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The role of left ventricular (LV) relaxation in the determination of transmitral flow dynamics was studied with pulsed Doppler flowmetry and high fidelity tip manometry in various cardiac diseases. Study population consisted of 14 cardiac patients (pts) with sinus rhythm, including 4 pts with chest pain syndrome, 4 with myocardial infarction, 3 with effort angina and 3 with hypertrophic cardiomyopathy. The acceleration of early diastolic inflow velocity (AC), the peak of early diastolic inflow velocity (peak EFV ) and the deceleration after the peak (DC) were determined from the phasic transmitral flow pattern. Hemodynamic parameters, i.e., cardiac index, mean pulmonary wedge pressure (PWP), peak positive dP/dt and the time constant of isovolumic LV pressure decay (T) were measured during cardiac catheterization. Decreases in AC, peak EFV and DC were accompanied by prolongation of T with correlation coefficient of -.851 (p less than .001), -.808 (p less than .001) and -.697 (p less than .01), respectively, indicating that impaired LV relaxation slows down the early diastolic LV filling irrespective of underlying cardiac disease. LV filling pressure did not appear as a predominant factor affecting the early diastolic filling in the pts studied, as indicated by an insignificant correlation between any of these flow indices and PWP. Also, no significant relations were found between the flow indices and other hemodynamic parameters. These results indicate that LV relaxation plays a primary role in determining the extent of the early diastolic filling. Pulsed Doppler flowmetry provides a new approach to evaluate the impairment of LV relaxation noninvasively and sensitively in cardiac disease.

We attempted to estimate transmitral pressure gradient and mitral valve area (MVA) noninvasively in mitral stenosis (MS) by a bi-directional pulsed Doppler flowmeter combined with an electronic two-dimensional echocardiograph. Eleven patients with MS in sinus rhythm were studied by cardiac catheterization. Fifteen healthy subjects (H) served as normal control. The pulsed Doppler flowmeter operated with a carrier frequency of 2.5 MHz, a pulse repetition rate of either 5 KHz or 10 KHz and a sample volume of 1 X 3 X 3 mm. The velocity of transmitral central flow was measured by this system, monitoring audible Doppler sounds and cardiac images which depict the anatomic location of the sampling site. The Doppler signal was analyzed by a sound spectrograph. In estimating the transmitral pressure gradient and MVA, we employed a Doppler parameter (half time) defined as the time for instantaneous maximal blood flow velocity to reduce to one-half from its rapid inflow peak, which is independent of the angle between the ultrasonic beam and blood flow. Transmitral pressure gradient (delta P100) was measured as the pressure gradient between either left atrial or pulmonary capillary pressure and left ventricular pressure at the point after 100 msec from the nadir of left ventricular early diastolic pressure [( LA or PC--LVDP]100). MVA was obtained using a Gorlin's formula. The transmitral blood flow velocity in both MS and healthy groups revealed a narrow frequency band pattern with two peaks, R and A, in diastole. The former peak occurred during rapid inflow phase and the latter following atrial contraction. In the healthy group, the descent rate of R wave was increased than that in the MS group. The square root of the pressure gradient also reduced linearly with transmitral flow velocity in the MS group. Thus in the MS group, the transmitral velocity was directly proportional to the square root of the pressure gradient as described by a Bernoulli theorem, and the half time was proportional to the transmitral velocity. The square of the half time (delta t2) was highly correlated with delta P100 (r = 0.97), and the inverse of the half time (delta t-1) was correlated with MVA (r = 0.76). There was no significant correlation between delta P100 and diastolic descent rate of anterior mitral leaflet (DDR). The present study indicates that the half time is useful in estimating transmitral pressure gradient and MVA in mitral stenosis.

Intracardiac flow dynamic alterations in patients (pts) with prosthetic mitral valve (PMV) were studied to assess prosthetic valve functions using pulsed Doppler technique and two-dimensional echocardiography. The study population consisted of 23 pts who underwent mitral valve replacement (11 with the Starr-Edwards disc valve, nine with the Björk-Shiley tilting disc valve, two with the Hancock porcine valve, and one with the homograft valve), 20 pts with mitral stenosis, and 17 control subjects (15 healthy persons and two with lone atrial fibrillation). All pts had a normal functioning PMV by clinical evaluation except for one patient with a dysfunctioning homograft valve, which was angiographically documented. Flow velocity patterns were obtained at various sites in the left ventricle (LV) and the left atrium (LA). Flow dynamic alterations in pts with PMV were evaluated from the half time of transmitral flow velocity descent in diastole, as an index of the atrioventricular pressure gradient, the extent of dispersion of Doppler frequency spectrum of intraventricular flow as an index of the degree of flow disturbances and the Doppler signals with broadening spectra indicating transvalvular regurgitant flow into the LA. The results were as follows: In pts with PMV, the velocity of transmitral flow decreased slowly and linearly throughout diastole. The half time was significantly prolonged for pts with PMV as compared with that for control subjects (272 + 94 ms [mean + SD] vs 79 + 15 ms, p less than .001), though it was shorter than that in pts with mitral stenosis (457 + 145 ms, p less than .001). In pts with PMV, the half time for pts with the Björk-Shiley valve was relatively short as compared with that for pts with other valve. Marked prolongation of the half time (483 ms) was observed in a patient with a dysfunctioning homograft valve. These findings indicate that any PMV is obstructive, even with normal valve function, as compared with healthy mitral valves and that the Björk-Shiley valve is superior to the other PMVs studied in regard to the pressure gradient across PMV. Diastolic flow velocity patterns in the LV were highly dependent on the type of PMV. Apparently, the flow characteristics in the LV were disturbed in every patient with PMV regardless of the type of PMV. The high pressure gradient across the PMV suggested by the prolonged half time in pts with PMV, may be partially caused by flow disturbances produced by PMV.(ABSTRACT TRUNCATED AT 400 WORDS)