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Mediastinitis-related right ventricular rupture is an unusual but potentially life-threatening complication of cardiac operations. Between January 1981 and December 1990, a total of 10,182 patients underwent heart operations for ischemic, valvular, and congenital heart disease at the Montreal Heart Institute. Forty-eight patients (0.5%) had postoperative mediastinitis necessitating surgical exploration and sternal debridement. The mediastinum was left open for daily irrigation with povidone-iodine and chest reconstruction was postponed. During treatment, seven patients (0.07%) had right ventricular rupture necessitating immediate surgical repair. All had ischemic heart disease before the operation. There were five women and two men, ages ranging from 52 to 65 years (mean 58 +/- 5 years). Surgical repair consisted of autologous patch covered with omentoplasty assisted with cardiopulmonary bypass. Two patients died, one during the operation of massive hemorrhage and the other 10 days after the operation of uncontrolled sepsis. Five patients survived 2 to 29 months (mean 23 +/- 10 months) after right ventricular rupture, with an overall survival of 71%. Obesity was more frequent in the patients with right ventricular rupture and was found to be a significant risk factor (multivariate analysis, p < 0.05, relative risk 3.22). Histologic examination of the right ventricle in the patient who died after a successful repair revealed fatty infiltration of the right ventricular wall. This may have predisposed the patient toward ventricular rupture. In conclusion, right ventricular rupture, an unusual event in heart surgery, is related to open sternal debridement. Favorable outcome of this complication depends on immediate surgical management, autologous repair, and the use of omentoplasty.

Rupture of the left ventricle in the atrioventricular (AV) groove is a rare and usually fatal complication of mitral valve replacement (MVR). The successful repair of a delayed type I left ventricular rupture is described. The technique of repair is described, the literature reviewed, and three further cases from the authors' experience are reported.

Eight patients (mean age 63.75 years) were operated upon for post-myocardial infarction ventricular septal rupture (PMI-VSD) within 1 to 21 days of the infarction and 8 hours to 18 days of rupture. All but one were in low cardiac output syndrome necessitating intra-aortic balloon pumping; all had cardiac catheterization. The VSD was closed via a transinfarct ventriculotomy with an oversized folded double patch, the folded edge being incorporated in the ventriculotomy closure. Five patients received seven saphenous vein coronary bypass grafts. None had recurrent shunts. Six patients (anterior VSD, five; posterior VSD, one) are survivors (18 months to 2.5 years) in Class I (five) or Class II (one). Two patients died postoperatively, one (anterior VSD) of an arrhythmia and the other (posterior VSD) while on biventricular bypass support. Two survivors in whom prolonged preoperative stabilization was attempted required emergency operation before the planned waiting period of 3 weeks had elapsed, and both had postoperative multiorgan complications. Our present approach is to operate as soon as clinical and catheterization diagnosis of VSD is made.

A 62-year-old man presented with a grand mal seizure, progressive abdominal distention, and refractory hypotension 18 years after colonic bypass of a benign stricture of the low middle third of the esophagus. He died 3 hours after admission to the hospital. The patient had a history of liniment ingestion in childhood plus a long history of dysphagia and substernal pain. Autopsy disclosed a large ulcer of the anterior wall of the distal esophagus, which had eroded through the posterior wall of the left atrium. Histologic examination revealed chronic esophagitis with fibrous obliteration of the esophageal wall, pericardium, and left atrial myocardium near the site of perforation. Foreign material was present within small arteries of multiple viscera, and in several of these fragments transverse striations were demonstrated. Esophageal-atrial perforation is a rare but fatal complication of chronic esophageal ulceration. The clinical and pathological features of this and previously reported cases of nontraumatic esophageal-atrial perforation are reviewed.

Damage to the posterolateral wall of the left ventricle was found in eight of approximately 700 sheep undergoing mitral valvular replacement as part of animal model studies of bioprosthetic valves. The damage consisted of left ventricular aneurysms in five animals, subacute rupture of the left ventricle in one, acute left ventricular laceration in one, and endocardial scarring in one. Six of the eight bioprostheses were bovine pericardial valves, including five low-profile valves and one standard valve; of the two porcine bioprostheses, one was intentionally oversized and the other was a low-profile supra-annular valve. In each of these animals the damage appeared to have been caused by contact between the most posterior strut of the bioprosthesis and the left ventricular wall.

Following a posterolateral myocardial infarction, a 57-year-old man developed severe shock which did not respond to catecholamine infusion and intra-aortic balloon counterpulsation. Implantation of a left ventricular assist pump was planned, but at sternotomy free ventricular rupture was identified and repaired. Repair of free-wall ventricular rupture is uncommon because of infrequent antemortem diagnosis. A more aggressive surgical approach of instituting left ventricular assist pumping in those patients with cardiogenic shock refractory to medical therapy and intra-aortic balloon pumping should yield the additional benefit of repair of the rather common but rarely recognized lesion of ventricular rupture.

This paper records an experience of 42 cases of cardiac rupture or syndromes simulating rupture. These include free wall rupture, hemopericardium without rupture, septal rupture associated with free wall rupture, pseudoaneurysm, and septal rupture. These groups constitute a series of syndromes with many features in common in terms of clinical presentation, difficulty in assessment, timing of operative intervention, and operative management. Free wall rupture, which can be simulated by hemopericardium without rupture, is not always rapidly fatal. Successful intervention was achieved in six of the 13 cases in the free wall group. Ventricular septal defect occurs less frequently than free wall rupture, is more easily diagnosed, and less frequently requires urgent medical intervention. In 12 of the 14 cases of acute rupture, stabilization of the patient by conservative measures could not be achieved and operation was undertaken within 1 week of infarction. There were seven survivors, in four of whom the defect reopened, with successful reoperation in three. In the remaining 15 cases, stabilization by conservative measures was achieved and operation was delayed until at least 2 weeks after infarction. There were 14 survivors and only one instance of reopening of the defect.

Experience with surgical treatment of 10 patients with aneurysms of the inferior wall of the left ventricle is presented. Six of the 10 aneurysms were false (pseudoaneurysms), and four were classified as true aneurysms. All except one resulted from myocardial infarction. Combined procedures, performed at the time of aneurysm resection, included mitral valve replacement (five patients), coronary artery bypass grafting (four patients), and closure of an interventricular septal defect (one patient). Three of four patients with true inferior aneurysms had mitral valve dysfunction, whereas only two of six patients with false aneurysms required mitral valve replacement (one because of infective endocarditis). Nine of the 10 patients survived operation, and all are functionally improved except one. On the basis of this and previously reported experience, it is concluded that a substantial proportion of inferior left ventricular aneurysms exhibit the pathological features of false aneurysms. Because of the associated propensity toward rupture of such lesions, an aggressive surgical approach is recommended.

Since 1973, 11 patients have had emergency valve replacement for severe mitral insufficiency and cardiogenic shock within 1 month (mean 10.0 days) of acute myocardial infarction. Mean age was 60 years (range 44 to 71 years). Nine infarcts affected the inferior wall, one patient had a prior myocardial infarction, and only two patients had a history of cardiac symptoms. Ten patients had pulmonary edema, five were oliguric (less than 0.5 ml/kg/hr for 12 hours), four required endotracheal intubation, nine required preoperative intra-aortic balloon support, and three had had a cardiac arrest. Preoperative cardiac index averaged 1.7 L/m2/min even with pharmacologic and circulatory support. Eight patients had cardiac catheterization and nine had echocardiograms. Left ventricular ejection fraction varied from 23% to 83% (mean 51%) and was not prognostic. Five patients had papillary muscle rupture and six patients had papillary muscle dysfunction. The mitral valve was replaced with a mechanical prosthesis in all patients. Five had simultaneous coronary artery bypass grafts. Three of five patients with papillary muscle rupture and two of six with papillary muscle dysfunction survived hospitalization. Two patients could not be weaned from cardiopulmonary bypass, two patients died within 24 hours of low cardiac output, and two patients died 3 weeks postoperatively of acute tubular necrosis and sepsis following prolonged preoperative cardiogenic shock. The interval from onset of shock to operative therapy averaged 1.7 days for survivors versus 9.3 days for nonsurvivors. Although the amount of viable left ventricular mass cannot be measured preoperatively, we recommend early operation, before other organ systems fail, for patients having severe mitral insufficiency and cardiogenic shock within 30 days of acute myocardial infarction.

A 62-year-old man sustained an acute myocardial infarction complicated on the thirteen hour by left ventricular rupture and acute periocardial tamponade. Echocardiography confirmed the suspicion of intrapericardial fluid, and immediate pericardiocentesis improved the hemodynamic state for a period sufficient to permit preparation for operation. Resection of ruptured and necrotic anteroapical left ventricular myocardium with primary reconstruction was successfully accomplished with the aid of temporary extracorporeal circulation. The patient has remained well for 1 year after the operation. Anatomic, clinical, and therapeutic features of acute cardiac rupture are discussed.

A patient with type I left ventricular rupture after mitral valve replacement was successfully treated by suturing a pericardial patch to the healthy endocardium around the tear.

Blowout rupture of the myocardium is intended to describe a syndrome of sudden hemodynamic deterioration after myocardial infarction. Characterized by abrupt hypotension, cardiac tamponade, or electromechanical dissociation, it is an emergency of the first order with no time for cardiac catheterization. Frequently one must make the diagnosis and race for the operating room almost simultaneously. We have managed four such patients, one with a ruptured false aneurysm and three patients with acute rupture of recently infarcted myocardium. All patients were placed on femoro-femoral bypass initially and all survived operation. Two patients died in the hospital of irreversible brain damage and two are long-term survivors. A high index of suspicion, a well-coordinated operating team, and a willingness to take the bold step to the operating room, frequently on the basis of clinical judgment alone, are necessary to salvage patients with this syndrome.