Weismüller S, Czernin J, Sun K T, Fung C, Phelps M E, Schelbert H R
Department of Molecular and Medical Pharmacology, UCLA School of Medicine 90095-1735, USA.
Am J Card Imaging. 1996 Jul;10(3):154-62.
Increases in wall stress because of left ventricular enlargement and/or alterations in coronary vasomotor tone might affect myocardial blood flow and vasodilatory capacity in patients with dilated cardiomyopathy. To test this hypothesis myocardial blood flow was measured at rest and during intravenous administration of dipyridamole (0.56 mg/kg) using dynamic nitrogen 13-ammonia positron emission tomography (two-compartment model) in 10 patients with dilated cardiomyopathy (mean left ventricular ejection fraction 28 +/- 8% 1 woman, 9 men; 47 +/- 13 years of age). Ten age and gender matched healthy volunteers served as controls. Coronary artery disease was ruled out by coronary angiography and left ventricular hypertrophy by two dimensional-echocardiography. Baseline heart rate (70 +/- 13 v 64 +/- 12 bpm), systolic blood pressure (111 +/- 20 v 114 +/- 12 mm Hg) and rate pressure product (7,686 +/- 1264 v 7,306 +/- 1,645) were similar in patients and controls. During dipyridamole administration, the rate pressure product increased similarly in both groups. Myocardial blood flow at rest did not differ between groups of patients and volunteers (0.69 +/ -0.27 v 0.67 +/- 0.17 mL/g/min) but correlated with the rate pressure product only in controls (myocardial blood flow, 0.18 + 0.000068214; rate pressure product, .67; P < .05). Hyperemic myocardial blood flow was lower in patients (1.57 +/- 0.39 v 1.92 +/- 0.31 mL/g/min, p < .05, whereas myocardial flow reserve did not differ between groups of patients and controls (2.57 +/- 1.15 v 3.02 +/- 0.94). Coronary vasodilatory capacity is reduced in patients with severe nonischemic cardiomyopathy. Increases in extravascular compressive forces or increased serum catecholamine levels, which in turn induce coronary vasoconstriction, might account for this finding.
由于左心室扩大和/或冠状血管舒缩张力改变导致的壁应力增加，可能会影响扩张型心肌病患者的心肌血流和血管舒张能力。为了验证这一假设，我们使用动态氮13 - 氨正电子发射断层扫描（双室模型），在10例扩张型心肌病患者（平均左心室射血分数28±8%，1名女性，9名男性；年龄47±13岁）中，于静息状态及静脉注射潘生丁（0.56mg/kg）期间测量心肌血流。10名年龄和性别匹配的健康志愿者作为对照。通过冠状动脉造影排除冠状动脉疾病，通过二维超声心动图排除左心室肥厚。患者和对照组的基线心率（70±13对64±12次/分钟）、收缩压（111±20对114±12mmHg）和心率血压乘积（7,686±1264对7,306±1,645）相似。在注射潘生丁期间，两组的心率血压乘积升高相似。患者组和志愿者组静息时的心肌血流无差异（0.69±0.27对0.67±0.17mL/g/min），但仅在对照组中与心率血压乘积相关（心肌血流，0.18 + 0.000068214；心率血压乘积，.67；P <.05）。充血性心肌血流在患者中较低（1.57±0.39对1.92±0.31mL/g/min，p <.05），而患者组和对照组之间的心肌血流储备无差异（2.57±1.15对3.02±0.94）。严重非缺血性心肌病患者的冠状血管舒张能力降低。血管外压力增加或血清儿茶酚胺水平升高，进而诱导冠状动脉收缩，可能是这一发现的原因。
