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The arrhythmogenic effects of endothelin-1 (ET-1) are mediated via ETA-receptors, but the role of ETB-receptors is unclear. We examined the pathophysiologic role of ETB-receptors on ventricular tachyarrhythmias (VT/VF) during myocardial infarction (MI). MI was induced by coronary ligation in two animal groups, namely in wild-type (n = 63) and in ETB-receptor-deficient (n = 61) rats. Using a telemetry recorder, VT/VF episodes were evaluated during phase I (the 1st hour) and phase II (2-24 h) post-MI, with and without prior beta-blockade. Action potential duration at 90% repolarization (APD90) was measured from monophasic epicardial recordings and indices of sympathetic activation were assessed using fast-Fourier analysis of heart rate variability. Serum epinephrine and norepinephrine were measured with radioimmunoassay. MI size was similar in the two groups. There was a marked temporal variation in VT/VF duration; during phase I, it was higher (p = 0.0087) in ETB-deficient (1,519 +/- 421 s) than in wild-type (190 +/- 34 s) rats, but tended (p = 0.086) to be lower in ETB-deficient (4.2 +/- 2.0 s) than in wild-type (27.7 +/- 8.0 s) rats during phase II. Overall, the severity of VT/VF was greater in ETB-deficient rats, evidenced by higher (p = 0.0058) mortality (72.0% vs. 32.1%). There was a temporal variation in heart rate and in the ratio of low- to high-frequency spectra, being higher (<0.001) during phase I, but lower (p < 0.05) during phase II in ETB-deficient rats. Likewise, 1 h post-MI, serum epinephrine (p = 0.025) and norepinephrine (p < 0.0001) were higher in ETB-deficient (4.20 +/- 0.54, 14.24 +/- 1.39 ng/ml) than in wild-type (2.30 +/- 0.59, 5.26 +/- 0.67 ng/ml) rats, respectively. After beta-blockade, VT/VF episodes and mortality were similar in the two groups. The ETB-receptor decreases sympathetic activation and arrhythmogenesis during the early phase of MI, but these effects diminish during evolving MI.

A 62-year-old man with prostate cancer underwent both 18F-PSMA-1007 and 18F-fluorocholine PET/CT studies for biochemical recurrence. 18F-PSMA-1007 PET/CT outperformed 18F-fluorocholine PET/CT in detecting lymph node metastases in the pelvis and retroperitoneum, whereas the former showed a focus of increased uptake in the spleen not seen on 18F-fluorocholine. The 18F-PSMA-1007 –avid lesion corresponded to a splenic hemangioma, which was initially detected in an MRI scan 10 years ago, unchanged in size. This case shows different features of 18F-PSMA-1007 and 18F-fluorocholine uptake, in an incidentally detected splenic hemangioma, alerting PET/CT reports for possible pitfall.

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Background: In recent years, concerns have been raised on the potential adverse effects of nonselective beta-blockers, and particularly carvedilol, on renal perfusion and survival in decompensated cirrhosis with ascites. We investigated the long-term impact of converting propranolol to carvedilol on systemic hemodynamics and renal function, and on the outcome of patients with stable cirrhosis and grade II/III nonrefractory ascites.Patients and Methods: Ninety-six patients treated with propranolol for esophageal varices' bleeding prophylaxis were prospectively evaluated. These patients were randomized in a 2:1 ratio to switch to carvedilol at 12.5 mg/d (CARVE group; n = 64) or continue propranolol (PROPRA group; n = 32). Systemic vascular resistance, vasoactive factors, glomerular filtration rate, and renal blood flow were evaluated at baseline before switching to carvedilol and after 6 and 12 months. Further decompensation and survival were evaluated at 2 years.Results: During a 12-month follow-up, carvedilol induced an ongoing improvement of systemic vascular resistance (1372 ± 34 vs. 1254 ± 33 dynes/c/cm 5 ; P = 0.02) along with significant decreases in plasma renin activity (4.05 ± 0.66 vs. 6.57 ± 0.98 ng/mL/h; P = 0.01) and serum noradrenaline (76.7 ± 8.2 vs. 101.9 ± 10.5 pg/mL; P = 0.03) and significant improvement of glomerular filtration rate (87.3 ± 2.7 vs. 78.7 ± 2.3 mL/min; P = 0.03) and renal blood flow (703 ± 17 vs. 631 ± 12 mL/min; P = 0.03); no significant effects were noted in the PROPRA group. The 2-year occurrence of further decompensation was significantly lower in the CARVE group than in the PROPRA group (10.5% vs. 35.9%; P = 0.003); survival at 2 years was significantly higher in the CARVE group (86% vs. 64.1%; P = 0.01, respectively). Conclusion:Carvedilol at the dose of 12.5 mg/d should be the nonselective beta-blocker treatment of choice in patients with cirrhosis and nonrefractory ascites, as it improves renal perfusion and outcome.