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Cystic lesion of the posterobasal portion of the heart in a 68-year-old woman. (Pathologic Quiz Case).

A 68-year-old Asian woman presented with a 1-day history of left-sided facial "droop" and weakness of the left arm and leg, which had evolved within a few hours. A week prior, she had an episode of diaphoresis associated with nausea. Her past medical history was significant for long-standing diabetes mellitus.

Physical examination revealed an alert patient with stable vital signs. She had mild weakness of the left hip and knee flexors. Laboratory investigations revealed normal laboratory values, except for an elevated troponin I level of 2.99 x [10.sup.6] mg/mL (normal, 0.1 x [10.sup.6] mg/mL). Electrocardiogram showed ST elevation in inferior leads. Computed tomographic scan of the brain showed multiple foci of cortical and white matter infarction in the right cerebral hemisphere. The patient was admitted to the hospital. Subsequent echocardiogram and magnetic resonance image of the heart showed a well-demarcated cystic lesion (Figure 1, arrow) within the posterobasal wall of the left ventricle just below the mitral valve annulus. On the third hospitalization day, the patient became suddenly unresponsive and underwent extensive resuscitative measures, including an emergency pericardiocentesis during which approximately 100 mL of fresh blood was removed. However, the resuscitative attempts were unsuccessful and the patient died.


At autopsy, the most significant findings were present in the heart. The pericardial cavity contained 25 mL of fresh blood. There was a hemorrhagic, soft, bulging, saccular lesion measuring 7.0 x 3.0 x 1.0 cm, located along the atrioventricular groove (Figure 2, arrow), predominantly involving the left ventricular posterior wall and focally extending into the right ventricle with a pinpoint area of rupture. Sectioning through the lesion revealed a hemorrhagic shaggy cystic space within the myocardium (Figure 2, inset). After fixation of the heart in formalin, the area was serially cut. There was a localized area of congested, mottled, and softened myocardium, with acute hemorrhagic necrosis dissecting through the posterobasal myocardium leading into the cystic lesion. The cystic space was focally bounded by hemorrhagic epicardial fat, which was focally disrupted. The left circumflex coronary artery showed severe calcific atherosclerosis. However, the vascular wall was intact without any aneurysmal dilation or communication with the hemorrhagic cystic lesion. There was also severe calcific atherosclerosis of the right coronary artery. Microscopically, multiple sections from the necrotic myocardium, including the cystic lesion, revealed recent myocardial necrosis with patchy acute inflammatory cell infiltration. The periphery of the lesion revealed scattered hemosiderin-laden macrophages and newly formed granulation tissue (Figure 3, A). The cystic space was lined by necrotic myocardium and recent granulation tissue with fibrin, but no epithelium (Figure 3, B).


The autopsy also disclosed multiple small foci of acute cerebral infarcts with recent microvascular thromboemboli.

What is your diagnosis?

Pathologic Diagnosis: Postinfarction Pseudoaneurysm of the Posterobasal Portion of the Heart With Rupture

Left ventricular pseudoaneurysm is a rare complication of myocardial infarction (MI), cardiac infection, cardiac surgery, or trauma. Mechanical complications following acute MI preferentially involve the ventricular free wall, interventricular septum, and papillary muscle in the descending order of frequency. Rupture of the posterobasal portion of the heart is very rare. Based on a large study, (1) the incidence of rupture of the posterobasal portion of the heart and pseudoaneurysm formation following MI was only 0.0026% (6 of 2600 consecutive patients).

Transmural MI involving the posterobasal portion of the heart may lead to a structural failure, resulting in complex cardiac rupture, and in a few cases it may be associated with pseudoaneurysm formation. Because of the inherent structural complexity of the posterobasal portion of the heart, the pseudoaneurysms are associated with a risk of rupture and subsequent hemopericardium and death. The posterobasal portion of the heart represents the zone of insertion of the ventricles on atrioventricular groove and heart cytoskeleton, and it is surrounded by important structures such as the posterior mitral annulus and leaflet on the inside, and the terminal branches of left circumflex coronary artery, right coronary artery, and coronary sinus on the outside. (2) This structural complexity results in an unusual appearance of rupture, which creates a difficult dilemma in making clinical and radiologic differential diagnoses.

The rupture of the posterobasal portion of the heart characteristically presents with a complex morphologic structure with serpiginous and hemorrhagic tracts away from the primary laceration. This is in sharp contrast to free ventricular wall rupture, which will show a simple and more direct defect.(3) Edwards et al (4) demonstrated an autopsy study in which 69% of posterior ruptures had a complex morphologic structure in contrast to only 21% of anterior ruptures with a complex morphologic structure. Cardiac rupture following a transmural acute MI involving posterobasal myocardium is temporarily contained by a hematoma or permanently by fibrous adhesions, resulting in a pseudoaneurysm formation. The pseudoaneurysm formation results within 3 to 7 days following an acute MI and has a propensity to spontaneously rupture between 10 and 90 days. (1,2) Cardiac rupture involving the posterobasal portion of the heart is indeed a "double rupture" and involves 2 stages in its evolution. The first stage is a primary and complex rupture of the myocardium, contained temporarily by a pseudoaneurysm, and the second stage is a spontaneous rupture of pseudoaneurysm that results in hemopericardium and death.

Morphologically, in this case, because of the unique location of the pseudoaneurysm involving the atrioventricular groove, a rare possibility of giant coronary aneurysm involving the left circumflex coronary artery could be an important differential diagnostic consideration. However, the presence of an intact coronary artery wall was sufficient to rule out coronary artery aneurysm. Mesothelial inclusion cysts can rarely involve the pericardium of the posterior basal portion of the heart and might be confused with pseudoaneurysm radiologically. However, the unilocular, thin-walled, translucent gross appearance of the cyst, combined with the characteristic mesothelial lining, should differentiate pericardial cyst from a ventricular pseudoaneurysm. Entities such as intramyocardial developmental or inflammatory cysts and intramyocardial abscess are other differential diagnostic considerations (more radiologic than morphologic).

With effective control of secondary arrhythmias, cardiogenic shock and myocardial rupture are the most frequent causes of in-hospital deaths in patients who present with acute MI, out of which cardiac rupture contributes to one third of the deaths. Early diagnosis of ventricular pseudoaneurysm is extremely important, because surgical repair of pseudoaneurysm can be successful. In a few cases, progressive enlargement of the aneurysm may cause symptoms of heart failure due to systolic regurgitation into the low-impedance aneurysmal reservoir. (1) Thrombus may develop within the aneurysm and might give rise to systemic thromboembolism, which may be the only clinical manifestation, since it happened in the current case under discussion.

In summary, pseudoaneurysm formation is a very rare complication following MI of the posterobasal portion of the heart. Since the postinfarction myocardial rupture of the posterobasal portion of the heart may be temporarily contained by pseudoaneurysm, it may represent a critical phase in the evolution of the catastrophic event, namely cardiac rupture. Therefore, early diagnosis of this condition is extremely important, and one should be aware of the possibility of complex rupture and pseudoaneurysm formation in patients with posterobasal MI.


(1.) Csapo K, Voith L, Szuk T, Edes I, Kerelakes D. Postinfarction left ventricular pseudoaneurysm. Clin Cardiol. 1997;20:898-903.

(2.) Pretre R, Stalder N, Ye Q, Grunenfelder J, Jenni R, Turina M. Surgical repair of postinfarction structural failure of the posterobasal part of the heart. Ann Thorac Surg. 1999;68:2152-2157.

(3.) Tanabe K, Sugamori T, Yoshiromi H, Asanuma T, Shimada T. Fatal cardiac rupture: a case of subepicardial aneurysm after myocardial infarction. J Am Soc Echocardiogr. 2000;13:951-952.

(4.) Edwards BS, Edwards WD, Edwards JE. Ventricular septal rupture complicating acute myocardial infarction: identification of simple and complex types in 53 autopsied hearts. Am J Cardiol. 1984;54:1201-1205.

Accepted for publication September 14, 2001.

From the Case Western Reserve University at MetroHealth Medical Center, Cleveland, Ohio.

Reprints: Santhi Ganesan, MD, Department of Pathology, MetroHealth Medical Center, 2500 MetroHealth Dr, Cleveland, OH 44109 (e-mail:
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Author:Ganesan, Santhi; Quealy, Kathleen; Chung-Park, Moonja
Publication:Archives of Pathology & Laboratory Medicine
Date:Jun 1, 2002
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