[Effects of isosorbide dinitrate of prolonged action on the prevention of myocardial ischemia induced by exercise: correlation with nitrate blood levels].
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The authors studied the effect of isoket on the central hemodynamics and myocardial contractility as well as on the conditions of myocardial functioning in 38 patients aged 28-53 years and suffering from coronary heart disease. The infusion of 2 mg of isoket at a rate of 400 micrograms/min was followed by a decrease in the arterial pressure with the maximum drop seen on the seventh minute (by 26% from the baseline value), a reduction in the end-diastolic pressure by 50%, and a lengthening of the preejection period without any significant changes in either the cardiac output or the total peripheral resistance. Taken as a whole these changes justify the conclusion that the influence of dinitrate isosorbite (isoket) on the central hemodynamics is largely due to its venodilating action leading to a reduction of the pre-load which in turn improves myocardial functioning.
When compared to the use of 12 hourly 200 microg vaginal misoprostol on its own, the addition of a single dose of 5 mg did not significantly increase the abortion or delivery rate in pregnancy termination at 13-29 weeks gestation. All patients were given intravenous syntocinon at 30 mU/min from the first dose of misoprostol onwards.
Sixteen patients with coronary heart disease (CHD) and three healthy volunteers were treated with a combination of a long-acting nitrite and a beta-receptor blocking agent. The drug proved effective in diminishing haemodynamic changes after physical and mental stress, respectively. The implications of these findings are discussed in the light of recent knowledge on CHD pathogenetic mechanisms.
In long-term, 1-year follow-up, uptitration of angiotensin-converting enzyme inhibitor and nitrate therapy over established doses can further improve severe functional mitral regurgitation in patients with dilated cardiomyopathy due to a reversal of heart failure-related left ventricular remodeling. With marked left ventricular enlargement, >6.8 cm end-diastolic diameter, heart failure remodeling may be irreversible and resistant to further medical intervention.