HISTORY

60-year-old man.

CHIEF COMPLAINT: Progressive shortness of breath of six

months duration.

PRESENT ILLNESS: At age 56 he had an acute myocardial infarction

complicated by pulmonary edema. He was clinically stable on digitalis and

diuretics until age 58 when he had an acute right femoral artery embolism with

successful embolectomy. For the last six months he has had progressive

orthopnea and dyspnea on minimal exertion in spite of therapy.

Question: What diagnoses are suggested by this history?

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Answer: With a history of myocardial infarction, atherosclerotic heart

disease is by far the the most likely basic diagnosis. To explain the embolism

and failure, some complication such as left ventricular remodeling, progressive

ischemia, arrhythmia or ventricular aneurysm must be considered.

PHYSICAL SIGNS a. GENERAL APPEARANCE – 60-year-old man who appears mildly

dyspneic at rest.

b. VENOUS PULSE - The CVP is estimated to be 7 cm H2O.

Question: How do you interpret the venous pulse?

PHONO

LOWER LEFT

STERNAL

EDGE

JUGULAR

VENOUS

PULSE

S1 S2

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Answer: The estimated central venous pressure is at the upper limits of

normal and the venous wave form is normal with a dominant “a” wave due to

atrial contraction.

c. ARTERIAL PULSE - (BP = 150/90 mm Hg)

Question: How do you interpret the arterial pulse?

ECG

CAROTID

UPPER RIGHT

STERNAL EDGE

S1 S2

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Answer: The arterial pulse is normal in upstroke, peak, and downstroke.

d. PRECORDIAL MOVEMENT

Question: How do you interpret the patient’s precordial movement?

ANTERIOR AXILLARY

LINE 6TH and 7TH ICS

ECG

Answer: The apical impulse is inferolaterally displaced due to left

ventricular enlargement. In this case, there is a sustained systolic impulse due

to a true “anatomic” fibrotic ventricular aneurysm. Similar bedside findings may

be present with a “physiologic” aneurysm (that is, an ischemic dyskinetic

muscle that moves outward as the rest of the ventricular muscle contracts) or

with primary myocardial disease (cardiomyopathy).

In addition, a presystolic impulse, corresponding to an S4, is present due to

atrial contraction into a poorly compliant left ventricle.

Proceed

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e. CARDIAC AUSCULTATION

Question: What is the likely cause of the systolic murmur at the apex?

APEXCARDIOGRAM

ECG

APEX

100 CPS

S2 S1

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Answer: The murmur is likely due to mitral regurgitation from papillary

muscle dysfunction associated with outward bulging of the ventricular wall.

This is also well heard posterolateral to the mitral area over the enlarged left

ventricle. A diagram of the ventricle during maximum ejection explains the

mechanism as shown below:

Question: What is the significance of the third heart sound ?

NORMAL PATIENT

AORTA AORTA LA LA

LV LV

PP PP AP

AP

LA = left atrium AP = anterior papillary muscle

LV = left ventricle PP = posterior papillary muscle

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Answer: The third heart sound reflects passive filling of the poorly

compliant left ventricle.

e. CARDIAC AUSCULTATION (continued)

Question: Based on information available by history and physical

examination, why is the second sound split in expiration?

EXPIRATION INSPIRATION

2L

ECG 2 1 1

A2 P2 A2 P2

1

0.1 sec

Answer: The second sound is paradoxically split due to the delay in aortic

valve closure associated with a prolonged pre-ejection period caused by left

ventricular dysfunction. The second sounds fuse in inspiration when the usual

prolongation of the right ventricular ejection occurs.

f. PULMONARY AUSCULTATION

Question: How do you interpret the acoustic events in the pulmonary lung

fields?

Proceed

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Answer: In all lung fields, there are inspiratory and expiratory crackles,

reflecting chronic severe congestive failure.

ELECTROCARDOGRAM

(At time of first admission 4 years ago)

Question: How do you interpret this ECG?

I II III aVR aVL aVF

V1 V2 V3 V4 V5 V6

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Answer: The ECG shows a left atrial abnormality and an extensive acute

anteroinferior infarction with Q waves, ST elevation and T inversion. This

implies anatomically that the entire apex of the heart is involved.

ELECTROCARDIOGRAM

(This admission)

Question: How do you interpret this ECG?

I II III aVR aVL aVF

V1 V2 V3 V4 V5 V6

Answer: The ECG shows persistence of ST-T elevation changes four years

after the infarction. Persistence of such changes for more than one month

suggests a ventricular aneurysm.

CHEST X RAY

Questions: 1. How do you interpret this chest X ray?

2. Based on the history, physical examination, ECG and chest X ray, what is

your diagnostic impression and plan to further evaluate this patient?

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Answers:

1. The chest X ray shows a large left ventricular aneurysm (solid arrows)

and signs of interstitial pulmonary edema (broken arrows).

2. The history, physical examination, ECG and chest X rays are essentially

diagnostic of ventricular aneurysm. The patient has had two of

the major complications of this disease: peripheral arterial embolism and

congestive failure.

Question: What further study is indicated?

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Answer: A two-dimensional echocardiogram will help define left ventricular

anatomy, function, and the presence of a clot.

LABORATORY- ECHOCARDIOGRAM

Proceed

APICAL FOUR CHAMBER

RV = right ventricle

RA = right atrium

LV = left ventricle

LA = left atrium

The echocardiogram shows a dilated left ventricle with an apical thrombus

(clot). In the real-time study it is also apparent that the apex of the left

ventricle is dyskinetic (i.e., moves paradoxically) confirming the presence of

an aneurysm.

Question: What is the third major complication of a ventricular aneurysm?

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Answer: Ventricular arrhythmias.

This patient demonstrated no significant arrhythmias. Because of refractory

congestive heart failure, cardiac catheterization was carried out.

LABORATORY- CATHETERIZATION DATA

The results of the coronary anatomy and hemodynamics follow.

LEFT VENTRICULAR ANGIOGRAM

Coronary angiography showed total obstruction of the left anterior descending

(LAD) and right coronary (RCA) arteries with poor distal runoff and without

collateral flow to the area.

The left ventricular end diastolic pressure was 18 mm Hg (normal <12 mm Hg).

The left atrial pressure curve showed prominent “v” waves. The cardiac index

was 2.0 (normal 2.5 - 3.5).

Questions: 1. How do you interpret the laboratory data?

2. How would you treat this patient?

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Answers:

1. The left ventricular angiogram demonstrates the ventricular aneurysm (solid

arrows) and mitral regurgitation (broken arrows outline left atrium). The

latter is supported by prominent “v” waves in the left atrial pressure curve.

The elevated left ventricular end diastolic pressure and low cardiac index

reflect the patient’s left ventricular failure.

2. If the patient’s congestive failure does not respond to maximizing his

medical therapy (i.e., adding ACE-I, anticoagulation, etc.), ventricular

aneurysmectomy is indicated. An additional though more remote indication

is his history of peripheral arterial embolism.

Proceed

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The patient underwent ventricular aneurysmectomy without complication. No

coronary bypass surgery was performed as the LAD and RCA were totally

occluded without distal runoff. The patient’s mitral regurgitation was no longer

present after surgery, as the cause of his papillary muscle dysfunction had

been treated. However, in similar cases, repair or replacement of the mitral

valve have been necessary.

The patient was discharged on aspirin, a beta-blocker, an ACE-inhibitor and a

statin. He was instructed to follow a low fat diet and an exercise program based

on outpatient stress testing.

Proceed for Summary

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SUMMARY

Ventricular aneurysm is almost always a complication of atherosclerotic heart

disease in which myocardial infarction, as a result of remodeling, becomes

organized into a thin, fibrous, wide-mouthed, sac-like structure which bulges

out under the force of systolic pressure. Physiologically, areas of dyskinetic or

akinetic motion are seen angiographically (and may be palpated at the bedside)

in many patients with myocardial infarction or ischemia. Persistent ST

elevation is an indication of likely ventricular aneurysm.

Proceed

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SUMMARY (continued)

True ventricular aneurysms must be differentiated from false aneurysms. False

aneurysms occur when myocardial infarctions rupture and the resulting

hematoma is contained by the pericardium and becomes organized. The

mouth of the aneurysm is characteristically small. Unlike true aneurysms, false

aneurysms may rupture. The typical gross pathology of a true ventricular

aneurysm follows.

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Proceed for Case Review

MITRAL VALVE

POSTERIOR

LEAFLET

LEFT ATRIUM

POSTEROMEDIAL

PAPILLARY

MUSCLE

LEFT

VENTRICULAR

ANEURYSM

MURAL

THROMBUS

APEX OF

LEFT VENTRICLE

INTERVENTRICULAR

SEPTUM

RIGHT VENTRICLE

AORTA

RIGHT ATRIUM

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To Review This Case of

Ventricular Aneurysm:

The HISTORY is typical, including previous infarction, embolism due to

mural thrombus formation, and congestive failure due to dyssynergic left

ventricular contraction. Another type of presentation not seen in this patient is

ventricular arrhythmia. Note that the patient had pulmonary edema at the time

of his initial infarct, which also suggests that the infarction was extensive.

PHYSICAL SIGNS

a. The GENERAL APPEARANCE shows the patient to be mildly

dyspneic at rest.

b. The JUGULAR VENOUS PULSE mean pressure is at the upper limits of

normal, and the wave form is normal.

Proceed

c. The CAROTID PULSE is normal. The patient’s borderline hypertension

may be due to congestive failure alone, as there is a reflex increase in

peripheral resistance when cardiac output is diminished.

d. PRECORDIAL MOVEMENT reveals an inferolaterally displaced,

enlarged and sustained apical impulse. In addition, presystolic expansion of

an S4 is present, reflecting poor ventricular distensibility.

e. CARDIAC AUSCULTATION reveals paradoxic splitting of the second

sound due to a prolonged pre-ejection period from pump dysfunction. A

third sound reflects poor ventricular compliance, and the palpable fourth

sound is confirmed. Finally there is a soft midsystolic murmur of mitral

insufficiency due to papillary muscle dysfunction associated with systolic

expansion of the aneurysm.

f. PULMONARY AUSCULTATION reveals inspiratory and expiratory

crackles in all lung fields, reflecting chronic severe congestive failure.

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The ELECTROCARDIOGRAM shows an anteroseptal current of

injury present for four years that is typical of ventricular aneurysm.

The CHEST X RAY reveals a large left ventricular aneurysm and signs

of interstitial pulmonary edema. Occasionally the aneurysm is calcified and this

may be seen on the X ray.

LABORATORY STUDIES including echocardiography show an

apical aneurysm and mural thrombus. Cardiac catheterization and angiography

confirm poor left ventricular function, a left ventricular aneurysm, mitral

regurgitation and total occlusion of the left anterior descending and right

coronary arteries.

TREATMENT is aneurysmectomy, as the patient has refractory failure.

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