PubMed · 15214293
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M Kozák. 2004. [Physiologic cardiostimulation].. https://pubmed.ncbi.nlm.nih.gov/15214293/
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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 (AV) 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 < or =80 (HR, 1.81; 95% CI, 0.94-3.50) versus DDDR Cum%VP < or =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 approximately 200 ms, normal- and low-EF patients had equivalent risk. HFH risk nearly doubled when VVIR Cum%VP was < or =80 or DDDR Cum%VP was >40 versus DDDR Cum%VP < or =40 and was additive with other risk factors. CONCLUSIONS: Differences in HFH risk can be explained by interactions between substrate (atrial fibrillation, AV conduction, heart failure, MI, EF) and pacing promoters (ventricular desynchronization-paced QRSd and Cum%VP, and AV desynchronization-pacing mode). Management of RVA pacing is important for reducing the risk of HFH, particularly among patients with low EF and heart failure.
BACKGROUND: Cardiac Resynchronization Therapy (CRT) leads to a reduction of left-ventricular dyssynchrony and an acute and sustained hemodynamic improvement in patients with chronic heart failure. Furthermore, an optimized AV-delay leads to an improved myocardial performance in pacemaker patients. The focus of this study is to investigate the acute effect of an optimized AV-delay on parameters of dyssynchrony in CRT patients. METHOD: 11 chronic heart failure patients with CRT who were on stable medication were included in this study. The optimal AV-delay was defined according to the method of Ismer (mitral inflow and trans-oesophageal lead). Dyssynchrony was assessed echocardiographically at three different settings: AVDOPT; AVDOPT-50 ms and AVDOPT+50 ms. Echocardiographic assessment included 2D- and M-mode echo for the assessment of volumes and hemodynamic parameters (CI, SV) and LVEF and tissue Doppler echo (strain, strain rate, Tissue Synchronisation Imaging (TSI) and myocardial velocities in the basal segments) RESULTS: The AVDOPT in the VDD mode (atrially triggered) was 105.5 +/- 38.1 ms and the AVDOPT in the DDD mode (atrially paced) was 186.9 +/- 52.9 ms. Intra-individually, the highest LVEF was measured at AVDOPT. The LVEF at AVDOPT was significantly higher than in the AVDOPT-50 setting (p = 0.03). However, none of the parameters of dyssynchrony changed significantly in the three settings. CONCLUSION: An optimized AV delay in CRT patients acutely leads to an improved systolic left ventricular ejection fraction without improving dyssynchrony.
BACKGROUND: Atrioventricular (AV) delay optimization can be an important determinant of the response to cardiac resynchronization therapy (CRT) in patients with medically refractory heart failure and a ventricular conduction delay. OBJECTIVES: The purpose of this study was to compare two Doppler echocardiographic methods of AV delay optimization after CRT. METHODS: Forty consecutive patients (age 59 +/- 12 years) with severe heart failure, New York Heart Association class 3.1 +/- 0.4, QRS duration 177 +/- 23 ms, and left ventricular ejection fraction 26% +/- 6% referred for CRT were studied using two-dimensional Doppler echocardiography. In each patient, the acute improvement in stroke volume with CRT in response to two methods of AV delay optimization was compared. In the first method, the AV delay that produced the largest increase in the aortic velocity time integral (VTI) derived from continuous-wave Doppler (aortic VTI method) was measured. In the second method, the AV delay that optimized the timing of mitral valve closure to occur simultaneously with the onset of left ventricular systole was calculated from pulsed Doppler mitral waveforms at a short and long AV delay interval (mitral inflow method). RESULTS: The optimized AV delay determined by the aortic VTI method resulted in an increase in aortic VTI of 19% +/- 13% compared with an increase of 12% +/- 12% by the mitral inflow method (P <.001). The optimized AV delay by the aortic VTI method was significantly longer than the optimized AV delay calculated from the mitral inflow method (119 +/- 34 ms vs 95 +/- 24 ms, P <.001). There was no correlation in the AV delay determined by the two methods (r = 0.03). CONCLUSION: AV delay optimization by Doppler echocardiography for patients with severe heart failure treated with a CRT device yields a greater systolic improvement when guided by the aortic VTI method compared with the mitral inflow method.