OBJECTIVES: Aim of our study was to evaluate the coronary flow patterns and therapeutic effects of nitroglycerin (NTG) in patients with isolated large coronary artery aneurysms (CA). CA are defined as nonobstructive lesions of the epicardial coronary arteries with a luminal dilation >or=two-fold of the normal diameters. The pathophysiology of a potential coronary insufficiency in this entity is still unknown. METHODS: A coronary sinus study with incremental atrial pacing before and after the administration of 0.2 mg NTG was performed in 19 patients with bilateral large fusiform nonstenotic CA to evaluate an exercise-induced myocardial ischemia. The average peak velocity in the aneurysmatic segment of the proximal left anterior descending artery was simultaneously measured by a 14/1000 inch Doppler flow wire. The coronary flow volumes and vascular resistances were calculated. RESULTS: Evidence of exercise-induced myocardial ischemia was found in all patients presenting with a frank cardiac lactate production (10.2+/-3.3%) which was significantly aggravated by NTG (26.0+/-7.5%, P<0.003). 0.2 mg NTG provoked a long-lasting and significant decrease in coronary flow volume (from 140.2+/-34.2 to 91.2+/-21.8 ml/min, P<0.002), a marked increase in coronary vascular resistance (from 0.62 to 0.92 mmHG x ml/min(-1), P<0.002) and an inadequate increase in coronary flow volume under cardiac pacing. CONCLUSION: CA were identified as an entity of nonobstructive ischemic coronary artery disease with an exercise-induced myocardial ischemia and impaired flow volume. NTG exerted an adverse vasoactive effect in CA.
OBJECTIVES: Aim of our study was to evaluate the coronary flow patterns and therapeutic effects of nitroglycerin (NTG) in patients with isolated large coronary artery aneurysms (CA). CA are defined as nonobstructive lesions of the epicardial coronary arteries with a luminal dilation >or=two-fold of the normal diameters. The pathophysiology of a potential coronary insufficiency in this entity is still unknown. METHODS: A coronary sinus study with incremental atrial pacing before and after the administration of 0.2 mg NTG was performed in 19 patients with bilateral large fusiform nonstenotic CA to evaluate an exercise-induced myocardial ischemia. The average peak velocity in the aneurysmatic segment of the proximal left anterior descending artery was simultaneously measured by a 14/1000 inch Doppler flow wire. The coronary flow volumes and vascular resistances were calculated. RESULTS: Evidence of exercise-induced myocardial ischemia was found in all patients presenting with a frank cardiac lactate production (10.2+/-3.3%) which was significantly aggravated by NTG (26.0+/-7.5%, P<0.003). 0.2 mg NTG provoked a long-lasting and significant decrease in coronary flow volume (from 140.2+/-34.2 to 91.2+/-21.8 ml/min, P<0.002), a marked increase in coronary vascular resistance (from 0.62 to 0.92 mmHG x ml/min(-1), P<0.002) and an inadequate increase in coronary flow volume under cardiac pacing. CONCLUSION: CA were identified as an entity of nonobstructive ischemic coronary artery disease with an exercise-induced myocardial ischemia and impaired flow volume. NTG exerted an adverse vasoactive effect in CA.