Abnormal subendocardial perfusion in cardiac syndrome X detected by cardiovascular magnetic resonance imaging.

N Engl J Med

Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital and National Heart and Lung Institute, Imperial College, London, United Kingdom.

Published: June 2002

Background: In cardiac syndrome X (a syndrome characterized by typical angina, abnormal exercise-test results, and normal coronary arteries), conventional investigations have not found that chest pain is due to myocardial ischemia. Magnetic resonance techniques have higher resolution and therefore may be more sensitive.

Methods: We performed myocardial-perfusion cardiovascular magnetic resonance imaging in 20 patients with syndrome X and 10 matched controls, both at rest and during an infusion of adenosine. Quantitative perfusion analysis was performed by using the normalized upslope of myocardial signal enhancement to derive the myocardial perfusion index and the myocardial-perfusion reserve index (defined as the ratio of the myocardial perfusion index during stress to the index at rest).

Results: In the controls, the myocardial perfusion index increased in both myocardial layers with adenosine (in the subendocardium, from a mean [+/-SD] of 0.12+/-0.03 to 0.16+/-0.03 [P=0.02]; in the subepicardium, from 0.11+/-0.02 to 0.17+/-0.05 [P=0.002]); in patients with syndrome X, the myocardial perfusion index did not change significantly in the subendocardium (0.13+/-0.02 vs. 0.14+/-0.03, P=0.11; P=0.09 as compared with controls) but increased in the subepicardium (from 0.11+/-0.02 to 0.20+/-0.04, P<0.001; P=0.11 for the comparison with controls). Adenosine provoked chest pain in 95 percent of patients with syndrome X and 40 percent of controls (P<0.001).

Conclusions: In patients with syndrome X, cardiovascular magnetic resonance imaging demonstrates subendocardial hypoperfusion during the intravenous administration of adenosine, which is associated with intense chest pain. These data support the notion that the chest pain may have an ischemic cause.

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Source
http://dx.doi.org/10.1056/NEJMoa012369DOI Listing

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