STRETCH-INDUCED ARRHYTHMIAS IN THE ISOLATED CANINE VENTRICLE - EVIDENCE FOR THE IMPORTANCE OF MECHANOELECTRICAL FEEDBACK
STRETCH-INDUCED ARRHYTHMIAS IN THE ISOLATED CANINE VENTRICLE - EVIDENCE FOR THE IMPORTANCE OF MECHANOELECTRICAL FEEDBACK
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DOI：
10.1161/01.cir.81.3.1094
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发表时间：
1990-03-01
期刊：
影响因子：
37.8
通讯作者：
HONDEGHEM, LM
中科院分区：
文献类型：
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作者：
HANSEN, DE;CRAIG, CS;HONDEGHEM, LM
负荷条件和肌肉长度的改变影响心室肌电生理，并可能在整体扩张或运动障碍心室的心律失常发生中发挥作用。为了验证拉伸可以引发正常心肌心律失常的假设，我们研究了7个离体血灌注犬心室对分级机械拉伸的反应。在他束起搏（2hz）产生八次调节收缩后，心室的整体拉伸由伺服控制泵产生，该泵在舒张早期突然以精确量（. delta . v）增加心室容积，然后将心室容积恢复到初始保持容积（Vi）。心室早缩易产生；偶有室性对联和室性心动过速的短暂发作。拉伸诱发心律失常的概率由多个交替序列确定，其中已知振幅的拉伸（. delta . v）或没有拉伸。.DELTA。V增大时，最初发生牵张性心律失常的概率较低，超过阈值后急剧增加，生理容积接近100%。将Vi设为20ml标准值，对应舒张末压为5.3±。5.2 mm Hg(平均+-。SD), delta。导致牵拉性心律失常的50%几率（. delta . v50）为15.0 +-。1.6毫升，delta下降。随着Vi的增加，V50持续存在。而.DELTA。V50值具有显著的相似性（变异系数为10.7%），不同心室触发心室过早去极化时的压力差异很大；这一发现表明，在这些心律失常的发生中，心肌应变比壁应力的绝对水平更重要。这些结果表明，心肌拉伸可预见地引发心律失常，心室扩张增强了对拉伸引起的心律失常的易感性。因此，局部或全局心脏扩张患者的心室异位可能部分由心肌拉伸机制引起。
Alterations in loading conditions and muscle length influence the electrophysiology of ventricular myocardium and may play a role in arrhythmogenesis in globally dilated or dyskinetic ventricles. To test the hypothesis that stretch can initiate arrhythmias in normal myocardium, the response to graded mechanical stretch was studied in seven isolated blood-perfused canine ventricles. After eight conditioning contractions produced by His bundle pacing (2 Hz), global stretch of the ventricle was produced by a servocontrolled pump that abruptly increased ventricular volume by a precise amount (.DELTA.V) during early diastole and then returned ventricular volume to the initial holding volume (Vi). Ventricular premature contractions were readily produced; ventricular couplets and short runs of ventricular tachycardia were occasionally elicited. The probability of a stretch-induced arrhythmia was determined from multiple alternating sequences in which a stretch of known amplitude (.DELTA.V) or no stretch was delivered. As .DELTA.V was increased, the probability of a stretch-induced arrhythmia was low initially, increased sharply after a threshold was exceeded, and approaching 100% with physiological volumes. With Vi set to a standard value of 20 ml, corresponding to end-diastolic pressure of 5.3 .+-. 5.2 mm Hg (mean .+-. SD), the .DELTA.V resulting in a 50% chance of a stretch-induced arrhythmia (.DELTA.V50) was 15.0 .+-. 1.6 ml. A decline in .DELTA.V50 was consistently observed when Vi was increased. While .DELTA.V50 values were remarkably similar (10.7% coefficient of variation), the pressure at the time the ventricular premature depolarization was triggered was highly variable for different ventricles; this finding suggests that myocardial strain is more important than absolute level of wall stress in the initiation of these arrhythmias. These results demonstrate that myocardial stretch predictably initiates arrhythmias and that the susceptibility to stretch-induced arrhythmias is enhanced by ventricular dilatation. Thus, ventricular ectopy in patients with regionally or globally dilated hearts may arise, in part, by a mechanism of myocardial stretch.