Myocardial Infarction (MDI) by coronary embolisms is considered rare. The explanations given call for: the narrowness of the coronaries in relation to the diameter of the aorta and the importance of the aortic flow; diastolic filling of the coronaries while most of the aortic flow is in systole; to the "protection" of the coronary ostia in systole by the opening of the aortic sigmoids.

72% of cases involve the left network and occlusions are most often distal. In 15% of cases, coronary embolisms are multiple. In 40% of cases, extracardiac embolic localizations are associated. They conclude that although "valve damage remains the leading cause of coronary embolism," bacterial endocarditis appears less frequently responsible.

Coronary embolisms are frequently associated with mur mur mur murbus, especially in patients with ACFA and those with dilated cardiomyopathy (CMD).

Coronary embolism infarction may be less rare than published observations suggest. This apparent rarity may be due to the difficulty of proving the mechanism of embolism, so that many cases are not published. Makino and Al-Sadir [13], for example, collect 12 cases of suspected coronary embolism found in three years in their center. 294 C. Gully et al. / Annales de Cardiologie et d'Angéologie 57 (2008) 290–294 Si.

These publications, like ours, most often carry out "suspicions of coronary embolisms". Indeed, "proof" of coronary embolism is not made. The criteria in principle required are: the coronarographic aspect; identification of the origin of the thrombus (ultrasound, CT, MRI); it is accepted that the existence of a spontaneous contrast in the OG in ETO is a strong argument to identify the origin of the thrombus; endodocron ultrasound with demonstration of the normality of the intima would be the third criterion.

However, the absence of stenosis at coronary angiography immediately after clot lysis or remotely is an accepted argument in favor of diagnosis. Clinically it is most often a caricatural picture of Acute Coronary Syndrome (ACS). Patients generally do not have a history of angina. Nevertheless, data from the literature demonstrate that the clinic can range from silent infarction to sudden death. In our series, these are limited infarctions revealed by chest pain.

The left coronary artery is the artery most often affected. The classic causes form a catalog from which valvulopathies and endocarditis emerge. ACFA is often associated with classical causes, but non-valvular ACFA is likely to be an increasingly common possibility due to the increase in the number of patients with ACFA and thromboembolic risk and the increase in coronarographic explorations in the elderly. In the same vein, we can ask ourselves the question of looking for unnoticed strokes in these patients. Clinical cases described in vivo as ours, it should be noted that absolute proof of the mechanism is only rarely provided and that these are most often diagnoses of (high) probability. This may explain why many suspicions of coronary embolisms are not published.

In acfa, published observations often report imperfect hypocoagulability, discontinuation of anticoagulant therapy or the possibility of an associated procoagulant factor. Treatment of early diagnosed acute infarction may involve thromboaspiration combined with distal protection. Background treatment depends on the suspected origin of the thrombus and the mechanism of embolism. He most often uses long-term VKAs.

In our case report, patients were medically managed with anti-vitamin K in addition to an antiplatelet agent P2Y12 given the absence of significant damage to coronary angiography.