Tailored therapy for heart failure: the role of biomarkers

Abstract

This editorial refers to ‘Galectin-3 predicts response to statin therapy in the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA)’, by L. Gullestad et al. , doi:10.1093/eurheartj/ehs077 The key process leading to heart failure (HF) is cardiac remodelling in response to chronic disease stresses. Several pathways, including those that regulate cardiomyocyte hypertrophy and processes that take place outside the cardiac myocyte, e.g. in the vasculature and extracellular matrix, play important roles in the remodelling process.1 Moreover, non-cardiac pathologies, such as renal dysfunction, anaemia, and skeletal myopathy, may develop in concert with left ventricular remodelling and contribute to the functional impairment in HF. Thus, HF, truly a syndrome rather than a disease, has many distinct subtypes. The heterogeneity of the HF syndrome implies that therapies have to be tailored to the individual patient to optimize the benefits and minimize the risks of a given drug or device. European Society of Cardiology (ESC) guidelines recommend using New York Heart Association (NYHA) class, left ventricular ejection fraction, and QRS width to guide most treatment decisions in chronic HF. The degree of tailoring achieved with these recommendations is low, and, today, most HF patients are prescribed the same medications. Still, the current ‘one size fits all’ approach to patients with symptomatic HF with reduced ejection fraction has been extremely successful, and the introduction of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, and aldosterone antagonists has resulted in a …