From the Department of Health and Social Development, Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Okanagan Campus, British Columbia, Canada (J.D.S., K.R.M., P.N.A.); Department of Physical Therapy, Faculty of Rehabilitation Medicine, University of Alberta and Mazankowki Alberta Heart Institute, Edmonton, Canada (M.J.H.); Cedars-Sinai Heart Institute, Los Angeles, CA (M.D.N.); Department of Surgery and Anaesthesia, Cardiovascular Systems Laboratory, Centre for Translational Physiology, University of Otago, Wellington, New Zealand (Y.-C.T.); and Department of Sport and Exercise Science, Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK (H.J.).
Hypertension. 2014 Dec;64(6):1314-20. doi: 10.1161/HYPERTENSIONAHA.114.04236. Epub 2014 Oct 6.
Heart transplant recipients are at an increased risk for cerebral hemorrhage and ischemic stroke; yet, the exact mechanism for this derangement remains unclear. We hypothesized that alterations in cerebrovascular regulation is principally involved. To test this hypothesis, we studied cerebral pressure-flow dynamics in 8 clinically stable male heart transplant recipients (62±8 years of age and 9±7 years post transplant, mean±SD), 9 male age-matched controls (63±8 years), and 10 male donor controls (27±5 years). To increase blood pressure variability and improve assessment of the pressure-flow dynamics, subjects performed squat-stand maneuvers at 0.05 and 0.10 Hz. Beat-to-beat blood pressure, middle cerebral artery velocity, and end-tidal carbon dioxide were continuously measured during 5 minutes of seated rest and throughout the squat-stand maneuvers. Cardiac baroreceptor sensitivity gain and cerebral pressure-flow responses were assessed with linear transfer function analysis. Heart transplant recipients had reductions in R-R interval power and baroreceptor sensitivity low frequency gain (P<0.01) compared with both control groups; however, these changes were unrelated to transfer function metrics. Thus, in contrast to our hypothesis, the increased risk of cerebrovascular complication after heart transplantation does not seem to be related to alterations in cerebral pressure-flow dynamics. Future research is, therefore, warranted.
心脏移植受者发生脑出血和缺血性卒中的风险增加;然而,这种紊乱的确切机制尚不清楚。我们假设主要涉及脑血管调节的改变。为了验证这一假设,我们研究了 8 名临床稳定的男性心脏移植受者(62±8 岁,移植后 9±7 年,平均值±标准差)、9 名年龄匹配的男性对照者(63±8 岁)和 10 名男性供体对照者(27±5 岁)的脑压力-血流动力学。为了增加血压变异性并改善压力-血流动力学的评估,受检者以 0.05 和 0.10 Hz 的频率进行蹲-站动作。在 5 分钟的坐姿休息期间和整个蹲-站动作期间,连续测量了每搏血压、大脑中动脉速度和呼气末二氧化碳。使用线性传递函数分析评估心脏压力感受器敏感性增益和脑压力-血流反应。与两个对照组相比,心脏移植受者的 R-R 间期功率和压力感受器敏感性低频增益降低(P<0.01);然而,这些变化与传递函数指标无关。因此,与我们的假设相反,心脏移植后脑血管并发症风险增加似乎与脑压力-血流动力学的改变无关。因此,有必要进行进一步的研究。