Pacing in heart failure: improved ventricular interaction in diastole rather than systolic re-synchronization.
OBJECTIVE
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.
Morris-Thurgood
J A
JA
Department of Cardiology, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff, U.K.
Turner
M S
MS
Nightingale
A K
AK
Masani
N
N
Mumford
C
C
Frenneaux
M P
MP
D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D005260:Female; D006333:Heart Failure / Q000175:diagnosis / Q000628:therapy*; D006334:Heart Function Tests; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011336:Probability; D011379:Prognosis; D012720:Severity of Illness Index; D013318:Stroke Volume; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology*