Catheter ablation in patients with LV dysfunction is feasible, not associated with higher procedural complications, and provides a significant improvement in LV performance, symptoms, and quality of life during follow-up.

Cardiovascular disease and cancer are leading causes of death. Both diseases share the same risk factors and, having the highest incidence and prevalence in the elderly, they often coexist in the same individual. Furthermore, the enhanced survival of cancer patients registered in the last decades and linked to early diagnosis and improvement of care, not infrequently exposes them to the appearance of ominous cardiovascular complications due to the deleterious effects of cancer treatment on the heart and circulatory system. The above considerations have led to the development of a new branch of clinical cardiology based on the principles of multidisciplinary collaboration between cardiologists and oncologists: Cardio-oncology, which aims to find solutions to the prevention, monitoring, diagnosis and treatment of heart damage induced by cancer care in order to pursue, in the individual patient, the best possible care for cancer while minimizing the risk of cardiac toxicity. In this consensus document we provide practical recommendations on how to assess, monitor, treat and supervise the candidate or patient treated with potentially cardiotoxic cancer therapy in order to treat cancer and protect the heart at all stages of the oncological disease. Cardiovascular diseases and cancer often share the same risk factors and can coexist in the same individual. Such possibility is amplified by the deleterious effects of cancer treatment on the heart. The above considerations have led to the development of a new branch of clinical cardiology, based on multidisciplinary collaboration between cardiologist and oncologist: the cardio-oncology. It aims to prevent, monitor, and treat heart damages induced by cancer therapies in order to achieve the most effective cancer treatment, while minimizing the risk of cardiac toxicity. In this paper, we provide practical recommendations on how to assess, monitor, treat and supervise patients treated with potential cardiotoxic cancer therapies.

The aim of this population‐based study was to evaluate the impact of being a cancer survivor (CS) on COVID‐19 risk and prognosis during the first wave of the pandemic (27 February 2020 to 13 May 2020) in Reggio Emilia Province. Prevalent cancer cases diagnosed between 1996 and 2019 were linked with the provincial COVID‐19 surveillance system. We compared CS' cumulative incidence of being tested, testing positive for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), being hospitalized and dying of COVID‐19 with that of the general population; we compared COVID‐19 prognosis in CS and in patients without cancer. During the study period, 15 391 people (1527 CS) underwent real‐time polymerase chain reaction for SARS‐CoV‐2, of whom 4541 (447 CS) tested positive; 541 (113 CS) died of COVID‐19. CS had higher age‐ and sex‐adjusted incidence rate ratios (IRR) of testing (1.28 [95% confidence interval, CI = 1.21‐1.35]), of positive test (IRR 1.06 [95% CI = 0.96‐1.18]) and of hospitalization and death (IRR 1.27 [95% CI = 1.09‐1.48] and 1.39 [95%CI = 1.12‐1.71], respectively). CS had worse prognosis when diagnosed with COVID‐19, particularly those below age 70 (adjusted odds ratio [OR] of death 5.03; [95% CI = 2.59‐9.75]), while the OR decreased after age 70. The OR of death was higher for CS with a recent diagnosis, that is, <2 years (OR = 2.92; 95% CI = 1.64‐5.21), or metastases (OR = 2.09; 95% CI = 0.88‐4.93). CS showed the same probability of being infected, despite a slightly higher probability of being tested than the general population. Nevertheless, CS were at higher risk of death once infected.

BackgroundImmune checkpoint inhibitors (ICIs) have significantly changed the oncology clinic in recent years, improving survival expectations in cancer patients. ICI therapy have a broad spectrum of side effects from endocrinopathies to cardiovascular diseases. In this study, pro-inflammatory and pro-fibrotic effects of short-term ICIs therapy in preclinical models were analyzed.MethodsFirstly, in a human in vitro model, human cardiomyocytes co-cultured with hPBMC were exposed to ICIs (with CTLA-4 or PD-1 blocking agents, at 200 nM) for 72 h. After treatment, production of DAMPs and 12 cytokines were analyzed in the supernatant through colorimetric and enzymatic assays. C57/Bl6 mice were treated with CTLA-4 or PD-1 blocking agents (15 mg/kg) for 10 days. Before (T0), after three days (T3) and after treatments (T10), ejection fraction, fractional shortening, radial and longitudinal strain were calculated by using bidimensional echocardiography (Vevo 2100, Fujfilm). Fibrosis, necrosis, hypertrophy and vascular NF-kB expression were analyzed through Immunohistochemistry. Myocardial expression of DAMPs (S100- Calgranulin, Fibronectin and Galectine-3), MyD88, NLRP3 and twelve cytokines have been analyzed. Systemic levels of SDF-1, IL-1β, and IL-6 were analyzed before, during and after ICIs therapy.ResultsRadial and longitudinal strain were decreased after 10 days of ICIs therapy. Histological analysis of NF-kB expression shows that short-term anti-CTLA-4 or anti-PD-1 treatment increased vascular and myocardial inflammation. No myocardial hypertrophy was seen with the exception of the pembrolizumab group. Myocardial fibrosis and expression of galectin-3, pro-collagen 1-α and MMP-9 were increased after treatment with all ICIs. Both anti-CTLA-4 or anti-PD-1 treatments increased the expression of DAMPs, NLRP3 inflammasome and MyD88 and induced both in vitro and in vivo the secretion of IL-1β, TNF-α and IL-6. Systemic levels of SDF-1, IL-1β and IL-6 were increased during and after treatment with ICIs.ConclusionsShort therapy with PD-1 and CTLA-4 blocking agents increases vascular expression of NF-kB, systemic SDF-1, IL-1β, IL-6 levels and myocardial NLRP3, MyD88 and DAMPs expression in preclinical models. A pro-inflammatory cytokine storm was induced in myocardial tissues and in cultured cardiac cells after ICIs therapy. The overall picture of the study suggests new putative biomarkers of ICIs-mediated systemic and myocardial damages potentially useful in clinical cardioncology.