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False aneurysm of the left ventricle
False aneurysm of the left ventricle Surgical treatment The clinical and pathological features in three cases of false aneurysm of the left ventricle are reported. In two instances the condition developed after myocardial infarction, and in the third case a mycotic pseudoaneurysm developed after purulent pericarditis. All three patients were in intractable heart failure before urgent operation. The correct diagnosis was establishedpreoperatively by angiography. In all three cases the aneurysms were successfully resected and the left ventricle reconstructed. An aggressive surgical approach is warranted in the management of this lesion. V. Yakierevitch, M . D . , B. Vidne, M . D . , R. Melamed, M . D . , and M. J. Levy, M . D . , Tel Aviv, Israel
IT seudoaneurysm of the left ventricle most commonly results from a recent myocardial infarction. Among the less frequent causes of pseudoaneurysm are myocardial abscess, infected embolic aneurysm, and erosive aneurysm. Myocardial abscesses usually result from pyemia and almost always are multiple. A single myocardial abscess, however, may be caused by a septic embolus and would more correctly be designated as a septic infarct or mycotic false aneurysm of the heart. Pseudoaneurysm of the left ventricle following acute myocardial infarction is rare, because in most instances rupture of this chamber leads to fatal hemopericardium. However, there are instances of survival following myocardial rupture because of the development of an extra chamber owing to pericardial adhesions. The present report deals with the clinical and pathological features of three cases of this unusual and rare complication and their successful treatment. Case reports CASE 1. A 66-year-old man with severe coronary insufficiency had a myocardial infarction and pericarditis in 1970. In 1972 he underwent resection of an aneurysm of the left ventricle, and after 8 months he was operated upon again because of the development of a pseudoaneurysm at the site of the previous aneurysmectomy. He was almost free of symptoms when, 2 years later, he began to have shortness of breath, tachycardia, and abnormal fatigability. From the Thoracic and Cardiovascular Surgery Department and the Cardiology Department, Beilinson Medical Center, Tel Aviv University Medical School, Tel Aviv, Israel. Received for publication April 12, 1978. Accepted for publication May 23, 1978.
556
Chest roentgenogram revealed marked enlargement of the cardiac silhouette (Fig. 1). Repeat cineangiography again revealed the formation of an aneurysm (Fig. 2). Urgent operation was decided upon, and dense adhesions were found between the pericardium and epicardium. A false aneurysm with a diameter of 7 cm. was found in the posterolateral part of the left ventricle in the region of the previously resected pseudoaneurysm. A tight 2 mm. communication between the false aneurysm and the left ventricular cavity allowed free blood flow between the two chambers. Microscopic examination showed the pseudoaneurysmal wall to consist entirely of fibrous tissue. The patient was discharged from the hospital in satisfactory condition and is well 2 years after the operation. CASE 2. A 6-year-old girl was hospitalized in the pediatric unit of this hospital because of osteomyelitis of the right femur. Her postoperative course following a sequestrectomy was complicated by sepsis and purulent pericarditis. She underwent pericardiocentesis on three occasions, with aspiration of purulent, staphylococcal fluid. After the third time, a shadow was noted on chest radiography close to the left border of the heart. Cineangiography revealed a large aneurysmal sac originating from the anterolateral wall of the left ventricle (Fig. 3). At operation on Feb. 15, 1976, there were adhesions between the pericardium and epicardium. A sac attached to the left ventricle by way of a narrow neck, with a diameter of 3 to 4 mm., was seen to pulsate during left ventricular systole. After the sac was opened and resected, this neck was closed. On microscopic examination, the wall of the false aneurysm was seen to consist of dense fibrous tissue with only a few scattered muscle bundles discernible. The girl was discharged from the hospital in satisfactory condition and is well 1 year after the operation. CASE 3. During hospitalization following a myocardial infarction, a 52-year-old woman began having signs of a ventricular septal defect which rapidly progressed to heart failure. The electrocardiogram showed persistent ST-segment elevation. Roentgenogram of die chest demonstrated marked
0022-5223/78/100556+03$00.30/0 © 1978 The C. V. Mosby Co.
Volume 76 Number 4 October, 1978
Fig. 1. Chest roentgenogram (posteroanterior view) showing the presence of a large mass adjacent to the border to the left ventricle, reminiscent of the left ventricular aneurysm present prior to the first operation (Case 1). left ventricular prominence suggestive of an aneurysm and prominent pulmonary vasculature. Urgent cardiac catheterization revealed a low systolic pressure and an elevated left ventricular end-diastolic pressure— 90/29 mm. Hg. Cineangiography disclosed a ventricular septal defect and a huge aneurysmal sac originating from the anterior apical and diaphragmatic walls of the left ventricle. Urgent operation was undertaken on July 7, 1976. When the sternum was divided, a taut pericardium was seen with no visible heart contraction. A sac was clearly demonstrated, formed by pericardium that was densely fused to the myocardium in the area thought to be an aneurysm. The pericardial sac was incised and 300 to 400 c.c. of blood was aspirated. When the operative field became dry, a fistulous tract was noted on the anterior apical ventricular wall; this tract led to a small true ventricular aneurysm and ejected blood to the false aneurysm. Opening the aneurysm revealed a hole, 1 cm. in diameter, in the posteroinferior part of the ventricular septum with fibrous tissue surrounding it. The ventricular septal defect was closed with a double suture supported by Dacron pledgets. The aneurysm was excised and the ventricular wall sutured. Microscopic examination revealed scarring of the left ventricular myocardium adjacent to the mouth of the aneurysm. In addition, pericardial tissue infiltrated by scar tissue represented the wall of the false aneurysm. The patient was discharged from the hospital in satisfactory condition and is well 12 months after the operation. Discussion The pathogenesis of true aneurysm of the heart is similar but not identical to that of false aneurysm. Both require damage to the myocardium resulting in its inability to withstand the intracardiac pressure, but false aneurysm requires an additional factor—fibrous thick-
False aneurysm of left ventricle
557
Fig. 2. Left ventriculogram (lateral view) showing a false aneurysm communicating with the left ventricle through a narrow neck (Case 1).
Fig. 3. Left ventriculogram (posteroanterior view). The contrast material in the cavity of the left ventricle can be seen passing through a narrow ostium into the large chamber of the false aneurysm (Case 2). ening and adhesions of the pericardium and epicardium sufficient to localize and retain the escaping blood within a restricted area. Without the latter there can be no false aneurysm, since the escaping blood would cause rapid death, either by producing cardiac tamponade or by rupturing through the parietal pericardium into the adjacent tissues and pleural cavities. 1 The hemodynamics of false aneurysm simulate mitral valve regurgitation, since a portion of the ventricular stroke volume is sequestered in the sac during systole. Because the sac is large in most cases, cardiac output is significantly reduced and intractable
The Journal of Thoracic and Cardiovascular Surgery
5 5 8 Yakierevitch et al.
heart failure or cardiogenic shock frequently results. In contrast to the true variety, false aneurysms may become very large, but the mouth of the aneurysm is always narrow. Because of the continuing enlargement, rupture of a false aneurysm is an imminent threat. By contrast, the chronic true aneurysm ruptures only rarely. 2,3 An interesting feature common to both varieties of aneurysm is the occurrence of thrombus in the sac, although these thrombi differ in nature. Thrombus in pseudoaneurysms frequently remains free because the sac is essentially avascular, whereas in true aneurysms thrombus usually becomes organized and adherent to the wall. However, the small ostia of false aneurysms apparently reduce the incidence of systemic embolism in these lesions.4 To avoid systemic and coronary embolism during operation, the surgeon should not handle these aneurysms before total cardiopulmonary bypass is instituted, the ascending aorta cross-clamped, and the heart fibrillated. A diagnosis of false aneurysm of the left ventricle can be suspected from the clinical picture, chest roentgenogram, and electrocardiogram, but the specific diagnosis can be confirmed only by angiocardiography, with the contrast material injected directly into the ventricle. This diagnostic procedure provides additional valuable preoperative information concerning the over-all condition, such as orifice size, relative position and mobility of the aneurysm, and the presence of clot. The indications for operation are usually the same for both false and true aneurysms, namely, intractable congestive heart failure, recurrent arrhythmias, and systemic embolization. The threat of rupture, however, is an added and prime indication for surgical resection in cases of false aneurysm, and aggressive surgical therapy for these lesions is warranted.
Our three cases, although identical in regard to hemodynamics, differ in regard to cause. The first case exemplifies the formation of pseudoaneurysm at the site of an old myocardial scar resulting from previous ventricular aneurysmectomy. The second case clearly demonstrates the relation between purulent pericarditis and the formation of myocardial abscess with consequent communication between the two. The last case illustrates the formation of a false aneurysm secondary to acute myocardial necrosis and rupture following infarction. In all cases, however, the presence of dense epicardial-pericardial adhesions adjacent to the ventricular wall fistula formed the anatomic basis for this rare formation. All were treated surgically with good results.
REFERENCES 1 Glyde OH, Fine G, Keves JW: Pseudoaneurysm of the heart. Circulation 28:427, 1963. 2 Bjornosson L: Pseudoaneurysm of the left ventricle of the heart. Am J Clin Pathol 41:302-306, 1964 3 Smith RC, Goldberg H, Bailey CP: Pseudoaneurysm of the left ventricle. Diagnosis by direct cardioangiography. Surgery 42:496-510, 1957 4 Roberts WC, Morrow AG: Pseudoaneurysm of the left ventricle. Am J Med 43:639-644, 1967 5 Abrams DL, Edelist A, Luria MH, Miller A: Ventricular aneurysm. Circulation 27:164-169, 1963. 6 Van Tassel RA, Edwards JE: Rupture of heart complicating myocardial infarction. Chest 61:104-116, 1972 7 Fadali MA: Successful surgical treatment of false ventricular aneurysm. Pa Med, p. 32, 1974 8 Fallah-nejad M, Abelson DM, Blakemore WS: Left ventricular pseudoaneurysm. Chest 61:90-92, 1972
IT seudoaneurysm of the left ventricle most commonly results from a recent myocardial infarction. Among the less frequent causes of pseudoaneurysm are myocardial abscess, infected embolic aneurysm, and erosive aneurysm. Myocardial abscesses usually result from pyemia and almost always are multiple. A single myocardial abscess, however, may be caused by a septic embolus and would more correctly be designated as a septic infarct or mycotic false aneurysm of the heart. Pseudoaneurysm of the left ventricle following acute myocardial infarction is rare, because in most instances rupture of this chamber leads to fatal hemopericardium. However, there are instances of survival following myocardial rupture because of the development of an extra chamber owing to pericardial adhesions. The present report deals with the clinical and pathological features of three cases of this unusual and rare complication and their successful treatment. Case reports CASE 1. A 66-year-old man with severe coronary insufficiency had a myocardial infarction and pericarditis in 1970. In 1972 he underwent resection of an aneurysm of the left ventricle, and after 8 months he was operated upon again because of the development of a pseudoaneurysm at the site of the previous aneurysmectomy. He was almost free of symptoms when, 2 years later, he began to have shortness of breath, tachycardia, and abnormal fatigability. From the Thoracic and Cardiovascular Surgery Department and the Cardiology Department, Beilinson Medical Center, Tel Aviv University Medical School, Tel Aviv, Israel. Received for publication April 12, 1978. Accepted for publication May 23, 1978.
556
Chest roentgenogram revealed marked enlargement of the cardiac silhouette (Fig. 1). Repeat cineangiography again revealed the formation of an aneurysm (Fig. 2). Urgent operation was decided upon, and dense adhesions were found between the pericardium and epicardium. A false aneurysm with a diameter of 7 cm. was found in the posterolateral part of the left ventricle in the region of the previously resected pseudoaneurysm. A tight 2 mm. communication between the false aneurysm and the left ventricular cavity allowed free blood flow between the two chambers. Microscopic examination showed the pseudoaneurysmal wall to consist entirely of fibrous tissue. The patient was discharged from the hospital in satisfactory condition and is well 2 years after the operation. CASE 2. A 6-year-old girl was hospitalized in the pediatric unit of this hospital because of osteomyelitis of the right femur. Her postoperative course following a sequestrectomy was complicated by sepsis and purulent pericarditis. She underwent pericardiocentesis on three occasions, with aspiration of purulent, staphylococcal fluid. After the third time, a shadow was noted on chest radiography close to the left border of the heart. Cineangiography revealed a large aneurysmal sac originating from the anterolateral wall of the left ventricle (Fig. 3). At operation on Feb. 15, 1976, there were adhesions between the pericardium and epicardium. A sac attached to the left ventricle by way of a narrow neck, with a diameter of 3 to 4 mm., was seen to pulsate during left ventricular systole. After the sac was opened and resected, this neck was closed. On microscopic examination, the wall of the false aneurysm was seen to consist of dense fibrous tissue with only a few scattered muscle bundles discernible. The girl was discharged from the hospital in satisfactory condition and is well 1 year after the operation. CASE 3. During hospitalization following a myocardial infarction, a 52-year-old woman began having signs of a ventricular septal defect which rapidly progressed to heart failure. The electrocardiogram showed persistent ST-segment elevation. Roentgenogram of die chest demonstrated marked
0022-5223/78/100556+03$00.30/0 © 1978 The C. V. Mosby Co.
Volume 76 Number 4 October, 1978
Fig. 1. Chest roentgenogram (posteroanterior view) showing the presence of a large mass adjacent to the border to the left ventricle, reminiscent of the left ventricular aneurysm present prior to the first operation (Case 1). left ventricular prominence suggestive of an aneurysm and prominent pulmonary vasculature. Urgent cardiac catheterization revealed a low systolic pressure and an elevated left ventricular end-diastolic pressure— 90/29 mm. Hg. Cineangiography disclosed a ventricular septal defect and a huge aneurysmal sac originating from the anterior apical and diaphragmatic walls of the left ventricle. Urgent operation was undertaken on July 7, 1976. When the sternum was divided, a taut pericardium was seen with no visible heart contraction. A sac was clearly demonstrated, formed by pericardium that was densely fused to the myocardium in the area thought to be an aneurysm. The pericardial sac was incised and 300 to 400 c.c. of blood was aspirated. When the operative field became dry, a fistulous tract was noted on the anterior apical ventricular wall; this tract led to a small true ventricular aneurysm and ejected blood to the false aneurysm. Opening the aneurysm revealed a hole, 1 cm. in diameter, in the posteroinferior part of the ventricular septum with fibrous tissue surrounding it. The ventricular septal defect was closed with a double suture supported by Dacron pledgets. The aneurysm was excised and the ventricular wall sutured. Microscopic examination revealed scarring of the left ventricular myocardium adjacent to the mouth of the aneurysm. In addition, pericardial tissue infiltrated by scar tissue represented the wall of the false aneurysm. The patient was discharged from the hospital in satisfactory condition and is well 12 months after the operation. Discussion The pathogenesis of true aneurysm of the heart is similar but not identical to that of false aneurysm. Both require damage to the myocardium resulting in its inability to withstand the intracardiac pressure, but false aneurysm requires an additional factor—fibrous thick-
False aneurysm of left ventricle
557
Fig. 2. Left ventriculogram (lateral view) showing a false aneurysm communicating with the left ventricle through a narrow neck (Case 1).
Fig. 3. Left ventriculogram (posteroanterior view). The contrast material in the cavity of the left ventricle can be seen passing through a narrow ostium into the large chamber of the false aneurysm (Case 2). ening and adhesions of the pericardium and epicardium sufficient to localize and retain the escaping blood within a restricted area. Without the latter there can be no false aneurysm, since the escaping blood would cause rapid death, either by producing cardiac tamponade or by rupturing through the parietal pericardium into the adjacent tissues and pleural cavities. 1 The hemodynamics of false aneurysm simulate mitral valve regurgitation, since a portion of the ventricular stroke volume is sequestered in the sac during systole. Because the sac is large in most cases, cardiac output is significantly reduced and intractable
The Journal of Thoracic and Cardiovascular Surgery
5 5 8 Yakierevitch et al.
heart failure or cardiogenic shock frequently results. In contrast to the true variety, false aneurysms may become very large, but the mouth of the aneurysm is always narrow. Because of the continuing enlargement, rupture of a false aneurysm is an imminent threat. By contrast, the chronic true aneurysm ruptures only rarely. 2,3 An interesting feature common to both varieties of aneurysm is the occurrence of thrombus in the sac, although these thrombi differ in nature. Thrombus in pseudoaneurysms frequently remains free because the sac is essentially avascular, whereas in true aneurysms thrombus usually becomes organized and adherent to the wall. However, the small ostia of false aneurysms apparently reduce the incidence of systemic embolism in these lesions.4 To avoid systemic and coronary embolism during operation, the surgeon should not handle these aneurysms before total cardiopulmonary bypass is instituted, the ascending aorta cross-clamped, and the heart fibrillated. A diagnosis of false aneurysm of the left ventricle can be suspected from the clinical picture, chest roentgenogram, and electrocardiogram, but the specific diagnosis can be confirmed only by angiocardiography, with the contrast material injected directly into the ventricle. This diagnostic procedure provides additional valuable preoperative information concerning the over-all condition, such as orifice size, relative position and mobility of the aneurysm, and the presence of clot. The indications for operation are usually the same for both false and true aneurysms, namely, intractable congestive heart failure, recurrent arrhythmias, and systemic embolization. The threat of rupture, however, is an added and prime indication for surgical resection in cases of false aneurysm, and aggressive surgical therapy for these lesions is warranted.
Our three cases, although identical in regard to hemodynamics, differ in regard to cause. The first case exemplifies the formation of pseudoaneurysm at the site of an old myocardial scar resulting from previous ventricular aneurysmectomy. The second case clearly demonstrates the relation between purulent pericarditis and the formation of myocardial abscess with consequent communication between the two. The last case illustrates the formation of a false aneurysm secondary to acute myocardial necrosis and rupture following infarction. In all cases, however, the presence of dense epicardial-pericardial adhesions adjacent to the ventricular wall fistula formed the anatomic basis for this rare formation. All were treated surgically with good results.
REFERENCES 1 Glyde OH, Fine G, Keves JW: Pseudoaneurysm of the heart. Circulation 28:427, 1963. 2 Bjornosson L: Pseudoaneurysm of the left ventricle of the heart. Am J Clin Pathol 41:302-306, 1964 3 Smith RC, Goldberg H, Bailey CP: Pseudoaneurysm of the left ventricle. Diagnosis by direct cardioangiography. Surgery 42:496-510, 1957 4 Roberts WC, Morrow AG: Pseudoaneurysm of the left ventricle. Am J Med 43:639-644, 1967 5 Abrams DL, Edelist A, Luria MH, Miller A: Ventricular aneurysm. Circulation 27:164-169, 1963. 6 Van Tassel RA, Edwards JE: Rupture of heart complicating myocardial infarction. Chest 61:104-116, 1972 7 Fadali MA: Successful surgical treatment of false ventricular aneurysm. Pa Med, p. 32, 1974 8 Fallah-nejad M, Abelson DM, Blakemore WS: Left ventricular pseudoaneurysm. Chest 61:90-92, 1972