Therapeutic Approaches Targeting Inflammation in Cardiovascular Disorders

Abstract

Cardiovascular disease is a leading cause of morbidity and mortality in the Western world and represents an enormous global health burden. Significant advances have been made in the conservative, medical and surgical management across the range of cardiovascular diseases however the inflammatory components of these diseases have traditionally been neglected. Inflammation is certainly a key component of atherosclerosis, a chronic inflammatory condition, but it is at least correlative and predictive of risk in many other aspects of cardiovascular medicine ranging from heart failure to outcomes following reperfusion strategies. Inflammation therefore represents significant potential for future risk stratification of patients as well as offering new therapeutic targets across cardiovascular medicine. This review explores the role of inflammation in several of the major aspects of cardiovascular medicine focusing on current and possible future examples of the targeting of inflammation in prognosis and therapy. It concludes that future directions of cardiovascular research and clinical practice should seek to identify cohorts of patients with a significant inflammatory component to their cardiovascular condition or reaction to cardiovascular intervention. These patients might benefit from therapeutic strategies mounted against the inflammatory components implicated in their condition.

Various aspects of inflammation in heart failure

“…Also, in clinical trials, the correlation between the degree of left ventricular dysfunction in patients with HF and both the circulating inflammation cells and the biomarkers of inflammation was confirmed [21]. Increased plasma concentrations of biomarkers such as TNF-alpha, ST2, IL-1, interleukin-6 (IL-6), interleukin-8 (IL-8), Gal-3 (Gal-3) or growth differentiation factor 15 (GDF15) are considered as characteristic for HF [2,19,21]. IL-1 acts on virtually all cells of the immune system, including neutrophils, macrophages, eosinophils and mast cells.…”

“…In addition, according to the timeline and the dynamics of the appearance of symptoms, either chronic HF (CHF) or acute HF may be diagnosed. The causes of HF can be divided into the following: (1) associated with myocardial disease (ischaemic heart disease, toxic damage, inflammation-related and immune-related damage-infectious and non-infectious, infiltrative diseases, metabolic disorders and genetic syndromes), (2) associated with abnormal preload/afterload of the heart (hypertension, valvular heart diseases, pericardial syndromes and endocarditis), (3) associated with arrhythmias and conduction disorders (tachyarrhythmia and bradyarrhythmia) [1].…”

“…The most important of these include inflammation and activation of the immune system, which, it has been confirmed, significantly stimulate cardiac fibrosis and remodelling and therefore contribute to the progression of HF. So far, a lot of experimental evidence has been gathered confirming the participation of inflammation in the development and course of different types of HF [2][3][4][5][6]. Several inflammatory biomarkers have also been evaluated, assessing their usefulness as diagnostic and prognostic indicators in HF [2,5,6].…”

“…So far, a lot of experimental evidence has been gathered confirming the participation of inflammation in the development and course of different types of HF [2][3][4][5][6]. Several inflammatory biomarkers have also been evaluated, assessing their usefulness as diagnostic and prognostic indicators in HF [2,5,6]. In addition, various anti-inflammatory therapeutic strategies in HF have also been assessed, which, unfortunately, most often have not met the hopes placed in them [2,7,8].…”

“…Several inflammatory biomarkers have also been evaluated, assessing their usefulness as diagnostic and prognostic indicators in HF [2,5,6]. In addition, various anti-inflammatory therapeutic strategies in HF have also been assessed, which, unfortunately, most often have not met the hopes placed in them [2,7,8]. Some of the aspects of inflammation in HF examined so far are presented in the following subsections of this paper.…”