IgM antibodies against apoptotic cells and phosphorylcholine in patients with acute myocardial infarction in relation to infarct size and inflammatory response.

BACKGROUND

Natural IgM antibodies, and anti-phosphorylcholine IgM (anti-PC IgM) in particular, may modulate the pathogenesis of acute myocardial infarction (AMI).

OBJECTIVES

An exploratory study was conducted to evaluate the hypothesis that circulating anti-PC IgM and IgM binding to damaged cells increases the infarct size and post-infarct inflammatory response in patients with AMI.

MATERIAL AND METHODS

Plasma IgM binding to apoptotic cells (anti-apop IgM) and anti-PC IgM levels were compared in plasma samples from 50 patients with AMI and 46 healthy controls after correction for hemodilution. The cumulative release of cardiac markers LDH (lactate dehydrogenase), CK or CK-MB in human myocardium at 48 hours was used as an indication of infarct size. The circulating levels of mediators such as activated complement, C-reactive protein (CRP), interleukin-6 (IL6), interleukin-8 (IL8) and secretory phospholipase A2 (sPLA2) were used to assess the post-infarct inflammatory response. Patients with low (< median) and high (> median) levels of anti-apop IgM or anti-PC IgM were compared regarding infarct size and post-infarct inflammatory response. An electrocardiographical scoring system (Selvester score) was used to asses myocardial infarct size in patients with a first AMI (n = 24).

RESULTS

AMI patients demonstrated lower levels of anti-PC IgM on admission (p < 0.01) and at 48 hours (p < 0.001) when compared to the healthy controls, whereas anti-apop IgM levels were comparable to control levels. In patients with a first infarct, patients with levels of anti-PC IgM above the median demonstrated larger electrocardiographic infarct sizes (p = 0.04) and a more pronounced response of the acute phase protein sPLA2 (p = 0.06), with a similar post-infarct course of LDH, CK and CK-MB.

CONCLUSIONS

These findings suggest that anti-PC IgM plasma levels may participatie in amplifying the inflammatory response of the ischemic heart and contribute to infarct size. However, the levels of anti-PC IgM in patients with AMI in this study do not show a significant effect on cardiac markers LDH, CK and CK-MB. Hence, conclusive evidence is not provided by this limited cohort.