Nitenberg A, Ledoux S, Valensi P, Sachs R, Attali J R, Antony I
Service de physiologie et d'explorations fonctionnelles, hôpital Louis-Mourier, centre hospitalier universitaire Xavier-Bichat, Colombes.
Arch Mal Coeur Vaiss. 2000 Aug;93(8):937-41.
A failure of coronary blood flow to increase during cold pressor test has been shown in patients with coronary atherosclerosis and impaired metabolic coronary vasodilatation in response to atrial pacing has been demonstrated in diabetic patients without significant epicardial artery stenoses. This study was designed to evaluate coronary microvascular adaptation to increased myocardial oxygen demand in response to sympathetic stimulation in diabetic patients with angiographically normal coronary arteries. Microvascular coronary adaptation to increased myocardial oxygen demand due to sympathetic stimulation evoked by the cold pressor test has been examined in 22 type 2 diabetic patients and in 15 control subjects with angiographically normal coronary arteries and no other risk factors. Coronary blood flow was calculated by measuring mean flow velocity in left anterior descending coronary artery by intracoronary Doppler and cross sectional area of the artery by digital angiography. Results show that despite a similar increase in rate-pressure product in the 2 groups (+22.6 +/- 12.4% in diabetic patients and +31.8 +/- 8.2% in control subjects, NS), coronary blood flow increase in left anterior descending artery 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 2 parameters in control subjects (R = 0.651, p < 0.01), there was no relationship in diabetic patients (R = 0.054). In conclusion, this study demonstrates that vasodilatation of coronary microcirculation in response to sympathetic stimulation evoked by 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 vasodilatation during current life stress episodes such as exercise, mental stress or cold exposure.
冠状动脉粥样硬化患者在冷加压试验期间冠状动脉血流量未能增加，而无明显心外膜动脉狭窄的糖尿病患者，在心房起搏时代谢性冠状动脉血管舒张功能受损。本研究旨在评估冠状动脉微血管对冠状动脉造影正常的糖尿病患者交感神经刺激引起的心肌需氧量增加的适应性。在22例2型糖尿病患者和15例冠状动脉造影正常且无其他危险因素的对照受试者中，研究了冷加压试验诱发的交感神经刺激引起的冠状动脉微血管对心肌需氧量增加的适应性。通过冠状动脉内多普勒测量左前降支冠状动脉的平均流速，并通过数字血管造影测量动脉的横截面积来计算冠状动脉血流量。结果显示，尽管两组的心率-血压乘积有相似的增加（糖尿病患者增加22.6±12.4%，对照受试者增加31.8±8.2%，无显著性差异），但糖尿病患者左前降支动脉的冠状动脉血流量增加显著低于对照受试者（分别为14.7±19.8%和75.5±13.5%，p = 0.0001）。此外，对照受试者中这两个参数呈正相关（R = 0.651，p < 0.01），而糖尿病患者中则无相关性（R = 0.054）。总之，本研究表明，在无心外膜动脉病变的2型糖尿病患者中，冷加压试验诱发的交感神经刺激引起的冠状动脉微循环血管舒张功能受损。交感神经刺激期间的这种微血管损伤可能解释了这些患者运动诱发的心肌灌注异常，并可能损害当前生活应激事件（如运动、精神压力或寒冷暴露）期间的冠状动脉微血管舒张功能。
