Review Article

Curbing Inflammation in the Ischemic Heart Disease

Table 2

Curbing inflammation in ischemic heart disease—key points.

(i) An anti-inflammatory therapy would provide real clinical value if an incremental benefit above and beyond existing therapies in a cost-efficient approach could be provided.
(ii) A potential new therapeutic target of ACS includes at least four anti-inflammatory treatment options: (1) nonspecific anti-inflammatory drugs; (2) specific antagonists of key cytokines; (3) immunomodulatory therapies; (4) immunization as promising therapeutic modality against atherosclerosis.
(iii) There is an early inflammatory response (innate inflammation) that would be a protective reaction in the acute phase of MI. Over time, persisting inflammatory response should be curbed.
(iv) The onset of AMI is determined with a certain safety margin. Thus, based on the concepts of ischemic myocardial protection emanating from the 1970s, it would be inappropriate “curbing” inflammation within 6 hours.
(v) General inhibition of the innate immune system is associated with adverse outcome after the challenge being to inhibit those parts of the innate immune system that cause injury, without affecting the myocardial infarct healing.
(vi) Would the sense of genetic predisposition, based on sensitive biomarkers, be an initial step to get strategies for AMI curbing inflammation?
(vii) It is well known that the inflammation occurs in the coronary artery wall, in the atherosclerotic plaque, and the myocardium. Would these alterations be considered individually or as a part of a single process of inflammation?
(viii) Would regular medications (ACE inhibitors, statins, aspirin, nitrates, and beta-blockers) be no longer functioning as curbing the AMI inflammatory process?