Myocardial Infarction Begets Myocardial Infarction
- Nahrendorf M, Swirski FK.
- Innate Immune Cells in Ischaemic Heart Disease: Does Myocardial Infarction Beget Myocardial Infarction? Eur Heart J 2015;Sep 8:[Epub ahead of print].
The following are points to consider from this review on innate immune cells in ischemic heart disease:
- Patients who experience a myocardial infarction (MI) are at increased risk of a subsequent adverse event (such as death, recurrent MI, and stroke), especially within the first year following the event.
- Some clinical studies have shown that the innate immune system is more active in patients who experience recurrent ischemic events.
- Preclinical studies in animals have demonstrated that experimentally induced MI leads to a systemic inflammatory response that is capable of accelerating the growth of atherosclerotic plaques, thus potentially contributing to recurrent ischemic events.
- The heart contains a network of resident macrophages positioned between myocytes; however, their function remains largely unknown.
- Following MI, recruitment of neutrophils and monocytes from the circulation to the myocardium occurs, largely replacing the pre-existing resident macrophages.
- Experimental MI leads to increased proliferative activity of hematopoietic stem and progenitor cells, an effect that may be mediated by circulating soluble factors such as damage-associated molecular patterns.
- Experimental MI also leads to a massive release of monocytes from the spleen, and these splenic monocytes account for a major portion of the myeloid cells infiltrating into the myocardium.
- Although post-MI leukocyte activation may lead to acceleration of atherosclerosis, this innate immune response may also be necessary for repair of injured myocardium, thus reducing the risk of cardiac rupture and heart failure.
- Further elucidation of mechanisms responsible for acceleration of atherosclerosis following MI may lead to improved secondary prevention strategies without compromising myocardial repair processes.
Keywords: Acute Coronary Syndrome, Atherosclerosis, Dyslipidemias, Heart Failure, Heart Rupture, Immunity, Innate, Macrophages, Metabolic Syndrome X, Monocytes, Myocardial Infarction, Myocardial Ischemia, Myocardium, Neutrophils, Plaque, Atherosclerotic, Secondary Prevention, Spleen, Stem Cells, Stroke
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