False Aneurvsm and Pseudo-False Aneurysm of the Left qentricle: ~tiology, Pathology; Diagnosis, and Operative Management

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1 False Aneurvsm and Pseudo-False Aneurysm of the Left qentricle: ~tiology, Pathology; Diagnosis, and Operative Management S. Stewart, M.D., R. Huddle, M.D., I. Stuard, M.D., B. F. Schreiner, M.D., and J. A. DeWeese, M.D. ABSTRACT Four patients are presented in whom either a false aneurysm or a "pseudo-false" aneurysm of the left ventricle developed following a myocardial infarction. False aneurysms of the left ventricle are unusual and are distinctly different from the more common true aneuryms. A false aneurysm is the result of a contained hematoma dissecting into a transmural infarct. It communicates with the left ventricle through a small orifice. Previous descriptions of false aneurysms have stressed that their wall consists of pericardium and mural thrombus and lack identifiable epicardial or myocardial elements. Two pseudo-false aneurysms are described. They communicated with the left ventricle through a small orifice but their wall contained myocardial tissue. False aneurysms have a tendency to rupture and therefore their presence alone is an indication for operation. One of the pseudo-false aneurysms discussed ruptured into the right ventricle. The operation for false aneurysm may be simpler than that for true aneurysm since it might be possible to close the small communication into the left ventricle without resecting the entire aneurysm wall. The incidence of true aneurysm of the heart following myocardial infarction is approximately 10% [l]. The incidence of false aneurysm is not known but it appears to be quite rare. Four patients in whom a false aneurysm of the left ventricle developed after a myocardial infarction were treated at the University of Rochester Medical Center. This report describes From the Division of Cardiothoracic Surgery, Department of Pathology, and the Cardiology Unit, University of Rochester School of Medicine, Rochester, NY. Supported in part by Postgraduate Research Training Grant in Cardiology HL from the National Heart and Lung Institute, National Institutes of Health. Accepted for publication April 3, Address reprint requests to Dr. Stewart, Division of Cardiothoracic Surgery, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY the clinical presentation, diagnostic evaluation, operative management, and pathological findings. Case Reports Patient 1 A 50-year-old woman experienced burning substemal chest pain radiating into the neck 18 months prior to operation. A chest roentgenogram showed mild cardiomegaly, and an electrocardiogram showed T wave inversion and a small Q wave in leads 11, 111, and avf. On physical examination there was a prominent pulsation in the epigastrium. During the next 12 months, the patient became progressively more disabled with dyspnea on exertion, paroxysmal nocturnal dyspnea, and easy fatigability. Cardiac catheterization demonstrated normal intracardiac pressures and a slightly reduced cardiac index. The right coronary artery was totally obstructed while the left coronary system was normal. There was an inferiorly positioned false aneurysm, which expanded during systole (Fig 1A) and emptied during diastole (Fig 1B). The aneurysm communicated with the ventricular cavity through a relatively small orifice. At operation a large posterior aneurysm was found to be densely adherent to the diaphragm, the inferior vena cava, and the posterolateral pericardium (Fig 2). Cardiopulmonary bypass was instituted, the aorta was cross-clamped, and cold cardioplegia was established. The aneurysm, which was opened directly without dissecting it from the surrounding structures, contained a large amount of old thrombus and communicated with the left ventricular cavity through a small, 2 cm by 4 cm orifice in the posterobasal wall of the left ventricle. The edge of the orifice was densely fibrotic and was closed primarily with heavy Tevdek suture (Fig by The Society of Thoracic Surgeons

2 . Y 260 The Annals of Thoracic Surgery Vol 31 No 3 March 1981 A B Fig 1. (Patient 2 J The catheter is positioned in the cavity of the false aneurysm. (A) The aneurysm expands in systole and (B) empties during diastole. 3). The patient s postoperative course was satisfactory. Patient 2 A 64-year-old man sustained a diaphragmatic myocardial infarction five years prior to operation. During the next several years electrocardiograms and chest roentgenograms suggested the presence of a left ventricular aneurysm but he was asymptomatic. Five years after the infarction, he experienced multiple episodes of confusion and amnesia thought to represent periods of transient global cerebral ischemia from systemic emboli. On physical examination, the patient had both a third heart sound and a fourth heart sound. The left ventricle was enlarged to palpation. At cardiac catheterization, the left ventricular end-diastolic pressure was 25 mm Hg. There was total occlusion of the right coronary artery and narrowing of the proximal left anterior descending coronary artery. The left ventricular cineangiogram showed a large, clot-filled aneurysm. A large* Posterior left aneurysm Fig 2. (Patient 7.) The aneurysm was located on the posterior aspect of the left ventricle, and was adherent to the surrounding structures including the diaphragm, containing old thrombotic debris was identi- pericardium, andhferior vena cava. -

3 261 Stewart et al: False and Pseudo-False Aneurysm of Left Ventricle Fig 4. (Patient 2.) An external view of the posterior left ventricle postmortem. The wall of the unroofed false aneurysm was composed of pericardium and organized mural thrombus. Here it is retracted by clamps to expose the small central orifice leading into the left ventricle from which the Teflon felt and sutures have been remozwd. Fig 3. (Patient 1.) A small opening into the cavity of the left ventricle was identified and closed. The aneurysm sac was not resected. fied at operation. There were adhesions between the aneurysm and the diaphragm. There was a 3 cm defect in the posterior wall of the left ventricle, which communicated with the cavity of the aneurysm. The defect was closed directly over Teflon felt. A saphenous vein graft was placed to the left anterior descending coronary artery. A hemorrhage developed from the area of the junction of the right atrium, inferior vena cava, and atrioventricular groove. It could not be completely controlled, and the patient died. At postmortem examination, the aneurysm and its small communication with the left ventricle were again visualized (Fig 4). The wall of the false aneurysm was formed by an outer layer of pericardium and an inner layer of organizing mural thrombus (Fig 5). There were no myocardial cellular elements or coronary remnants present. Patient 3 A 37-year-old man sustained both an anterior and a diaphragmatic myocardial infarction in the year preceding operation. He had severely limiting angina and mild dyspnea on exertion following the second infarction. Physical examination was normal. The electrocardiogram was diagnostic of both an old anterior and a diaphragmatic infarction. At cardiac catheterization, the intracardiac pressures were normal. Coronary angiography demonstrated substantial proximal disease in all three major vessels. The left ventricular cineangiogram showed an apical aneurysm containing a filling defect. At operation, the aneurysm was located at the apex of the left ventricle and contained a large amount of clot and necrotic debris. It communicated with the cavity of the left ventricle through a 3 mm orifice. There were some fine, thin adhesions between the aneurysm and the pericardium. The aneurysm was excised, and saphenous veins were grafted to the posterior descending branch of the right coronary artery and to the left anterior descending coronary artery. The postoperative course was uneventful.

4 262 The Annals of Thoracic Surgery Vol 31 No 3 March 1981 A Fig 5. (Patient 2.) (A) A low-power microscopic view of the wall of the false aneurysm. It is composed of an outer layer of pericardial connective tissue and an inner layer of organized mural thrombus. There is neither an endothelial lining nor are there elements of myocardial muscle or coroniry vessels. (B) A higher magnification of the same section demonstrating the absence of an endothelial lining and confirming the absence of any myo- cardial elements. (Both, H6E; A: x22 before 25% reduction; B: ~ 8 before 4 35% reduction.) Microscopic examination of the aneurysm wall showed myocardial tissue mixed with infarct and scar. Patient 4 A 60-year-old man sustained a diaphragmatic infarction complicated by systemic hypertension and sporadic ventricular tachycardia. Four days after the infarction, a holosystolic murmur was heard for the first time. An M mode echocardiogram suggested a ventricular septal defect. A Swan-Ganz catheter was inserted. There was an oxygen step-up in the right ventricle and a pulmonary to systemic flow ratio B of 3 to 1. Congestive heart failure developed. Blood urea nitrogen and pulmonary artery diastolic pressure rose. The patient was treated with diuretics and large doses of nitroprusside and experienced progressive hemodynamic improvement. Four weeks after the myocardial infarction, coronary angiography demonstrated severe three-vessel disease. A left ventricular cineangiogram was not performed. At operation five weeks after the infarction, the pericardial space was entirely free from adhesions. An aneurysm was found on the diaphragmatic surface of the left ventricle. The aneurysm was opened, and a small 3 cm orifice at its base leading into the true left ventricular cavity was identified. In addition, a second opening from the aneurysm cavity across the ventricular septum into the right ventricle was present. The aneurysm apparently had developed as an expanding hematoma within the left ventricular wall near the septum and had ruptured through the septum into the right ventricle. The septal defect was closed with a patch. The opening from the aneurysm into the

5 263 Stewart et al: False and Pseudo-False Aneurysm of Left Ventricle ~ Fig 6. (Patient 4.) A low-power microscopic view of the wall of the pseudo-false aneurysm. The outer layer is epicardium and below that are myocardial muscle elements and coronary vessels interspersed with diffuse areas of fibrosis. (H6E; X25 before 25% reduction.) left ventricle was obliterated with large sutures taken from the right side of the septum below that opening and out the left ventricle adjacent to the aneurysm border. A sequential saphenous vein bypass graft was placed to the left anterior descending coronary artery and to its diagonal branch. Atrial and ventricular arrhythmias were satisfactorily controlled in the early postoperative period, and the patient was discharged twenty-four days after operation. Microscopic section of the partially resected aneurysm wall showed diffuse fibrosis interspersed with myocardial muscle elements and coronary vessels (Fig 6). Comment Both true and false aneurysms of the heart are sequelae of myocardial infarction but their etiology, effect on ventricular performance, diagnostic findings, potential complications, pathological findings, and operative management can be strikingly different. A true ventricular aneurysm results from the gradual thinning of a segment of ventricular wall following a transmural infarction. The wall often becomes adherent to the overlying pericardium. The thinned area can expand gradually so that its surface area far exceeds the original surface area of the infarct. The end result is a noncontractile, and perhaps expansile, segment which forms part of the true circumferential wall limits of the left ventricle. In general, the orifice into a true aneurysm is the largest diameter of the aneurysm. The wall of a true aneurysm is composed of pericardium adherent to underlying epicardium. Beneath this is the residual fibrous scar tissue of the infarcted myocardial muscle. There may also be remnants of myocardial muscle cells or coronary vessels. An inner layer of endothelium completes the wall of the aneurysm. There often is fresh or old organized thrombus within the aneurysm cavity L2, 31. In contrast, a false aneurysm occurs following hemorrhagic dissection into an area of transmural infarction [4, 51. Most commonly, such a process ends in free intrapericardial rupture of the heart, cardiac tamponade, and death [6]. However, if the overlying pericardium has become adherent to the epicardium along the surface of the infarction, it could contain a hematoma that has dissected through the myocardium. The left ventricular pressure is then transmitted through the tract of the hematoma to the fused epicardium and pericardium. This area then can stretch and form a false aneurysm, communicating with the true cavity of the left ventricle through the relatively small orifice created by the initial dissection which itself does not enlarge as the aneurysm enlarges 161 (Fig 7). Occasionally the hematoma does not dissect completely through to the epicardium but is contained within the area of the infarct. This segment of the infarcted wall can then expand under the transmitted left ventricular pressure and form a pseudo-false aneurysm as suggested in Patients 3 and 4 (see Fig 7). In each of these patients, a large aneurysm of the left ventricle communicated with that chamber through a small opening but in Patient 3 there were only a few fine adhesions between the epicardium and pericardium while in Patient 4 there were none. The absence of a dense fusion between these structures suggests that the dissecting

6 264 The Annals of Thoraac Surgery Vol 31 No 3 March 1981.) False aneum Pseudo-false aneurysm Fig 7. The mechanism of formation of false and pseudo-false aneurysms of the left ventricle following myocardial infarction. Both occur as a result of a hmatoma dissecting into tke area of infarction. The false aneurysm is contained by densely fused pericardium and epicardium while the pseudo-false aneurysm is contained by elements of the ventricular wall. hematoma was contained by the ventricular wall itself and not by an overlying fused layer of pericardium. The wall of most false aneurysms has an outer layer of fused pericardium and epicardium and beneath that is a layer of dense fibrous, collagenous tissue without evidence of any muscle elements except in the rare instance of a pseudo-false aneurysm 151. This layer is the product of organized thrombus material. False aneurysms often contain old thrombotic debris not unlike the material found in abdominal aortic aneurysms. The most striking difference between the two types of aneurysms on gross examination is their relationship to the cavity of the left ventricle. The true aneurysm forms part of the perimeter of the left ventricular cavity and communicates with it through an orifice whose diameter is usually equivalent to the diameter of the aneurysm itself. The false aneurysm does not form part of the perimeter of the left ventricular cavity and communicates with it through a relatively small orifice. Although the diagnosis of left ventricular aneurysm can be suspected clinically, it can be confirmed only by left ventricular cineangiography. A true aneurysm appears as a relatively smooth extension of the outline of the left ventricle and can be akinetic or dyskinetic. A false aneurysm often appears as a separate cavity which fills from the left ventricle through a small orifice during systole and empties back into the left Ventricle during diastole (see Fig 1B). It has a "dumbbell" appearance with a narrow neck between the two cavities. Both types of aneurysms can affect ventricular performance adversely but do so through different mechanisms. When the size of a true aneurysm exceeds 20 to 25% of the surface area of the ventricle, the myocardium is placed at a mechanical disadvantage which can be overcome only by dilatation of the ventricular cavity [7]. This results in an increase in systolic wall tension and increased myocardial oxygen consumption. The false aneurysm does not interfere with muscle function directly but acts to unload the ventricle during systole in a manner similar to mitral valve incompetence. This can reduce cardiac output and, indirectly, result in left ventricular dilatation. The major indications for the resection of a true aneurysm have been congestive heart failure and systemic emboli. Rupture of a chronic true aneurysm is extremely rare and has not been considered an indication for prophylactic resection. Although false aneurysms can result in similar symptoms, their propensity for producing systemic emboli may be less since they communicate with the left ventricle through a relatively small opening. They seem to have a much greater proclivity toward rupture and operation is indicated for that reason alone, even in the absence of symptoms [6, 81. The operative management of false aneurysms of the left ventricle is often simpler than that of true aneurysms. Since the aneurysm is not functionally part of the body of the left ventricle, it does not need to be excised. After cardiopulmonary bypass is established and the aorta is cross-clamped, the aneurysm needs only to be opened, the thrombotic debris removed, and the communication with the cavity

7 265 Stewart et al: False and Pseudo-False Aneurysm of Left Ventricle of the left ventricle closed directly. There is no need to dissect the aneurysm from the surrounding tissue or excise it from the ventricle. The clinical presentation, diagnostic evaluation, operative management, and pathological findings of false aneurysm or pseudo-false aneurysm of the left ventricle in 4 patients are described. False aneurysms differ from true aneurysms in their gross and, frequently, microscopic pathology and in their operative management. The indications for operative intervention are the same as those for true aneurysm. However, since they have a tendency toward rupture which is not shared by true aneurysms, prophylactic repair is a further indication for operation even in the asymptomatic patient. References 1. Abrams DL, Edlelist A, Luria MD, Miller AJ: Ventricular aneurysm. Circulation 27:164, Parkinson J, Bedford DE, Thomson WA: Cardiac aneurysm. Q J Med 7:455, Schlichter J, Hellerstein HK, Katz LN: Aneurysm of the heart: a correlative study of one hundred and two proved cases. Medicine (Baltimore) 33:43, Hurst CO, Fine G, Keyes JW: Pseudoaneurysm of the heart. Circulation 28:427, Roberts WC, Morrow AG: Pseudoaneurysm of the left ventricle. Am J Med 43:639, Van Tassel RA, Edwards JE: Rupture of the heart complicating myocardial infarction. Chest 61:104, Klein MD, Herman MV, Gorlin R: A hemodynamic study of left ventricular aneurysm. Circulation 35:614, Vlodaver Z, Coe JI, Edwards JE: True and false left ventricular aneurysms. Circulation 51:567, 1975 Notice from the American Board of Thoracic Surgery The American Board of Thoracic Surgery will give a voluntary recertification examination in the fall of Diplomates interested in participating in this examination should maintain a documented list of their cardiothoracic operations performed two years prior to application for recertification. They should also keep a record of their attendance at thoracic surgical meetings and other continuing medical education activities for the two years prior to application for recertification. A recertification brochure has been prepared outlining the rules and requirements. It also contains information about applying for the voluntary recertification examination. The brochure has been mailed to all Diplomates except those certified in 1979 and If you have not received yours and wish a brochure, please write the American Board of Thoracic Surgery, E Seven Mile Road, Detroit, MI