Lefroy D C, de Silva R, Choudhury L, Uren N G, Crake T, Rhodes C G, Lammertsma A A, Boyd H, Patsalos P N, Nihoyannopoulos P
Medical Research Council (MRC) Cyclotron Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London, England, United Kingdom.
J Am Coll Cardiol. 1993 Nov 15;22(6):1653-60. doi: 10.1016/0735-1097(93)90591-n.
This study was conducted to determine the myocardial beta-adrenoceptor density as a marker of sympathetic function in patients with hypertrophic cardiomyopathy and normal control subjects.
Although some cases of hypertrophic cardiomyopathy are familial with an autosomal dominant pattern of inheritance, there remains a substantial proportion of cases in which neither a family history nor genetic abnormalities can be demonstrated. Additional abnormalities, both genetic and acquired, may be important in the phenotypic expression of this condition. Clinical features of the disease and metabolic studies suggest an increased activity of the sympathetic nervous system.
Eleven patients with hypertrophic cardiomyopathy, none of whom had previously received beta-blocking drugs, and eight normal control subjects underwent positron emission tomography to evaluate regional left ventricular beta-adrenoceptor density and myocardial blood flow using carbon-11-labeled CGP 12177 and oxygen-15-labeled water as tracers. Plasma catecholamines were also measured.
Mean (+/- SD) myocardial beta-adrenoceptor density was significantly less in the hypertrophic cardiomyopathy group than in the control group (7.70 +/- 1.86 vs. 11.50 +/- 2.18 pmol/g tissue, p < 0.001). Myocardial blood flow was similar in both groups (0.91 +/- 0.22 vs. 0.91 +/- 0.21 ml/min per g, p = NS). The distribution of beta-adrenoceptor density was uniform throughout the left ventricle in both groups. In the hypertrophic cardiomyopathy group, there was no correlation between regional wall thickness and myocardial beta-adrenoceptor density. There were no significant differences in either plasma norepinephrine or epinephrine concentrations between the two groups.
There is a diffuse reduction in myocardial beta-adrenoceptor density in patients with hypertrophic cardiomyopathy in the absence of significantly elevated circulating catecholamine concentrations. This most likely reflects downregulation of myocardial beta-adrenoceptors secondary to increased myocardial concentrations of norepinephrine and is consistent with the hypothesis that cardiac sympathetic drive is increased in this condition.
本研究旨在确定肥厚型心肌病患者和正常对照者的心肌β - 肾上腺素能受体密度，作为交感神经功能的标志物。
虽然部分肥厚型心肌病病例为家族性，呈常染色体显性遗传模式，但仍有相当比例的病例无法证明有家族史或基因异常。其他遗传和后天获得的异常可能对该疾病的表型表达很重要。该疾病的临床特征和代谢研究提示交感神经系统活性增加。
11例肥厚型心肌病患者（均未接受过β受体阻滞剂治疗）和8名正常对照者接受正电子发射断层扫描，使用碳 - 11标记的CGP 12177和氧 - 15标记的水作为示踪剂，评估左心室局部β - 肾上腺素能受体密度和心肌血流。同时测量血浆儿茶酚胺水平。
肥厚型心肌病组的平均（±标准差）心肌β - 肾上腺素能受体密度显著低于对照组（7.70±1.86 vs. 11.50±2.18 pmol/g组织，p < 0.001）。两组的心肌血流相似（0.91±0.22 vs. 0.91±0.21 ml/min per g，p = 无显著差异）。两组左心室内β - 肾上腺素能受体密度分布均一。在肥厚型心肌病组中，局部室壁厚度与心肌β - 肾上腺素能受体密度之间无相关性。两组间血浆去甲肾上腺素或肾上腺素浓度均无显著差异。
在循环儿茶酚胺浓度未显著升高的情况下，肥厚型心肌病患者心肌β - 肾上腺素能受体密度弥漫性降低。这很可能反映了去甲肾上腺素心肌浓度增加导致的心肌β - 肾上腺素能受体下调，与该疾病中心脏交感神经驱动增加的假说一致。
