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Background: We document dual antiplatelet therapy (DAPT) use from discharge to 4 years after acute myocardial infarction (AMI), and investigate whether prolonged DAPT (beyond 1 year) is related to 5-year mortality., Methods: The French Registry of Acute ST-elevation or non-ST-elevation Myocardial Infarction (FAST-MI 2005) included 3670 patients with AMI in 223 French centres. We identified predictors of DAPT (aspirin+clopidogrel) beyond 1 and 2 years, and relation with all-cause 5-year mortality., Results: Among 3319 (96%) patients with discharge data, 2432 (73%) had DAPT, 582 (17%) single antiplatelet therapy (SAPT), and 305 (9%) no antiplatelet treatment. DAPT decreased from 75% at 1 year to 29% at 4 years, with a corresponding increase in SAPT (p<0.05 for trend). Patients with DAPT were more often male, treated with a drug-eluting stent (DES), and without oral anticoagulants. Independent predictors at 1 year of prolonged DAPT were age<75 years, in-hospital bleeding, history of MI, use of DES, discharge use of beta-blockers or statins and no chronic anticoagulation. Predictors at 2 years were age<75 years, male gender, previous MI, diabetes, DES implantation, no chronic oral anticoagulation. By multivariate analysis, there was no difference in 5-year mortality between those on SAPT vs DAPT at 1 year. DAPT at 2 years was also not significantly related to 5-year mortality (Hazard Ratio 1.3, 95% CI [0.9; 1.8], p=0.21)., Conclusion: Prolonged DAPT in selected AMI patients, observed in 47% at 1 year and 21% at 2 years, had no impact on 5-year mortality. These findings do not support the use of DAPT beyond 1 year after an initial ACS., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

A 60-year-old male presented a myocardial infarction after a voluntary overdose of Asasantine(®) started after strokes. He took chronically this association and some psychotropic drugs with vasodilator effects. After an intake of 40 tablets, he presented a cardiogenic shock with a myocardial infarction confirmed by biological samples, EKG, echocardiography and angiocoronarographie. No recent change of his treatment was found and symptoms regressed when dipyridamole was stopped while other vasodilators drugs were continued. Chronological analysis of events led us to suspect dipyridamole as a starter of the myocardial infarction secondary to a coronary artery steal reinforced by the vasodilator effect of combined treatments, in a patient at risk of ischemia. This case shows that, in such particular conditions, a change in dipyridamole dosage can induce a myocardial infarction even if its blood level remains in the therapeutic range., (Copyright © 2010. Published by Elsevier SAS.)

Some pulmonary embolism may present electrocardiogram changes, which suggest the diagnosis of myocardial infarction. We report the case of a patient with such a confounding presentation. In this patient, the wrong diagnosis of myocardial infarction led to a primary coronarography which was normal and finally, echocardiogram gave us the key leading to a fibrinolitic treatment which improved the patient.

A 50-year-old male patient treated with mesalazine for Crohn's disease was admitted in our unit for a chest pain, associated with nonspecific ST depression or ECG and troponin elevation. Coronarography showed minimal changes while SPECT imagery suggested a posterobasal subendocardial infarction, so that the diagnosis was unclear between ischemic disease and mesalazine-induced myocarditis. Eventually, MRI demonstrated clearly a subendocardial posterior infarction eliciting the diagnosis of mesalazine-induced myocarditis. This case report illustrates, in our opinion, that MRI is of invaluable interest in evaluating the characteristics of myocardium, and must be the cornerstone in the diagnosis of myocardial diseases.

Abstract: A 60-year-old male presented a myocardial infarction after a voluntary overdose of Asasantine® started after strokes. He took chronically this association and some psychotropic drugs with vasodilator effects. After an intake of 40 tablets, he presented a cardiogenic shock with a myocardial infarction confirmed by biological samples, EKG, echocardiography and angiocoronarographie. No recent change of his treatment was found and symptoms regressed when dipyridamole was stopped while other vasodilators drugs were continued. Chronological analysis of events led us to suspect dipyridamole as a starter of the myocardial infarction secondary to a coronary artery steal reinforced by the vasodilator effect of combined treatments, in a patient at risk of ischemia. This case shows that, in such particular conditions, a change in dipyridamole dosage can induce a myocardial infarction even if its blood level remains in the therapeutic range. [Copyright &y& Elsevier]