Abnormal elevations of plasma brain natriuretic peptide levels are difficult to explain on the basis of hemodynamic and echocardiographic data and are a special feature of hypertrophic obstructive cardiomyopathy.

The response of atrial natriuretic peptide (ANP) release to haemodynamic influences after cardioversion of atrial fibrillation has not been fully examined. We measured plasma concentrations of ANP and assessed haemodynamic changes 60-120 min after DC cardioversion in 22 patients with non-valvular chronic atrial fibrillation. Passive leg elevation to enhance volume expansion was performed 60 min after DC cardioversion. Sinus rhythm was restored in 18 of the 22 patients (successful DC cardioversion group). The control group consisted of seven patients with non-valvular chronic atrial fibrillation who did not undergo DC cardioversion (atrial fibrillation control group). In the successful DC cardioversion group, the mean pulmonary artery wedge pressure decreased significantly 15 min after cardioversion (P < 0.05) and then remained unchanged. Plasma concentrations of ANP also decreased significantly 15 min after cardioversion (P < 0.05). Furthermore, there was an additional significant decrease in ANP levels for up to 60 min after cardioversion (P < 0.05 from 15 min). Passive leg elevation for 15 min led to an increase in the mean pulmonary artery wedge pressure (P < 0.01) and right atrial pressure (P < 0.05), but did not result in increased plasma concentrations of ANP (47.1 +/- 27.6 vs 43.9 +/- 34.4 pg.ml-1, mean +/- SD, P = ns). In the atrial fibrillation control group, passive leg elevation increased the mean pulmonary artery wedge pressure (P < 0.01), the mean right atrial pressure (P < 0.05) and plasma concentrations of ANP (139.9 +/- 85.8 vs 168.1 +/- 108.2, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

During the ventricular slow-filling period, both the left atrium and left ventricle fill passively, and their respective internal pressures equalize, becoming evenly elevated. If the diastolic chamber compliance of the left atrium is smaller than that of the left ventricle, we expect the inflowing blood to be distributed more to the left ventricle than to the left atrium during this period. We examined the magnitude of the diastolic compliance of the left atrium and the left ventricle at the end of the slow-filling period. We studied 10 patients, mostly with a mild degree of coronary artery disease, in whom hemodynamic variables were almost within normal limits. To estimate the compliance of the left atrium, we recorded the left atrial pressure directly (by the Brockenbrough technique) and determined the left atrial volume by biplane cineatriography. We determined the diastolic compliance of the left atrium from the pressure-volume relations between the nadir of the x trough and the peak of the v wave by fitting them to an exponential equation. P = b.eaV (P = pressure, V = volume, a, b = constants). The diastolic compliance of the left ventricle was determined from the pressure-volume relations during the ventricular slow-filling period. The compliances of the left atrium and the left ventricle at the pressure at the end of the ventricular slow-filling period were 1.60 +/- 0.41 (mean +/- SD) ml.mmHg-1.m-2 and 4.22 +/- 1.12, respectively. The ratio of compliance of the left ventricle to that of the left atrium was 2.60 +/- 0.71.(ABSTRACT TRUNCATED AT 250 WORDS)

We aimed to study the time-course of recovery of atrial contraction after cardioversion of chronic atrial fibrillation (duration of more than 3 months) to sinus rhythm. Using M-mode, two-dimensional and pulsed Doppler echocardiography, we determined left atrial (LA) and ventricular (LV) dimensions, peak velocities, and velocity-time integrals of early and atrial filling velocity-time profiles in both LV and right ventricular (RV) inflows (peak E and peak A, Ea and Aa). Results of the LA and LV functions in seven elderly patients (an initial study group) were as follows. The extent of the LA dimensional reduction resulting from atrial contraction was significantly increased up to 5-8 weeks compared with values 0-1 day after cardioversion [from 1.3 +/- 0.8 (mean +/- SD) mm to 3.9 +/- 1.1, P < 0.01]. In conjunction with the progressive increase in peak A, the ratio of peak E to peak A (peak E/A) was significantly decreased and reached a plateau at 5-8 weeks (from 1.93 +/- 0.59 to 0.67 +/- 0.11, P < 0.01). LV fractional shortening was increased significantly 5-8 weeks after cardioversion (from 0.20 +/- 0.06 to 0.29 +/- 0.05, P < 0.01). Since a large part of the improvement in LA contraction was expected to occur in an early stage after cardioversion, we studied eight additional patients more frequently in the early stage (an additional study group). Furthermore, we studied the time course of LA and right atrial (RA) contractions.(ABSTRACT TRUNCATED AT 250 WORDS)

SummaryBackgroundarid hypothesis: Flow velocity of the left atrial appendage (LAA) is thought to be important in thrombus formation in association with blood stasis and the development of spontaneous echo contrast. The effects of heart rate on peak flow velocity of the LAA have not been studied in patients with nonvalvular atrial fibrillation.Methods: Using transesophageal Doppler echocardiography, peak flow velocity of the LAA was measured at the junction between the left atrium and the LAA during left ventricular (LV) systole and diastole in 21 patients with nonvalvular atrial fibrillation. In six cases, the average peak flow velocity