Postprandial myocardial perfusion in healthy subjects and in type 2 diabetic patients
Postprandial myocardial perfusion in healthy subjects and in type 2 diabetic patients
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DOI：
10.1161/circulationaha.104.495127
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发表时间：
2005-07-12
期刊：
影响因子：
37.8
通讯作者：
Avogaro, A
中科院分区：
文献类型：
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作者：
Scognamiglio, R;Negut, C;Avogaro, A
背景-在糖尿病患者中，餐后高血糖是比空腹高血糖本身更强的心血管疾病危险因素。急性高血糖对全身内皮功能（肱动脉）有负面影响。然而，在餐后高血糖心肌灌注还没有investigated.Methods和结果-我们评估了20名健康受试者和20例连续2型糖尿病患者的心肌灌注的标准化混合餐没有大血管或微血管并发症的影响。通过心肌声学造影评估空腹和餐后状态下的心肌灌注。对照组和糖尿病患者的空腹心肌血流速度（β，0.65 +/- 0.27对0.67 +/- 0.24; P=NS）、心肌血容量（MBV; 8.3 +/- 1.2对8.4 +/- 2; P=NS）和心肌血流量（5.4 +/- 1.5对5.6 +/- 2; P=NS）无差异。在餐后状态下，对照组受试者的β（0.67 +/- 0.24对0.92 +/- 0.35; P < 0.01）、MBV（8.4 +/- 2对10.9 +/- 2.7; P < 0.01）和心肌血流量（5.6 +/- 2对9.9 +/- 2.8; P < 0.01）显著增加。在糖尿病患者中，β增加（0.65 +/- 0.27对0.8 +/- 0.24; P < 0.01），但MBV（8.3 +/- 1.2对4.3 +/- 1.3; P < 0.01）和心肌血流量（5.4 +/- 1.5对3.4 +/- 0.9; P < 0.01）显著降低。MBV的变化（表示为[（MBVpostprandial-MBVfasting）/MBVfasting]x100）与糖尿病患者餐后血糖水平显著相关。结论-餐后高血糖决定2型糖尿病患者的心肌灌注缺陷。它们继发于微血管功能恶化，导致MBV降低。在无微血管或大血管并发症的糖尿病患者中，餐后心肌灌注缺损可能代表冠状动脉循环中致动脉粥样硬化过程的早期标志物;因此，其逆转构成了潜在的治疗目标。
Background - In diabetic patients, postprandial hyperglycemia is a more powerful risk factor for cardiovascular disease than fasting hyperglycemia itself. A negative influence of acute hyperglycemia on systemic endothelial function (brachial artery) has been shown. However, myocardial perfusion during postprandial hyperglycemia has not been investigated.Methods and Results - We evaluated the effects of a standardized mixed meal on myocardial perfusion in 20 healthy subjects and 20 consecutive patients with type 2 diabetes mellitus without macrovascular or microvascular complications. Myocardial perfusion was assessed in fasting and postprandial states by myocardial contrast echocardiography. Fasting myocardial flow velocity (beta, 0.65 +/- 0.27 versus 0.67 +/- 0.24; P=NS), myocardial blood volume (MBV; 8.3 +/- 1.2 versus 8.4 +/- 2; P=NS), and myocardial blood flow (5.4 +/- 1.5 versus 5.6 +/- 2; P=NS) did not differ between control subjects and diabetic patients. In the postprandial state, beta(0.67 +/- 0.24 versus 0.92 +/- 0.35; P < 0.01), MBV (8.4 +/- 2 versus 10.9 +/- 2.7; P < 0.01), and myocardial blood flow (5.6 +/- 2 versus 9.9 +/- 2.8; P < 0.01) increased significantly in control subjects. In diabetic patients, beta increased (0.65 +/- 0.27 versus 0.8 +/- 0.24; P < 0.01) but MBV (8.3 +/- 1.2 versus 4.3 +/- 1.3; P < 0.01) and myocardial blood flow (5.4 +/- 1.5 versus 3.4 +/- 0.9; P < 0.01) decreased significantly. Changes in MBV (expressed as [(MBVpostprandial-MBVfasting)/MBVfasting]x100) were significantly correlated with postprandial glycemia levels in diabetic patients.Conclusions - Postprandial hyperglycemia determines myocardial perfusion defects in type 2 diabetic patients. They are secondary to deterioration in microvascular function causing a decrease in MBV. In diabetic patients without microvascular or macrovascular complications, postprandial myocardial perfusion defects may represent an early marker of the atherogenic process in the coronary circulation; hence, its reversal constitutes a potential goal of treatment.