The contribution of tricuspid valve closure to the first heart sound. An intracardiac micromanometer study.

The sound-pressure correlates of the second high frequency component of a split first heart sound (S1) were investigated in 27 patients. An external phonocardiogram was recorded with high fidelity sound and pressure from the left and right atria in 21 patients, from the pulmonary artery in 14 of these, and from the central aorta in 11. In the remaining six patients, high fidelity recordings from the central aorta and right-sided chambers were obtained with an external phonocardiogram. The external component of S1 that coincided with a left atrial C wave and "internal sound" was defined as M1. In those cases where the left atrial pressure was not recorded, this component could be identified by a low frequency transient in the central aortic pressure trace. The other external high frequency component of S1 that was synchronous with a separate right atrial C wave and "internal sound" was defined as T1; with two exceptions, M1 preceded T1. The two exceptions which caused reversal of this order, so that T1 preceded M1, were due to chronic left bundle branch block and mitral stenosis. In both cases, T1 was shown to be distinctly separated from the upstroke of pressure rise in the central aorta. This finding was also demonstrated in three cases of right bundle branch block and one case with aortic valvular disease. The usual asynchrony of ventricular contraction was altered by induction of ventricular premature systoles; the separation of externally identifiable M1 and T1 components and their internal markers was predictably altered by this maneuver. The occurrence of T1 was variable in relation to the upstroke of the pulmonary artery pressure, which suggests that it is not related to pulmonic ejection. It is concluded that micromanometrically recorded right and left atrial C waves can serve as markers for externally recordable M1 and T1 components of the first heart sound. In addition, T1 is frequently an externally recordable and audible event.

Sound pressure correlates of the Austin Flint murmur. An intracardiac sound study.

Mitral valve motion and pressure correlates of the Austin Flint murmur (AFM) were investigated in nine patients with aortic regurgitation using high fidelity catheter tip micromanometers and the mitral valve echocardiogram (MVE). External phonocardiography demonstrated a mid-diastolic murmur (MDM) in eight subjects and a presystolic murmur (PSM) in five. Maximum intensity of both AFM components was found in the left ventricular (LV) inflow tract; the murmur was not recordable in the left atrium (LA). In two patients, an apparent AFM was recorded in the intracardiac phonocardiogram when absent externally. Only one subject had a significant late diastolic "reversed" or LV to LA gradient; in this patient, presystolic mitral regurgitation was shown angiographically but no PSM was present and MVE revealed absence of atriogenic mitral valve re-opening. In two subjects, a PSM disappeared from the external phono when a "reversed" gradient occurred during the diastolic pause following a ventricular premature systole; this LV to LA gradient was associated with diastolic mitral regurgitation recordable in the left atrial phono. In two patients, LV inflow phono showed the MDM to begin 80-120 msec after the aortic second sound and during the D to E phase of the MVE. The rate of early diastolic mitral valve closure in patients (152 +/- 24 mm/sec) was not significantly different from 13 normals (232 +/- 10 mm/sec). With regard to the genesis of the AFM, the present study concludes: 1) diastolic mitral regurgitation plays no role, and 2) antegrade mitral valve flow is required but simultaneous retrograde aortic flow may also be necessary.

Determination of site of infection in endocarditis.

Medical-surgical treatment of antibiotic refractory endocarditis requires determination of the site of infection, which is not always possible with conventional cardiac catheterization. The cases of two patients with right-sided endocarditis who survived after combined medical-surgical therapy are presented. One had persistent Pseudomonas aeruginosa bacteremia and three possible sites of infection. Multiple quantitative blood cultures proximal and distal to each suspected site indicated the pulmonary valve alone was infected. The second had sustained bacteremia with three enteric organisms and no apparent valvular abnormality. Quantitative cultures excluded the abdomen as the continuing source of bacteremia and suggested the tricuspid valve was infected. This was confirmed by a second catheterization using multiple cultures in conjuction with dye dilution studies, intracardiac phonocardiography, and angiography. These bacteriologic and cardiologic techniques may be especially useful in detecting right-sided endocarditis and may also be helpful in detecting concomitant infection of both sides of the heart.