Pacing in heart failure: improved ventricular interaction in diastole rather than systolic re-synchronization

Aims To determine the mechanism by which left ventricular and biventricular pacing works. Background Pacing for congestive heart failure patients is employed in thos e with left bundle branch block on the basis that it will improve discoordi nated contraction; however, the response is unpredictable. The authors prop ose that the mechanism of benefit is rather related to improvement of ventr icular 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 l eft ventricular filling before the onset of VID. Methods The study group consisted of 18 congestive heart failure patients w ith an ejection fraction <30% and with no more than Grade 1 mitral regurgit ation. Group I comprised 10 patients with pulmonary capillary wedge pressur e >15 mmHg, four patients had a normal QRS duration and six had left bundle branch block. Group II comprised eight patients with pulmonary capillary w edge pressure <15 mmHg, of whom five had a normal QRS duration. Haemodynami cs were measured at baseline and during VDD pacing from either the left ven tricle or right ventricle. Results The ratio of stroke volume/pulmonary capillary wedge pressure was c alculated as an index of the relationship between left ventricular end-dias tolic pressure and contractile function. This ratio was lower in group I th an in group II patients (P=0.005). In group I, haemodynamics were improved with left ventricular pacing (stroke volume/ pulmonary capillary wedge pres sure 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 failu re patients with pulmonary capillary wedge pressure >15 mmHg irrespective o f left bundle branch block. The present data suggest that the mechanism of response may be an improvement in left ventricular filling rather than vent ricular systolic re-synchronization. (Europace 2000; 2: 271-275) (C) 2000 T he European Society of Cardiology.