[Mitral component of the first heart sound in complete left bundle branch block: the mechanism of the decreased intensity].

To clarify the mechanism of the reduced intensity of the mitral component of the first heart sound (IM) in complete left bundle branch block (LBBB), electrocardiograms, phonocardiograms, apexcardiograms and mitral valve echograms of 12 patients with LBBB (LBBB group) and 13 normal subjects (normal group) were simultaneously recorded. The first derivative of the apexcardiogram was also studied. One of the 12 patients had an intermittent LBBB. There was no significant difference in the P-Q interval between the two groups. The following results were obtained: 1. In the LBBB group; 1) The intensity of the IM, expressed as a ratio of the amplitude of the IM to that of the aortic component of the second heart sound (IIA) on the apical phonocardiograms, was significantly reduced except in one patient who had a relatively short P-Q interval. 2) The timings of the onset of the upstroke of the apexcardiogram and mitral valve closure were significantly and equally delayed. 3) The amplitude of the mitral valve echogram at the onset of the upstroke of the apexcardiogram (end-diastolic amplitude of the mitral valve) was significantly decreased. The closing velocity of the mitral valve was also decreased. 4) The amplitude ratio (H2/H1) and the rate of rise (A) of the apexcardiogram at the onset of the IM were significantly decreased. 2. The intensity of the IM, H2/H1 and A of the apexcardiogram at the onset of the IM were compared for three cases with nearly equal end-diastolic mitral valve amplitudes in each group. The intensity of the IM was apparently reduced in the LBBB group, compared with that of the normal group, and its intensity correlated inversely with H2/H1 and A. These results indicate that the reduced intensity of the IM in LBBB is caused mainly by the decreased amplitude of the mitral valve excursion at the onset of left ventricular contraction. An additional cause is the decreased tension on the closed mitral valve resulting from the slow rate of left ventricular pressure rise at the onset of the IM.