Sympathetic nervous system activation in postextrasystolic potentiation: role of catecholamine release in enhancement of ventricular function

The role of catecholamines in postextrasystolic potentiation was assessed in 30 patients during continuous coupled right ventricular pacing. Hemodynamic data were recorded in 15 patients (group 1); in the other 15 patients (group 2), coronary blood flow and metabolic variables, including catecholamines, were measured. Data were recorded in the control state and after 10 minutes of coupled pacing. Both groups had similar control pulse rates and mean aortic pressures: these variables decreased abruptly by 32 beats/min and 12 mm Hg, respectively, (p less than 0.001 for each) after the initiation of coupled pacing. In group 1, all indexes of left ventricular function and contractility increased during coupled pacing (p less than 0.001 for each), thus confirming postextrasystolic potentiation. In group 2, coupled pacing increased coronary blood flow, myocardial oxygen consumption and free fatty acid uptake (p less than 0.001 for each) but not lactate extraction. Plasma epinephrine was unchanged, but norepinephrine levels increased in arterial (421 +/- 27 to 576 +/- 41 ng/liter) and coronary sinus plasma (611 +/- 46 to 836 +/- 46 ng/liter) (p less than 0.001 for both). Indirectly calculated norepinephrine release within the myocardium increased from 25.6 +/- 2.8 to 39.7 +/- 5.2 ng/min (SEM) (p less than 0.05), suggesting a sympathetic nervous system activation. It is argued that coupled pacing acutely lowered mean aortic pressure, leading to baroreflex sympathetic activation which may contribute to augmented cardiac contractility in postextrasystolic potentiation.