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PubMed1986

[Infarct rupture of the heart. A clinical case operated on with success].

A 48-year-old woman was admitted for acute myocardial infarction with a normal clinical course. On the fifth day a new chest pain occurred, with low cardiac output and high central venous pressure; a pericardial effusion was present at the echocardiogram. The clinical picture improved with intensive medical care but, on the tenth day, there was a relapse with a life-threatening heart tamponade. An emergency operation was performed without previous heart catheterization. The pericardium was tense and contained about 300 ml of clots; in a wide infarcted area of the lateral wall of the left ventricle two small perforations were evident. Primary reconstruction was accomplished with interrupted stitches supported by Teflon felt strips. The bypass weaning was easy and the postoperative clinical course uneventful. We believe that the cardiac rupture is a surgical emergency; the non-invasive diagnosis is possible; the coronary angiography and revascularization must be postponed.

Emergencies↗
PubMed1986

[Anatomic features of postmortem experimental ruptures of the human heart].

Comparison of postmortem performed experimental cardiac ruptures with post-infarction lesions reveals uniformity of their localization. The ruptures are found to occur at places of a sharp change in the relief of the cardiac internal surface. These areas should be considered as concentrators of strain, promoting cardiac ruptures. In the left ventricle six concentrators of strain are revealed. They are: the place where the anterior part of the interventricular septum passes into the anterior wall of the left ventricle, the right edge of the papillary muscle, the left edge of the anterior papillary muscle, the left edge of the posterior papillary muscle, the right edge of the posterior papillary muscle, the place where the posterior part of the interventricular septum passes into the posterior wall of the left ventricle. Frequency of the experimental ruptures of the interventricular septum, under loading of the left ventricle, is demonstrated to depend on pressure in the right cardiac part.

Biomechanical Phenomena↗
PubMed1988

Management of post-infarction angina.

Post-infarction angina includes a syndrome of ischemic chest pain occurring either at rest or during minimal activity 24 hours or more following an acute MI. It develops in approximately 10 to 15 per cent of patients and is particularly common in non Q-wave infarcts involving the anterior myocardial wall. Post-infarction angina may result from ischemia either within the infarct zone or at a distance and frequently portends a poor long term prognosis. Platelet aggregation, coronary vasospasm, and thrombus formation at the site of a ruptured atherosclerotic plaque are each involved in its pathogenesis. The initial treatment of post-infarction angina includes identification and correction of factors that increase myocardial demand including congestive heart failure and arrhythmias. beta-Adrenergic blockers, calcium channel blockers, and nitrate preparations constitute the first line of medical therapy. The role of heparin is controversial, yet it continues to be used in clinical practice. Although thrombolytic agents are currently being investigated, early experience suggests that they may accelerate clinical stabilization and allow time for elective revascularization when required. Antiplatelet therapy with aspirin has proven benefit in the long term management of unstable angina. Patients unresponsive to medical therapy should be considered for intra-aortic balloon pump placement and early coronary angiography. Revascularization with either coronary angioplasty or coronary artery bypass grafting may then be performed as dictated by the overall clinical status, available facilities, and coronary anatomy.

Angina Pectoris↗
PubMedDate not supplied

Apparent rupture of the ventricular septum after myocardial infarction in an infant with congenital heart disease.

Clinical and angiocardiographic simulation of rupture of the interventricular septum, in an infant with an endocardial cushion defect and documented myocardial infarction is reported. Close straddling of a proven congenital muscular apical ventricular septal defect by trabeculae carne is believed to have led to the angiocardiographic simulation of a post-infarction apical ventricular septal defect. In the surgical approach to post-infarction ventricular septal defects, the implication of such a simulation could be important.

Heart Rupture↗
PubMed1989

[Surgical therapy of post-infarct aneurysm of the left ventricle. Immediate and long-term results].

Between January 1982 and December 1986, 62 patients (59 male and 3 female) ranging in age from 37 to 69 years (mean 53) underwent resection of postinfarction left ventricular aneurysm. The indication for operation was angina in 23 cases (37%), congestive heart failure (CHF) in 7 (11.2%), angina and CHF in 29 (46.8%), rupture in 1; 2 patients were low symptomatic. Ventricular arrhythmias were present in 6 (9.7%) cases and previous systemic embolism in 4 (6.4%). Forty-seven (75.8%) patients had lesions of three coronary arteries with involvement of left main coronary artery in 4 cases; 10 (16.1%) had lesions of two vessels [left anterior descending (LAD) and/or right coronary artery]; 4 (6.4%) had only LAD artery involvement, and 1 had no significant coronary artery stenoses. Left ventricular ejection fraction (EF) was less than 0.30 in 22% of cases, between 0.30 and 0.40 in 25.4% and greater than 0.40 in 50%. The location of the aneurysm was anterolateral or apical (83.8%), posterior (14.5%) and lateral (1.6%). Left ventricular aneurysmectomy with myocardial revascularization was performed in 61 patients (bypass/patient = 2.7), with ventricular septoplasty in 20 and concomitant mitral valve replacement in 3 patients. LAD was grafted in 59.6% of anterior aneurysm. Operative mortality (30 days) was 4.8%, the late mortality, with a follow-up between 12 and 72 months (mean 38), was 6.7% and the actuarial 5 year survival rate was 85% (91% without operative mortality). In our experience, despite no evidence of any operative risk factors, no improvement was noted in radionuclide left ventricular ejection fraction in patients undergoing aneurysmectomy with ventricular septoplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Major causes of death from acute myocardial infarction in a coronary care unit.

In order to define indications for newly developing aggressive managements for patients with acute myocardial infarction, an analysis of therapeutic results was made on 1,060 patients admitted to our coronary care unit (CCU). The total mortality was 14.9%, and 143 patients (13.5%) died from cardiac complications. These 143 patients were divided according to causes of death listed in Killip's classification. In the Killip class 4 group, mortality was as high as 86.6%, and all patients with previous infarction and/or hemodynamic abnormality of Forrester's subset 4 died. Pump failure caused death in 100 patients, of whom 69 were in a state of cardiogenic shock at the time of their admission. On the other hand, 58 patients, accounting for 40.6% of the cardiac deaths, were in Killip's class 1 or 2 at admission. In these 58 patients, 23 died from free wall rupture and/or perforation of the interventricular septum. Another 27 patients expired from reinfarction or infarct size extension and/or post-infarction angina. Thus, we can say that the major causes of death of patients in CCU are cardiogenic shock, reinfarction and cardiac rupture. We could not save these patients by using conventional CCU managements. Newly developing aggressive techniques, such as intracoronary thrombolysis and artificial hearts, seem to be indicated for these potentially fatal patients, while the effectiveness of these techniques should be verified as to such patients.

Adult↗
PubMed1988

Rupture of the right ventricular free wall. An unusual complication of mediastinitis after cardiac surgery.

Of 2171 patients who underwent open heart surgery between 1981 and 1986, 41 (1.8%) developed postoperative mediastinitis and were treated by closed irrigation drainage or open chest therapy. Six patients, (mean age 59 years) developed rupture of the right ventricular free wall. The primary procedures were: resection of akinetic fibrous plaque (2), mitral valve replacement (1), coronary bypass grafting (1), removal of a left atrial myxoma (1) and repair of post-infarction rupture of the left ventricle (1). In 2 patients, rupture occurred in the operating theatre during revision of the irrigation drainage. Both patients died after repair. In 4 patients, rupture occurred during coughing. One died before surgery. In the 3 other cases, the defects were repaired either by direct suture (2 patients) or with a pericardial patch (1 patient) with the aid of normothermic extracorporeal circulation. Three days later, a muscular flap (pectoral or dorso-lumbar) was mobilized to protect the mediastinal viscera. All 3 patients are alive and well. When bleeding occurs during treatment of mediastinitis, an immediate exploration with extracorporeal circulation to close the defect should be considered.

Aged↗
PubMed1979

[Surgery of ventricular aneurysms and akinetic zones].

Operation was performed in 180 patients with post-infarction ventricular aneurysm (12 cases) or akinesia (92 cases). Simultaneously in 2 cases mitral valve replacement was performed and in 2 cases ruptured ventricular septum was treated by patch. The results are reported and discussed.

Adult↗
PubMed1979

[False aneurysm associated with mitral insufficiency due to rupture of the heart at the point of insertion of the anterior papillary muscle. A successfully operated case].

Although rupture of a mitral papillary muscle during myocardial infarction is well known, and post-infarction transmural ruptures causing false aneurysms occasionally reported, the association of rupture of the anterior papillary muscle and a underlying transmural parietal rupture giving rise to a false aneurysm is quite exceptional, and, to the best of our knowledge, has not previously been reported. Despite the serious nature of the disease, surgical cure of the aneurysm with mitral valve replacement was successful, due to the limitation of the anatomical disruption by early pericardial symphysis.

Aneurysm↗
PubMed1976

Post-infarction cardiac rupture.

Three allied conditions are described in this paper: (i) haemopericardium with cardiac rupture (5 cases); (ii) haemopericardium without rupture (2 cases); (iii) pseudoaneurysm (1 case). In the first 2 of these, the significant features were clinical deterioration with shock 3 or more days after infarction, recurrent cardiac pain, cardiac tamponade, and immediate or later ineffectiveness of counterpulsation. An additional feature in the second group was the development of haemopericardium after heparin therapy. In the third group, infarction followed by left ventricular failure and progressive cardiac enlargement was the significant feature. An apical systolic murmur was not present, as a false sac had not been formed. Ante-mortem diagnosis depends upon an appreciation of these features. Without it successful surgery is impossible. There were 4 survivors in this group of 8 patients.

Aged↗
PubMed1990

[Mitral valve replacement in post-infarction rupture of the papillary muscle. Apropos of 13 cases surgically treated during the acute phase of infarction].

Between 1983 and 1988, thirteen patients (12 men and 1 women, average age 63 years) were operated in the acute phase of myocardial infarction for papillary muscle rupture (PMR). The rupture involved the posterior papillary muscle in 12 cases. The average left ventricular ejection fraction was 47 +/- 9 per cent (range 34 to 63%). Pulmonary capillary pressures ranged from 76 to 41 mmHg (average 35 mmHg). Eleven patients presented with acute pulmonary oedema and 7 had cardiogenic shock. Coronary arteriography showed triple vessel disease in 3 cases, double vessel disease in 7 cases and single vessel disease in 3 cases. Surgery was carried out on average 2.7 days after the rupture and 10 days after the initial infarct. In addition to mitral valve replacement (N = 13), 11 patients underwent a myocardial revascularisation procedure. The operative mortality was 15 per cent (N = 2). Papillary muscle rupture in the acute phase of myocardial infarction causes cardiac failure which is related more to the mechanical abnormality than to an alteration of left ventricular function. Considering the operative mortality and the natural history of PMR treated medically, the authors recommend early surgery as the only management which can improve the precarious haemodynamic status of patients with this complication.

Aged↗
PubMed1990

[Post-infarction pseudoaneurysm of the left ventricle as a cause of heart failure. Presentation of a surgically treated case].

Pseudoaneurysm of the left ventricle is an unusual complication of myocardial infarction. Surgical resection is justified by the high risk of rupture. Patients may be asymptomatic, more often a clinical state of chronic heart failure is present. We report on a patient who successfully underwent urgent resection of a large pseudoaneurysm which was the cause of acute heart failure.

Emergencies↗