Adamson P B, Huang M H, Vanoli E, Foreman R D, Schwartz P J, Hull S S
Department of Internal Medicine, University of Oklahoma, HSC, Oklahoma City.
Circulation. 1994 Aug;90(2):976-82. doi: 10.1161/01.cir.90.2.976.
Heart rate (HR) variability is a marker of tonic cardiac autonomic activity and contributes in assessing risk for sudden death after myocardial infarction. Recent clinical observations have indicated that attenuation of HR variability, which occurs after myocardial infarction, may be transient. This study addresses the issue of whether autonomic control of heart rate recovers at different rates after myocardial infarction in subjects at high and low risk for ventricular fibrillation (VF).
Thirty dogs, 22 with myocardial infarction and 8 sham-prepared animals, completed the study. Changes and recovery in cardiac autonomic activity after myocardial infarction were examined by measuring HR variability before and at defined intervals during the first 30 days after infarction. Each HR variability measurement was made before and after beta-blockade in dogs at high (n = 10) and low (n = 12) risk for VF. Arrhythmia risk was determined on the basis of development of VF during exercise and transient myocardial ischemia 30 days after infarction. No sham-prepared animals developed VF. Preinfarction measurements of HR variability were not different between the groups before beta-blockade, but HR variability increased much more in response to beta-blockade in animals destined to be resistant compared with susceptible animals (289 +/- 26 to 369 +/- 35 msec, delta 27.7%, versus 270 +/- 36 to 283 +/- 34 milliseconds, delta 4.8%, respectively, P < .01). Immediately after infarction, HR variability was significantly attenuated in all dogs, but in the resistant dogs it recovered to pre-myocardial infarction levels within 10 days. After the infarction, beta-blockade did not increase HR variability in either group of animals. Postoperative increases in HR variability from beta-blockade were preserved in the sham group. Susceptible animals were characterized by a persistent attenuation of HR variability throughout the 30 days.
The depression in HR variability produced by myocardial infarction has a clearly different temporal recovery pattern between low- and high-risk animals. After myocardial infarction, beta-adrenergic blockade does not alter HR variability, thus preserving its predictive value. Before myocardial infarction, however, beta-blockade increases HR variability only in the animals destined to be at low risk for lethal arrhythmias after the infarction. The recovery pattern of HR variability after myocardial infarction may contribute to the early recognition of individuals at high risk for sudden death.
心率（HR）变异性是心脏自主性张力活动的一个指标，有助于评估心肌梗死后猝死的风险。最近的临床观察表明，心肌梗死后发生的HR变异性减弱可能是短暂的。本研究探讨了在心室颤动（VF）高风险和低风险受试者中，心肌梗死后心率的自主控制是否以不同速率恢复的问题。
30只犬，22只患有心肌梗死，8只为假手术制备动物，完成了本研究。通过测量梗死后前30天内定义时间点及梗死前的HR变异性，研究心肌梗死后心脏自主活动的变化和恢复情况。在VF高风险（n = 10）和低风险（n = 12）的犬中，在β受体阻滞剂给药前后进行每次HR变异性测量。根据梗死后30天运动期间VF的发生情况和短暂性心肌缺血来确定心律失常风险。假手术制备动物未发生VF。在β受体阻滞剂给药前，两组之间梗死前HR变异性测量值无差异，但与易感性动物相比，注定具有抗性的动物对β受体阻滞剂的反应中HR变异性增加更多（分别为289±26至369±35毫秒，变化27.7%， versus 270±36至283±34毫秒，变化4.8%，P <.01）。梗死后立即，所有犬的HR变异性均显著减弱，但在抗性犬中，其在10天内恢复到心肌梗死前水平。梗死后，β受体阻滞剂在两组动物中均未增加HR变异性。假手术组中由β受体阻滞剂引起的术后HR变异性增加得以保留。易感性动物的特征是在整个30天内HR变异性持续减弱。
心肌梗死引起的HR变异性降低在低风险和高风险动物之间具有明显不同的时间恢复模式。心肌梗死后，β肾上腺素能阻滞剂不会改变HR变异性，从而保留其预测价值。然而，在心肌梗死前，β受体阻滞剂仅在梗死后注定发生致死性心律失常风险低的动物中增加HR变异性。心肌梗死后HR变异性的恢复模式可能有助于早期识别猝死高风险个体。
