title: Influence of left ventricular filling profile during preceding control beats on the occurrence of pulse deficit caused by ventricular premature contractions.
abstract: This study was designed to investigate whether the left ventricular filling profile during preceding control beats significantly affects the pulse deficit caused by ventricular premature contractions (VPCs). The study group consisted of 18 patients (10 men, eight women, 15-85 years old) who underwent electrophysiological catheterization because of sinus bradycardia. Using a temporary pacing lead inserted in the right ventricular apex, isolated VPCs with various coupling intervals were produced by electrical stimulation of the right ventricle. During the production of the VPCs, the mitral filling flow velocity using pulsed wave Doppler echocardiography, the femoral arterial pressure curve and the electrocardiogram were simultaneously recorded. The right ventricle was stimulated 800, 750, 700, 650, 600, 550, 500, 450 and 400 ms after the triggered control beat QRS complex. Pulse pressures during VPCs gradually decreased in relation to the shortening of the extrasystolic beat coupling interval. The longest coupling interval for each subject, which caused complete abolition of the pressure pulse during the VPC, was defined as the pulse deficit coupling interval. The early to late diastolic velocity-time integral ratio (Ei/Ai ratio) of the mitral filling flow velocity during the control beats which precede the VPC was obtained as an index expressing the left ventricular filling profile. The Ei/Ai ratio of the mitral filling flow velocity ranged from 0.7 to 4.5 (1.8 +/- 1.0). The pulse deficit coupling interval ranged from 440 to 640 ms (510 +/- 60 ms).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: First Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Otsuji
authors.forename: A
authors.initials: A
authors.lastname: Kisanuki
authors.forename: H
authors.initials: H
authors.lastname: Toda
authors.forename: R
authors.initials: R
authors.lastname: Kuroiwa
authors.forename: T
authors.initials: T
authors.lastname: Murayama
authors.forename: R
authors.initials: R
authors.lastname: Matsushita
authors.forename: K
authors.initials: K
authors.lastname: Toyonaga
authors.forename: Y
authors.initials: Y
authors.lastname: Miyazono
authors.forename: S
authors.initials: S
authors.lastname: Nakao
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001783:Blood Flow Velocity / Q000502:physiology; D001919:Bradycardia / Q000503:physiopathology; D006328:Cardiac Catheterization; D005117:Cardiac Complexes, Premature / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003971:Diastole / Q000502:physiology; D015150:Echocardiography, Doppler; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000000981:diagnostic imaging / Q000503:physiopathology; D009200:Myocardial Contraction / Q000502:physiology; D011446:Prospective Studies; D011674:Pulse / Q000502:physiology*; D013599:Systole / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*