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Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage:
Congestive heart failure in adults
Ary L. Goldberger
To cite this article: Ary L. Goldberger (1981) Congestive heart failure in adults, Postgraduate
Medicine, 69:3, 151-160, DOI: 10.1080/00325481.1981.11715713
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Published online: 07 Jul 2016.
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Download by: [Johann Christian Senckenberg]
Date: 28 October 2017, At: 13:11
Downloaded by [Johann Christian Senckenberg] at 13:11 28 October 2017
Second of three
symposium articles
in this issue
heart failure
in adults
Six considerations in
systematic diagnosis
Can "congestive heartjailure" ever be
considered diagnosis?
What is the "high-output syndrome"? How can
it be identifled?
What are curable causes of heartjailure?
Ary L. Goldberger, MD
Assessment of padents with congestive heart
fallure should focus on underlying pathophysiology and exacerbadng factors. A slmpllfled
dlagnosdc classlflcadon ls presented. Special
consideradon should be glven to the mode of
presentadon (acute vs chronlc) and possible
reversible causes. Important elues to dlagnosls
that can be obtalned by nonlnvasive tesdng are
The term "congestive heart failure" refers to a
complex syndrome generally charactertzed by
systolic or diastolic abnormalities of cardiac
function. Relatively low cardiac output commonly results in the symptom of fatigue and sets
the pathophysiologic basis for increased renal
sodium retention and edema formation ("forward failure theory"). Abnormally high filling
pressures in the left or rtght atrium may result
from abnormal ventrtcular function or atrtoventrtcular valvular lesions. Elevated atrtal pressures, in turn, lead to systemic venous or pulmonary venous hypertension ("backward failure
The purpose of this review is to provide a simplifted, yet comprehensive approach to the diagnosis of congestive heart failure in adults. Particular attention will be devoted to six tapies: (1)
diagnostic classification of heart failure. (2) elues
to the etiology of congestive heart failure from
noninvasive tests, (3) acute vs chronic heart fanure, (4) factors exacerbating chronic heart failure. (5) congestive heart failure with acute myecardial infarction, and (6) potentially reversible
causes of heart fallu re.
Dlagnosdc classlflcadon
Congestive heart failure should not be considered a final diagnosis for any patient. Instead,
the precise etiology should always be sought.
Inadequate attention to the underlying cause(s)
Sustained systemic or pulmonary arterial hypertension
can lead to left or right heart
failure, respectively.
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Table 1. Diagnostic classification of congestive heart
fallu re
Low or normal basal cardlac output
Pericardial disease
Pericardial tamponade
Pericardial constriction
Coronary artery disease
Primary myocardial disease (cardiomyopathy)
Restrictive (eg, amyloidosis)
Congestive (eg. idiopathie. alcoholic. viral)
Hypertrophie (idiopathie hypertrophie subaortic
Endocardial disease
Cyanotic (eg. tetralogy of Fallot)
Acyanotic (eg. bicuspid aortic valve. atrial septal
Systemic hypertension
Pulmonary arterial hypertension
With precedent pulmonary venous hypertension
Left ventricular tai lure
Mitral valve disease or rare forms of obstruction
at left atriallevel (myxoma. cor triatriatum)
Pulmonary venoocclusive disease
Without precedent pulmonary venous hypertension
Primary pulmonary hypertension
Recurrent pulmonary emboli
Chronic obstructive or restrictive lung disease
Eisenmenger syndrome
Hlgh basal cardiac output
Arteriovenous fistula
Severe anemia
Paget's disease
has resulted in failure to diagnose such treatable
lesions as severe aortic stenosis, chronic constrictive pericarditis, and recurrent pulmonary
To avoid such omissions. a systematic approach to diagnosis is necessary. A simple. comprehensive classification of congestive heart failure is presented in table 1. The causes have been
divided into two basic subgroups. depending on
whether heart failure is present ( l) with a relatively law or normal basal cardiac output or (2)
despite a high basal cardiac output.
associated wi th a law or normal basal cardiac
output generally results from sorne primary abnormality in cardiopulmonary function. Clinicians can best conceptualize the many causes in
this subgroup in a topographie way. starting at
the outside of the heart (pericardial disease) and
working inward through the coronaxy arteries
(ischemie heart disease). myocardium (cardiomyopathy). and endocardium (valvular lesions.
myxomas. and congenital heart disease). The
ventricles. in tum. are "connected" to two outflow networks: systemic (aorta) and pulmonary
(pulmonary artexy). Sustained systemic or pulmonaxy arterial hypertension can lead to left or
right heart failure. respectively.
These general categories of heart failure can.
in tum. be further subdivided. Pericardial diseases causing heart failure include chronic constrictive pericarditis and pericardial tamponade.
Cardiomyopathies have been subdivided into
restrictive. congestive. and hypertrophie types. 1
Restrictive cardiomyopathy resembles constrictive pericarditis hemodynamically. The ventricles
may be normal in size. with well-preserved systolic function but high filling pressures due to
abnormal ventricular compliance. Restrictive
cardiomyopathy may be idiopathie or may be
due to such factors as amyloidosis, hemochromatosis, or eosinophilic infiltration.
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ECG evidence of left ventricular
hypertrophy in a patient without
systemic hypertension should
prompt a careful search for
valvular heart disease.
In congestive cardiomyopathy the left ventricle
is typically dilated. with markedly reduced ejection fraction. Congestive cardiomyopathy is most
often idiopathie but may be due to specifie factors such as toxins (alcohol. cobalt), drugs (doxorubicin). infection (viral diseasel. metabolic disorders (hypophosphatemia). or neuromuscular
disease (Duchenne muscular dystrophy). Hypertrophie cardiomyopathy is characterized by
asymmetric septal hypertrophy with or without
actual subaortic obstruction (idiopathie hypertrophie subaortic stenosis). 2
Valvular lesions causing congestive heart failure are predominantly either stenotic or regurgitant. Myxomas may also produce heart failure.
particularly left atrial myxoma causing mitral
Congenital lesions can be divided into cyanotic
and acyanotic subgroups.~ The most common
cyanotic condition with survival into adulthood
is tetralogy of Fallot. Patients with Ebstein's
anomaly of the tricuspid valve may also survive
into adulthood (with or without cyanosis) and
may present with rtght heart failure.
Lesions in the acyanotic subgroup may occur
with or without a left-to-right shunt.:1 Bicuspid
aortic valve is a common cause of acyanotic
heart disease (without a shunt) and may lead to
aortic stenosis or regurgitation. Mitral valve prolapse may produce significant mitral regurgitation in occasional cases. Lesions with a left-toright shunt may occur at the atrial (atrial septal
defect). ventricular (ventricular septal defect). or
aortic (patent ductus arteriosus) level. Patients
with atrial septal defect may first present in
adulthood with complaints of fatigue and dyspnea and evidence of right heart failure or atrial
Congestive heart failure may result from longstanding systemic hypertension. which is most
commonly idiopathie (essential) or due to renal
disease (vascular or parenchymall. However.
Ary L Goldberger
Dr Goldberger is assistant professor of medicine. division of
cardiology. University of California School of Medicine. and
director of electrocardiography, Veterans Administration Medical
Center. San Diego.
rarer causes of hypertension (eg. aortic coarctation. primary hyperaldosteronism. pheochromocytoma) should not be overlooked.
Pulmonary arterial hypertension. a common
forerunner of right ventricular failure. can be
subdivided into conditions with and those without precedent pulmonary venous hypertension.
The former category includes common conditions. such as left ventricular failure of any cause
and mitral valve disease. and very rare abnormalities. such as left atrial myxoma. cor triatrlatum
(a congenital lesion which may simulate mitral
stenosis). and pulmonary venoocclusive disease.
Pulmonary arterial hypertension may also occur
in the absence of prior pulmonary venous hypertension. as ln primary pulmonary hypertension,
continued on page 156
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Calcification of the aortic or
mitral valve, indicative of signif·
icant valvular disease, may be
overlooked unless sought with
severe chronic obstructive or restrictive lung
disease (cor pulmonale), Eisenmenger syndrome, or recurrent pulmonary emboli.
IDGH CARDIAC OUTPUT- The second major category of congestive heart failure includes patients
with high basal cardiac output-the so-called
high-output failure syndrome. Such patients
have evidence of hyperkinetic circulation, with
wide pulse pressure and bounding pulses.
While uncommon, the syndrome of high-output failure is important because it includes a
number of treatable conditions: hyperthyroidism, beriberi, arteriovenous fistula, and severe
anemia. Other causes of high-output failure inelude the idiopathie hyperkinetic heart syndrome and Paget's disease. Thus, in contrast to
cardiac failure associated with a low or normal
basal cardiac output which may be due to a variety of intrinsic cardiopulmonary abnormalities.
the high-output syndrome is caused primarily by
extracardiac abnormali ti es.
The diagnostic categories in table 1 are not
intended to be mutually exclusive. For example,
ischemie heart disease may cause severe congestive heart failure by producing myocardial infarction, mitral regurgitation (papillary muscle
dysfunction), or ventricular septal defects. Similarly in scleroderma,4 numerous factors may contribu te to the development of heart failure, including pericardial effusion, myocardial involvement. papillary muscle dysfunction, hypertension from renal failure. cor pulmonale from interstitial lung disease, or primary pulmonary
Clues to etiology
Clues to the etiology of heart failure can often be
obtained by careful attention to the results of
noninvasive tests, including electrocardiography,
chest x-ray studies, and echocardiography.
ECG pattern in congestive heart failure. Low
limb-lead voltage is a common finding with heart
failure of multiple causes but should always
raise the suspicion of pericardial disease. The
ECG pattern of left ventricular hypertrophy may
be seen with either excessive volume (eg, aortic
regurgitation) or pressure loads (aortic stenosis,
hypertension) causing congestive heart failure.
In a patient without systemic hypertension, ECG
evidence of left ventricular hypertrophy should
prompt a careful search for valvular heart disease, especially aortic stenosis. It should be
emphasized that. particularly in older patients
with congestive failure, even critical aortic stenosis may be overlooked. In such cases, the characteristic murmur may not be as evident because
of low output. In other cases, the murmur may
be most apparent at the apex, mimicking mitral
regurgitation (Gallavardin murmur).
Pathologie Q waves in a patient with congestive failure suggest ischemie heart disease. However, noninfarctional Q waves due to myocardial
fibrosis can also occur with other cardiomyopathies (eg, idiopathie, alcoholic).5 The presence of
low voltage and Q waves (particularly in leads V1
to V3 ) in a patient with refractory failure should
raise the suspicion of cardiac amyloidosis.6
The ECG combination of right ventricular
hypertrophy (tall R wave in lead V1 ) with left
atrial abnormality (P mitrale pattern) should
suggest mitral stenosis. Right bundle-branch
black or right ventricular hypertrophy may also
suggest atrial septal defect. Wolff-ParkinsonWhite syndrome type B (negative delta wave in
lead V1 ) is a common finding with Ebstein's
anomaly of the tricuspid valve. Congestive failure
in a patient with Q waves and persistent STsegment elevation should raise suspicion of a
ventricular aneurysm.
CHEST X-RAY S1l1DIES-Chest x-ray studies may
also be helpful in the initial assessment of the
patient with congestive heart failure. Calcification of the aortic or mitral valve, indicative of
Downloaded by [Johann Christian Senckenberg] at 13:11 28 October 2017
lncreased aortic valve echoes
on echocardiography are elues to
the diagnosis of aortic stenosis.
significant valvular disease. may be overlooked
unless sought with fluoroscopy. Pericardial calcification may help confirm the diagnosis of constrictive pericarditis. In patients presenting with
congestive cardiomyopathy of uncertain etiology,
coronary artery calcification seen on fluoroscopy
usually indicates an ischemie cause; the absence
of coronary calcification in such patients suggests idiopathie (nonlschemic) congestive myopathy?
Pulmonary arterial overcirculation suggests a
left-to-right shunt at the ventricular. aortlc. or
atrial level. In adults. the most common cause of
such a shunt is an atrial septal defect. Congestive heart failure with a normal-sized cardiac
silhouette is most commonly seen with ischemie
heart disease but may also occur with stenotic
valvular lesions (aortlc or mitral) or constrictive
pericardi tl s.
The slze of the aorta may also provide Important elues in the diagnosis of congestive failure.
Poststenotlc dilatation of the ascending aorta ls
characteristic of aortic stenosls. Dilatation of the
ascending aorta and aortic knob is seen with
chronic aortic insufficiency.
ECHOCARDIOGRAPHY-In patients with congestive cardiomyopathy of multiple causes. the
echocardiogram characteristically shows a dilated left ventricle. In certain cases. the echocardiogram may hold specifie diagnostic clues.8
Aortic regurgitation may cause fine diastolic fluttering of the mitral valve. In addition, severe
acute aortic regurgitation may cause premature
closure of the mitral valve (before the QRS complex). owtng to rapldly rising diastolic pressure.9
Acute mitral regurgitation due to rupture of
chordae or of the papillary muscle may result ln
a flail leaflet (chaotlc motion of the anterior or
posterior leaflet). Increased aortic valve echoes
suggest aortic stenosis. Concentric left ventricular hypertrophy ls also seen with severe aortic
stenosis. Rheumatlc mitral valve disease causes
thlckening of mitral leaflets, usually with concordant motion of the anterior and posterior
The echocardiogram will, of course, be diagnostic ln cases of pericardial effusion and may
suggest the dlagnosls in cases of chronlc constrictive dlsease, showtng lncreased pericardial
echoes. Echocardiography is of key importance
in the diagnosls of myxomas and also of hypertrophie cardiomyopathy. which is characterized
by asymmetric septal hypertrophy with or without systolic anterior motion of the mitral valve.
Finally, the echocardiogram may suggest the
presence of congenital heart dlsease. For example, with atrial septal defect. a dilated right ventricle with paradoxical septal motion is typically
Acute vs chronic
One of the key points in the differentiai diagnosls of heart failure ls the distinction between
acute and chronlc modes of presentation. Acute
failure (onset within hours or days) in previously
asymptomatic patients is most commonly due to
acute myocardial infarction. Not ali patients with
infarctlon have chest pain. Such "silent" lnfarctions often present with signs of acute left heart
failure. Acute left ventricular failure may also
occur with valvular heart disease, particularly
aortic or mitral regurgitation.
Infective endocarditis is a major cause of acute
aortlc regurgitation. Acute aortic insufficiency
may also result from such factors as aortic dissection or chest trauma. 9 Acute mitral regurgitation most commonly results from infective endocarditis, ruptured chordae tendineae in a previously healthy persan, or papillary muscle dysfunction or rupture with acute myocardial infarction. The cllnical picture of heart failure with
law output and distended neck veins may be
produced abruptly by pericardial tamponade.
Finally, tachyarrhythmias, such as atrial fibrillaconttnued
Worsening of congestive heart
failure in a patient with
valvular heart disease should
prompt a careful search
for infective endocarditis.
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Table 2. Factors thal commonly exacerbate chronic
heart fallure
Myocardial ischemia or infarction
Tachyarrhythmias (eg, atrial tachycardia, atrial
fibrillation, ventricular tachycardia)
Bradyarrhythmias (sinus bradycardia,
atrioventricular junctional rhythm, complete
heart block)
Excessive sodium intake (oral or intravenous) or
administration of salt-retaining drugs (estrogens,
Noncompliance with drug therapy (failure to take
digitalis, diuretics, or vasodilators as prescribed)
Use of negative inotropic drugs (eg. beta blockers,
lnfective endocarditis
Other infections
Pulmonary emboli
Accelerated systemic hypertension
Hypoxemia (eg. due to bronchospasm, pneumonia)
"Stress" (emotional or physical)
Renal failure
Thyroid disease (hyperthyroidism or hypothyroidism)
tian, may acutely induce congestive heart failure,
particularly when underlying heart disease (eg,
mitral stenosis) is present.
Exacerbating factors
In many cases of heart failure, patients present
with a history of subacute or chronic syrnptoms
which have increased in severity over weeks or
even months. In such cases. one of the causes of
chronic heart failure listed in table 1 (most
commonly ischemie, valvular. cardiomyopathie,
or hypertensive heart disease) is present. along
with sorne recent exacerbating factor(s).
Factors which frequently precipitate or worsen
chronic heart failure are listed in table 2. 10 The
net effect of these factors is to decrease the ratio
of cardiac output (supply) to metabolic requirements (demand). lt should be emphasized that
an increase in the severity of congestive heart
failure in a patient with valvular heart disease
should prompt a careful search for infective
endocardi ti s. Superimposed renal insufficiency
may also worsen heart failure by increasing fluid
Congestive heart failure with acute myocardial
Congestive failure is a major complication of
acute myocardial infarction. In most cases. it
reflects extensive damage to the left ventricle,
resulting in abnormal systolic and diastolic
function (pump failure). Occasionally, patients
may have significant infarction of the right ventricle, resulting in decreased cardiac output with
elevated central venous pressure (distended neck
veins). The ECG in cases of right ventricular
infarction typically shows the pattern of acute
inferior myocardial infarction. 11
The acute onset of congestive heart failure
with a new systolic murmur in a patient with
acute myocardial infarction may be a sign of
ruptured ventricular septum or acute mitral
regurgitation due to papillary muscle dysfunction with or without frank rupture of a papillary
muscle. 12 Swan-Ganz catheterization in the case
of ruptured ventricular septum will show an
oxygen step-up (increase in oxygen content) between right atrium and right ventricle. With
acute mitral regurgitation, a giant systolic (V)
wave will appear in the pulmonary artery wedge
Finally. progressive congestive failure following
infarction may be due to ventricular aneurysm.
The ECG in such cases may show persistent STsegment elevations severa! weeks after the infarction. A rarer cause of heart failure following
acute myocardial infarction is so-called false
aneurysm due to incomplete myocardial rupture,
Progressive congestive failure
following myocardial infarc·
lion may be due to a ventricular
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in which the pericardium alone covers the
myocardial tear.
Reversible causes
Patients with heart failure due to such causes as
ischemie disease. valvular lesions, hypertension.
or cardiomyopathy are rarely "cured." Rather.
therapy with diet. drugs, and regulation of activity is palliative without reversing the primary
In rarer cases. medical or surgical therapy can
afford complete or virtually complete relief. For
example. congestive cardiomyopathy due to
severe hypophosphatemia. a newly described
disorder, 13 can be reversed with appropriate
phosphate repletion. Pheochromocytoma is another potentially reversible metabolic cause of
heart failure. ~ Patients with congestive heart
failure due to aortic stenosis may show major
improvement or even normalization of left ventricular function following aortic valve replacement.15
Atrial septal defect is a surgically correctable
lesion. Left or right atrial myxoma is resectable.
Chronic constrictive pericarditis and recurrent
pulmonary emboli are two potentially treatable
causes of predominant "right-heart" failure.
Treatable causes of high-output congestive heart
failure have already been mentioned.
This review has emphasized the importance of
making a specifie etiologie diagnosis in patients
with congestive heart failure. However. it should
also be mentioned that there is a tendency in
clinical practice to indiscriminately apply the
diagnosis "congestive heart failure" without
adequate documentation. For example. pedal
edema is a common finding in chronic heart
failure. but it also may occur with venous insufficiency of the lower extremities in a patient with
normal cardiac function. Peripheral edema may
also occur in various noncardiac conditions, including nephrotic syndrome and chronic liver
disease. Similarly. raies may be heard in the
chest in noncardiac settings, including chronic
lung disease. atelectasis, and pneumonitis.
ln sorne cases, it may be difficult to decide if
such signs reflect cardiac or noncardiac abnormalities. Important elues concerning cardiac
function can be obtained noninvasively with
echocardiographyB and radionuclide angiography.16 In more difficult-to-diagnose cases. cardiac catheterization may be required.
There are two key clinical questions to be answered in any patient with documented congestive heart fallure. 10 First, what is the underlying
etiology? Second, what exacerbating factors
are present? The ECG, the echocardiogram,
and chest x-ray films may provide important
diagnostic elues. The mode of presentation
(acute vs chronic) is also of major importance.
Attention should be paid to treatable or reversible factors, including infective endocarditis,
occult aortic stenosis, recurrent pulmonary
emboli, and chronic constrictive pericarditis.
Finally, the possibility ofunrecognized congenital heart disease (eg, atrial septal defect)
should not be overlooked. ~
Reprints of this article w111 not be available.
1. Goodwin JF. Congestive and hypertrophie cardiomyopathies: a decade of study. Lancet 1970:1:732-9
2. Henry WL, Clark CE, Epstein SE. Asymmetrlc septal
hypertrophy (ASH)-the underlylng llnk ln the IHSS dlsease
spectrum: observations regarding lts pathogenesls. pathophyslology. and course. Circulation 1973:47:827-32
3. Per1off JK. The cllnlcal recognition of congenital heart
disease. 2nd ed. Philadelphia: WB Saunders. 1978:4-5
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4. Buckley BH, Ridolfi RL, Salyer WR, et al. Myocardial
lesions of progressive systemic sclerosis. Circulation 1976:
5. Goldberger AL. Myocardial infarction: electrocardiographie differentiai diagnosis. 2nd ed. St Louis: CV Mosby.
6. B~a LM, Khoi NB, Roberts WC. Clinically significant cardiac amyloidosis: clinicopathologic findings in 15 patients.
Am J Cardiol 1970:26:394-405
7. Johnson AD, Laiken SL, Sbabetai R. Noninvasive diagnosis of ischemie cardiomyopathy by fluoroscopic detection
of coronary artery calcification. Am Heart J 1978:96:521-4
8. Feigenbaum H. Echocardiography. 2nd ed. Philadelphia:
Lea & Febiger, 1976
9. Morganroth J, Perloff JK, Zeldis SM, et al. Acute severe
aortic regurgitation: pathophysiology, clinical recognition,
and management. Ann Intem Med 1977:87:223-32
10. Braunwald E. Heart failure. ln: Thom GW, Adams RD,
Braunwald E, et al, eds. Harrison's principles of internai medicine. 8th ed. New York: McGraw-Hill, 1978:1178-87
11. Cohn JN, Guiba NH, Broder Ml, et al. Right ventricular
infarction: clinical and hemodynamic features. Am J Cardiol
12. Wei JY, Hutchins GM, Bulkley BH. Papillary muscle
rupture in fatal acute myocardial infarction:Ann lntem Med
1979:90: 149-52
13. Daraee JR, Nutter DO. Reversible severe congestive cardiomyopathy in three cases of hypophosphatemia. Ann
lntem Med 1978:89:867-70
14. Daraee JR, Nutter DO. Two distinct catecholamine cardiomyopathies from norepinephrine and epinephrine secreting pheochromocytomas. Circulation 1980:62(Suppl III):317
15. Smith N, McAnulty JH, Rahimtoola SH. Severe aortic
stenosis with impaired left ventricular function and clinical
heart failure: results of valve replacement. Circulation 1978:
16. Holman BL. Radioisotopic examination of the cardiovascular system. ln: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine. Philadelphia: WB Saunders,
Self-assessment test
Select the best answer for each of the following. Answers are given on page 70.
1. Which of the following statements regarding congestive
cardiomyopathy is not correct?
4. ln adults, an atrial septal defect is the most common cause of
a. Left ventricle is typically normal in size
a. True
findings on chest x-ray films indicating a left-to-right shunt.
b. False
b. Cause is usually idiopathie
c. Infection may be responsible
d. Ejection fraction is markedly reduced
2. High-output heart failure may be due to which of the following
treatable conditions?
1. Hyperthyroidism
2. Arteriovenous fistula
3. Severe anemia
4. Paget's disease
5. The echocardiogram can be expected to provide specifie
diagnostic information in patients with congestive heart failure
1. Pericardial effusion
2. Myxomas
3. Hypertrophie cardiomyopathy
4. Viral myocarditis
a. 1, 2, 3
b. 1, 3
1, 2, 3
b. 1, 3
d. 4
6. Congestive heart failure following acute myocardial infarction
usually reflects extensive damage to the right ventricle.
3. Congestive heart failure in a patient with Q waves and
persistent ST-segment elevation on ECG should raise
suspicion of
2, 4
1, 2, 3, 4
2, 4
a. Ischemie heart disease
b. Valvular heart disease
d. 4
1, 2, 3, 4
a. True
b. False
c. Ventricular aneurysm
d. Cardiac amyloidosis
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