This study assessed whether Doppler-derived mitral and pulmonary venous flow parameters were predictors of pulmonary artery hypertension in patients with left ventricular dysfunction. Doppler echocardiographic examinations were performed in patients (n = 100) with dilated cardiomyopathy in sinus rhythm either symptomatic or asymptomatic before and after optimized therapy with ACE inhibitors, diuretics, and vasodilators. In case of weak or poor Doppler signals, measurable tricuspid regurgitation and pulmonary venous flow tracings were obtained after intravenous administration of 2.5 grams of Levovist at 400 mg/ml. At baseline, left ventricular ejection fraction was 30% +/- 7% and pulmonary artery systolic pressure was 48 +/- 14 mmHg. At the follow-up study carried out after 6 +/- 2 months, reversibility of pulmonary artery hypertension was apparent only in those patients exhibiting favorable changes of mitral flow curve from the restrictive or pseudonormal to impaired relaxation pattern (53 +/- 7 mmHg vs 38 +/- 8 mmHg; P < 0.0001). Numerous variables correlated significantly with pulmonary artery systolic pressure at baseline, while the correlations were generally weaker at the follow-up study. The closest correlations were found with E wave deceleration rate (r = 0.73) at baseline and with the systolic fraction of pulmonary venous flow forward peak velocities (r = -0.67) at follow-up. The stepwise regression model showed that the E wave deceleration rate and the degree of mitral regurgitation were the strongest independent predictors of pulmonary hypertension at baseline, while the ratio between pulmonary venous flow reverse and mitral wave velocities at atrial systole and ejection fraction added minor contributions, leading to a cumulative r value of 0.81. The systolic fraction was the strongest at the follow-up study, with minor contributions provided by the E wave deceleration rate and the left atrial dimension index, leading to a cumulative r value of 0.71.
Ninety patients with cirrhosis undergoing elective distal splenorenal shunt (DSRS) for variceal bleeding between January, 1977 and September, 1988 comprised the study group. In 63 cases, the original technique of Warren was used and, in 15, the modified Britton procedure was employed. Twelve patients had a DSRS plus splenopancreatic disconnection. Thirty-four had alcoholic cirrhosis and 56 had nonalcoholic cirrhosis. Intraoperative portal pressure remained high after the shunt (29.4 cm H2O) even if its initial value was probably decreased by the loss of the splenic flow. Splenic pressure was reduced to 21 cm H2O. The hepatic artery diameter enlarged even after selective shunt (from 6.5 to 7.1 mm). The persistence of a high portal pressure allowed for the preservation of hepatopedal portal flow in 87% of cases. Disconnection between the high-pressure mesenteric area and the low-pressure splenic area seemed to be ideal in only 17% of cases. Fifty-five percent of cases had the early development of minimal or moderate portomesenteric gastrosplenic (PM-GS) collateral pathways. In 33%, the PM-GS collaterals were generally abundant and often allowed visualization of the splenic and caval veins during the venous phase of the superior mesenteric arteriograms. In this group, portal flow was generally highly reduced and even abolished. The incidence of portal thrombosis was 11%. Early angiographic checks after DSRS did not show a different hemodynamic behavior between alcoholics and nonalcoholics. Splenopancreatic disconnection seems to prevent the development of collaterals and the loss of portal perfusion after shunt surgery.
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