Repair of ventricle free wall rupture after acute myocardial infarction: a case report

Abstract

IntroductionAcute myocardial infarction (AMI) may culminate in sudden death by ventricular fibrillation, cardiogenic shock, and cardiac rupture. We present a case of postinfarction rupture treated by direct closure and coronary artery bypass grafting after thrombolytic therapy.Case reportA 67-year-old woman with cardiac risk factors of hypertension, diabetes mellitus, and being post-menopausal was admitted complaining of chest pain and sweating. Thrombolytic therapy with streptokinase was started due to acute myocardial infarction. But, reperfusion criteria were not achieved. Echocardiography revealed a moderate pericardial effusion with mild right chamber collapse and pericardial thrombus. Cardiac catheterization revealed totally occluded left anterior descending (LAD) and circumflex coronary arteries. She was taken to the operating-room immediately. The pericardium was opened and a large amount of blood with thrombus was removed. Her hemodynamic indices improved immediately. There was active bleeding from multiple sites with a 4 mm rupture. Cardiopulmonary bypass was established. Direct closure of rupture was carried out. Reversed autogenous saphenous vein bypass grafts were placed to the LAD and second obtuse margin coronary arteries. Postoperative recovery was uneventful and she was discharged from hospital in good condition. She remained asymptomatic during first year following the surgery.ConclusionThis case demonstrates that left ventricular free wall rupture is not always fatal and that early diagnosis and emergency surgical therapy may be successful. The combination of surgical repair with revascularization should be considered, because 80% of patients who experience LVFWR have multivessel coronary artery disease.

The implications of serum enzymes and coagulation activities in postinfarction myocardial

“…2) A previous history of systemic hypertension [8]; 3) A new heart murmur associated with a thrill [9,10]; 4) Progressive hemodynamic deterioration (refractory hypotensive condition, pulmonary edema, left heart failure, cardiogenic shock) usually within 6 hours after the onset of acute myocardial infarction, and mechanical ventilation and intra-aortic balloon counterpulsation are often required [8]; 5) Echocardiographic or magnetic resonance imaging signs of myocardial rupture and (or) pericardial effusion, or tamponade [11][12][13]; and, 6) In case of papillary muscle rupture, severe mitral incompetence could be visualized on echocardiography [14]. rupture, ventricular septal or papillary muscle rupture, and between the survivors and non-survivors were made.…”

Acute tamponade due to postinfarction myocardial rupture successfully managed with urgent pericardiotomy

“…Sutureless repair with TachoComb was praised to be the most effective technique for myocardial rupture repair with rapid hemostasis and without the need of cardiopulmonary bypass [8]. However, sutureless techniques may be associated with some problems, such as diffi culty in locating and exposing the coronary arteries in coronary artery bypass grafting in a later stage, risks of recurrent rupture, left ventricular pseudoaneurysm formation and mitral regurgitation [9]. There have been several reports describing the non-surgical treatment of oozing type myocardial rupture, by percutaneous injection of fi bringlue into the pericardium [10], by combined prolong rest, blood pressure control and -blocker [11], or by percutaneous cardiopulmonary support [12].…”

Adjuvant Role of CT in the Diagnosis of Post-Infarction Left Ventricular Free-Wall Rupture

“…Awareness of the risk factors associated with post-infarction LVFWR is important to maintain a high-degree of suspicion in the appropriate clinical circumstances. These include age over 65, female gender, hypertension without significant left ventricular hypertrophy and late presenters [ 12 ]. Diabetes, prior myocardial infarction and peripheral vascular disease are significantly less prevalent in patients with LVFWR and shock, and pulmonary edema is less frequently found on physical examination [ 3 ].…”