OBJECTIVE:Onco-cardiology services are expanding rapidly in Japan. To provide a better service, it is important to consider the needs of oncologists. However, little is known regarding specific needs for which oncologists should consult cardiologists to manage cardiovascular problems of their patients. We analysed cardiology consultations sought by oncologists to evaluate the role of cardiologists in cancer treatment. METHOD:We retrospectively investigated consecutive 2064 cardiology consultations of cancer patients in the University of Tsukuba Hospital, Tsukuba, Japan, between January 2014 and December 2018. RESULTS:The most common timing of cardiology consultation was before the commencement of cancer treatment (n = 1355; 65.7%), followed by after the commencement of cancer treatment (n = 686; 33.2%). Among the 361 consultations before the administration of anticancer drugs, 235 (65.1%) were for anthracycline-based regimens. There were 506 (24.5%) consultations for the management of cardiovascular emergencies developing after the commencement of cancer treatment; venous thromboembolism was the most frequent (n = 125; 24.7%), followed by atrial fibrillation (n = 110; 21.7%) and heart failure (n = 74; 14.6%). There were marked differences in the types of cardiovascular emergencies depending on the type of cancer. CONCLUSIONS:This survey revealed the various cardiovascular problems for which oncologists sought interventions by cardiologists. A multidisciplinary approach in an onco-cardiology service is essential to achieve optimal long-term outcomes.

Renal dysfunction results in the accumulation of various uremic toxins, including indoxyl sulphate (IS), and is a major risk factor for atrial fibrillation (AF). Experimental studies have demonstrated that IS exacerbates atrial remodelling via oxidative stress, inflammation, and fibrosis. However, its clinical impact on AF-promoting cardiac remodelling has not been described. Therefore, the purpose of this study was to clarify the relationship between basal IS levels and the 1-year outcomes after catheter ablation for the treatment of AF. Our prospective observational study included data from 125 patients with AF who underwent catheter ablation. Over a 1-year follow-up period, AF recurrence was identified in 21 patients. The 1-year AF-free survival was significantly lower in patients with high serum IS levels (≥0.65 μg/mL) than in those with low IS levels (60.1 ± 10.4% versus 85.2 ± 3.9%, P = 0.007). Univariable analysis identified that an IS concentration ≥ 0.65 μg/mL was associated with AF recurrence (hazard ratio [HR] = 3.10 [1.26–7.32], P = 0.015), and this association was maintained in multivariate analysis (HR = 3.67 [1.13–11.7], P = 0.031). Thus, in patients undergoing AF ablation, serum IS levels at baseline independently predict the recurrence of arrhythmia.

Introduction: The Glucagon-like peptide-1 receptor (GLP-1R) agonist, liraglutide is an incretin hormone mimetics, a drug for diabetes mellitus. Recently, it is reported that the GLP-1R agonist inhibits endothelial dysfunction, inflammation, and cell proliferation, which are the major molecular findings for pathophysiology of pulmonary arterial hypertension (PAH). However, it is unclear whether the GLP-1R agonist ameliorates PAH. Objective: To investigate the effect of a GLP-1R agonist on the development of PAH. Methods: 8 week-old C57BL6/J mice were injected liraglutide (0.3 mg/kg/day) or saline for total 5 weeks. One week after starting injection, mice were placed in room air or exposed to chronic hypoxia (10% O2) for further 4 weeks. Results: Right ventricular systolic pressure of hypoxia + liraglutide group were significantly reduced compared with that of hypoxia + saline group (30.0 ± 1.5 mmHg vs 34.3 ± 2.2 mmHg, P < .01, n = 7). Right ventricular/body weight ratio of hypoxia + liraglutide group were significantly smaller than that of hypoxia + saline group (P < .01). The expression of eNOS mRNA and the protein expression of phospho-eNOS in the lung was significantly augmented by liraglutide administration under hypoxia (P < .05). Conclusion: The GLP-1R agonist liraglutide reduces right ventricular pressure in hypoxia-induced PAH mice model. This effect is suggested to be through the eNOS activation in pulmonary artery.

Aims: Vascular remodeling results from aberrations in the balance between cell proliferation and death, which is seen in the obstructive vasculature of pulmonary arterial hypertension (PAH). Endothelin (ET)-1 has a potent proliferative activity on vascular smooth muscle cells, and ET receptor inhibitors are used to treat PAH; however, it remains unclear whether ET receptor inhibition contributes to the apoptosis of pulmonary arterial smooth muscle cells (PASMCs), another cause of pulmonary vascular remodeling.Main methods: Cultured human PASMCs were treated with the ETA receptor antagonist BQ-123 (100 mu M), or the ETB antagonist A-192621 (1 - 100 mu M) or BQ-788 (1 - 100 mu M) for 48 h. The cells were then incubated for another 24 h with or without doxorubicin (DOX, 1 mu M), an anthracyclin antitumor antibiotic that promotes p53-mediated apoptosis. Cell viability and apoptosis were evaluated by MTT assays, caspase-3/7 activity assays, and Western blots for cleaved caspase-3 expression.Key findings: The viability of PASMCs was significantly decreased by A-192621 and BQ-788, in a dose-dependent manner. A-192621 and BQ-788 significantly increased the caspase-3/7 activity and cleaved caspase-3 expression in PASMCs. The PASMCs' susceptibility to DOX-induced apoptosis was significantly higher in the presence of A-192621 and BQ-788 than with vehicle. However, BQ-123 did not affect these parameters.Significance: Blockade of the ETB receptor increases the extent of apoptosis and susceptibility to DOX-induced apoptosis in PASMCs. Apoptosis caused by ETB receptor blockade in PASMCs may be one of the mechanisms by which vascular remodeling is reduced in ET receptor inhibitor-based PAH treatments. (C) 2016 Elsevier Inc. All rights reserved.