Most patients with severe congestive heart failure have secondary pulmonary hypertension (PHT). Elevation of pulmonary vascular resistance (PVR) to greater than 480 dynes sec cm-5 (6 Wood units) is currently the principle hemodynamic contraindication to orthotopic cardiac transplantation. We performed serial two-dimensional Doppler echocardiographic examinations and right heart catheterizations in 24 recipients (21 men, 14-58 years old) of orthotopic cardiac transplants to determine the time course of resolution of PHT and the concomitant remodeling of the donor right ventricle. Right and left heart filling pressures declined in parallel and reached the upper normal range at 2 weeks after the transplant procedure and remained unchanged at 1 year follow-up. Mean pulmonary arterial pressure (mm Hg) decreased from 38 + 9 preoperatively to 22 ± 5 at 2 weeks and was 19 + 5 at 1 year after the transplantation procedure. At 1 year after surgery, PVR had decreased from 202 + 89 dynes.sec-cm-5 preoperatively to 99 + 36 dynes-sec cm-5 (p < .001), while cardiac output increased from 3.7 + 1.2 to 6.3 1.5 liters/min (p < .001). Echocardiographic analysis showed that transplant recipients had an enlarged right ventricle on day 1 after surgery, and a volume overload contraction pattern and tricuspid regurgitation was present in the majority. This increase in right ventricular size was maintained at 1 year follow-up while the incidence of tricuspid regurgitation decreased. We conclude that there is rapid resolution of moderately elevated pulmonary arterial pressures after cardiac transplantation. The donor right ventricle responds to the abnormal recipient pulmonary circulatory dynamics by developing early dilatation and tricuspid regurgitation that persists despite resolution of PHT. Circulation 76, No. 4, 819-826, 1987. PATIENTS with severe class IV congestive heart fail-

Atraumatic splenic rupture is an uncommon complication of acute pancreatitis. This article presents a case of a 35-year-old patient presenting with acute pancreatitis who subsequently developed a splenic vein thrombosis and splenic rupture requiring a laparotomy and splenectomy. This rare but life-threatening complication requires prompt recognition and management in patients with pancreatitis who develop sudden hemodynamic instability.

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Objective: Chronic inflammatory disease increase arterial stiffness and are associated with accelerated atherosclerosis. Our aim was to determine augmentation index (AIx) and pulse wave velocity (PWV) in patients with chronic autoimmune liver disease. Design and method: We have enrolled 38 patients (3m 35w; age 58.7 ± 9.6) with chronic autoimmune liver disease (autoimmune hepatitis 4, primary biliary cholangitis 24, primary sclerosing cholangitis 10). Office blood pressure (BP) was using Omron M6; PWV and AIx by Arteriograph. The assessment of liver cirrhosis was determined with FibroScan. Fasting blood and 24-hour urine samples were collected. Hypertension was diagnosed in 42.1% patients (18.7% were treated) and diabetes in 8.4%. Results: PWV was 9.7 m/s while AIx was also increased (32.8%). PWV was positively correlated with age, sedimentation rate, CRP and central systolic BP and negatively with eGFR. AIx was positively correlated with heart rate and central systolic BP. Linear regression analysis showed positive association of Aix with duration of disease, sedimentation rate, total cholesterol,triglycerides and FibroScan stiffness. PWV was positively associated with age, duration of disease, sedimentation rate, total cholesterol and triglycerides. We found that patients with PWV > 9 m/s were significantly older, had higer sedimentation rates, lower GFR, higher total cholesterol, LDL cholesterol, systolic/diastolic BPr and central systolic BP values. Conclusions: Patients with chronic autoimmune liver diseases have increased arterial stiffness than general population which confirmed our hypothesis on impact of chronic inflammation on increased arterial stiffness. However, this should be confirmed on larger number of patients.