Occhetta E, Bortnik M, Francalacci G, Sarasso G, Piccinino C, Pistono M, Marenna B, Paffoni P, Sacchetti M, Inglese E, Trevi G
Cattedra e Divisione Clinicizzata di Cardiologia, Università degli Studi di Torino, Sede di Novara.
Cardiologia. 1998 Dec;43(12):1327-35.
Effectiveness of dual-chamber pacing in patients with dilated cardiomyopathy is still controversial. Our study was performed: to select the most favorable individual atrioventricular (AV) delay; to compare hemodynamic short-term effects in each patient after 2 periods of DDD pacing and sinus rhythm (AV spontaneous); to assess hemodynamic long-term (1 year) effects after DDD pacing at optimum AV delay. In 1996, 9 patients (7 men, 2 women; mean age 69 +/- 5 years) with dilated cardiomyopathy (5 idiopathic, 4 ischemic), NYHA functional class III-IV, ejection fraction < 30%, end-diastolic volume > 60 ml/m2, mitral regurgitation +2/+3, PR interval > or = 200 ms, were enrolled. All patients were implanted with DDD pacemakers and monitored for: ejection fraction and end-diastolic volume (measured by echocardiography and radionuclide angiography); clinical conditions; exercise tolerance and maximum oxygen consumption (by Weber exercise protocol); neurohormonal activity (plasma renin, aldosterone, atrial natriuretic factor). Data were recorded: before DDD implantation; after 2 randomized, single-blind periods of 3 months in VVI mode (at ventricular "sentinel" rate of 50 b/min) and in DDD mode with the optimum AV delay, corresponding for each patient to the minimum end-diastolic volume measured by radionuclide angiography and to the highest cardiac output recorded by echocardiography; after 6 months of DDD pacing with most favorable AV delay. Three more patients died 6 months after (between sixth and twelfth month of follow-up), due to refractory heart failure; 1 patient dropped out because his pacemaker was programmed in VVI mode at low rate, due to intolerance of DDD pacing. Among the other 4 patients no clinical and laboratory parameters were significantly different after 1 year of follow-up. In conclusion, DDD pacing in selected patients with dilated cardiomyopathy showed disappointing results, despite a strict and laboratory monitoring; DDD pacing could be of major benefit in larger populations, according to Doppler mitral flow pattern: those patients with a larger A-wave amplitude could be more sensitive to DDD pacing than those with evidence of poor atrial systole. Moreover, biatral and/or biventricular pacing could also play a significant role.
双腔起搏在扩张型心肌病患者中的有效性仍存在争议。我们开展了本研究：选择最适宜的个体化房室（AV）延迟；比较每位患者在DDD起搏和窦性心律（房室自主）两个阶段后的短期血流动力学效应；评估在最佳AV延迟下DDD起搏后的长期（1年）血流动力学效应。1996年，纳入了9例扩张型心肌病患者（7例男性，2例女性；平均年龄69±5岁）（5例特发性，4例缺血性），纽约心脏协会（NYHA）心功能分级为III-IV级，射血分数<30%，舒张末期容积>60 ml/m²，二尖瓣反流+2/+3，PR间期≥200 ms。所有患者均植入DDD起搏器，并监测：射血分数和舒张末期容积（通过超声心动图和放射性核素血管造影测量）；临床状况；运动耐量和最大耗氧量（采用Weber运动方案）；神经激素活性（血浆肾素、醛固酮、心房利钠因子）。记录数据：在植入DDD起搏器前；在VVI模式（心室“警戒”频率为50次/分钟）和具有最佳AV延迟的DDD模式下进行两个3个月的随机、单盲阶段后，最佳AV延迟对每位患者而言对应通过放射性核素血管造影测量的最小舒张末期容积以及通过超声心动图记录的最高心输出量；在采用最适宜AV延迟进行DDD起搏6个月后。另外3例患者在6个月后（随访的第6至12个月之间）因难治性心力衰竭死亡；1例患者退出研究，因为其起搏器因不耐受DDD起搏而被程控为低频率的VVI模式。在其他4例患者中，随访1年后临床和实验室参数无显著差异。总之，尽管进行了严格的临床和实验室监测，但在选定的扩张型心肌病患者中DDD起搏显示出令人失望的结果；根据二尖瓣血流频谱模式，DDD起搏在更大规模人群中可能具有更大益处：A波幅度较大的患者可能比心房收缩功能不良的患者对DDD起搏更敏感。此外，双心房和/或双心室起搏也可能发挥重要作用。
