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Single coronary artery anomaly without previous myocardial infarction does not cause ischemic mitral insufficiency

We read with great interest the recent report of Ay and colleagues, describing ‘‘the case of a 58-year-old man with single coronary artery anomaly, which stemmed from the left coronary sinus and caused ischemic mitral insufficiency due to left anterior descending artery (LAD) stenosis’’. We would like to make the following remarks in this regard, since whether the revealed severe mitral insufficiency, diagnosed by transthoracic echocardiography, was really caused by coronary ischemia, is in our opinion, still a matter for an open debate. On the contrary, the provided clinical history and symptomatology of this patient and the electrocardiography and echocardiography findings do not evidently support the authors’ presumption that the revealed severe mitral insufficiency was really of ischemic coronary origin. Ischemic mitral insufficiency (IMI) is a common (approximately 20%) complication after myocardial infarction, which follows more frequently an inferior infarction (38%) rather than an anteroseptal one (10%). IMI may be classified into acute and chronic types. Acute IMI occurs as a result of papillary muscle rupture and infarction, complicating acute myocardial infarction, or as a result of acute ischemic episodes involving the left circumflex or right coronary artery, resulting in cardiogenic shock. Chronic IMI should be defined as mitral regurgitation occurring more than 1 week after myocardial infarction with one or more left ventricular segmental wall motion abnormalities, significant coronary disease in the territory supplying the wall motion abnormality, and structurally normal mitral valve leaflets and chordae tendinae. Based on this information relating to either acute or chronic IMI, the clinical data and evidence provided by Ay and colleagues do not, in our opinion, support their assertion that the diagnosed severe mitral insufficiency was really caused by single coronary artery anomaly and left anterior descending artery stenosis. In this regard, Ay and colleagues stated in their report: ‘‘a telecardiogram was normal, and an electrocardiogram showed sinus rhythm with no signs of ischemia. Transthoracic echocardiography revealed severe mitral insufficiency, mild aortic and tricuspid insufficiency, an ejection fraction of 50%, a systolic pulmonary artery pressure of 45mmHg, and a borderline large left ventricle’’. Neither signs of myocardial ischemia nor history of myocardial infarction (acute or more than 1 week), which may be responsible for IMI, were claimed by the authors. Despite the presence of 80% stenosis of the left anterior descending artery, no left ventricular segmental wall motion abnormalities, which may explain the occurrence of IMI, were evidenced by the echocardiography. Furthermore, it was stated that: ‘‘the circumflex artery was normal, extending to the right coronary area after the origin of the posterior descending artery’’, which is further evidence that either acute or chronic myocardial ischemia, which may explain the severe mitral insufficiency, is highly improbable. Therefore, based on all above mentioned considerations, an another potential underlying pathology (degenerative or organic), which might explain the described severe mitral insufficiency in the case reported by Ay and colleagues cannot, in our opinion, be excluded.