LAUSR

SEE PAGE 386 P ersonalized treatment, namely the ability to target treatments and doses to an individual based on their specific phenotype and risk, has become a holy grail for modern medicine (1). The aim is for patients who are most likely to benefit to receive target doses of a treatment, whereas for those not expected to benefit, unnecessary treatments or side effects from higher dosages may be avoided. For conditions where the disease phenotype is closely linked to a single-gene or -protein defect, a high degree of targeted treatment can be achieved. In contrast, the expression of heart disease in most individuals is complex and influenced by an extensive range of clinical, biochemical, and genomic factors. This is especially true for the heart failure phenotype, which can be a final common pathway for a large array of cardiovascular conditions and is frequently accompanied by significant comorbidity (2). With modern tools, the phenotypic expression of heart failure in an individual can now be robustly characterized. Detailed assessment and quantitation are now possible for cardiac structure and function, circulating peptides, and genetic markers. There is, additionally, a large body of research supporting our understanding of circulating markers that reflect heart failure pathophysiology and can act as heart failure biomarkers (3). Some biomarkers, such as the B-type natriuretic peptides (BNP) and N-terminal pro– B-type natriuretic peptide (NT-proBNP), have been studied extensively, and we have a thorough