It is well known that those who have just had a heart attack are at highest risk for future events. The “culprit” lesion for the event, may not, however be the only one lurking in the near term, just the only one exposed at the moment. A recent study published in the Journal of the American Heart Association was designed to investigate systemic atherosclerotic acceleration in relation to the acute inflammatory response surrounding acute myocardial infarction (MI). They analyzed details from subjects who had thoracic 18F-fluorodeoxyglucose (18F-FDG) positron emission and combined computed tomography aortic images from 1000 subjects with recent MI from the GRACE registry as a comparator to results from 40 patients with recent MI and 40 patients with stable coronary disease. The amount of uptake of 18F-FDG was highest in those who had transmural infarcts, which aligns with outcome trials where subjects with larger infarcts were more likely to have early recurrent MI. The investigators concluded that recent myocardial infarction (<30 days post event) along with the extent of myocardial damage is significantly associated with increased inflammation. These study results support the hypothesis that increases in inflammation with acute MI can lead to remote plaque destabilization and early MI recurrence.
According to the commentary by Benjamin M. Scirica MD, “These results highlight the clinically important distinction between acute and stable atherosclerotic disease.” Because of the increased inflammatory state early post MI, “these are the patients who require the most intense therapy, be it revascularization, high-intensity lipid-lowering therapy, or extended and more potent antiplatelet and antithrombotic therapy. Furthermore, in these patients specifically, novel, targeted anti-inflammatory therapy may be of greatest benefit.”