起搏可治心衰，也可致心衰
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起搏可以治心衰（CRT），也可致心衰。后者在最近10年才得到重视。研究显示，cum％ VP （心室起搏比例）与心衰发生成正比。基线的起搏QRS时限或QRS时限，也是一个重要影响因素。MOST研究小组的提出一个概念叫心室不同步负荷＝cum％ VP × QRS时限。认为这是最重要的致心衰起搏因素。 有过心肌梗死得病人，装了起搏器后，发生心衰得比例也会明显升高。Circulation 上有篇文章，我看了近10遍，写得非常好，对这个问题研究得很透。文章结果显示，起搏器导致心衰可以看成是患者基质特性与起搏因素相互作用得结果。前者包括患者基础心功能，EF值，有无心肌梗死，房颤，后者包括起搏模式、起搏QRS时限宽度，心室起搏部位。在EF正常，无心肌梗死，基线QRS<120ms的病人，心衰发生率是很低，这些病人是能长期耐受右室心尖部起搏的。而这些病人是占置入起搏器患者中大多数。这跟我们临床经验很相符，我们经常碰到更换了几个起搏器还心功能良好的病人。所以可以得出这样一个结论，对于心功能良好的患者，或者没有MI的患者，心室同步意义不大。机体有较强耐受能力。而对于EF<40%的患者，心室同步是相当重要的，这可以由PAVE研究及HOBIPACE研究得出这样推论。对于EF<0。40伴高度AVB的病人，条件好的话可以直接行CRT，没钱的话本人认为还是行RVOT起搏。最近国内有许多医院，（包括我们医院），开始搞右室流出道起搏（RVOT）与心尖部起搏（RVA）对比研究，我认为很难得出阳性结果。应该只入选EF<40％人群才能得出结果。
PS:有研究这问题的战友欢迎发言。附circulation 上的一篇文章。有兴趣大家可以去读读。
Michael O. Sweeney, MD; Anne S. Hellkamp, MS。 Heart Failure During Cardiac Pacing (Circulation. 2006;113:2082-2088.)
Background—Right ventricular apical (RVA) pacing creates abnormal left ventricular contraction, hypertrophy, and
reduced pump function. The adverse effects of ventricular desynchronization may explain the association of RVA
pacing with an increased risk of heart failure hospitalization (HFH) in clinical trials.
Methods and Results—Baseline and postimplantation variables were used to predict HFH in the Mode Selection Trial, a
2010-patient, 6-year trial of dual-chamber (DDDR) versus ventricular (VVIR) pacing in sinus node dysfunction. A Cox
model showed that New York Heart Association (NYHA) class at baseline and follow-up predicted HFH (hazard ratio
[HR], 3.99; 95% confidence interval [CI], 2.74 –5.79 for NYHA class III/IV and HR, 2.17; 95% CI, 1.54 –3.04 for
NYHA class II versus class I); other predictors were heart failure (HR, 2.30; 95% CI, 1.70 –3.11), atrioventricular (**)
block (HR, 1.48; 95% CI, 1.11–1.97), and myocardial infarction (MI)(HR, 1.37; 95% CI, 1.00 –1.86). Postimplantation
predictors were VVIR cumulative percent ventricular pacing (Cum%VP) 80 (HR, 3.58; 95% CI, 1.72–7.45), DDDR
Cum%VP 40 or VVIR Cum%VP 80 (HR, 1.81; 95% CI, 0.94 –3.50) versus DDDR Cum%VP 40; whether QRS
duration (QRSd) was paced or spontaneous (HR, 2.21; 95% CI, 1.39 –3.54; spontaneous versus paced); and drugs for
atrial fibrillation (HR, 1.60; 95% CI, 1.19 –2.15). Low baseline ejection fraction (EF) and postimplantation RVA-paced
or spontaneous QRSd predicted HFH; the increased risk with QRSd was steeper for normal versus low EF (HR, 1.18;
95% CI, 1.11–1.27; versus HR, 1.08; 95% CI, 1.01–1.15; for a 10-ms increase); at a QRSd of 200 ms, normal- and
low-EF patients had equivalent risk. HFH risk nearly doubled when VVIR Cum%VP was 80 or DDDR Cum%VP was
40 versus DDDR Cum%VP 40 and was additive with other risk factors.
Conclusions—Differences in HFH risk can be explained by interactions between substrate (atrial fibrillation, **
conduction, heart failure, MI, EF) and pacing promoters (ventricular desynchronization-paced QRSd and Cum%VP, and
** desynchronization-pacing mode). Management of RVA pacing is important for reducing the risk of HFH,
particularly among patients with low EF and heart failure. (Circulation. 2006;113:2082-2088.)
PS:有研究这问题的战友欢迎发言。附circulation 上的一篇文章。有兴趣大家可以去读读。
Michael O. Sweeney, MD; Anne S. Hellkamp, MS。 Heart Failure During Cardiac Pacing (Circulation. 2006;113:2082-2088.)
Background—Right ventricular apical (RVA) pacing creates abnormal left ventricular contraction, hypertrophy, and
reduced pump function. The adverse effects of ventricular desynchronization may explain the association of RVA
pacing with an increased risk of heart failure hospitalization (HFH) in clinical trials.
Methods and Results—Baseline and postimplantation variables were used to predict HFH in the Mode Selection Trial, a
2010-patient, 6-year trial of dual-chamber (DDDR) versus ventricular (VVIR) pacing in sinus node dysfunction. A Cox
model showed that New York Heart Association (NYHA) class at baseline and follow-up predicted HFH (hazard ratio
[HR], 3.99; 95% confidence interval [CI], 2.74 –5.79 for NYHA class III/IV and HR, 2.17; 95% CI, 1.54 –3.04 for
NYHA class II versus class I); other predictors were heart failure (HR, 2.30; 95% CI, 1.70 –3.11), atrioventricular (**)
block (HR, 1.48; 95% CI, 1.11–1.97), and myocardial infarction (MI)(HR, 1.37; 95% CI, 1.00 –1.86). Postimplantation
predictors were VVIR cumulative percent ventricular pacing (Cum%VP) 80 (HR, 3.58; 95% CI, 1.72–7.45), DDDR
Cum%VP 40 or VVIR Cum%VP 80 (HR, 1.81; 95% CI, 0.94 –3.50) versus DDDR Cum%VP 40; whether QRS
duration (QRSd) was paced or spontaneous (HR, 2.21; 95% CI, 1.39 –3.54; spontaneous versus paced); and drugs for
atrial fibrillation (HR, 1.60; 95% CI, 1.19 –2.15). Low baseline ejection fraction (EF) and postimplantation RVA-paced
or spontaneous QRSd predicted HFH; the increased risk with QRSd was steeper for normal versus low EF (HR, 1.18;
95% CI, 1.11–1.27; versus HR, 1.08; 95% CI, 1.01–1.15; for a 10-ms increase); at a QRSd of 200 ms, normal- and
low-EF patients had equivalent risk. HFH risk nearly doubled when VVIR Cum%VP was 80 or DDDR Cum%VP was
40 versus DDDR Cum%VP 40 and was additive with other risk factors.
Conclusions—Differences in HFH risk can be explained by interactions between substrate (atrial fibrillation, **
conduction, heart failure, MI, EF) and pacing promoters (ventricular desynchronization-paced QRSd and Cum%VP, and
** desynchronization-pacing mode). Management of RVA pacing is important for reducing the risk of HFH,
particularly among patients with low EF and heart failure. (Circulation. 2006;113:2082-2088.)
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