Haemodynamic Effects of Nitroglycerin in Patients with Coronary Heart Disease.

The usefulness of nitroglycerin (glyceryl trinitrate) in relieving angina pectoris is undisputed: it has one of the clearest pharmacological effects in man. However, the mechanism of its action is not well understood (Gorlin, 1962; Case and Roven, 1963). In animal experiments the nitrites cause relaxation of smooth muscle, notably in the vessels, and an increased coronary flow can easily be demonstrated (Charlier, 1961). However, it is doubtful whether nitroglycerin relieves angina pectoris by dilatation of the coronary arteries. In the first place, ischemia by itself provides a very powerful vasodilator stimulus due to the accumulation of vasodilating substances in the anoxic tissue, so that it is unlikely that artificial vasodilator agents can act upon vessels already under a maximal influence of endogenous metabolites. An action of nitroglycerin on the larger arteriosclerotic coronary arteries also seems unlikely. Another mechanism of action of nitrites may be through reduction of the work of the heart. Brunton (1867) pointed out that amyl nitrite diminished the tension of the pulse, and it has also been found that the cardiac output at rest is decreased after nitroglycerin (Gorlin, 1962). Other mechanisms of action have also been proposed but so far none has been found acceptable, and the general opinion appears to favour a direct dilatation of coronary vessels (or collaterals) in combination with a reduction of cardiac work as the most likely mode of action of nitrites. In the course of a study of the hwmodynamic pattern during exercise in patients with coronary heart disease it was sometimes necessary to give nitroglycerin. Observations could, therefore, be made of the action of the drug on cardiac output and arterial blood pressure during exercise in such patients. Similar observations have apparently not been made hitherto. A short account of the main findings has been given (Christensson, Karlefors, and Westling, 1964).