Cibenzoline improves coronary flow velocity reserve in patients with hypertrophic obstructive cardiomyopathy.

The effect of cibenzoline, a class-Ia antiarrhythmic drug, on coronary flow velocity reserve (CFVR) was examined in patients with hypertrophic cardiomyopathy using transthoracic Doppler echocardiography. Coronary flow velocity reserve was assessed in 11 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 12 patients with hypertrophic nonobstructive cardiomyopathy (HNCM), before and after the intravenous administration of cibenzoline (1 mg/kg). Coronary hyperemia was induced by an intravenous infusion of adenosine triphosphate and CFVR was calculated as the ratio of hyperemic to basal mean coronary diastolic flow velocity. At baseline, CFVR was significantly correlated with left ventricular outflow tract pressure gradient (LVPG) in patients with HOCM (r = 0.67, P < 0.03). In patients with HOCM, administration of cibenzoline significantly improved impaired CFVR (2.0 +/- 0.8 to 3.0 +/- 1.0, P < 0.001), and reduced LVPG (55 +/- 30 to 23 +/- 18 mmHg, P < 0.001), while CFVR remained unchanged in patients with HNCM (2.6 +/- 0.9 to 2.9 +/- 0.8, P not significant). Cibenzoline not only reduces LVPG but also improves CFVR in patients with HOCM. In addition left ventricular outflow obstruction plays an important role in impaired coronary circulation in patients with HOCM.

Effect on coronary flow velocity reserve in patients with type 2 diabetes mellitus: comparison between angiotensin-converting enzyme inhibitor and angiotensin II type 1 receptor antagonist.

BACKGROUND: The effects of angiotensin antagonists on coronary circulation in type 2 diabetes are unclear. We aimed to assess whether 4 weeks of treatment with angiotensin-converting enzyme inhibitor or angiotensin II type 1 receptor antagonist improves coronary flow velocity reserve (CFVR) in patients with type 2 diabetes. METHODS: Twenty-four asymptomatic patients with type 2 diabetes were randomly assigned to temocapril (2 mg/d) or candesartan (8 mg/d). Coronary flow velocity reserve, calculated as the ratio of adenosine-induced hyperemic to basal coronary flow velocity, was measured with transthoracic Doppler echocardiography. Coronary flow velocity reserve measurement and venous blood sampling were performed before and after 4 weeks of treatment. We also obtained CFVR and venous blood data in the 8 healthy controls. RESULTS: Coronary flow velocity reserve was significantly lower in patients than controls (temocapril group 2.74 +/- 0.28, candesartan group 2.65 +/- 0.30, controls 3.53 +/- 0.23, P < .0001 for both, respectively). Blood pressure was reduced in both diabetic groups (n = 12 each) similarly 4 weeks after treatment. There were no significant differences between the 2 groups in venous blood data before or after treatment. However, CFVR increased significantly in the temocapril group (2.74 +/- 0.28 to 3.31 +/- 0.36, P < .0001), but not in the candesartan group (2.65 +/- 0.30 to 2.71 +/- 0.43, P = ns). CONCLUSIONS: Coronary flow velocity reserve in patients with type 2 diabetes improved after treatment with temocapril but not with candesartan, suggesting that angiotensin-converting enzyme inhibitor, but not angiotensin II type 1 receptor antagonist, might have beneficial effects on coronary microangiopathy associated with type 2 diabetes.

Acute effect of oral vitamin C on coronary circulation in young healthy smokers.

BACKGROUND: Recent studies suggest that smokers' coronary endothelial function is impaired because of increased oxidative stress, and their coronary flow velocity reserve (CFVR) is reduced. It is uncertain whether oral antioxidant vitamin C restores impaired CFVR in smokers. Recent technological advances in transthoracic Doppler echocardiography (TTDE) have resulted in the successful measurement of coronary flow velocity and noninvasive CFVR assessment. METHODS: We studied 13 healthy young male smokers and 12 nonsmokers. Coronary flow velocities in the left anterior descending coronary artery (LAD) were recorded with TTDE at rest and during hyperemia induced with intravenous infusion of adenosine triphosphate (ATP). CFVR was calculated as the ratio of hyperemic to basal mean diastolic flow velocity. CFVR and plasma concentrations of vitamin C were assessed at baseline and 2 and 4 hours after oral intake (2 g). RESULTS: Heart rate and blood pressure responses to ATP infusion were not affected by oral vitamin C, but plasma concentrations of vitamin C increased to physiological levels in both groups. CFVR was significantly higher in nonsmokers than in smokers at baseline (4.3 +/- 0.4 vs 3.8 +/- 0.8, P <.05). After oral vitamin C, it was increased significantly in smokers (3.8 +/- 0.8 to 4.5 +/- 0.7, P <.005, 4.5 +/- 0.8, P <.005, respectively), but not in nonsmokers (4.3 +/- 0.4 to 4.3 +/- 0.3, 4.4 +/- 0.7). CONCLUSIONS: This study demonstrated that oral vitamin C restores coronary microcirculatory function and impaired CFVR against oxidative stress in smokers.