Showing papers by "Elliott M. Antman published in 1983"
TL;DR: It is concluded that NAC potentiates the vasodilator effects of NTG in man and suggests that sulfhydryl availability and/or redox state may be determinants of in vivo responsiveness to NTG.
Abstract: The biochemical basis of the mechanism of vasodilatation by nitroglycerin (NTG) has not been previously investigated in man. However, evidence from in vitro studies suggests that NTG induces activation of guanylate cyclase via a series of enzymatic reactions that are modulated by the availability of sulfhydryl groups. Cysteine appears to be particularly effective in potentiating guanylate cyclase activation by NTG. To determine whether hemodynamic responsiveness to NTG in man might be modulated by sulfhydryl availability, concentration-response curves for effects of intravenously infused NTG on mean arterial pressure (MAP) and mean pulmonary capillary wedge pressure (PCW) were obtained in 10 patients undergoing cardiac catheterization for investigation of chest pain. NTG infusion was repeated 10 min after the intravenous infusion of 100 mg/kg of the cysteine source N-acetylcysteine (NAC). NAC induced no significant hemodynamic effect, but after NAC infusion there was a significant reduction both in the NTG infusion rate associated with a 10% fall from control values in MAP (25.8 +/- 8.3 to 9.3 +/- 2.7 micrograms/min; p less than .01) and in the infusion rate inducing a 30% reduction in PCW (13.6 +/- 4.6 to 4.2 +/- 1.6 micrograms/min; p less than .02). In a control group of five patients who received no NAC, there was no significant change in responsiveness to NTG between infusions. It is concluded that NAC potentiates the vasodilator effects of NTG in man. This suggests that sulfhydryl availability and/or redox state may be determinants of in vivo responsiveness to NTG.
202 citations
TL;DR: In this paper, the authors analyzed the ambulatory electrocardiographic recordings of 12 patients who sustained ventricular fibrillation or torsade de pointes while wearing a long-term ECG monitor and found that ventricular arrhythmias leading to sudden death in an ambulatory population do not occur in isolation but are preceded by increased ventricular ectopic activity.
76 citations
TL;DR: Observations of the case of a 62‐year‐old man with severe aortic stenosis and hypertrophic cardiomyopathy, who could not be weaned from cardiopulmonary bypass until buccal administration of the calcium‐blocking agent nifedipine led to achievement of adequate hemodynamics, suggest an important peri‐ and intraoperative role for calcium‐ blocking agents in their management.
Abstract: We report the case of a 62-year-old man with severe aortic stenosis and hypertrophic cardiomyopathy, who could not be weaned from cardiopulmonary bypass after aortic valve replacement until buccal administration of the calcium-blocking agent nifedipine led to achievement of adequate hemodynamics These observations demonstrate the importance of diastolic dysfunction in patients with hypertrophic cardiomyopathy, and suggest an important peri- and intraoperative role for calcium-blocking agents in their management Recent hemodynamic studies have shown the importance of diastolic myocardial dysfunction in patients with hypertrophic cardiomyopathy, and demonstrated that calcium-blocking agents may enhance myocardial performance by reducing this dysfunction (Goodwin, 1982; Lorell et al, 1980, 1982; Sanderson et al, 1977) Although this new class of drugs has been increasingly used as an adjunct to cardioplegia, there is little information thus far on their application as treatment of intraoperative diastolic abnormalities We report the case of a 62-year-old man with severe aortic stenosis and hypertrophic cardiomyopathy, who could not be weaned from cardiopulmonary bypass after aortic valve replacement until buccal administration of the calcium-blocking agent nifedipine led to an increase in cardiac output and blood pressure
7 citations