[Prolonged hemodynamic effects of nitroglycerin ointment in acute myocardial infarction (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Previtali.
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A patient admitted for evaluation of repeated episodes of faintness not associated with chest pain is presented. The episodes were caused by marked sinus bradyarrhythmias secondary to ischemic attacks with inferior ST-segment elevation, no accompanied by anginal pain. Medical treatment with nifedipine was able to prevent both the ischemic attacks and cardiac rhythm disturbances associated with acute ischemia. This case shows that ischemic pathogenesis of syncopal attacks should not be ruled out even in the absence of chest pain and that the attacks may be prevented by treating their primary cause.
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The effectiveness of nifedipine in treating angina pectoris at rest was evaluated in 14 patients with frequent ischemic episodes associated with S-T segment elevation or depression. The trial consisted of (1) a 48 hour control period; (2) a placebo period and a period of treatment with nifedipine of 48 hours each; and (3) a second placebo period and a second period of treatment with nifedipine of 24 hours each. The efficacy of treatment was evaluated by continuous electrocardiographic recording to detect painless ischemic episodes. During coronary angiography coronary spasm was demonstrated in five patients. The ergonovine maleate test was positive in seven of eight patients. No statistically significant difference was found in the mean daily number of ischemic episodes between the control period and the first placebo period, or between the control and the second placebo periods. Nifedipine produced a highly significant reduction in the mean daily number of episodes compared with the response to placebo during the first as well as the second period. Nifedipine is effective in angina at rest caused by coronary arterial spasm. The prevention of ischemia may be related to the ability of nifedipine to decrease calcium-dependent coronary muscle tone and to prevent coronary spasm.
The effect on exercise tolerance of nitroglycerin (NTG) ointment was studied by exercise test on bicycle ergometer in a selected group of patients with effort angina and angiographically proven critical coronary lesions. NTG ointment (15 mg) and placebo were administered in a double-blind cross-over randomized trial on two consecutive days; exercise test was carried out before the administration of NTG ointment and placebo, and repeated after one hour, 2 and 1/2 hours and 4 hours. Compared to control and placebo tests, NTG ointment produced a highly significant increase of duration of exercise and of total work load in all tests, as well as a significant decrease of maximal ST segment depression. After NTG ointment administration resting systolic blood pressure showed a significant decrease after one hour, 2 and 1/2 hours and 4 hours, resting heart rate a significant increase after 2 and 1/2 and 4 hours, and peak exercise heart rate a significant increase after 4 hours. Double product at rest was unaffected by NTG ointment, while at peak exercise it showed a significant increase only after 4 hours. Our data show that in patients with effort angina NTG ointment produces an important increase of exercise capacity which persists at least for 4 hours after the administration. Therefore NTG ointment seems to be of high value in the treatment of effort angina.
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Fifty patients who suffered from an acute myocardial infarction at age 40 or below and underwent coronary arteriography, were studied from 8 to 184 months after the infarction (mean follow-up 56 months). Hyperlipidaemia (60%) and cigarette-smoking (82%) were the most common risk factors, while hypertension and diabetes mellitus were found in 10% of all patients. Thirty-seven patients had two or more risk factors. Preinfarction angina was present in 7 subjects. Death rate was 14% within five years and was related to the severity of symptoms. Out of the patients with normal coronary arteriogram (6 patients) or with a single vessel disease 21 were free of angina and 30 did not suffer a reinfarction. Out of 17 patients with two or more coronary vessel disease, angina was present in 14 and reinfarction was seen in 5.
We investigated ex vivo spontaneous platelet aggregation (SPA) in platelet-rich plasma in 37 patients with acute myocardial infarction. It occurred in about 50% of subjects receiving heparin after streptokinase treatment, while it rarely took place in patients who did not receive either streptokinase or heparin and in those treated with streptokinase alone. The study of patients receiving heparin for deep vein thrombosis suggested that SPA may derived from adenosine diphosphate released from platelets during sample handling. We suggest that heparin infusion may facilitate ex vivo platelet activation and that this mechanism is operative in patients with acute myocardial infarction who have undergone thrombolytic therapy.