Farmakis, D. (Dimitrios)

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2018 - 20202

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    Classification, prevalence, and outcomes of anticancer therapy-induced cardiotoxicity: the CARDIOTOX registry
    (2020) Cardinale, D. (Daniela); González-Costello, J. (José); Rodríguez-Rodríguez, I. (Isabel); Lyon, A.R. (Alexander R.); López-Fernández, T. (Teresa); Feliu-Batlle, J. (Jaime); Farmakis, D. (Dimitrios); Gómez-Prieto, P. (Pilar); González-Juanatey, J. R. (José Ramón); Zamora-Auñon, P. (Pilar); Cadenas-Chamorro, R. (Rosalía); Martínez-Monzonis, A. (Amparo); Buño-Soto, A. (Antonio); Canales-Albendea, M. A. (Miguel Ángel); Álvarez-Ortega, C. (Carlos); Albaladejo, A. (Ainara); Serrano-Antolín, J. M. (José María); López-Sendón, J.L. (J. L.); Mediavilla, G. (Guimoar); Rodríguez-Fraga, O. (Olaia)
    Aim: Cardiotoxicity (CTox) is a major side effect of cancer therapies, but uniform diagnostic criteria to guide clinical and research practices are lacking. Methods and results: We prospectively studied 865 patients, aged 54.7 ± 13.9; 16.3% men, scheduled for anticancer therapy related with moderate/high CTox risk. Four groups of progressive myocardial damage/dysfunction were considered according to current guidelines: normal, normal biomarkers (high-sensitivity troponin T and N-terminal natriuretic pro-peptide), and left ventricular (LV) function; mild, abnormal biomarkers, and/or LV dysfunction (LVD) maintaining an LV ejection fraction (LVEF) ≥50%; moderate, LVD with LVEF 40–49%; and severe, LVD with LVEF ≤40% or symptomatic heart failure. Cardiotoxicity was defined as new or worsening of myocardial damage/ventricular function from baseline during follow-up. Patients were followed for a median of 24 months. Cardiotoxicity was identified in 37.5% patients during follow-up [95% confidence interval (CI) 34.22–40.8%], 31.6% with mild, 2.8% moderate, and 3.1% with severe myocardial damage/dysfunction. The mortality rate in the severe CTox group was 22.9 deaths per 100 patients-year vs. 2.3 deaths per 100 patients-year in the rest of groups, hazard ratio of 10.2 (95% CI 5.5–19.2) (P < 0.001). Conclusions: The majority of patients present objective data of myocardial injury/dysfunction during or after cancer therapy. Nevertheless, severe CTox, with a strong prognostic relationship, was comparatively rare. This should be reflected in protocols for clinical and research practices.
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    Heart failure and diabetes: metabolic alterations and therapeutic interventions: a state-of-the-art review from the Translational Research Committee of the Heart Failure Association-European Society of Cardiology
    (European Society of Cardiology, 2018) Staels, B. (Bart); Heinzel, F.R. (Frank R.); Rosano, G. (Giuseppe); Huelsmann, M. (Martin); Hulot, J.S. (Jean-Sebastien); Ruschitzka, F. (Frank); Lyon, A.R. (Alexander R.); Laake, L.W. (Linda W.) van; Maack, C. (Christoph); Cosentino, F. (Francesco); Brutsaert, D. (Dirk); Rena, G. (Graham); Bauersachs, J. (Johann); Farmakis, D. (Dimitrios); Boer, R.A. (Rudolf A.) de; Keulenaer, G. (Gilles) de; Taegtmeyer, H. (Heinrich); Lunde, I.G. (Ida G.); Iaccarino, G. (Guido); Dei-Cas, A. (Alessandra); Clarke, K. (Kieran); Heymans, S. (Stephane); Pollesello, P. (Piero); Gonzalez, A. (Arantxa); Seferovic, P. (Petar); Paulus, W.J. (Walter J.); Wanner, C. (Christoph); Backs, J. (Johannes); Bugger, H. (Heiko); Riksen, N.P. (Niels P.); Lehrke, M. (Michael); Filippatos, G. (Gerasimos); Marx, N. (Nikolaus); Rossignol, P.(Patrick); Bayes-Genis, A. (Antoni)
    Heart failure (HF) is growing to a modern epidemic and despite advances in therapy, it still carries an ominous prognosis and a significant socioeconomic burden. Many novel agents that emerged as promising HF drugs failed to improve residual morbidity and mortality.2,3 Since developing and testing new agents has become increasingly costly,4 the concept of repurposing existing drugs for new indications has gained considerable importance. Conceptually, comorbidities such as type 2 diabetes mellitus (T2DM), obesity or chronic kidney disease, all highly prevalent in HF populations, have shifted from being innocent bystanders to drivers of HF. This applies especially to HF with preserved ejection fraction (HFpEF), a phenotype that accounts for more than 50% of HF patients and for which no effective therapy exists thus far.5,6 In particular, the prevalence of T2DM, thereby its combination with HF is rapidly increasing, mainly due to the obesity epidemic. Cardiovascular (CV) outcomes are addressed by an increasing number of clinical studies in T2DM, mainly as safety endpoints for anti-diabetic agents. Some of those drugs have beneficial CV effects independent of their glucose-lowering action. Consequently, antidiabetic agents have gained interest for their potential repurposing in HF treatment. In this context, the Translational Research Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC) organized a workshop on HF and T2DM, focusing on the pathophysiological and therapeutic aspects of this relationship. Here, we summarize the main points raised during this workshop, providing an overview of current evidence and open issues.