Haemodynamic effects of nitroglycerin in patients with mitral valvular disease.

Nitrites are widely used for the treatment of angina pectoris, but their mechanism of action is still not clear. Animal experiments have shown that nitrites dilate arteries, arterioles, capillaries, and veins (for a review: see Charlier, 1961). Most workers feel that nitroglycerin acts by dilating coronary vessels, though such an effect has been difficult to show in patients with coronary heart disease. Moreover, Gorlin et al. (1959), Weiss, WiLkins, and Haynes (1937), Wilkins, Haynes, and Weiss (1937), and Johnsson, Henning, and Ablad (1965) have shown that the most important circulatory effect of nitrites in man is probably a dilatation of peripheral veins, which may lead to a fall in central blood volume and a reduction of the work of the heart. Others, e.g. Christensson, Karlefors, and Westling (1965), maintain that this may be a sufficient explanation for the relief of anginal pain, since they found a reduced stroke volume after nitroglycerin, particularly when the drug was given during anginal pain provoked by sitting exercise. However, these findings were not confirmed by Hoeschen et al. (1966): they found increased cardiac output and stroke volume when nitroglycerin was given to patients with angina pectoris under experimental conditions which appear similar to those of Christensson et al. (1965). It has also been observed by 0. Muller (1963, personal communication), Arborelius et al. (1968), and Najmi et al. (1967) that nitroglycerin may prevent anginal pain during supine exercise without a reduction of cardiac output, but with reduced pressures in the lesser circulation. Variations in the patients and the experimental methods may possibly explain the different results, but nevertheless these findings and those of Hoeschen et al. (1966) appear to cast doubt on the theory