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MAC and Aortic Atheroma in Stroke
Abstract & Commentary
By Michael H. Crawford, MD, Professor of Medicine, and Chief of Clinical Cardiology, at the University of California, San Francisco. Dr. Crawford is on the speaker's bureau for Pfizer.
Source: Karas MG, et al. Relation Between Mitral Annular Calcium and Complex Aortic Atheroma in Patients with Cerebral Ischemia Referred for Transesophageal Echocardiography. Am J Cardiol. 2007;999:1306-1311.
Although Mitral Annular Calcium (MAC) is a risk for stroke, the mechanism is unclear. MAC is associated with complex proximal aorta (before the left subclavian) aorta atheromatous plaques and is seen in patients with risk factors for atherosclerosis. Thus, these investigators from New York explored the relationship between MAC and aortic atheroma (AA) in patients with cerebral ischemia. This was a retrospective cross-sectional study of patients referred for transesophageal echocardiography (TEE) to evaluate the source of cardioembolism over 6 years. Those with endocarditis, congenital heart disease or valvular disease were excluded. Complex plaques were those ≥ 4 mm in height or with mobile elements. The inclusion criteria were met by 419 patients; mean age 59; 47% women; and 24% with transient ischemic attacks. Patients with MAC were older (mean 72 years), were more likely to have traditional risk factors for coronary heart disease and had more previous cardiovascular events including atrial fibrillation. MAC patients had more carotid and intracranial atherosclerosis, especially in the ipsilateral cerebral territory. On echo MAC patients had more aortic valve calcium, left atrial enlargement, and left ventricular hypertrophy. MAC was associated with complex AA in the proximal aorta after adjustment for clinical and echo confounders. The severity of MAC was related to the incidence of complex AA. The authors concluded that MAC is associated with complex proximal aorta atheroma in patients with cerebral ischemia. These results suggest that proximal aorta complex atheroma are the cause of cerebral ischemia in patients with MAC.
Several studies have shown that MAC shares the same risk profile as atherosclerosis. Thus, it is not surprising that by focusing on patients with cerebral ischemic events that MAC would be associated with complex aortic atheroma and head and neck artery atherosclerosis. No patients in this study had evidence of thrombi on their MAC. It is reasonable then to presume that the reason MAC is associated with cerebral ischemic events is because it is a marker of proximal aorta and large-vessel head and neck complex atheroma, which are likely the cause of embolic events.
There are other possible confounders that accompany MAC such as left atrial enlargement, aortic valve calcification and diabetes. After correction for several clinical and echocardiographic variables, MAC was still associated with complex proximal AA. When patients with other possible causes of cerebral ischemia were excluded, the relationship between MAC and complex AA was strengthened. So the authors argued that the referral bias of only studying patients with cerebral ischemia suspected of having a cardiovascular etiology, actually strengthened the association between MAC and proximal AA and buttresses the concept that aortic atheroma are the cause of cerebral ischemia in patients with MAC and no other discernable cause. Of course, this will need to be confirmed in a prospective study.
The practical implications of this study are that MAC is a strong marker of proximal aortic atheroma and aggressive risk factor modifications are indicated to prevent the development of complex plaques and subsequent stroke.