High-speed Cine-left-ventriculographic Study on Ventricular Premature Contraction
1975 Volume 27 Issue 1 Pages 94-109
Details
1975 Volume 27 Issue 1 Pages 94-109
Left ventricular hemodynamics and angiocardiographic morphology in ventricular premature contraction were studied in 8 closed-chest dogs by means of high-speed cineleftventriculography (35mm,130 frames per second).
Ventricular premature beats were artificially induced by bipolar electrodes indwelled in the 'left ventricular wall. The timing and duration of mitral regurgitation, the sequential changes of the left ventricular shape and pressure were investigated for the ventricular premature contraction originated from septal portion as well as for those from free wall of the ventricle. The ventricular premature contraction following normal beat was called 1st VPC and those following 1st VPC was 2nd VPC in this study.
Results obtained were as follows.
1) Mitral regurgitation was observed cineangiographically in every ventricular premature contraction studied.
2) The duration of mitral regurgitation was 7.3±2.3 frames (mean±1 SD) in septal VPC group and 11.8±3.2 frames in free wall VPC group. The difference of the groups was statistically significant (P<0.01).
3) Abnormal systolic bulge was almost always demonstrated during every VPC studied at the stimulating electrodes site. The extent of bulging was greater in 1st VPC than in 2nd. However there was no relationship between the left ventrieular peak pressure and the extent of bulging.
4) The coupling interval ratio of ventricular premature contraction had a relationship to left ventricular systolic pressure (r=0.823, P<0.01), but not to the duration of mitral regurgitation.
5) It was discussed that mitral regurgitation associated with VPC would result mainly from abnormal sequence of ventricular contraction with abnormal systolic bulge as well as in part from the absence of atrial contribution to mitral valve closure.
The decrease in left ventricular pressure at the time of VPC may as well be postulated by the decreased ventricular filling due to shortening of the proceeding diastole, absence of atrial kick, mitral regurgitation and change of sequence in ventricular contraction
