Editorial (Thematic Issue: Targeting Inflammation in Cardiovascular Disease)

Title:Editorial (Thematic Issue: Targeting Inflammation in Cardiovascular Disease)

Volume: 10 Issue: 7

Author(s): Spyridon Deftereos and Georgios Bouras

Affiliation:

Abstract: Cardiovascular mortality remains the leading cause of death all over the world, despite recent advances in early diagnosis, interventional techniques and pharmacological treatment targeting several risk factors of cardiovascular disease (CVD) [1]. The inflammatory process, as an integral part of the immune system, plays an important role in tissue homeostasis. Atherosclerosis has been identified early as a chronic inflammatory disease, giving another perspective in the nature of CVD and a new field to explore for the scientific community [2]. In this research, inflammatory biomarkers have been a great ally by helping to clarify the pathophysiological mechanisms linking inflammation to CVD and identify novel therapeutic targets [3]. Dyslipidemias, Acute Coronary Syndromes (ACSs), Atrial Fibrillation (AF), Essential Hypertension (HT) and Chronic Heart Failure (CHF) have been chosen for this special issue as some of the “hottest representatives” regarding CVD. The following series of original mini-review papers attempt to summarize the acquired so far knowledge of the relation of inflammation with the aforementioned conditions, evaluate the utility and prospects of the newly discovered mediators of inflammation in CVD and highlight promising anti-inflammatory therapeutic agents. In the first of this series of articles, Papoutsidakis et al. [4] summarize what is known today about the ways inflammation interacts with lipid metabolism and whether there is therapeutic potential in exploiting this interaction. Although inflammation pathways have been shown to play an important role on the road from dyslipidemia to atherogenesis, there is relatively little data on the ways inflammation promotes changes in total cholesterol, HDL, LDL and triglyceride metabolism. There is accumulating evidence that chronic inflammatory states can aggravate atherogenesis not only by directly promoting the formation of atherosclerotic plaque inside coronary vessels but also indirectly, by impairing lipid metabolism towards a more atherogenic profile, while anti-lipidemic therapies have not focused so far in inflammation pathways that could be contributing to the rise in cholesterol and triglyceride levels. Deftereos et al. [5] in a brief and comprehensive review article deal with the role of the innate immune system in the acutely ischemic myocardium. Since originally described in the 1930s the role of inflammation in the setting of acute myocardial infarction has been extensively studied. Myriads of animal models provided critical insight into the pathways governing the inflammatory responses and revealed the role of the innate immune system in initiating and perpetuating those responses. Despite the newly acquired knowledge, success was never met in the clinical field. Today with more than seven million people dying every year from coronary artery disease and with a rapidly increasing pool of heart failure patients as a result of an acute coronary event, it is compelling to identify possible new targets that modify the inflammatory cascades, attenuating tissue damage without affecting tissue healing. AF is the most common chronic arrhythmia and a source of significant morbidity and mortality. In their paper, Giannopoulos et al. [6] focus on the existing evidence supporting the ‘inflammatory’ hypothesis for AF pathophysiology. They also provide a review of potential biomarkers of inflammation in AF and comprehensively refer to therapeutic means that could counteract the full interplay between this arrhythmia and inflammation. Tsounis et al. [7] provide a detailed review of the current literature on the most important and most studied traditional and novel inflammation markers in HT. Recent evidence suggests that the immune system and inflammation processes are important contributors in the pathophysiology of HT. Inflammation markers have been associated with the risk of developing HT in normotensives and in hypertensive patients many of these have emerged as potent prognosticators for target organ damage and for future cardiovascular events. Additionally, antihypertensive agents that seem to exhibit a kind of antiinflammatory action and novel agents targeting inflammation have been studied and provide new insights for the treatment of HT. Finally, the article of Bouras et al. [8] is dedicated to the inflammatory mechanisms in CHF and provides an elucidating review of the most potent and novel biomarkers of ongoing inflammatory processes in the setting of CHF. Inflammatory mediators participate in CHF pathophysiology by various ways like exerting direct impact on cardiac myocytes, fibroblasts and α-adrenergic receptors leading to hypertrophy, fibrosis and impaired cardiac contractility, respectively, or inducing apoptosis by stimulation of the proper genes. They utter a brief and essential reference to the anti-inflammatory effects of current CHF therapeutic strategies, while providing an up-to-date and intriguing summary of the most novel and promising antiinflammatory drugs that may gain a place in CHF treatment in the years to come. The purpose of this series of mini-reviews is to highlight the most potent biomarkers of inflammation in pathophysiology of dyslipidemias, HT, AF, ACSs and CHF, clarify their utility as possible indicators of diagnosis and disease progression and present current and promising future therapeutic strategies. We would like to express our sincere thanks to the Editor-in-Chief, Professor Atta-ur-Rahman for giving us the opportunity to contribute to this special issue. Finally, we would like to thank all the authors for their effort and the quality of their work.

Cite this article as:

Deftereos Spyridon and Bouras Georgios, Editorial (Thematic Issue: Targeting Inflammation in Cardiovascular Disease), Medicinal Chemistry 2014; 10 (7) . https://dx.doi.org/10.2174/1573406410666140811161803