© 2000 by European Society of Cardiology
LEADING ARTICLE
Pacing in heart failure: improved ventricular interaction in diastole rather than systolic re-synchronization
1Department of Cardiology, Wales Heart Research Institute, University of Wales College of Medicine Cardiff, U.K.; 2Department of Cardiology, University Hospital of Wales Cardiff, U.K.
AIMS: To determine the mechanism by which left ventricular and biventricular pacing works.
BACKGROUND: Pacing for congestive heart failure patients is employed in those with left bundle branch block on the basis that it will improve discoordinated contraction; however, the response is unpredictable. The authors propose that the mechanism of benefit is rather related to improvement of ventricular interaction in diastole (VID). VID is found in patients with a high left ventricular end-diastolic pressure (>15 mmHg). Left ventricular pacing in these patients will delay right ventricular filling and allow greater left ventricular filling before the onset of VID.
METHODS: The study group consisted of 18 congestive heart failure patients with an ejection fraction <30% and with no more than Grade 1 mitral regurgitation. Group I comprised 10 patients with pulmonary capillary wedge pressure >15 mmHg, four patients had a normal QRS duration and six had left bundle branch block. Group II comprised eight patients with pulmonary capillary wedge pressure <15 mmHg, of whom five had a normal QRS duration. Haemodynamics were measured at baseline and during VDD pacing from either the left ventricle or right ventricle.
RESULTS: The ratio of stroke volume/pulmonary capillary wedge pressure was calculated as an index of the relationship between left ventricular end-diastolic pressure and contractile function. This ratio was lower in group I than in group II patients (P=0·005). In group I, haemodynamics were improved with left ventricular pacing (stroke volume/pulmonary capillary wedge pressure increased from 2·2±0·9 to 4·4±3·6, P=0·03). In group II there was no response to either left ventricular or right ventricular pacing. The improvement with left ventricular pacing was unrelated to QRS duration (r=0·09).
CONCLUSIONS: Left ventricular pacing acutely benefits congestive heart failure patients with pulmonary capillary wedge pressure >15 mmHg irrespective of left bundle branch block. The present data suggest that the mechanism of response may be an improvement in left ventricular filling rather than ventricular systolic re-synchronization.
Key Words: Pacing, heart failure, haemodynamics, physiology, left ventricular pacing
Correspondence: M. P. Frenneaux, Department of Cardiology, Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, U.K.
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