Acute postinfarction septal rupture: long-term results.

From 1973 to 1989, 66 patients received early surgical repair for acute postinfarction ventricular septal rupture. Mean age was 64 +/- 7 years (range, 45 to 80 years). Ventricular septal rupture occurred soon after acute myocardial infarction (3.

[Early septal rupture after acute myocardial infarction. Reflections on the immediate operative risk and long-term results].

Sixty-one patients with septal rupture immediately consecutive to acute myocardial infarction underwent emergency surgery after a period of intensive care which included diastolic counterpulsation in 25 cases. The operation was performed in 37 patients with controlled haemodynamic status and in 24 patients still in a state of shock. The surgical procedure comprised wide exposure of the lesions, septal reinforcement, closure of the ventricular septal defect, removal of the infarct and correction of associated valve lesions.

[Uncommon aspect of electrocardiographic ischemia. Correlations with coronarography].

It has long been known that the morphology of ventricular repolarization is extremely sensitive to acute or chronic myocardial anoxia. In patients with coronary disease, we are used to observe a wide variety of ST segment, T wave and sometimes U wave abnormalities. The classical description of "lesions" or "ischaemia", as well as their anatomical locations called, perhaps rather arbitrarily, "subendocardial" or "subepicardial" account for ST segment displacements and T wave inversions the patterns of which are well known to all of us.

[Sinusal dysfunction secondary to the ingestion of diltiazem, cured by the administration of intravenous calcium].

An elderly patient, receiving long-term oral diltiazem at the usual dosage, presented a sudden attack of junctional bradycardia at 35 b X min-1; this was badly tolerated by the patient. The diltiazem blood level was normal. After recovery, nodal investigations were also normal.

[Study of a marker of free radical activity in myocardial infarction and in the prodromal syndrome].

Myocardial ischemia is accompanied by a release of free radicals (FR) derived from oxygen, elements having an important cytotoxic activity. These FR react with unsaturated lipids from the membrane fatty acids, leading possibly to a lysis of the membrane. This lipidic peroxidation of the fatty acids generates, in fact, endoperoxides, unstable lipid by-products and also with a cytotoxic activity.