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Results for “Heart Rupture, Post-Infarction”

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PubMed1988

Treatment of the hemodynamically unstable patient.

The pathogenesis, diagnosis, and management of six clinical syndromes associated with acute myocardial infarction and hemodynamic instability are discussed: (1) autonomic disturbances with hypertension-tachycardia or hypotension-bradycardia; (2) pulmonary edema; (3) cardiogenic shock; (4) right ventricular infarction; (5) rupture of ventricular free wall or septum; and (6) papillary muscle rupture.

Cardiotonic Agents↗
PubMed1988

Transvenous closure of acquired ventricular septal defects.

Post infarction ventricular septal defect is an uncommon but frequently fatal complication of myocardial infarction. In this report a method for creating experimental ventricular septal defects is described and the use of a transvenous balloon catheter for closure of septal perforations reported. Ventricular septal defects were created with a specially designed punch in 25 adult mongrel dogs. Severe hemodynamic compromise occurred immediately following septal perforation in 15 animals which failed to permit sufficient time to pass the transvenous balloon catheter. However, passage of the catheter and occlusion of the ventricular septal defect was accomplished in the remaining 10 animals. Perforation of the ventricular septum resulted in a marked left-to-right shunt as indicated by changes in interventricular pressure and a step-up in the right ventricular PO2 saturations. Passage of the double balloon catheter and inflation of the balloons prevented left-to-right shunting and completely occluded the ventricular septal defect. Further refinements of this experimental catheter may result in the development of a balloon catheter that may be used to stabilize patients after spontaneous ventricular perforation, thus allowing them to recover from their infarction and undergo delayed repair of the ventricular septal defect.

Animals↗
PubMed1988

[Morphologic characteristics of the evolution of myocardial infarct after effective thrombolytic therapy].

Stroma and vessels which remain in the zone of myocardial infarction (MI) after thrombolytic therapy has restored impaired circulation during early hours of MI onset may produce foci of necrosis responsible for accelerated MI formation both in the periphery and centre of the foci. Hemorrhagic MI development can be related to microvascular and intramural vein spasms at early stages of the blood supply recovery. Fibrinoid necrosis of the wall and thrombosis of the lumen were observed in relevant vessels later on. These were associated with disturbed blood outflow from the infarction zone and hemorrhagic saturation of the interstice and cardiomyocytes.

Aged↗
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↗
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↗