Neunteufl T, Katzenschlager R, Abela C, Kostner K, Niederle B, Weidinger F, Stefenelli T
Department of Cardiology, University of Vienna, Austria.
Cardiovasc Res. 1998 Nov;40(2):396-401. doi: 10.1016/s0008-6363(98)00177-1.
Patients with primary hyperparathyroidism (PHPT) and/or hypercalcemia are at increased risk for myocardial ischemia. Whether PHPT is associated with altered endothelium-dependent dilation, vascular smooth muscle cell function, or both is unknown. This study was performed to test the hypothesis that endothelium-dependent, flow-mediated dilation (FMD) and/or endothelium-independent, nitroglycerin-induced dilation (NMD) is impaired in the preclinical phase of vascular disease in patients with PHPT.
Twenty-six PHPT patients (mean +/- SD; age 55 +/- 15 y, serum calcium 3.00 +/- 0.37 mmol/l, serum phosphate 0.79 +/- 0.21 mmol/l, iPTH 249 +/- 262 pg/ml) with no evidence of coronary artery disease (CAD) as well as 26 normocalcemic control subjects (CTL; age 51 +/- 12 y) were studied. FMD following reactive hyperemia and NMD after 0.8 mg nitroglycerin (NTG) were assessed in the brachial artery by using high resolution ultrasound (7 MHz).
NMD was impaired in PHPT patients compared to CTL (11.9 +/- 3.9% vs. 15.6 +/- 5.7%; p = 0.012). FMD was similar in both study groups (11.6 +/- 4.6% vs. 12.6 +/- 4.9; NS). The ratio of FMD to NMD was significantly different between PHPT patients and CTL (0.98 +/- 0.19 vs 0.81 +/- 0.25, p = 0.0009). On multiple stepwise regression analysis serum calcium was independently associated with the FMD/NMD ratio (r = 0.34, p = 0.017).
Endothelium-independent vasodilation is impaired in PHPT patients without clinical evidence of coronary artery disease compared to normocalcemic CTL, while endothelium-dependent dilation was similar in both study groups. Thus, altered arterial reactivity in the course of PHPT may predominantly involve the arterial media and not the endothelium as observed previously in patients with various stages of atherosclerosis.
原发性甲状旁腺功能亢进症（PHPT）患者和/或高钙血症患者发生心肌缺血的风险增加。PHPT是否与内皮依赖性舒张功能改变、血管平滑肌细胞功能改变或两者均有关尚不清楚。本研究旨在验证以下假设：在PHPT患者血管疾病的临床前期，内皮依赖性血流介导的舒张功能（FMD）和/或非内皮依赖性硝酸甘油诱导的舒张功能（NMD）受损。
研究了26例无冠状动脉疾病（CAD）证据的PHPT患者（平均±标准差；年龄55±15岁，血清钙3.00±0.37 mmol/L，血清磷0.79±0.21 mmol/L，iPTH 249±262 pg/ml）以及26例血钙正常的对照受试者（CTL；年龄51±12岁）。通过高分辨率超声（7 MHz）评估肱动脉在反应性充血后的FMD以及在给予0.8 mg硝酸甘油（NTG）后的NMD。
与CTL相比，PHPT患者的NMD受损（11.9±3.9%对15.6±5.7%；p = 0.012）。两个研究组的FMD相似（11.6±4.6%对12.6±4.9；无显著性差异）。PHPT患者与CTL之间FMD与NMD的比值显著不同（0.98±0.19对0.81±0.25，p = 0.0009）。在多元逐步回归分析中，血清钙与FMD/NMD比值独立相关（r = 0.34，p = 0.017）。
与血钙正常的CTL相比，无冠状动脉疾病临床证据的PHPT患者非内皮依赖性血管舒张功能受损，而两个研究组的内皮依赖性舒张功能相似。因此，在PHPT病程中动脉反应性改变可能主要累及动脉中膜，而不像先前在动脉粥样硬化各阶段患者中观察到的那样累及内皮。
