Butler, J. (Javed)
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- Time to reconsider the perception and management of hypertensive heart disease(Wiley, 2023) Rosano, G. (Giuseppe); Butler, J. (Javed); Diez, J. (Javier)Heart failure (HF) is a global pandemic. Its prevalence is increas-ing with the aging of the population, with improved treatmentof ischemic heart disease (IHD) and the availability of effectiveevidence-based therapies that prolong survival of patients with HF.Despite the age-standardized stable worldwide prevalence of sys-temic arterial hypertension, but considering that the rates of hyper-tension control with treatment have worsened in recent years,hypertension remains one of the main causes of HF with a globalimpact. In the last two decades, the presence of hypertension hasincreased in incident cases of HF either with reduced (HFrEF) orwith preserved ejection fraction (HFpEF).1Additionally, the lifetimerisk of HF is higher in people with hypertension than in those withnormal blood pressure (BP), especially in women and the elderly.1On the other hand, the incidence of de novo HF in 23 hyperten-sion trials involving193 424 patients was 28.9% (n=7171)oftheall major cardiovascular events reported.2Therefore, HF continuesto represent a major concern in hypertension management.
- Rationale of the FIBROTARGETS study designed to identify novel biomarkers of myocardial fibrosis(Wiley, 2018) Gyöngyösi, M. (Mariann); Pizard, A. (Anne); Thum, T. (Thomas); Jaisser, F. (Frederic); Machu, J.L. (Jean-Loup); Ferreira, J.P. (João Pedro); McDonald, K. (Kenneth); Firat, H. (Hueseyin); Heymans, S. (Stephane); Butler, J. (Javed); Zannad, F. (Faiez); Gonzalez, A. (Arantxa); Girerd, N. (Nicolas); Rossignol, P.(Patrick); Diez, J. (Javier)Aims Myocardial fibrosis alters the cardiac architecture favouring the development of cardiac dysfunction, including arrhythmias and heart failure. Reducing myocardial fibrosis may improve outcomes through the targeted diagnosis and treatment of emerging fibrotic pathways. The European-Commission-funded ‘FIBROTARGETS’ is a multinational academic and industrial consortium with the main aims of (i) characterizing novel key mechanistic pathways involved in the metabolism of fibrillary collagen that may serve as biotargets, (ii) evaluating the potential anti-fibrotic properties of novel or repurposed molecules interfering with the newly identified biotargets, and (iii) characterizing bioprofiles based on distinct mechanistic phenotypes involving the aforementioned biotargets. These pathways will be explored by performing a systematic and collaborative search for mechanisms and targets of myocardial fibrosis. These mechanisms will then be translated into individualized diagnostic tools and specific therapeutic pharmacological options for heart failure. Methods and results The FIBROTARGETS consortium has merged data from 12 patient cohorts in a common database available to individual consortium partners. The database consists of >12 000 patients with a large spectrum of cardiovascular clinical phenotypes. It integrates community-based population cohorts, cardiovascular risk cohorts, and heart failure cohorts. Conclusions The FIBROTARGETS biomarker programme is aimed at exploring fibrotic pathways allowing the bioprofiling of patients into specific ‘fibrotic’ phenotypes and identifying new therapeutic targets that will potentially enable the development of novel and tailored anti-fibrotic therapies for heart failure.