We conducted a multicenter, double-blind, placebo-controlled randomized trial of aspirin treatment (324 mg in buffered solution daily) for 12 weeks in 1266 men with unstable angina (625 taking aspirin and 641 placebo). The principal end points were death and acute myocardial infarction diagnosed by the presence of creatine kinase MB or pathologic Q-wave changes on electrocardiograms. The incidence of death or acute myocardial infarction was 51 per cent lower in the aspirin group than in the placebo group: 31 patients (5.0 per cent) as compared with 65 (10.1 per cent); P = 0.0005. Nonfatal acute myocardial infarction was 51 per cent lower in the aspirin group: 21 patients (3.4 per cent) as compared with 44 (6.9 per cent); P = 0.005. The reduction in mortality in the aspirin group was also 51 per cent--10 patients (1.6 per cent) as compared with 21 (3.3 per cent)--although it was not statistically significant; P = 0.054. There was no difference in gastrointestinal symptoms or evidence of blood loss between the treatment and control groups. Our data show that aspirin has a protective effect against acute myocardial infarction in men with unstable angina, and they suggest a similar effect on mortality.

We conducted a prospective study in which 554 patients with chronic bifascicular and trifascicular conduction abnormalities were followed for an average of 42.4 +/- 8.5 months. Heart block occurred in 19 patients, and 17 were successfully treated. The actuarial five-year mortality from an event that could conceivably have been a bradyarrhythmia was 6 per cent (35 per cent from all causes). Of the 160 deaths 67 (42 per cent) were sudden; most of these were not ascribable to bradyarrhythmia but to tachyarrhythmia and myocardial infarction. Mortality was higher in patients with coronary-artery disease (P less than 0.01) and congestive heart failure (P less than 0.05). Patients in whom syncope developed before or after entry into the study had a 17 per cent incidence of heart block (2 per cent in those without syncope)(P less than 0.05); however, no single variable was predictive of which patients were at high risk of death from a bradyarrhythmia. The predictors of death were increasing age, congestive heart failure, and coronary-artery disease; the predictors of sudden death were coronary-artery disease and increasing age. The risks of heart block and of death from a bradyarrhythmia are low; in most patients, heart block can be recognized and successfully treated with a pacemaker.

The effectiveness of an intermittent regimen of transdermal nitroglycerin in chronic stable angina was evaluated in 206 patients using serial treadmill testing. After a placebo stabilization phase, patients were randomized to 4 weeks of double-blind treatment with transdermal nitroglycerin, 10 or 20 cm2 (equivalent to 5 or 10 mg/24 h) (Group A); transdermal nitroglycerin, 30 or 40 cm2 (equivalent to 15 or 20 mg/24 h) (Group B), or placebo. Patches were applied at 8:00 AM and removed at 8:00 PM each day throughout the study. Treadmill testing was performed 0, 4, 8 and 12 h after patch application at baseline (day 0) and on days 1, 15 and 29. After short-term application of the transdermal patches, treadmill walking time was greater for patients in both Group A and Group B than for the placebo group at all time points tested; differences from placebo were statistically significant at 12 h for Group A and at 4, 8 and 12 h for Group B. After 2 and 4 weeks of long-term therapy, treadmill walking time was again greater for Group B than for the placebo group at all postapplication time points; differences from placebo reached statistical significance at 4 h (2 weeks) and 8 h (2 and 4 weeks). The improvement in the treadmill walking time seen over the short-term in Group A was largely lost after 4 weeks of long-term therapy. Potentially important differences in the patient characteristics of the two active treatment groups, particularly the greater use of a beta-adrenergic blocker among patients in Group A, may have contributed to these observed differences in treatment effect. An unexpected finding was the ability of the placebo group to exercise longer than either active treatment group just before patch application during long-term therapy; nonetheless, absolute responsiveness to transdermal nitroglycerin after patch application remained virtually unchanged in both active treatment groups during the 4 week treatment period. Intermittent transdermal nitroglycerin therapy was well tolerated in the vast majority of patients; nine patients experienced an increase in nonexertional angina during the patch-off periods but completed the study uneventfully.

Echocardiographic and phonocardiographic findings in 35 patients with Marfan's Syndrome and ten patients without Marfan's or other clinically apparent connective tissue disorders but with angiographic and echocardiographic evidence of mitral prolapse are reported and compared. Echocardiography revealed aortic root dilatation and/or mitral valve prolapse in 97% of the patients with Marfan's Syndrome. Aortic root dilatation was found in 60% of this group (74% of males, 33% of females) while mitral valve prolapse was found in 91% (87% of males, 100% of females). The incidence of aortic dilatation and mitral prolapse in patients with Marfan's syndrome was essentially equal in children and adults of the same sex. None of the nine adults or one child with mitral prolapse but without evidence of Marfan's Syndrome or other clinically apparent connective tissue disorder had aortic root enlargement. Ausculatory examination and phnocardiography revealed abnormalities in 54% of the patients with Marfan's Syndrome. Aortic regurgitation was found in 23% of this group (35% of males, 0% of females) while mitral regurgitation and/or mitral clicks were found in 46% (39% of males, 58% of females). Aortic regurgitation was much more frequent in adult males with Marfan's Syndrome (7/14, 50%) than male children (1/9, 11%), while the incidence of abnormal mitral sounds was essentially the same in adults (33% of males, 60% of females) and children (43% of males, 57% of females) of the same sex with Marfan's Syndrome. Abnormal mitral sounds were more frequent in patients without Marfan's who had mitral prolapse (90%) than in those with Marfan's (46%). It appears that cardiac abnormalities are a consistent manifestation of Marfan's Syndrome and that ultrasound is a more sensitive indicator of these abnormalities in such patients than ausculation or phonocardiography.

No abstract