Giannattasio Cristina, Vincenti Antonio, Failla Monica, Capra Anna, Cirò Antonio, De Ceglia Sergio, Gentile Gaetano, Brambilla Roberta, Mancia Giuseppe
Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Università di Milano, Milano Bicocca e Pavia, Italy.
Hypertension. 2003 Sep;42(3):253-6. doi: 10.1161/01.HYP.0000085199.33254.15. Epub 2003 Aug 11.
In rats, an increase in heart rate by pacing is accompanied by progressive large-artery stiffening. Whether this is also the case in humans is unknown. We enrolled 20 patients who were chronically implanted with a pacemaker because of atrioventricular block or sick sinus syndrome. Arterial distensibility was measured by an echo-tracking device. In 10 patients, the evaluation was performed on the radial artery by using continuous finger blood pressure measurements, whereas in the remaining 10 patients, the common carotid artery was studied with a semiautomatic measure of brachial artery blood pressure. Diastolic diameter, systodiastolic diameter change, and distensibility were obtained at baseline (heart rate 63+/-2 beats/min) and after atrial and ventricular sequential pacing at a heart rate of 90 and 110 beats/min. At baseline, the diameter was 7.8+/-0.3 mm in the carotid artery and 2.4+/-0.1 mm in the radial artery; the respective systodiastolic diameter change values were 375.4+/-31.0 and 55.9+/-9.0 (microm) and the distensibility values were 1.4+/-0.1 and 0.7+/-0.1 (1/mm Hg 10-3). Blood pressure and diameter were not significantly modified by increasing heart rate, which markedly modified systodiastolic diameter change and distensibility. In the radial artery, distensibility was reduced by 47% (P<0.05) at a heart rate of 90 beats/min with no further reduction at 110 beats/min. In the carotid artery, distensibility was reduced by 20% at a heart rate of 90 beats/min (P<0.05) with a further reduction at 110 beats/min (45%, P<0.05). These data provide the first evidence in humans that acute increases in heart rate markedly affect arterial distensibility and that this occurs in both large- and middle-size muscle arteries within the range of "normal" heart rate values.
在大鼠中，通过起搏使心率增加会伴随大动脉硬化程度逐渐加重。在人类中是否也是如此尚不清楚。我们纳入了20例因房室传导阻滞或病态窦房结综合征而长期植入起搏器的患者。通过回声跟踪装置测量动脉扩张性。10例患者通过连续手指血压测量对桡动脉进行评估，而其余10例患者则通过半自动测量肱动脉血压对颈总动脉进行研究。在基线时（心率63±2次/分钟）以及心房和心室顺序起搏使心率达到90次/分钟和110次/分钟后，获取舒张期直径、收缩期-舒张期直径变化以及扩张性。基线时，颈总动脉直径为7.8±0.3毫米，桡动脉直径为2.4±0.1毫米；各自的收缩期-舒张期直径变化值分别为375.4±31.0和55.9±9.0（微米），扩张性值分别为1.4±0.1和0.7±0.1（1/毫米汞柱×10⁻³）。心率增加时血压和直径未发生显著改变，但显著改变了收缩期-舒张期直径变化和扩张性。在桡动脉中，心率为90次/分钟时扩张性降低了47%（P<0.05），心率为110次/分钟时未进一步降低。在颈总动脉中，心率为90次/分钟时扩张性降低了20%（P<0.05），心率为110次/分钟时进一步降低（45%，P<0.05）。这些数据首次在人类中证明，心率急性增加会显著影响动脉扩张性，且这种情况发生在“正常”心率值范围内的大、中尺寸肌肉动脉中。
