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Thirty patients admitted to the ICCU with a first myocardial infarction (MI) of any localization, with left ventricular dysfunction revealed by echo-Doppler ejection fraction (EF) < 40%, where randomly divided in three groups of ten: GROUP 1 who was treated with captopril 25 mg orally between the 5th and 7th day post MI, and sustained until the end of the study. GROUP 2 received nifedipine, 10 mg capsules t.i.d. also started between days 5 and 7 post MI. GROUP 3 as a control group was treated conventionally, according to the ICCU routine. The treatment was maintained during 12 months. All patients had a second echo-Doppler at the 5th day post MI to confirm the EF criteria. Also left ventricular end-systolic and end-diastolic diameters were measured. At the 5th day post MI and before the drug administration, a low level treadmill stress test was performed in all patients. Subsequently a maximal stress test (Bruce protocol) was done at the first month and at 6 and 12 months of the study. The results showed a significant increase EF in patients of GROUP 1 from an average basal value of 38 +/- 2 to 54 +/- 5 at six months (p < 0.01) and to 60 +/- 3 at 12 months (p < 0.005). The increments observed in patients of GROUP 2 and 3 were more modest; only the 12 month value in GROUP 3, from a basal figure of 41 +/- 3 to 50 +/- 4, had a p < 0.05.(ABSTRACT TRUNCATED AT 250 WORDS)

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Twenty seven patients, 43 to 69 years of age, all with disabling stable angina and positive Bruce stress test, no amendable for revascularization procedures mainly because of poor distal coronary run-off by angiography, were studied with two calcium-channel blockers, the recently developed gallopamil hydrochloride and nifedipine hydrochloride. According to a double blind, cross-over protocol of 12 week duration and after a 2-week washout period, the patients randomly received during 4 weeks 50 mg gallopamil capsules t i d, or 10 mg nifedipine capsules t i d. After a second 2-week wash-out, the alternative drug was administered for another 4 weeks. The number of anginal episodes decreased significantly (p less than 0.01) with both treatments (from 6.4 to 1.8 crisis with gallopamil and from 6.2 to 2.1 with nifedipine). Heart rate (HR) was progressively reduced with gallopamil (-7.9%, p less than 0.05) but increased with nifedipine (+5.7%) in relation to basal figures. Both medications reduced the level of ST depression during the stress test (52.4% with gallopamil and 41.8% with nifedipine, N.S.). The time for angina at the stress test increased 92.5% with gallopamil and 40.7% with nifedipine (p less than 0.05). HR systolic product at peak exercise was 23,101 with gallopamil and 24,906 with nifedipine (p less than 0.001). Both calcium-channel blockers are drugs with significant anti-anginal effects in patients with stable, disabling angina.(ABSTRACT TRUNCATED AT 250 WORDS)

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We studied four patients with ruptured aneurysms of the sinus of Valsalva. All were men with a mean age of 33 years. The presenting illness was insidious in three and of abrupt onset in one. Physical examination showed a continuous murmur in all. Chest X ray film showed moderate cardiomegaly. Electrocardiogram disclosed left ventricular hypertrophy. Echocardiogram revealed the site of the rupture which was corroborated by aortography. Two aneurysms ruptured to the right ventricle and two to the right atrium. All were corrected by surgery. All patients became asymptomatic.

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To evaluate the characteristics that the renin and aldosterone profile could present in essential hypertensive patients complicated with ischemic heart disease, and as a contribution to the knowledge of the roll that these hormones could have as possible "risk factors" of coronary heart disease, sixty male patients were studied. These were divided in three groups: group I, formed by 15 essential hypertensive patients with objectively demonstrated ischemic heart disease; group II integrated by 15 essential hypertensives with no ischemic heart disease and group III with 30 normal volunteers. Serum levels of plasma renin activity (PRA) and aldosterone determined by radioimmunoassay, and of urinary sodium excretion were measured in all the patients. The distribution of cases with high, normal and low renin and aldosterone were similar in group I and in group II. It was interesting to find that the four patients of group I who were non-smokers, presented the lower renin levels (from 0.36 to 2.8 ng/ml/h). The relation between PRA and the number of occluded coronary arteries revealed an increased number of patients and affected arteries in the subgroup with renin levels above 5 ng/ml/h in comparison with the subgroup with PRA from 0 to 5, although the difference was not statistically significant. By our study, we cannot conclude that the PRA and aldosterone behave in a different fashion in essential hypertensives from those complicated with ischemic heart disease.

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The frequency of the different types of cellular necrosis in patients who died of myocardial infarction was investigated, in search of a possible correlation between the various types of myocardial necrosis and the clinical history and death characteristics of the patients. The significance of the microscopic alterations as a manifestations of the physiopathologic derangements was analyzed. Clinically, the time of appearance of pump failure with recognizable manifestations of cardiac failure or shock, arrhythmias, myocardial rupture or rupture of other cardiac structures, infarct extention or sudden death was recorded. Pathologically, coagulative necrosis was considered an obligatory finding for study.

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