Coronary vasodilator reserve is impaired in patients with hypertrophic cardiomyopathy and left ventricular dysfunction

Background We tested the hypothesis that a reduced delivery of blood to the myocardium is involved in the develop ment of systolic dysfunction of patients with hypertrophic cardiomyopathy (HCM). Methods and Results Eighty-four patients with HCM (62 men, age 43 +/- 12 years) were studied. Left ventricular dimensions and function (fractional shortening) were evaluated by 2-dimensional echocordiography. Myocardial blood flow (MBF) was measured by N-13-ammonia or O-15-water and positron emission tomography at baseline and after dipyridamole; coronary vasodilator reserve (CVR) was calculated as dipyridamole/baseline MBF. Patients with HCM in advanced New York Heart Association (NYHA) classes had lower dipyridamole MBF (NYHA class I = 1.57 +/- 0.64 vs class II = 1.52 +/- 0.58 vs class III = 0.96 +/- 0.32 mL/min per gram; analysis of variance, P < .05) and CVR (NYHA class I = 1.93 +/- 0.64 vs class II = 1.69 +/- 0.54 vs class III = 1.40 +/- 0.43; analysis of variance, P < .05). A positive linear correlation between fractional shortening and dipyridamole MBF was demonstrated (R = 0.23, P < .05), and patients with abnormal fractional shortening had lower dipyridamole MBF (1.07 +/-: 0.43 vs 1.58 +/- 0.62 mL/min per gram, P < .01). Conclusions systolic dysfunction in HCM may be caused by a more severe alteration of the coronary vasodilator capacity.