Electrical modulation of cardiac contractility: clinical aspects in congestive heart failure.
Heart failure is a highly prevalent disease in western society. Drug therapies aimed at increasing myocardial contractility have been associated with decreased survival. Several short and mid term clinical studies have suggested adjuvant or alternative therapies to congestive heart failure using modified pacing techniques that were aimed to increase contractility (e.g. Paired pacing) or restore synchrony of contraction (biventricular pacing). While delivery of paired pacing was abandoned during the early 70's, biventricular pacing has recently emerged as an adjuvant treatment to limited group of congestive heart failure patients with aberrant left ventricular conduction. In this brief review, we describe our initial safety and efficacy experience in patients with heart failure using a novel non-stimulatory electrical approach to the delivery of positive inotropic therapy to the failing myocardium. The study suggests that unlike modified pacing techniques, delivery of the signal to the left ventricle during the refractory period resulted in a rapid increase in myocardial contractility and improved hemodynamic performance. The near instantaneous contractility improvement achieved by this type of stimulus was shown to be safe and effective independently of the primary cause of heart failure or the function of the conduction system. Unlike pharmacologic treatments, which have a relatively constant effect, use of electrical stimuli may prove useful as a new therapeutic modality in the treatment of heart failure with which contractility can be improved when and as needed.
Department of Cardiology, Hospital San Raffaele, Milan, Italy. pappone.carlo@hsr.it
C
C
Pappone
G
G
Vicedomini
A
A
Salvati
C
C
Meloni
W
W
Haddad
R
R
Aviv
Y
Y
Mika
N
N
Darvish
Y
Y
Kimchy
I
I
Shemer
Y
Y
Snir
D
D
Pruchi
S A
SA
Ben-Haim
I
I
Kronzon
D002304:Cardiac Pacing, Artificial / Q000379:methods; D004599:Electric Stimulation Therapy / Q000379:methods*; D006333:Heart Failure / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology