The pathophysiology of angina pectoris with normal coronary arteriograms. Histopathological and metabolic correlations with coronary vasospasm.

Angina pectoris may occur in the presence of normal major coronary vessels (NCA) in 10-20 per cent of patients investigated by coronary arteriography. Whilst hypertrophic cardiomyopathy, mitral valve prolapse and hyperthyroidism are excluded by routine investigation, in the remainder coronary vasospasm may be demonstrated. An organic basis for angina may not always be found. In order to document the pathophysiological basis for angina pectoris with NCA we have investigated patients using atrial pacing stress with measurement of coronary sinus blood flow and lactate metabolism, together with myocardial biopsy to determine biochemical and histopathological abnormalities. These have been correlated with localised coronary vasospasm induced by ergometrine (E). Thallium scintigraphy has also been used to detect the myocardial changes. Fifteen patients were investigated: 5 of 15 patients developed abnormal lactate metabolism on atrial pacing (change greater than 0.8 mg per cent in A/V lactate difference) and all had greater than 50 per cent coronary luman reduction after E. In 10 of 15 patients no lactate change occurred and in 7 no significant response to E was seen. However, significantly lower myocardial enzyme activities were found in the first group (lactate dehydrogenase p less than 0.01, malate dehydrogenase p less than 0.05, alpha hydroxy-butyrate dehydrogenase p less than 0.02). The change in myocardial enzyme activities in angina with NCA may indicate a metabolic basis for angina in those patients who develop both abnormal lactate metabolism on pacing and coronary vasospasm after ergometrine. The enzyme activities and histological changes in angina with NCA are similar to these in dilated cardiomyopathy.