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-

ABSTRACT. We assessed fetoplacental blood volume flow human fetuses using pulsed-wave Doppler. Our aims were 3-and placental resistance prospectively with Doppler sonog-fold: I ) to quantitate the changes in placental blood volume flow raphy in 74 normal human fetuses of 19 to 42 wk gestation with gestational age and fetal body weight, 2) to determine to determine the changes in placental perfusion with ges-whether placental blood volume flow falls in postdate fetuses tational age. Placental blood volume flow was assessed (greater than 40 wk), and 3 ) to examine the relation between from the umbilical vein as the product of the mean flow umbilical arterial velocity ratio and placental blood volume flow. velocity integral and the cross-sectional area of the umbilical vein. Placental resistance was assessed as the ratio of MATERIALS AND METHODS maximum systolic and minimum diastolic blood flow velocities from an umbilical artery. Umbilical vein blood volumeWe studied 74 normal human fetuses ranging in age from 19 flow increased exponentially ( r = 0.86) with gestational to 42 wk, whose mothers were referred for routine obstetric age from 19 wk to term, and did not decrease in postdate ultrasound examination to assess fetal gestational age and/or fetuses. Umbilical vein blood volume flow increased lin-placental location. Mothers with diabetes, hypertension, preearly with fetal weight ( r = 0.77), although volume flow eclampsia, rhesus-incompatibility, multiple gestations, and preper unit body weight changed little with gestational age. vious fetuses with congenital malformations were excluded. HuUmbilical artery velocity ratio decreased progressively, man fetuses were only included in this study if their biophysical indicating diminishing placental resistance with gestational profiles were normal for their gestational age and any congenital age, but did not correlate closely with umbilical vein blood abnormalities involving the cardiovascular system or any other volume flow. We submit that fetoplacental blood volume organ system were excluded. Each human fetus was studied only flow can be readily calculated directly from the umbilical once to minimize any potential hazard from the Doppler ultravein with Doppler ultrasound and may provide a better sound. Written informed consent was obtained from each index of placental perfusion than the umbilical artery mother, and the protocol was approved by the Brigham and velocity ratio. (Pediatr Res 28: 383-387, 1990) Women's Hospital Human Subjects Committee. Two-dimensional imaging and pulsed-wave Doppler flow studies were performed using a model 77020 AC/AR ultrasonoscope (Hewlett Packard Co., Palo Alto, CA) with either a 3.5-mHz or, more frequently, a 5.0-mHz transducer. Normal fetal growth and viability depend directly upon the The transducer was placed on the maternal abdomen after the fetoplacental circulation for the supply of nutrients, gas, and mother had rested semi-recumbent for 15 min, and each fetus metabolite exchange. Impaired placental blood flow has been was...

No abstract

To determine the effect of metoprolol on silent ischemia and platelet aggregability, 10 patients with coronary artery disease were studied with a randomized, double-blind, placebo-controlled, crossover trial. Patients were treated with metoprolol (200 mg b.i.d.) or placebo for 1 week and then received the alternate therapy. Two days before the end of each treatment period, platelet aggregability was studied for 24 hours, and a 48-hour ambulatory electrocardiogram was obtained. Compared with placebo, metoprolol significantly decreased the total number (from 26 to 4, p < 0.01) and duration (from 735 to 84 minutes, p < 0.01) of silent ischemic episodes. This decrease was accompanied by a decrease in the mean blood pressure (from 127/81 to 118/71 mm Hg, p < 0.01) and the mean heart rate (from 70 to 54 beats/min, p < 0.01). The incidence of silent ischemic episodes in the morning was significantly higher in untreated patients than in treated patients. The few episodes observed during metoprolol treatment occurred at the same time as the peak incidence observed during placebo treatment. During placebo treatment, platelet aggregability increased from 6:00 to 9:00 AM as reflected by a decrease in the threshold concentrations of ADP and epinephrine required to induce biphasic platelet aggregation (from 4.8±0.8 to 2.6±0.4 pM, p <0.02; and from 7.3±2.3 to 1.8±0.9 ,M, respectively, p <0.02). Metoprolol did not alter the basal level nor blunt the morning increase of platelet aggregability. We conclude that patients with coronary artery disease have a marked increase in platelet aggregability from 6:00 to 9:00 AM that is not alfected by P-adrenergic blockade with metoprolol. Despite not affecting platelet aggregability, metoprolol compared with placebo decreases the number and duration of silent ischemic episodes. The decrease in the frequency of silent ischemic episodes is accompanied by a decrease in blood pressure and heart rate, suggesting that the beneficial effect of metoprolol is due, at least in part, to a reduction of myocardial oxygen demand and not to inhibition of transient platelet aggregation. The morning surge of transient ischemic events can be effectively blocked without changing platelet aggregability. (Circulation 1989;79:557-565)