It has been suspected that inflammation contributes to the atherosclerotic process and that increased inflammation can worsen the risk of having a heart attack. Inflammatory markers are studied in an effort to identify ones that can help predict a patient’s risk of cardiovascular disease. Inflammation is thought to worsen atherosclerotic lesions by causing an oxidative cascade that leads to worsening coronary artery disease and progression of stenotic lesions.
Researchers, lead by Dr. Matthias Nahrendorf of the Massachusetts General Hospital Center for Systems Biology, have found that inflammation can also contribute to an increased risk of developing a second heart attack after a first has occurred. The results of their study were published in the journal Nature. The researchers use a mouse model to study the inflammatory response after an induced myocardial infarction. The study results showed that there was a marked inflammatory response after an induced myocardial infarction, and that the inflammation caused worsening of previously existing atherosclerotic lesions. More specifically, the researchers found that there was increased inflammatory enzymatic activity at the atherosclerotic lesions that caused breakdown of the fibrous cap, potentially leading to future plaque rupture. In addition, there was increased accumulation of inflammatory cells, specifically monocytes, within atherosclerotic plaques and within the spleen. Finally, it was found that induced myocardial infarction caused increased release of blood cells from the bone marrow that would eventually develop into mediators of the exaggerated inflammatory response.
The authors wrote, “We have shown that acute [myocardial infarction] or stroke increases inflammation in atherosclerotic plaques at a distance. After an ischaemic event, atherosclerotic plaques grew faster and displayed higher protease activity. We identified an increased supply of innate immune cells as a driving force for this phenomenon… Despite growing understanding of the chronic inflammatory nature of atherosclerosis, specific anti-inflammatory therapy has yet to materialize. Given the central role of myeloid cells in disease promotion and their rapid turnover in inflamed tissue, interrupting the monocyte supply chain may attenuate atherosclerosis”.
This study suggests that inflammation after a heart attack contributes to the increased risk of developing a second heart attack through worsening of pre-existing atherosclerotic lesions. Future research should focus on determining whether a similar physiological response occurs in humans. In addition, treatments targeted at decreasing the inflammatory response after a heart attack may be of benefit to post-myocardial infarction patients and in preventing or decreasing the risk of a second heart attack.
Partha Dutta et al. “Myocardial infarction accelerates atherosclerosis” Nature published online June 27, 2012 doi:10.1038/nature11260