDd, Left ventricular internal diastolic diameter; IVST, Interventricular septal thickness; PWT, Posterior wall thickness; LVMI, Left ventricular mass index; LVH, Left ventricular hypertrophy; MR, Mitral regurgitation; AI, Aortic insufficiency; TR, Tricuspid regurgitation a: male >4 cm, female >3.8 cm; b: male >5.9 cm, female >5.3 cm; c: male >1 cm, female >0.9 cm; d: male >1 cm, female >0.9 cm; e: male LVMI >115 female LVMI >95
Table 4. Association between the ETT false results and the clinical characteristics and echocardiographic findings
ETT, Exercise tolerance test; LVH, Left ventricular hypertrophy; LVIDd, Left ventricular internal diastolic diameter a: male LVMI >115 female LVMI >95; b: male >5.9 cm, female >5.3 cm Area under the curve =69.8% (95% CI: 67.9 – 71.6%; P <0.001), P for Hosmer–Lemeshow goodness-of-fit statistic =0.383
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Echocardiographic and Clinical Factors Related to False Results of Exercise Tolerance Test Sadeghian H, et al.
42
Table 5. Association between the ETT false-positive results and the clinical characteristics and echocardiographic findings in the patients with <50% stenosis on angiography
ETT, Exercise tolerance test; LVIDd, Left ventricular internal diastolic diameter a: male >5.9 cm, female >5.3 cm Area under the curve =64.7% (95% CI: 59.8 – 69.5%; P <0.001), P for Hosmer–Lemeshow goodness-of-fit statistic =0.383
Table 6. Association of ETT false negative result with clinical characteristics and echocardiographic findings in patientswith≥50%stenosisinangiography
Total population (n=2925) Univariable OR (95% CI)
p-value multivariable OR (95% CI)
p-value
Age 0.970 (0.954-0.986) <0.001 0.968 (0.952-0.984) <0.001
Echocardiographic and Clinical Factors Related to False Results of Exercise Tolerance Test Sadeghian H, et al.
43
in producing subendocardial current of injury
and ST depression on ECG, may be altered by
those changes and ischemic ST response is
likely to be reduced.23
Previous studies have argued that LVH
increases the probability of false-positive
results in the ETT.24,25
In our study, we did
not obtain this result. It may be argued that in
the previous studies, specific criteria
accounting for the diagnosis of LVH were
based on ECG and not on echocardiography.
As it has been revealed that the sensitivity of
ECG for ECG-defined LVH is only 6.9%,26
ECG is a poor screening test for detecting
LVH compared to echocardiography. To our
knowledge, there is no study to report the role
of echocardiographically defined LVH in the
false-positive results of the ETT. Further
studies are required to confirm our results.
Study Limitations
First and foremost among the limitations of
the present study is its retrospective design. In
addition, eligibility for angiography was
based on the clinician’s assessment in patients
with negative ETT results. Therefore,
coronary angiography was not performed on
all the subjects and the patients with true-
negative ETT results but without angiography
were excluded. Another weakness of note is
that although all the ETT examinations were
done according to the current guidelines of
the ACC/AHA, variables such as the Duke
treadmill score were not included in the
angiography registry—resulting in the
unavailability of such variables for reporting.
Moreover, because of the retrospective nature
of the study, echocardiographic findings
reported by different physicians were drawn
upon—which may have influenced the
results.
CONCLUSIONS
The diagnostic value of the ETT in patients
with suspected CAD should be adjusted
according to sex, presence of resting ECG
changes, CAD risk factors, and traditional
measurements on echocardiography. Based on
clinical, paraclinical, and echocardiographic
variables—other stress tests for the initial
assessment of patients with suspected CAD or
confirmation of the ETT results should be
considered. A dilated LV increases the risk of
false-negative results and decreases the
likelihood of a false-positive result in the
ETT.
REFERENCES
1. Gianrossi R, Detrano R, Mulvihill D,
Lehmann K, Dubach P, Colombo A,
McArthur D, Froelicher V. Exercise-induced
ST depression in the diagnosis of coronary
artery disease: A meta-analysis. Circulation
1989; 80: 87-98.
2. Review.
3. Miller TD, Roger VL, Milavetz JJ,
Hopfenspirger MR, Milavetz DL, Hodge DO,
Gibbons RJ. Assessment of the exercise
electrocardiogram in women versus men using
tomographic myocardial perfusion imaging as
the reference standard. Am JCardiol 2001; 87:
868-873.
4. Detrano R, Gianrossi R, Froelicher V. The
diagnostic accuracy of the exercise
electrocardiogram: a meta-analysis of 22 years
of research. Prog Cardiovasc Dis 1989; 32:
173-206.
5. Kwok Y, Kim C, Grady D, Segal M, Redberg
R. Meta-analysis of exercise testing to detect
coronary artery disease in women. Am J
Cardiol 1999; 83: 660-666.
6. Detrano R, Gianrossi R, Mulvihill D,
Lehmann K, Dubach P, Colombo A,Froelicher
V. Exercise-induced ST segment depression in
the diagnosis ofmultivessel coronary disease:
a meta analysis. J Am Coll Cardiol 1989; 14:
1501-1508.
7. Curzen N, Patel D, Clarke D, Wright C,
Mulcahy D, Sullivan A, Holdright D,Fox K.
Women with chest pain: is exercise testing
worthwhile? Heart 1996; 76: 156-160.
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nia
n H
eart Jo
urn
al; 2
016
; 17 (3
)
Echocardiographic and Clinical Factors Related to False Results of Exercise Tolerance Test Sadeghian H, et al.
44
8. Lang RM, Bierig M, Devereux RB,
Flachskampf FA, Foster E, Pellikka PA,
Picard MH, Roman MJ, Seward J, Shanewise
JS, Solomon SD, Spencer KT, Sutton MS,
Stewart WJ; Chamber Quantification Writing
Group; American Society of
Echocardiography's Guidelines and Standards
Committee; European Association of
Echocardiography. Recommendations for
Chamber Quantification: A Report from the
American Society of Echocardiographyʼs
Guidelines and Standards Committee and the
Chamber Quantification Writing Group,
Developed in Conjunction with the European
Association of Echocardiography, a Branch of
the European Society of Cardiology. J Am
Soc Echocardiogr 2005; 18: 1440-1463.
9. BraunBalady GJ and Morise AP. Exercise
Testing. In Mannn DL, Zipes DP, Libby P,
Bonow R, Eugene, Braunwald E. Braunwald’s
heart disease: a textbook of cardiovascular
medicine. 10 th edition. Philadelphia, Elsevier
Saunders 2015 P 180-203.
10. Richie RC. Non-invasive assessment of the
risk of coronary heart disease. J InsurMed
2002; 34: 31-42.
11. Sketch MH, Mohiuddin SM, Lynch JD,
Zencka AE, Runco V. Significant sex
differences in the correlation of
electrocardiographic exercise testing and
coronary arteriograms. Am J Cardiol 1975;
36: 169-73.
12. Manca C, Dei Cas L, Bernardini B, Barilli
AL, Tsialtas D, Vasini P, Visioli O.
Comparative evaluation of exercise ST
response in healthy males and females: a
computer study. Cardiology. 1984; 71: 341-7.
13. Osbakken MD. Exercise stress testing in
women: diagnostic dilemma. In: Douglas PS,
ed. Heart Disease in Women. Philadelphia:
FA Davis, 1989:187-9.
14. Ellestad MH. Stress testing: principles and
practice. Fifth ed. Stress testing in women.
Oxford university press: 2003: 309-16.
15. Kansal S, Roitman D, Sheffield LT. Stress
testing and ST segment depression at rest.
Circulation 1976; 54: 636-9.
16. Meyers DG, Bendon KA, Hankins JH,
Stratbucker RA. The effect of baseline
electrocardiographic abnormalities on the
diagnostic accuracy of exercise-induced ST
segment changes. Am Heart J 1990; 119: 272-
6.
17. Miranda CP, Lehmann KG, Froelicher VF.
Correlation between resting ST segment
depression, exercise testing, coronary
angiography, and long-term prognosis. Am
Heart J 1991; 122: 1617-28.
18. Fearon WF, Lee DP, Froelicher VF. The
effect of resting ST segment depression on the
diagnostic characteristics of the exercise
treadmill test. J Am Coll Cardiol2000; 35:
1206-1211.
19. Kwok JM, Miller TD, Christian TF.
Prognostic value of a treadmill exercise score
in symptomatic patients with nonspecific ST-
T abnormalities on resting ECG. JAMA 1999;
282: 1047-1053.
20. Kannel WB, Anderson K, McGee DL,
Degatano LS, Stampfer MJ. Nonspecific
electrocardiographic abnormality as a
predictor of coronary heart disease: the
Framingham Stydy. Am Heart J 1987; 113:
377-382.
21. Kreger BE, Cupples LA, Kannel WB. The
electrocardiogram in prediction of sudden
death: Framingham Study experience. Am
Heart J 1987; 113: 377-382.
22. Sigurdsson E, Sigfusson N, Sigvaldason H,
Thorgeirsson G. Silent ST-T changes in an
epidemiologic cohort study-a marker of
hypotension or coronary heart disease, or
both: the Reykjavik Study. J Am Coll Cardiol
1996; 27: 1140-1147.
23. Ellestad MH. Stress testing: principles and
practice. Fifth ed. Predictive implications.
Oxford university press: 2003: 271-307.
Ira
nia
n H
eart Jo
urn
al; 2
016
; 17 (3
)
Echocardiographic and Clinical Factors Related to False Results of Exercise Tolerance Test Sadeghian H, et al.
45
24. Tavel ME. Stress testing in cardiac evaluation,
current concepts with emphasis on the ECG.
Chest 2001; 119: 907-925.
25. Smith RH, LePetri B, Moisa RB, Studzinski
M, Flaster E, Steingart RM. Association of
increased left ventricular mass in the absence
of electrocardiographic left ventricular
hypertrophy with ST depression during
exercise. Am J Cardiol 1995; 76: 973-974.
26. Levy D, Labib SB, Anderson KM,
Christiansen JC, Kannel WB, Castelli WP.
Determinants of sensitivity and specificity of
electrocardiographic criteria for left
ventricular hypertrophy. Circulation 1990; 81:
815-820.
Ira
nia
n H
eart Jo
urn
al; 2
016
; 17 (3
)
AML and Cardiac MRI Nikdoust F, et al.
46
Case Report AML and Cardiac MRI Nikdoust F, et al.
Right Ventricle Tumoral Mass in Acute Promyelocytic Leukemia
(AML M3): Cardiac Magnetic Resonance Findings
Farahnaz Nikdoust1, MD; Zahra Alizadeh Sani
2, MD;
Seyed Abdolhussein Tabatabaei1*, MD
ABSTRACT
Intracardiac masses found on 2D echocardiography in patients with leukemia can present diagnostic
challenges. A correct differentiation between thrombi, metastases, and infective vegetations is
important in the management of patients with leukemia.
We describe a 24-year-old male patient, who was diagnosed with acute myelogenous leukemia
(APL, AML M3). 2D transthoracic echocardiography showed 2 inhomogeneous highly mobile
masses (10×13 and 6×9 mm) in the right ventricle (RV). The masses were attached to the chordae
tendineae and exhibited movements compatible with the cardiac cycle. Cardiac magnetic resonance
imaging revealed 3 mobile masses in the RV attached to the RV trabeculations with isosignal
intensity on steady-state free precession sequence. There was no obvious evidence of mass invasion
or necrosis. On the last transesophageal echocardiography (6 months after the initial admission), the
mass did not exist anymore. At the time of paper compilation, the patient has no complaints and is
in remission.
This report underscores the importance of cardiac magnetic resonance imaging in differentiating
intracardiac thrombi from aggregations of tumoral cells in APL, AML M3. (Iranian Heart Journal
2016; 17(3):46-50)
Keywords: Right ventricle Mass Tumor Leukemia Cardiac magnetic resonance imaging
1 Department of Cardiology, Shariati Hospital, Tehran University of Medical Sciences, Tehran, I.R. Iran. 2 Department of MRI, Shahid Rajaie Cardiovascular, Medical, and Research Center, Iran University of Medical Sciences, Tehran, I.R. Iran.
Corresponding Authors: Seyed Abdolhussein Tabatabaei, MD; Shariati Hospital, Tehran University of Medical Sciences, Tehran, I.R. Iran.
precession (SSFP) image shows small and round mobile right ventricular (RV) masses, which are attached to the RV trabeculations. (B) Short T1 inversion recovery (STIR) image shows an RV mass with isosignal intensity. (C) T1-weighted image shows an RV mass with isosignal intensity. (D) First-pass perfusion image in the SAX plane does not show Gadolinium enhancement.
Figure 1. Parasternal right ventricular inflow
view of transthoracic echocardiography shows 2 inhomogeneous highly mobile masses (10×13 and 6×9 mm) in the right ventricle attached to the chordae tendineae.
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AML and Cardiac MRI Nikdoust F, et al.
49
Chemotherapy with arsenic and all-trans
retinoic acid (ATRA) was initiated along with
warfarin. Antibiotics (vancomycin and
gentamicin), started earlier for the
presumptive diagnosis of infective
endocarditis, were discontinued. After 1
month, repeated TTE showed a 50% decrease
in the size of the mass. The chemotherapy
was then continued for 4 more cycles with
arsenic and hydroxyurea. Warfarin has been
continued since the patient’s discharge from
the hospital. On the last TEE (6 months after
the initial admission), the mass did not exist
anymore. At the time of the compilation of
this paper, the patient has no complaints and
is in remission.
DISCUSSION
APL is a distinct subtype of AML. APL is
characterized by a balanced chromosomal
translocation between chromosomes 15 and
17, young age of the patients at the time of
diagnosis, and unique response to ATRA
treatment.6 It constitutes about 15% to 20% of
all cases of AML. Vegetations secondary to
infections caused by defective leukocyte
function, thrombus formation owing to
coagulopathy seen in AML, and tumoral
masses secondary to the aggregation of
tumoral leukemic cells are the differential
diagnoses regarding the intracardiac masses
seen in patients with AML.
Here, initially, echocardiography enabled us
to detect 2 intracardiac masses in the patient’s
RV. The approach to such masses can be
challenging. First, in light of consultation
with the hematology services, a diagnosis of
thrombus was high on our differential list.
Indeed, thrombi in APL have been reported
previously in the literature, with 10% of
patients with APL known to have thrombosis
upon admission.3-6
As regards our patient,
however, after a long-term follow-up and in
light of the CMR images, we are of the belief
that that this mass was likely an aggregate of
blastocysts and not a thrombus. Evidence
favoring the tumoral nature of the mass
secondary to AML is that the size of the
tumor decreased significantly by half after the
1st month of chemotherapy. This evidence
was further bolstered by CMR appearance.
And as for echocardiography, in case of a
mass, echo appearance will show central
necrosis and peripheral calcification, whereas
in case of a thrombus, echo appearance will
demonstrate clot lysis—which usually starts
from its periphery. Another finding that rules
out a thrombus here is that we did not find
deep vein thrombosis on Doppler studies. A
thrombus in the right heart usually is found in
the setting of embolization from a deep vein
thrombosis in the pelvis or lower extremities.4
Cahill et al.5 described a 29-year-old female
patient, who presented with sudden-onset
chest pain. Her ECG as well as cardiac
biomarkers showed myocardial infarction.
Echocardiogram revealed a mass at the left
ventricular apex. CMR demonstrated apical
scarring, suggestive of myocardial infarction
as well as apical thrombi in the left ventricle
and the RV. Early gadolinium image
differentiated the thrombus from the
myocardium. Diagnostic coronary
angiography did not reveal coronary artery
disease. The patient had elevated D-dimer,
dropping neutrophil count, and prolonged
prothrombin time and partial thromboplastin
time. Based on bone marrow biopsy, the
diagnosis of APL was made for the patient.
CMR of the patient showed that the mass was
isointense to the myocardium. The patient
received ATRA and idarubicin chemotherapy
and remained in remission at the last follow-
up after 2 months. Repeated CMR showed a
reduction but not the resolution of the cardiac
thrombus.
Potenza et al.6 described a 22-year-old male
patient, who presented with the initial
complaint of palpitation. 2D
echocardiography showed a mobile
heterogeneous bilobate mass in the RV. CMR
demonstrated a mass with heterogeneous
signal intensity on T1-weighted images with
no contrast enhancement. With leukopenia
found on laboratory investigations, bone
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AML and Cardiac MRI Nikdoust F, et al.
50
marrow biopsy was done and it demonstrated
90% blasts. With the diagnosis of APL,
ATRA was ordered for the patient. Then, after
the recovery of the bone marrow, the mass
was removed surgically. Histological
examination showed amorphous eosinophilic
material with inflammatory cells, consistent
with thrombosis as a result of APL. The
patient remained in remission until the last
follow-up.
To the best of our knowledge, our report of an
APL patient with a tumoral mass—as
demonstrated by CMR and
echocardiography—is the 1st of its kind in the
literature. Our report highlights not only the
importance of the correct diagnosis of such
masses with the use of CMR but also the
advantages of CMR over 2D
echocardiography. Echocardiography was not
sufficiently informative in differentiating the
thrombus from the aggregation of tumoral
cells. It can be concluded that when faced
with a patient diagnosed with APL, clinicians
can draw upon CMR as a useful method to
differentiate between thrombi and tumoral
masses.
Disclosure: None.
REFERENCES
1. Narin B, Arman A, Arslan D, Simsek M,
Narin A. Assessment of cardiac masses:
magnetic resonance imaging versus
transthoracic echocardiography. Anadolu
kardiyoloji dergisi : AKD = the Anatolian
journal of cardiology. 2010;10(1):69-74.
2. Reynen K, Kockeritz U, Strasser RH.
Metastases to the heart. Annals of oncology :
official journal of the European Society for
Medical Oncology / ESMO. 2004;15(3):375-
81.
3. De Stefano V, Sora F, Rossi E, Chiusolo P,
Laurenti L, Fianchi L, et al. The risk of
thrombosis in patients with acute leukemia:
occurrence of thrombosis at diagnosis and
during treatment. Journal of thrombosis and
haemostasis : JTH. 2005;3(9):1985-92.
4. Nanjappa MC, Shankarappa RK, Kalpana SR,
Bhat P, Moorthy N. Intracardiac thrombi in
acute myeloid leukemia: an echocardiographic
and autopsy correlation. Echocardiography
(Mount Kisco, NY). 2010;27(1):E4-8.
5. Cahill TJ, Chowdhury O, Myerson SG,
Ormerod O, Herring N, Grimwade D, et al.
Myocardial infarction with intracardiac
thrombosis as the presentation of acute
promyelocytic leukemia: diagnosis and
follow-up by cardiac magnetic resonance
imaging. Circulation. 2011;123(10):e370-2.
6. Potenza L, Luppi M, Morselli M, Riva G,
Saviola A, Ferrari A, et al. Cardiac
involvement in malignancies. Case 2. Right
ventricular lesion as presenting feature of
acute promyelocytic leukemia. Journal of
clinical oncology : official journal of the
American Society of Clinical Oncology.
2004;22(13):2742-4.
7. Peters PJ, Reinhardt S. The echocardiographic
evaluation of intracardiac masses: a review.
Journal of the American Society of
Echocardiography : official publication of the
American Society of Echocardiography.
2006;19(2):230-40.
8. Torromeo C, Latagliata R, Avvisati G, Petti
MC, Mandelli F. Intraventricular thrombosis
during all-trans retinoic acid treatment in
acute promyelocytic leukemia. Leukemia.
2001;15(8):1311-3.
9. O'Donnell DH, Abbara S, Chaithiraphan V,
Yared K, Killeen RP, Cury RC, et al. Cardiac
tumors: optimal cardiac MR sequences and
spectrum of imaging appearances. AJR
American journal of roentgenology.
2009;193(2):377-87.
10. Gulati G, Sharma S, Kothari SS, Juneja R,
Saxena A, Talwar KK. Comparison of echo
and MRI in the imaging evaluation of
intracardiac masses. Cardiovascular and
interventional radiology. 2004;27(5):459-69.
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urn
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016
; 17 (3
)
Neonatal Tuberous Sclerosis Complex Ramesh Bhat Y, et al.
51
Case Report Neonatal Tuberous Sclerosis Complex Ramesh Bhat Y, et al.
Neonatal Tuberous Sclerosis Complex with
Large and Multiple Cardiac Rhabdomyomas
Ramesh Bhat Y1, MD;
Leslie E Lewis
1, MD;
Jayashree P
1, MD;
Prakashini K2, MD;
Ranjan S
3, MD; Krishnananda N
3, MD
ABSTRACT
The tuberous sclerosis complex (TSC) is most commonly diagnosed around the age of 5 years.
Neonatal TSC is rare. The important neonatal manifestations include cardiac rhabdomyomas,
central nervous system abnormalities, and skin manifestations. We describe a neonate suffering
from the TSC with large and multiple cardiac rhabdomyomas. The largest rhabdomyoma measured
3.6 cm × 2 cm almost filling the right ventricle. The neonate did not have any symptoms. She
continued to remain asymptomatic until 8 months’ follow-up. (Iranian Heart Journal 2016;
1Department of Pediatrics, Kasturba Medical College, Manipal University, Manipal-576104, Udupi District, Karnataka, India. 2Department of Radiodiagnosis and Imaging, Kasturba Medical College, Manipal University, Manipal-576104, Udupi District,
Karnataka, India. 3Department of Cardiology, Kasturba Medical College, Manipal University, Manipal-576104, Udupi District, Karnataka, India.
Corresponding Author: Ramesh Bhat Y, MD; Kasturba Medical College, Manipal University, Manipal-576104, Udupi District,
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Introduction to Aortic Surgery Thursday, March 16, 2017 to Saturday, March 18, 2017 EACTS House Windsor United Kingdom See map: Google Maps 35th Cardiovascular Surgical Symposium Saturday, March 18, 2017 to Saturday, March 25, 2017 Robinson Select Alpenrose Zürs Zürs am Arlberg
Austria See map: Google Maps Master Class on Aortic Valve Repair: A Step-by-Step Approach Wednesday, March 22, 2017 to Friday, March 24, 2017 L'Institut Mutualiste Montsouris (IMM) Paris France See map: Google Maps The 25th Annual Meeting of the Asian Society for Cardiovascular and Thoracic Surgery (ASCVTS 2017) Thursday, March 23, 2017 to Sunday, March 26, 2017 Coex Convention and Exhibition Center Seoul South Korea See map: Google Maps 13th International Congress of Update in Cardiology and Cardiovascular Surgery Thursday, March 23, 2017 to Sunday, March 26, 2017 Cesme Sheraton Convention Center Izmir Turkey See map: Google Maps Thoracic Surgery: Part I Monday, March 27, 2017 to Friday, March 31, 2017 EACTS House Windsor United Kingdom See map: Google Maps 23th Annual Conference of the Egyptian Society of Cardiothoracic Surgery Tuesday, April 4, 2017 to Thursday, April 6, 2017 Mena House Hotel, Giza, Egypt Cairo Egypt See map: Google Maps 32nd EACTA Annual Congress 2017 Wednesday, April 19, 2017 to Friday, April 21, 2017 Maritime Hotel Berlin Germany See map: Google Maps ESTS Skill Track Course "Elancourt in Copenhagen" Wednesday, April 19, 2017 to Friday, April 21, 2017 Denmark See map: Google Maps
AATS Mitral Conclave 2017 Thursday, April 27, 2017 to Friday, April 28, 2017 New York Hilton Midtown New York, NY United States See map: Google Maps AATS Centennial Saturday, April 29, 2017 to Wednesday, May 3, 2017 Boston Hynes Convention Center Boston, MA United States See map: Google Maps Massachusetts General Hospital Postgraduate Course in General Thoracic Surgery Thursday, May 25, 2017 to Friday, May 26, 2017 Royal Sonesta Hotel Cambridge, MA United States See map: Google Maps 25th European Conference on General Thoracic Surgery Sunday, May 28, 2017 to Wednesday, May 31, 2017 Congress Messe Innsbruck Austria See map: Google Maps Fundamentals in Cardiac Surgery: Part II Monday, June 5, 2017 to Friday, June 9, 2017 EACTS House Windsor United Kingdom See map: Google Maps Thoracic Surgery: Part II Monday, June 12, 2017 to Wednesday, June 14, 2017 EACTS House Windsor United Kingdom See map: Google Maps Ventricular Assist Device Co-ordinators Training Course Thursday, June 15, 2017 to Saturday, June 17, 2017 Deutsches Herzzentrum Berlin (German Heart Institute Berlin) Berlin Germany See map: Google Maps Magna Græcia AORtic Interventional Project® (MAORI) 5th Symposium Complex Diseases of Thoracic and Thoraco-Abdominal Aorta Tuesday, June 20, 2017 to Wednesday, June 21, 2017 University Campus “Salvatore Venuta” Italy Building H, Auditorium Room B, level 2
Catanzaro Italy See map: Google Maps ASAIO 63rd Annual Conference Wednesday, June 21, 2017 to Saturday, June 24, 2017 Hyatt Regency Chicago Chicago, IL United States See map: Google Maps The New Orleans Conference - Las Vegas Edition Wednesday, June 28, 2017 to Saturday, July 1, 2017 The Four Seasons Resort Las Vegas, NV United States See map: Google Maps 27th Annual Congress of the World Society of Cardiovascular &Thoracic Surgeons Friday, September 1, 2017 to Sunday, September 3, 2017 The Palace Of Independence Astana Kazakhstan See map: Google Maps 2nd International Conference on Hypertension & Healthcare Monday, September 11, 2017 to Wednesday, September 13, 2017 Hyatt Place Amsterdam Airport Rijnlanderweg 800 Hoofddorp 2132 NN Amsterdam Netherlands
See map: Google Maps Annual Conference on Heart Diseases Monday, September 18, 2017 to Tuesday, September 19, 2017 Holiday Inn Toronto International Airport 970 Dixon Road Toronto, ON M9W 1J9 Canada See map: Google Maps 37th Annual Cardiothoracic Surgery Symposium Thursday, September 28, 2017 to Sunday, October 1, 2017 Westin San Diego Gaslamp Quarter San Diego, CA United States See map: Google Maps Fundamentals in Cardiac Surgery: Part III Monday, October 23, 2017 to Friday, October 27, 2017 EACTS House Windsor United Kingdom See map: Google Maps Thoracic Surgery: Part III Monday, December 4, 2017 to Wednesday, December 6, 2017 EACTS House Windsor United Kingdom See map: Google Maps