Modena M G, Rossi R, Carcagnì A, Molinari R, Mattioli G
Department of Internal Medicine, Institute of Cardiology, Modena, Italy.
Pacing Clin Electrophysiol. 1996 Nov;19(11 Pt 1):1595-604. doi: 10.1111/j.1540-8159.1996.tb03186.x.
We assessed the influence and clinical consequences of different AV delay on ventricular filling in 30 patients (mean age 60 +/- 5 years) who had DDD pacemakers for AV block. All 30 patients presented a normal ejection fraction, but in 18 cases (Group I), an echo-Doppler examination revealed ventricular hypertrophy (mean end-diastolic wall thickness of 1.4 +/- 0.16 cm, LV mass index 155 +/- 17 g/m2), and an abnormal relaxation pattern (isovolumetric relaxation time = 124.72 +/- 11.82; early to late peak velocity = 0.6 +/- 0.03; deceleration time = 296.83 +/- 34.02 ms). Group II included the remaining 12 patients who had a normal filling pattern. In all 30 patients, the pattern was reassessed following modification of the AV delay (200, 150, 100, and 75 ms). Patients at baseline (AV delay of 200 ms) also underwent an exercise test with determination of respiratory gas exchange. In Group I, 13 (72.5%) patients were classified as Weber class B (VO2 Max 16.8 +/- 1.7 mL/min per kg); and 5 (27.5%) were Class A (VO2 Max 22.5 +/- 1.4 mL/min per kg). In Group II, all 12 patients were classified as Weber Class A. In Group II, changes in AV delay caused no consistent variations in filling pattern, and therefore AV delay was not modified. In Group I patients, since reduction to 100 ms resulted in normalization of the filling pattern, the AV delay was programmed to 100 ms. A graded exercise test repeated after 6 months' follow-up showed an improved Weber class in 13 patients (from B to A) and greater VO2 Max in the remaining five already in Class A. We concluded that, in sequential paced patients with normal ejection fraction but abnormal relaxation pattern, modification in AV delay can induce normalization of filling and improvement in cardiac functional capacity.
我们评估了30例因房室传导阻滞植入DDD起搏器的患者(平均年龄60±5岁)中不同房室延迟对心室充盈的影响及临床后果。所有30例患者射血分数均正常,但18例患者(I组)经超声心动图 - 多普勒检查显示心室肥厚(平均舒张末期室壁厚度为1.4±0.16 cm,左心室质量指数为155±17 g/m²),且舒张模式异常(等容舒张时间 = 124.72±11.82;早期与晚期峰值速度 = 0.6±0.03;减速时间 = 296.83±34.02 ms)。II组包括其余12例充盈模式正常的患者。对所有30例患者,在改变房室延迟(200、150、100和75 ms)后重新评估其模式。基线时(房室延迟200 ms)的患者还进行了运动试验并测定呼吸气体交换。I组中,13例(72.5%)患者被分类为Weber B级(最大摄氧量16.8±1.7 mL/min per kg);5例(27.5%)为A级(最大摄氧量22.5±1.4 mL/min per kg)。II组中,所有12例患者均被分类为Weber A级。在II组中,房室延迟的改变未引起充盈模式的一致变化,因此未改变房室延迟。在I组患者中,由于将房室延迟减至100 ms可使充盈模式正常化,故将房室延迟程控为100 ms。6个月随访后重复进行的分级运动试验显示,13例患者的Weber分级得到改善(从B级变为A级),其余5例已为A级的患者最大摄氧量增加。我们得出结论,在射血分数正常但舒张模式异常的顺序起搏患者中,改变房室延迟可使充盈正常化并改善心功能能力。