Momose Mitsuru, Abletshauser Claudia, Neverve Jodi, Nekolla Stephan G, Schnell Oliver, Standl Eberhard, Schwaiger Markus, Bengel Frank M
Nuklearmedizinische Klinik und Poliklinik der Technischen Universität München, Klinikum rechts der Isar, Ismaninger Strasse 22, 81675 Munich, Germany.
Eur J Nucl Med Mol Imaging. 2002 Dec;29(12):1675-9. doi: 10.1007/s00259-002-0977-0. Epub 2002 Sep 21.
In diabetic patients, a number of studies have suggested an impairment of vascular reactivity in response to vasodilatory stimuli. The pattern of dysregulation at the coronary microcirculatory level, however, has not been clearly defined. Thus, it was the aim of this study to characterise coronary microvascular function non-invasively in a homogeneous group of asymptomatic type 2 diabetic patients. In 46 patients with type 2 diabetes, myocardial blood flow (MBF) was quantified at baseline, in response to cold pressor test (CPT) and during adenosine-mediated vasodilation using positron emission tomography and nitrogen-13 ammonia. None of the patients had been treated with insulin, and none had symptoms of cardiac disease. Decreased MBF during CPT, indicating microvascular dysregulation, was observed in 16 patients (CPT-), while 30 patients demonstrated increased MBF during CPT (CPT+). Response to CPT was mildly, but significantly correlated with response to adenosine ( r=0.44, P=0.0035). There was no difference in HbA1c, serum lipid levels or serum endothelial markers between the groups. Microvascular dysregulation in the CPT- group was associated with elevated baseline MBF ( P<0.0001), reduced baseline vascular resistance ( P=0.0026) and an abnormal increase in resistance during CPT ( P=0.0002). In conclusion, coronary microvascular dysregulation is present in approximately one-third of asymptomatic, non-insulin-treated type 2 diabetic patients. Elevated baseline blood flow and reduced microvascular resistance at rest are characteristics of this dysregulation. These data suggest a state of activation of endothelial-dependent vasodilation at baseline which appears to limit the flow response to stress conditions.
在糖尿病患者中，多项研究表明血管对血管舒张刺激的反应性受损。然而，冠状动脉微循环水平的失调模式尚未明确界定。因此，本研究的目的是在一组同质的无症状2型糖尿病患者中无创地表征冠状动脉微血管功能。对46例2型糖尿病患者，使用正电子发射断层扫描和氮-13氨在基线、冷加压试验（CPT）期间以及腺苷介导的血管舒张期间对心肌血流量（MBF）进行定量。所有患者均未接受胰岛素治疗，也没有心脏病症状。16例患者（CPT-）在CPT期间观察到MBF降低，表明微血管失调，而30例患者在CPT期间MBF增加（CPT+）。对CPT的反应与对腺苷的反应呈轻度但显著的相关性（r = 0.44，P = 0.0035）。两组之间的糖化血红蛋白、血脂水平或血清内皮标志物无差异。CPT-组的微血管失调与基线MBF升高（P < 0.0001）、基线血管阻力降低（P = 0.0026）以及CPT期间阻力异常增加（P = 0.0002）相关。总之，约三分之一的无症状、未接受胰岛素治疗的2型糖尿病患者存在冠状动脉微血管失调。基线血流升高和静息时微血管阻力降低是这种失调的特征。这些数据表明在基线时内皮依赖性血管舒张处于激活状态，这似乎限制了对应激条件的血流反应。
