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Background— A “renal dose” of dopamine is often used to increase renal blood flow; however, data on the magnitude of effect and site of action in patients with heart failure are scarce. Methods and Results— Renal effects of intravenous dopamine (1, 2, 3, 5, and 10 μg · kg −1 · min −1 ) were evaluated in 13 patients with chronic heart failure. Renal blood flow was calculated from renal artery cross-sectional area measured with intravascular ultrasound and renal blood flow velocity-time integral measured by the intravascular Doppler technique. Cross-sectional area increased and was significantly higher than baseline (0.30±0.04 cm 2 ) at 5 μg · kg −1 · min −1 (0.36±0.05 cm 2 ) and 10 μg · kg −1 · min −1 (0.38±0.06 cm 2 ). The velocity-time integral was significantly higher than baseline (22±3 cm) at doses of 3 and 5 μg · kg −1 · min −1 (both 31±4 cm). Renal blood flow increased, whereas renal vascular resistance decreased, reaching statistical significance at 2 μg · kg −1 · min −1 through 10 μg · kg −1 · min −1 . Cardiac output gradually increased, reaching statistical significance at doses of 5 and 10 μg · kg −1 · min −1 (5.5±0.5 and 6.1±0.7 versus 4.5±5.2 L/min at baseline), but the increase in renal blood flow appeared proportionately larger than corresponding increases in cardiac output. Conclusions— Dopamine is associated with an increase in renal blood flow in patients with heart failure. This effect is due to dilation of both the large conductance and small resistance renal blood vessels. Further evaluation of the efficacy and safety of dopamine for improvement of renal function in hospitalized patients with heart failure is warranted.

BackgroundLong‐term corticosteroid therapy is the standard of care for treatment of cardiac sarcoidosis (CS). The efficacy of long‐term corticosteroid‐sparing immunosuppression in CS is unknown. The goal of this study was to assess the efficacy of methotrexate with or without adalimumab for long‐term disease suppression in CS, and to assess recurrence and adverse event rates after immunosuppression discontinuation.Methods and ResultsRetrospective chart review identified treatment‐naive CS patients at a single academic medical center who received corticosteroid‐sparing maintenance therapy. Demographics, cardiac uptake of 18‐fluorodeoxyglucose, and adverse cardiac events were compared before and during treatment and between those with persistent or interrupted immunosuppression. Twenty‐eight CS patients were followed for a mean 4.1 (SD 1.5) years. Twenty‐five patients received 4 to 8 weeks of high‐dose prednisone (>30 mg/day), followed by taper and maintenance therapy with methotrexate±low‐dose prednisone (low‐dose prednisone, <10 mg/day). Adalimumab was added in 19 patients with persistently active CS or in those with intolerance to methotrexate. Methotrexate±low‐dose prednisone resulted in initial reduction (88%) or elimination (60%) of 18‐fluorodeoxyglucose uptake, and patients receiving adalimumab‐containing regimens experienced improved (84%) or resolved (63%) 18‐fluorodeoxyglucose uptake. Radiologic relapse occurred in 8 of 9 patients after immunosuppression cessation, 4 patients on methotrexate‐containing regimens, and in no patients on adalimumab‐containing regimens.ConclusionsCorticosteroid‐sparing regimens containing methotrexate with or without adalimumab is an effective maintenance therapy in patients after an initial response is confirmed. Disease recurrence in patients on and off immunosuppression support need for ongoing radiologic surveillance regardless of immunosuppression regimen.

Background: Pulmonary hypertension carries significant maternal and fetal risk during pregnancy and the postpartum period. As maternal mortality is high, specific targeted therapy for pulmonary hypertension may be required during pregnancy. Cases: We describe 2 pregnant patients who presented with severe secondary pulmonary arterial hypertension during their last trimester. They were electively treated in the late antepartum and early postpartum periods with sildenafil and intravenous epoprostenol and successfully delivered healthy infants via cesarean section without postpartum complications. Conclusion: Although pulmonary hypertension is associated with a risk of maternal mortality and most women are advised against pregnancy, new therapies may improve the outcome of pregnancy in patients with pulmonary hypertension.

Recent guidelines by the Heart Failure Society of America have recommended consideration for use of nitroprusside, nitroglycerin, or nesiritide in addition to diuretics to achieve hemodynamic and symptomatic improvement. This article reviews the results of previous studies evaluating the pharmacologic and clinical effects and safety profiles of these drugs in patients with heart failure.

BACKGROUND: A long-term trial showed that the oral prostacyclin (PGl 2) receptor (IP) agonist, selexipag, delayed disease progression in patients with pulmonary arterial hypertension (PAH). Transition to selexipag in patients treated with more burdensome inhaled therapies that target the prostacyclin pathway may be considered by patients and physicians. The Phase 3b, prospective, open-label TRANSIT-1 (Tolerability and Safety of the Transition From Inhaled Treprostinil to Oral Selexipag in Patients With Pulmonary Arterial Hypertension) study evaluated the safety and tolerability of transition from inhaled treprostinil to oral selexipag. METHODS: Patients receiving non-prostanoid oral PAH therapy and inhaled treprostinil at stable doses, in World Health Organization Functional Class II/III, with 6-minute walk distance ≥ 300 meters were enrolled. The 16-week main treatment period included downtitration of inhaled treprostinil over 8 weeks and parallel uptitration of selexipag over 12 weeks. Sustained treatment transition at Week 16 was defined as (1) receiving selexipag at Week 16; (2) no selexipag interruption(s) totaling ≥ 8 days; and (3) no inhaled treprostinil or other prostanoids after Week 8. Clinical parameters and patientreported treatment satisfaction outcomes were assessed at Week 16.

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Coronary artery endothelial function is heterogeneous in patients with idiopathic dilated cardiomyopathy. Endothelial dysfunction is present in approximately half of the cases and involves both resistance as well as conductance coronary blood vessels. Furthermore, coronary endothelial function cannot be predicted by demographic and hemo-dynamic parameters or left ventricular ejection fraction.