Inflammatory Biomarkers and Therapeutic Targets in Heart Failure

Improved outcomes of acute cardiac conditions, population aging, prevalent lifestyle-related risk factors, and advances in heart failure (HF) therapy, all have led to an ever-increasing prevalence of HF, currently considered a public health priority in developed countries and a major noncommunicable syndrome in developing regions. Heart failure is a complex syndrome with a host of pathophysiological mechanisms in action. Inflammation, an integral component of homeostasis, is a complex tissue response to stressors that attempts to mitigate their effect and initiate healing. Inflammation plays a critical role in the development, course, severity and outcomes of HF. The delicate balance of pro- and antiinflammatory processes can lead to beneficial or detrimental effects to the failing heart. In this article, we review the evidence on inflammatory biomarkers and their potential role in prognosis and therapeutic decisions for patients with HF. Although attempts to directly disrupt the inflammatory cascade in HF have been largely abandoned due to lack of efficacy and potential harm, there are still important gaps in our knowledge. Despite the strong association of levels of inflammatory biomarkers with HF severity and comorbidities, the causal association of certain markers and pathways with specific types or aspects of HF remains to be elucidated. When used as treatment response markers in conjunction with other risk factors, inflammatory markers have the potential to improve risk stratification of patients with HF and personalize HF treatment, with the ultimate goal to improve quality of life and prolong survival in these patients.