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Inflammation and the induction of acute myocardial infarction (AMI)

It is well known that the inflammatory protein type IIA secretory Phospholipase A2 (sPLA2-IIA) is involved in the pathogenesis of atherosclerosis. sPLA2-IIA releases fatty acids from membrane phospholipids that form precursors for inflammation inducing eicosanoids. Membrane phospholipids from which sPLA2-IIA has freed a fatty acid are lysophospholipids. These lysophospholipids act as binding sites for another inflammatory protein C-reactive protein (CRP), which in turn can activate complement. Furthermore, sPLA2-IIA can also kill cells by itself. In chapter 2 we show that sPLA2-IIA is significantly more expressed in culprit coronary atherosclerotic plaques that caused AMI than in coronary plaques that caused angina pectoris. This sPLA2-IIA may be involved in the death of smooth muscle cells in the plaque, which contributes to plaque instability. This implies that sPLA2-IIA is involved in the induction of plaque complications and therefore also AMI. Branched off from the coronary arteries that lie on the heart (epicardial) are the arteries that lie embedded in the heart muscle; the so-called intramyocardial arteries. In chapter 3 we investigated the accumulation of advanced glycation end products (AGEs), in this case N-carboxymethyllysine (CML), in these intramyocardial arteries. AGEs are the product of non-enzymatic glycation of proteins which disrupts the functioning of these proteins. AGEs accumulate during aging and at an accelerated rate in diabetes. We found significantly more accumulation of CML in the intramyocardial arteries of the left ventricle in AMI patients than in control patients. These patients did not have diabetes. CML was found in intramyocardial arteries throughout the left ventricle, not just the infarction area, and was found shortly after the onset of infarction. Furthermore, we found in vitro and in a rat AMI model that CML was likely not formed as a result of AMI, but accumulated prior to the onset of AMI. The CML in the intramyocardial arteries did not correlate with CML in the epicardial arteries. It has been shown before that CML, via the receptor for AGEs (RAGE), can upregulate adhesion molecules (E-selectin, ICAM-1) on endothelial cells, thereby inducing a pro-inflammatory state of these cells. This implicates a possible role for intramyocardial arteries and CML-induced inflammation herein, in the pathophysiology of AMI and perhaps in the induction of AMI. These two studies, sPLA2-IIA in the epicardial coronary arteries and CML in the intramyocardial arteries endorse the role of inflammation in aberrations of cardiac blood vessels that may lead to infarction.