Coronary Embolism Among ST-Segment-Elevation Myocardial Infarction Patients: Mechanisms and Management.

BACKGROUND: Coronary artery embolism (CE) is recognized as an important nonatherosclerotic cause of ST-segment-elevation myocardial infarction. The objective was to describe clinical characteristics and long-term outcomes and to identify risks factors of CE in a large consecutive series of ST-segment-elevation myocardial infarction patients. METHODS AND RESULTS: We studied 1232 consecutive patients who presented with de novo ST-segment-elevation myocardial infarction. CE was diagnosed based on criteria encompassing clinical, angiographic, and diagnostic imaging findings. A total of 53 patients were identified in the CE group including 12 (22.6%) patients with multisites CE and 9 patients with other extracoronary localization. Compared with the non-CE group, age and coronary risks factors were not significantly different in the CE group except for smoking (P=0.03) and body mass index (P<0.001). Interventional coronary procedures were characterized by a higher use of glycoprotein IIb/IIIa inhibitors (P<0.001) and lower use of angioplasty (P<0.001) in the CE group. The most frequent underlying cardiac diseases were atrial fibrillation (n=15, 28.3%) followed by dilated cardiomyopathy (n=5), endocarditis (n=4), and intracardiac tumor (n=3), whereas among systemic diseases, malignancy (n=8) and systemic autoimmune disease or antiphospholipid syndrome (n=4) were present. No etiopathological mechanisms could be identified in 14 patients (26.4%). Coronary embolism was associated with a higher risk of death (crude hazard ratio, 4.87; 95% confidence interval, 2.52-9.39; P<0.0001). CONCLUSIONS: Etiopathogenesis of ST-segment-elevation myocardial infarction secondary to CE is diverse ranging from cardiac to systemic disease, and patient long-term survival is worse than expected according to the baseline cardiovascular risk.

Possible relationship between antiphospholipid antibodies and embolic events in infective endocarditis.

OBJECTIVE: Antiphospholipid (aPL) antibodies may activate platelets and contribute to vegetation growth and embolisation in infective endocarditis (IE). We aimed to determine the value of aPL as predictors of embolic events (EE) in IE. METHODS: We studied 186 patients with definite IE (Duke-Li criteria, all types of IE) from the Nanc-IE prospective registry (2007-2012) who all had a frozen blood sample and at least one imaging procedure to detect asymptomatic or confirm symptomatic EE. Anticardiolipin (aCL) and anti-ß2-glycoprotein I (ß2GPI) antibodies (IgG and IgM) were assessed after the end of patients' inclusion. The relationship between antibodies and the detection of EE after IE diagnosis were studied with Kaplan-Meier and Cox multivariate analyses. RESULTS: At least one EE was detected in 118 (63%) patients (52 cerebral, 95 other locations) after IE diagnosis in 80 (time interval between IE and EE diagnosis: 5.9±11.3 days). At least one aPL antibody was found in 31 patients (17%).Detection of EE over time after IE diagnosis was more frequent among patients with anti-ß2GPI IgM (log-rank P=0.0036) and that of cerebral embolisms, among patients with aCL IgM and anti-ß2GPI IgM (log-rank P=0.002 and P<0.0001, respectively).Factors predictive of EE were anti-ß2GPI IgM (HR=3.45 (1.47-8.08), P=0.0045), creatinine (2.74 (1.55-4.84), P=0.0005) and vegetation size (2.41 (1.41-4.12), P=0.0014). Those of cerebral embolism were aCL IgM (2.84 (1.22-6.62), P=0.016) and anti-ß2GPI IgM (4.77 (1.79-12.74), P=0.0018). CONCLUSION: The presence of aCL and anti-ß2GPI IgM was associated with EE, particularly cerebral ones, and could contribute to assess the embolic risk of IE.