BACKGROUND: New left ventricular systolic dysfunction affects 500,000 Americans and coronary artery disease (CAD) is responsible for two-thirds of cases. Identifying CAD has both prognostic and therapeutic implications. We evaluated the ability of late gadolinium enhancement (LGE) by cardiovascular magnetic resonance imaging (CMR) to detect CAD as the etiology of recent onset congestive heart failure (CHF). METHODS: CMR and LGE were performed in 26 patients with new onset left ventricular systolic dysfunction. All patients received an x-ray angiography for identification of CAD. Patients with an acute coronary syndrome with troponin I > 1.0 ng/ml or a history of CAD were excluded. The presence and distribution of LGE was evaluated. RESULTS: Significant coronary stenoses were present in 5 of 26 patients (19%). LGE in an infarct pattern was found in 2 of the 5 patients with CAD. Of the 21 patients without CAD, 2 had midwall enhancement but none had evidence of LGE in an infarct pattern. CONCLUSIONS: When present, LGE in an infarct pattern suggests CAD as the etiology of new onset CHF. However, the absence of LGE does not exclude CAD as the underlying etiology. A small proportion of patients with a nonischemic cause of new onset CHF have LGE limited to the midwall.
BACKGROUND: New left ventricular systolic dysfunction affects 500,000 Americans and coronary artery disease (CAD) is responsible for two-thirds of cases. Identifying CAD has both prognostic and therapeutic implications. We evaluated the ability of late gadolinium enhancement (LGE) by cardiovascular magnetic resonance imaging (CMR) to detect CAD as the etiology of recent onset congestive heart failure (CHF). METHODS: CMR and LGE were performed in 26 patients with new onset left ventricular systolic dysfunction. All patients received an x-ray angiography for identification of CAD. Patients with an acute coronary syndrome with troponin I > 1.0 ng/ml or a history of CAD were excluded. The presence and distribution of LGE was evaluated. RESULTS: Significant coronary stenoses were present in 5 of 26 patients (19%). LGE in an infarct pattern was found in 2 of the 5 patients with CAD. Of the 21 patients without CAD, 2 had midwall enhancement but none had evidence of LGE in an infarct pattern. CONCLUSIONS: When present, LGE in an infarct pattern suggests CAD as the etiology of new onset CHF. However, the absence of LGE does not exclude CAD as the underlying etiology. A small proportion of patients with a nonischemic cause of new onset CHF have LGE limited to the midwall.
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