Electrical restitution and conduction intervals of ventricular premature beats in man: influence of heart rate.
Monophasic action potentials (MAP) were obtained from the outflow tract of the right ventricle during apical pacing in 20 patients with coronary artery disease. The electrical restitution was studied by interpolation of extrasystoles with various coupling intervals to the preceding steady-state beat at basic paced cycle lengths (CL) of 700, 600, and 500 msec. At higher frequencies the ventricular effective refractory periods (V-ERP) and duration of MAPs became shorter and the electrical restitution curves were displaced downwards (P less than 0.001). With increasing diastolic intervals preceding the extrasystole up to a maximum of 100 msec, the duration of premature MAPs increased at all frequencies. An obvious hump of the electrical restitution curve was observed at coupling intervals of 100 msec due to a later transient decrease (P less than 0.01) in duration of MAPs at the basic CL of 500 msec. No significant hump was observed at lower heart rates. Thus, a different time course of the electrical restitution was observed at various CLs. The intraventricular conduction intervals were shorter at the shorter basic CLs when compared to the 700 msec cycles (P less than 0.05). The conduction intervals were also modified by the coupling interval between the interpolated stimulus and the preceding steady-state action potential (AP). The premature beats elicited 30 msec or earlier after refractoriness were conducted more slowly at all basic cycle lengths (P less than 0.005), and those between 60 and 150 msec after the V-ERP more rapidly (P less than 0.01) than the steady-state beats. These observations have implications for the protocols used for introducing two or more frequencies during programmed stimulation in man. Furthermore, the conduction pattern in vivo cannot be interpreted from single cell studies.
Endresen
K
K
Medical Department B, Rikshospitalet, Oslo University Hospital, Norway.
Amlie
J P
JP
D000200:Action Potentials; D005117:Cardiac Complexes, Premature / Q000503:physiopathology* / Q000628:therapy; D002304:Cardiac Pacing, Artificial; D005069:Evaluation Studies as Topic; D006329:Heart Conduction System / Q000503:physiopathology*; D006339:Heart Rate; D006352:Heart Ventricles; D006801:Humans; D008297:Male