Ito M, Tsumabuki S, Maeda Y, Arita M, Saikawa T, Ito S, Fujino T, Fukumoto T, Yamada K, Kikuchi Y
Jpn Circ J. 1987 Feb;51(2):217-29. doi: 10.1253/jcj.51.217.
The clinical importance of triggered activity as a cause of arrhythmias is uncertain. We assumed that ventricular premature contractions (VPCs) caused by triggered activity could be increased at higher heart rates and be suppressed by calcium channel blockers and beta-adrenoceptor blocker. Thus, we evaluated VPC frequency as a function of underlying heart rate and examined the efficacy of diltiazem and atenolol on VPCs, using 24 hour ECG recording. Plots of VPC frequency vs. heart rate were made at 1-beat/min intervals for all heart rates recorded for at least 5 min during 24 hours. Diltiazem (90-180 mg/day) and atenolol (50 mg/day) were given orally for 4 weeks, respectively in 36 and 16 patients with VPCs of more than 2000/day. Patterns of relationship between VPC frequency and heart rate observed before diltiazem therapy included: an increase of VPCs at higher heart rates (positive correlation) in 16 patients, an increase at low heart rates and a decrease at high heart rates (bidirectional correlation) in 13 patients, an increase at low heart rates and flat curve at high heart rates (positive-flat correlation) in 5 patients, a linear decrease (negative correlation) in 1 patient, and flat curve (flat correlation) in 1 patient. The patterns of correlation in patients treated with atenolol were positive in 6, bidirectional in 7, positive-flat in 2 and negative in 1. Both drugs significantly reduced the VPC frequency per 24 hours for patients with a positive correlation (P group), but induced no significant change for those with the other patterns of correlation (NP group). At the 70% VPC suppression level, diltiazem was effective in 9 of 16 patients of P group and only 1 of 20 patients of NP group (p less than 0.01); atenolol was effective in 5 of 6 patients of P group and only 1 of 10 patients of NP group (p less than 0.05). Both drugs reduced the slope of a positive correlation. These results suggest that: VPCs which increase at higher heart rates may be related to triggered activity, and an evaluation of VPC frequency as a function of heart rate predicts the response of VPCs to diltiazem and atenolol, and probably to other calcium antagonists and beta blockers.
触发活动作为心律失常病因的临床重要性尚不确定。我们假设由触发活动引起的室性早搏（VPC）在较高心率时会增加，并可被钙通道阻滞剂和β-肾上腺素能受体阻滞剂抑制。因此，我们使用24小时心电图记录，评估VPC频率与基础心率的关系，并研究地尔硫卓和阿替洛尔对VPC的疗效。在24小时内，对至少记录5分钟的所有心率，以每分钟1次心跳的间隔绘制VPC频率与心率的关系图。分别给予36例和16例每日VPC超过2000次的患者口服地尔硫卓（90 - 180毫克/天）和阿替洛尔（50毫克/天），持续4周。地尔硫卓治疗前观察到的VPC频率与心率的关系模式包括：16例患者在较高心率时VPC增加（正相关），13例患者在低心率时增加而在高心率时减少（双向相关），5例患者在低心率时增加而在高心率时呈平坦曲线（正-平坦相关），1例患者呈线性下降（负相关），1例患者呈平坦曲线（平坦相关）。接受阿替洛尔治疗的患者的相关模式为：6例为正相关，7例为双向相关，2例为正-平坦相关，1例为负相关。两种药物均使正相关患者（P组）每24小时的VPC频率显著降低，但对其他相关模式的患者（NP组）无显著影响。在地尔硫卓治疗中，在VPC抑制水平达到70%时，P组16例患者中有9例有效，而NP组20例患者中仅1例有效（p<0.01）；阿替洛尔治疗中，P组6例患者中有5例有效，而NP组10例患者中仅1例有效（p<0.05）。两种药物均降低了正相关的斜率。这些结果表明：在较高心率时增加的VPC可能与触发活动有关，评估VPC频率与心率的关系可预测VPC对地尔硫卓和阿替洛尔的反应，可能也能预测对其他钙拮抗剂和β受体阻滞剂的反应。
