[Acute hemodynamic effects of biventricular and left ventricular pacing in chronic pacemaker-dependent patients with advanced heart failure].
The beneficial hemodynamic effects of cardiac resynchronization in patients with intraventricular conduction delay have been demonstrated. The potential hemodynamic effects of cardiac resynchronization to compensate the pacing-induced left ventricular conduction delay in chronically paced heart failure patients are not as well established. The aim of the study was to evaluate the acute hemodynamic effects of biventricular and left ventricular pacing in chronically paced patients with advanced heart failure. Fourteen consecutive pacemaker or defibrillator patients with permanent atrial fibrillation and AV block (11 male, 3 woman, mean age: 68 +/- 7 years) were enrolled in this study. There were 5 ischemic (36%) and 9 nonischemic (64%) patients (mean left ventricular ejection fraction: 19 +/- 5%; mean end-diastolic left ventricular diameter: 71 +/- 11 mm). In all patients a right ventricular and left ventricular (via coronary sinus) pacing lead was placed. The aortic and left ventricular hemodynamic measurements were performed using a two-channel micro-tip catheter. The measurements of the aortic pulse pressure (APP) and (dP/ dtmax) were performed during right ventricular apical pacing (RVP), left ventricular (LVP), and biventricular pacing (BVP) (70 bpm). Compared to RVP, LVP and BVP increased APP and dP/dtmax (35.8 +/- 4.2 vs 43.3 +/- 4.5 and 41.2 +/- 4 mmHg; p < 0.001) and (758 +/- 56 vs 967 +/- 60 and 961 +/- 62 mmHg/s; p < 0.001). LVP and BVP showed a comparable hemodynamic response. The hemodynamic effects were not related to the width of the paced QRS complex. Every patient showed improved hemodynamics during LVP and BVP unrelated to the underlying heart disease and to the baseline level of left ventricular dysfunction. BVP and LVP pacing acutely improve contractile left ventricular function in chronically paced patients with advanced heart failure.
Direktor der Medizinischen Klinik II, Klinikum Kassel, Mönchebergstrasse 41-43, 34125 Kassel, Germany.
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Hansen
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Sperzel
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Neumann
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Pitschner
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Neuzner
D000368:Aged; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000628:therapy; D002303:Cardiac Output, Low / Q000503:physiopathology / Q000628:therapy; D002908:Chronic Disease; D017147:Defibrillators, Implantable; D004567:Electrodes, Implanted; D005260:Female; D005500:Follow-Up Studies; D006327:Heart Block / Q000503:physiopathology / Q000628:therapy; D006329:Heart Conduction System / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology; D010138:Pacemaker, Artificial; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology*; D016278:Ventricular Function, Right / Q000502:physiology*