Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 Study.

OBJECTIVES: The purpose of this study was to determine the incidence and demographic characteristics of patients experiencing cardiac rupture after thrombolytic and adjunctive anticoagulant therapy and to identify possible associations between the mechanism of thrombin inhibition (indirect, direct) and the intensity of systemic anticoagulation with its occurrence. BACKGROUND Cardiac rupture is responsible for nearly 15% of all in-hospital deaths among patients with myocardial infarction (MI) given thrombolytic agents. Little is known about specific patient- and treatment-related risk factors. METHODS Patients (n = 3,759) with MI participating in the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9A and B trials received intravenous thrombolytic therapy, aspirin and either heparin (5,000 U bolus, 1,000 to 1,300 U/h infusion) or hirudin (0.1 to 0.6 mg/kg bolus, 0.1 to 0.2 mg/kg/h infusion) for at least 96 h. A diagnosis of cardiac rupture was made clinically in patients with sudden electromechanical dissociation in the absence of preceding congestive heart failure, slowly progressive hemodynamic compromise or malignant ventricular arrhythmias. RESULTS A total of 65 rupture events (1.7%) were reported-all were fatal, and a majority occurred within 48 h of treatment Patients with cardiac rupture were older, of lower body weight and stature and more likely to be female than those without rupture (all p < 0.001). By multivariable analysis, age >70 years (odds ratio [OR] 3.77; 95% confidence interval [CI] 2.06, 6.91), female gender (OR 2.87; 95% CI 1.44, 5.73) and prior angina (OR 1.82; 95% CI 1.05, 3.16) were independently associated with cardiac rupture. Independent predictors of nonrupture death included age >70 years (OR 3.68; 95% CI 2.53, 5.35) and prior MI (OR 2.14; 95%, CI 1.45, 3.17). There was no association between the type of thrombin inhibition, the intensity of anticoagulation and cardiac rapture. CONCLUSIONS Cardiac rupture following thrombolytic therapy tends to occur in older patients and may explain the disproportionately high mortality rate among women in prior dinical trials. Unlike major hemorrhagic complications, there is no evidence that the intensity of anticoagulation associated with heparin or hirudin administration influences the occurrence of rupture.

[Occlusion of interventricular septal rupture in 2 patients with an infarction]. / Oclusión de ruptura septal interventricular en dos pacientes con infarto.

We describe two women with interventricular septal rupture secondary to a myocardial infarction due to a total obstruction of the anterior descendent coronary artery. With the aim to stabilize the hemodynamic state of the patients before the surgical closure of the defect, we inserted a balloon-catheter introducing it to the left ventricle from the aorta and inflating it in the right ventricle after passing it through the septal orifice. After occlusion, we observed decreases in the pulmonary to systemic blood flow ratio (6% in one patient and 26% in the other) and in the arteriovenous blood flow shunt (8 and 31%); a 10% systemic blood flow increase was observed in one patient. Since the pulmonary arterial pressure did not change and the pulmonary blood flow increased, an increase of the pulmonary arterial resistance was observed but no modification of the pulmonary and systemic arterial pressure occurred. In the following days, the oxymetric differences between the pulmonary artery and the right atrium showed a tendency to remain below the figures before occlusion and the pulmonary blood flow and pressure showed a tendency to decrease. One patient died 14 days after the surgical closure of the rupture, and the other, seven days after the balloon occlusion of the rupture before any surgery. We present the physiological evolution of the patients.

[The pathogenesis of heart rupture in myocardial infarct]. / O patogeneze razryva serdtsa pri infarkte miokarda.

Examination of 166 patients with primary transmural myocardial infarction (MI) of the anterior site has shown that the blood of MI patients (n = 34) complicated by cardiorrhexis manifests the maximal increase of the stress reaction components, lipid peroxidation products and an appreciable lowering of the content of adaptogens. It is emphasized that the development of the maladaptation syndrome underlies the pathogenesis of cardiorrhexis during MI as the result of the failure of the compensatory-adaptive potentialities of the body in response to the excessive stress reaction. It has been discovered that the high rise of the ST segment on the ECG and pronounced arterial hypoxemia are informative indicators mirroring the high probability of cardiorrhexis occurrence in MI patients. A scheme of cardiorrhexis pathogenesis in MI patients is offered.

[Biochemical blood indices of patients with a myocardial infarct complicated by heart rupture]. / Biokhimicheskie pokazateli krovi u bol'nykh infarktom miokarda, oslozhnennym razryvom serdtsa.

Adrenal function, blood kallikrein-kinin status and the levels of serotonin, histamine, electrolytes and enzymes were repeatedly assessed in 97 patients with myocardial infarction and external cardiorrhexis. Certain patterns were identified as common to the pre-rupture period and the time of the rupture proper that can have a pathogenetic, and sometimes also diagnostic and predictive, significance.