[Mechanism of discrepancy between mean pulmonary capillary wedge pressure and left ventricular end-diastolic pressure].

It is well known that discrepancies between mean pulmonary capillary wedge pressure (man-PCWP) and left ventricular end-diastolic pressure (LVEDP) exist in the pathological heart with sinus rhythm. We discussed the mechanism of these discrepancies in the aspect of increased LV end-diastolic stiffness. Fifty-two patients observed in this study included 23 with old myocardial infarction (OMI), 4 with hypertrophic cardiomyopathy and 9 with hypertensive heart disease (LVH group), 6 with dilated cardiomyopathy (DCM), and 10 normal subjects (N). All 52 patients had sinus rhythm. Those with significant mitral and aortic regurgitation were excluded. End-diastolic LV stiffness was evaluated by the ratio of increases in LV pressure and volume during atrial systole (delta P/delta V), as proved by cardiac catheterization and cine-angiography. Discrepancies between m-PCWP and LVEDP were 5.9 +/- 4.3 mmHg in OMI group, 4.5 +/- 4.6 mmHg in LVH group, 5.8 +/- 4.5 mmHg in DCM, and 1.6 +/- 1.8 mmHg in N group. These discrepancies correlated well with delta P/delta V (r = 0.74). More significant discrepancies were observed in patients with so-called pseudo-normalized left ventricular inflow velocities proved by pulsed Doppler echocardiography, and in patients with marked concentric LV hypertrophy with increased delta P/delta V. In clinical observation, symptoms of heart failure may be determined by m-PCWP rather than LVEDP. We concluded that discrepancies between m-PCWP and LVEDP were caused by the booster pump function of the left atrium against increased LV end-diastolic stiffness. By the use of apexcardiogram and echocardiogram including the pulsed Doppler method, it was possible to predict these discrepancies non-invasively.