No abstract

This study shows that (1) responses of angiographically normal CAs to CPT and to flow increase are impaired in diabetic patients; (2) abnormal responses are not improved by L-arginine, suggesting that a deficit in substrate for nitric oxide synthesis is not involved; and (3) deferoxamine restores a vasodilator response to the two tests, suggesting that inactivation of NO by oxygen species might be partly responsible for the impairment of CA dilation in diabetic patients.

Coronary microcirculation dysfunction may be associated with myocardial perfusion defects on thallium imaging in diabetic patients without coronary artery stenosis. Microvascular coronary adaptation to increased myocardial oxygen demand in response to sympathetic stimulation evoked by the cold pressor test was examined in 22 type 2 diabetic patients with thallium imaging defects and in 15 control subjects. Both the diabetic patients and control subjects had angiographically normal coronary arteries and no other risk factors. Despite a similar increase in the rate-pressure product in the two groups (22.6 ؎ 12.4% in diabetic patients and 31.8 ؎ 8.2% in control subjects, NS), coronary blood flow increase in the left anterior descending artery (mean flow velocity measured by intracoronary Doppler multiplied by the cross-sectional area measured by digital angiography) was significantly lower in diabetic patients than in control subjects (14.7 ؎ 19.8 vs. 75.5 ؎ 13.5%, respectively; P ‫؍‬ 0.0001). In addition, when there was a positive correlation between the two parameters in control subjects (r ‫؍‬ 0.651, P < 0.01), there was no relationship in diabetic patients (r ‫؍‬ 0.054). In conclusion, vasodilation of the coronary microcirculation in response to sympathetic stimulation evoked by the cold pressor test is impaired in type 2 diabetic patients without epicardial artery lesions. This microvascular impairment during sympathetic stimulation may explain exercise-induced myocardial perfusion abnormalities observed in these patients and may impair microcirculatory coronary vasodilation during current life stress episodes such as exercise, mental stress, or cold exposition. Diabetes 50:1180 -1185, 2001 I t has been shown that endothelium-dependent epicardial coronary artery vasodilation in response to acetylcholine (1) or physiological stimuli (2) is impaired in diabetic patients with angiographically normal coronary arteries. Microvascular functional abnormalities have also been reported by Nasher et al. (3), who have shown that metabolic vasodilation of coronary microcirculation evoked by atrial pacing is reduced in diabetic patients. Similar impairment has also been reported in hypertensive patients with angiographically normal coronary arteries (4) and by Zeiher et al., who showed that coronary blood flow failed to increase during exercise (5) or during the cold pressor test (CPT) in patients with early atherosclerosis (6) and without significant coronary artery stenosis, suggesting that the endothelial function is impaired at the microvascular level. Such coronary microcirculation dysfunction may be associated with myocardial perfusion defects on 99m Tc sestamibi single photon emission computed tomography (SPECT) imaging in humans with angina and minimally obstructive coronary artery disease (7) and might contribute to myocardial ischemia when myocardial oxygen demand is increased, even in the absence of coronary artery stenosis.In diabetes, it has been suggested that coronary functional abnormalities and microvas...