Kawasaki Tatsuya, Azuma Akihiro, Kuribayashi Toshiro, Akakabe Yoshiki, Yamano Michiyo, Miki Shigeyuki, Sawada Takahisa, Kamitani Tadaaki, Matsubara Hiroaki, Sugihara Hiroki
Department of Cardiology, Matsushita Memorial Hospital, Osaka, Japan.
Int J Cardiol. 2008 Sep 16;129(1):59-64. doi: 10.1016/j.ijcard.2007.05.023. Epub 2007 Jul 24.
Patients with hypertrophic cardiomyopathy (HCM) often develop myocardial ischemia in association with abnormal blood pressure response to exercise. Vagal nerves mediate cardioinhibitory stimuli, with little knowledge regarding vagal response to myocardial ischemia in patients with HCM.
Exercise Tc-99m-tetrofosmin myocardial scintigraphy was performed in 59 HCM patients and 39 controls who had no evidence of cardiac disease. We examined how reversible regional perfusion abnormality and transient left ventricular cavity dilation, a parameter of subendocardial ischemia, are related to vagal modulation as assessed by coefficient of high frequency component variance (CCV(HF)) on heart rate variability. We then correlated the results with abnormal blood pressure response to exercise, defined as failed increase >or=25 mm Hg during exercise.
Regional perfusion abnormality and left ventricular cavity dilation were observed in 26 and 21 HCM patients, respectively. The percentage change of CCV(HF) from before to after exercise was higher in HCM patients with left ventricular cavity dilation than without or controls (5.2+/-9.8%, -23.5+/-5.7%, -14.5+/-5.5%, P=0.004). By contrast, the change of CCV(HF) was similar in HCM patients with regional perfusion abnormality, those without, and controls. The change of CCV(HF) was correlated with exercise-induced increase in systolic blood pressure (rho=-0.64, P<0.001); HCM patients with abnormal blood pressure response were characterized by a higher percentage change in CCV(HF) (50.0+/-18.3%).
Subendocardial ischemia provoked vagal enhancement in patients with HCM, which may be related to the development of abnormal blood pressure response to exercise.
肥厚型心肌病(HCM)患者常伴有运动时血压异常反应,并出现心肌缺血。迷走神经介导心脏抑制性刺激,但对于HCM患者迷走神经对心肌缺血的反应了解甚少。
对59例HCM患者和39例无心脏病证据的对照者进行运动Tc-99m-替曲膦心肌闪烁显像。我们通过心率变异性高频成分方差系数(CCV(HF))评估可逆性局部灌注异常和短暂性左心室腔扩张(心内膜下缺血的一个参数)与迷走神经调节之间的关系。然后将结果与运动时异常血压反应相关联,运动时异常血压反应定义为运动期间收缩压升高未达到或超过25 mmHg。
分别在26例和21例HCM患者中观察到局部灌注异常和左心室腔扩张。左心室腔扩张的HCM患者运动前后CCV(HF)的百分比变化高于无左心室腔扩张的HCM患者或对照者(5.2±9.8%,-23.5±5.7%,-14.5±5.5%,P = 0.004)。相比之下,有局部灌注异常的HCM患者、无局部灌注异常的HCM患者和对照者的CCV(HF)变化相似。CCV(HF)的变化与运动引起的收缩压升高相关(ρ = -0.64,P < 0.001);血压反应异常的HCM患者CCV(HF)的百分比变化更高(50.0±18.3%)。
心内膜下缺血可引起HCM患者迷走神经功能增强,这可能与运动时异常血压反应的发生有关。