Coronary care unit CDK Cyclin-dependent kinase CHA 2 DS 2 -VASc Congestive heart failure, Hypertension, Age ≥ 75 years (2 points), Diabetes mellitus, Stroke (2 points)-Vascular disease, Age 65-74 years, Sex category (female) CIED Cardiac implantable electronic device CML Chronic myeloid leukaemia CMR Cardiac magnetic resonance COMPASS-CAT Prospective COmparison of Methods for thromboembolic risk assessment with clinical Perceptions and AwareneSS in real-life patients-Cancer Associated Thrombosis CPET Cardiopulmonary exercise testing CrCl Creatinine clearance CRF Cardiorespiratory fitness CRS Cytokine release syndrome CS Cancer survivors CT Computed tomography CTLA-4 Cytotoxic T lymphocyte-associated antigen-4 cTn Cardiac troponin CTRCD Cancer therapy-related cardiac dysfunction CTR-CVT Cancer therapy-related cardiovascular toxicity CV Cardiovascular CVD Cardiovascular disease CVRF Cardiovascular risk factorsData derived from a single randomized clinical trial or large non-randomized studies.Consensus of opinion of the experts and/or small studies, retrospective studies, registries.©ESC 2022 ESC Guidelines © ESC 2022This table refers to anthracycline equivalence dose using doxorubicin as a reference. Note that these isoequivalent doses are derived from paediatric CS. CS, cancer survivors; CV, cardiovascular.a Data for idarubicin are based upon an estimated anticancer efficacy ratio, not derived from cardiotoxicity data. The CV toxicity dose ratio provides the value that should be used to multiply the dose of the anthracycline of interest to convert to isoequivalent doses of doxorubicin; e.g. to convert 125 mg/m 2 of epirubicin to doxorubicin isoequivalent, multiply the dose by 0.8 (125 mg/m 2 × 0.8 = 100 mg/m 2 of doxorubicin).

Heavy alcohol intake increases the risk of hypertension, but the relationship between light to moderate alcohol consumption and incident hypertension remains controversial. The authors sought to analyze the dose-response relationship between average daily alcohol consumption and the risk of hypertension via systematic review and meta-analysis. Electronic databases were searched for prospective control studies examining quantitative measurement of alcohol consumption and biological measurement of outcome. The primary endpoint was the risk of developing hypertension based on alcohol consumption. The level of alcohol consumption from each study was assigned to categorical groups based on the midpoint of their alcohol consumption classes to make possible the comparison of heterogeneous classification of alcohol intake. A total of 16 prospective studies (33,904 men and 193,752 women) were included in the analysis. Compared with nondrinkers, men with alcohol consumption with <10 g ⁄ d and 11 to 20 g ⁄ d had a trend toward increased risk of hypertension (relative risk [RR], 1.03; 95% confidence interval [CI], 0.94-1.13; P=.51) and (RR, 1.15; 95% CI, 0.99-1.33; P=.06), respectively, whereas a significantly increased risk of hypertension was found with heavy alcohol consumption of 31 to 40 g ⁄ d (RR, 1.77; 95% CI, 1.39-2.26; P<.001) and >50 g ⁄ d (RR, 1.61; 95% CI, 1.38-1.87; P<.001). Among women, the meta-analysis indicated protective effects at <10 g ⁄ d (RR, 0.87; 95% CI, 0.82-0.92; P<.001) and a trend toward decreased risk of hypertension with alcohol consumption 11 to 20 g ⁄ d (RR, 0.9; 95% CI, 0.87-1.04; P=.17), whereas a significantly increased risk of hypertension was indicated with heavy alcohol consumption of 21 to 30 g ⁄ d (RR, 1.16; 95% CI, 0.91-1.46; P=.23) and 31 to 40 g ⁄ d (RR, 1.19; 95% CI, 1.07-1.32; P=.002). In men, heavy alcohol consumption is associated with increased risk of hypertension, whereas there is a trend toward increased risk of hypertension with low and moderate alcohol consumption. The relationship between alcohol consumption and hypertension is J-shaped in women. Limiting alcohol intake should be advised for both men and women. J Clin Hypertens (Greenwich). 2012;14:792-798. Ó2012 Wiley Periodicals, Inc. Hypertension is a prevalent condition that affects approximately 65 million individuals in the UnitedStates based on a preliminary report from the National Health and Nutrition Examination Survey (NHANES) [2005][2006] and coincident US population estimates. 1 Due to its increasing clinical and public health importance, examining the risks or benefits of alcohol consumption in patients with hypertension is needed to assist clinicians in developing appropriate strategies of prevention. In observational studies, moderate alcohol consumption has been associated with lower incidence of cardiovascular diseases such as coronary artery disease, stroke, heart failure, and peripheral vascular disease. [2][3][4] Epidemiologic evidence suggests that heavy alcohol consumption is strongly associated ...

Recent data suggest a suboptimal antibody response to COVID-19 vaccination in patients with hematological malignancies. Neutralizing antibodies (NAbs) against SARS-CoV-2 were evaluated in 276 patients with plasma cell neoplasms after vaccination with either the BNT162b2 or the AZD1222 vaccine, on days 1 (before the first vaccine shot), 22, and 50. Patients with MM (n = 213), SMM (n = 38), and MGUS (n = 25) and 226 healthy controls were enrolled in the study (NCT04743388). Vaccination with either two doses of the BNT162b2 or one dose of the AZD1222 vaccine leads to lower production of NAbs in patients with MM compared with controls both on day 22 and on day 50 (p < 0.001 for all comparisons). Furthermore, MM patients showed an inferior NAb response compared with MGUS on day 22 (p = 0.009) and on day 50 (p = 0.003). Importantly, active treatment with either anti-CD38 monoclonal antibodies (Mabs) or belantamab mafodotin and lymphopenia at the time of vaccination were independent prognostic factors for suboptimal antibody response following vaccination. In conclusion, MM patients have low humoral response following SARS-CoV-2 vaccination, especially under treatment with anti-CD38 or belamaf. This underlines the need for timely vaccination, possibly during a treatment-free period, and for continuous vigilance on infection control measures in non-responders.

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Chronic inflammation underlies a variety of seemingly unrelated conditions including coronary artery disease. The interest in exploring the role of inflammation in heart failure (CHF) arises from earlier observations that circulating pro-inflammatory biomarker levels are elevated in patients with both ischaemic and non-ischaemic cardiomyopathies and correlate with severity of disease and prognosis (McMurray et al. in Eur Heart J 33:1787-1847, 2012; Mosterd and Hoes in Heart 93:1137-1146, 2007; Owan et al. in New Engl J Med 355:251-259, 2006). In acute decompensated HF, pro-inflammatory biomarker levels have been associated with mortality and readmission rates (Cowie et al. in Heart 83:505-510, 2000). Similar to neurohormonal activation and inflammation, production of pro-inflammatory cytokines is a response to stress in an attempt to restore cellular function. However, sustained expression and exposure to cytokines can lead to left ventricular dysfunction, negative inotropic effects, altered cardiac metabolism, myocardial remodelling and HF progression. However, it is unclear whether elevated levels of pro-inflammatory biomarkers, such as high-sensitivity C-reactive protein, signify an ongoing inflammatory process that leads to HF progression, or are merely markers of advanced disease. Beta-blockers, renin-angiotensin-aldosterone axis antagonists, statins and immunosuppressants have been found to decrease the levels of cytokines in small clinical studies of patients with HF (Hobbs et al. in Heart J 28:1128-1134, 2007). However, 'immunomodulatory' approaches applied in the RECOVER, RENAISSANCE, ATTACH, IMAC and ACCLAIM double-blind, placebo-controlled studies had neutral or negative effects on outcomes of patients with HF. In the present review, we focus on the role of inflammation in pathogenesis and progression of the HF, the value of pro-inflammatory cytokines as biomarkers and the potential therapeutic applications of immunomodulation in HF patients.