Why the study?
Does sublingual nitroglycerin alter coronary and systemic hemodynamics to alleviate exercise-induced angina in patients with coronary artery disease?
Does sublingual nitroglycerin alter coronary and systemic hemodynamics to alleviate exercise-induced angina in patients with coronary artery disease?
Sublingual nitroglycerin attenuates exercise-induced ischemia by altering systemic and coronary circulation to reduce myocardial oxygen demand and increase supply, reversing exercise-induced vasoconstriction of stenosed segments.
Supports mechanistic coronary effects of nitroglycerin during exercise; hypothesis-generating for angina relief, needing randomized confirmation.
BACKGROUND: The mechanisms governing exercise-induced angina and its alleviation by the most commonly used antianginal drug, nitroglycerin, are incompletely understood. The purpose of this study was to develop a method by which the effects of antianginal drugs could be evaluated invasively during physiological exercise to gain further understanding of the clinical impact of angina and nitroglycerin. METHODS: Forty patients (mean age, 65.2±7.6 years) with exertional angina and coronary artery disease underwent cardiac catheterization via radial access and performed incremental exercise using a supine cycle ergometer. As they developed limiting angina, sublingual nitroglycerin was administered to half the patients, and all patients continued to exercise for 2 minutes at the same workload. Throughout exercise, distal coronary pressure and flow velocity and central aortic pressure were recorded with sensor wires. RESULTS: <0.0001), in keeping with exercise-induced vasoconstriction of stenosed epicardial segments and dilatation of normal segments, with trends toward reversal with nitroglycerin. CONCLUSIONS: The catheterization laboratory protocol provides a model to study myocardial ischemia and the actions of novel and established antianginal drugs. Administration of nitroglycerin causes changes in the systemic and coronary circulation that combine to reduce myocardial oxygen demand and to increase supply, thereby attenuating exercise-induced ischemia. Designing antianginal therapies that exploit these mechanisms may provide new therapeutic strategies.
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Asrress et al. (2017) studied this question.
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