Contrast-enhanced myocardial inversion time at the null point for detection of left ventricular myocardial fibrosis in patients with dilated and hypertrophic cardiomyopathy: a pilot study
- PMID: 20308473
- DOI: 10.2214/AJR.09.3414
Contrast-enhanced myocardial inversion time at the null point for detection of left ventricular myocardial fibrosis in patients with dilated and hypertrophic cardiomyopathy: a pilot study
Abstract
Objective: The purpose of this article is to investigate a noninvasive method for quantifying diffuse myocardial fibrosis with cardiac MRI in patients with dilated cardiomyopathy and hypertrophic cardiomyopathy.
Materials and methods: We performed cardiac MRI on 35 patients (24 patients with dilated cardiomyopathy and 11 patients with hypertrophic cardiomyopathy) and 10 control subjects, on a clinical 1.5-T cardiac MRI scanner. Delayed hyperenhancement images were obtained 15 minutes after injection of a bolus of gadopentetate dimeglumine (0.2 mmol/kg), to identify fibrosis using an inversion recovery gradient-echo technique (inversion time scout sequence: TR, 20.8 milliseconds; TE, 1.3 milliseconds; inversion time, individually determined to null the myocardial signal [range, 85-800 milliseconds]). An inversion time mapping sequence was used to calculate the contrast-enhanced myocardial inversion time at the null point of a single midventricular slice as an index of diffuse fibrosis.
Results: The mean contrast-enhanced myocardial inversion time at the null point was significantly shorter in the patient group than the control group (343. 7 +/- 27.9 vs 390.4 +/- 19.3 milliseconds; p < 0.0001). In the patient group, the mean contrast-enhanced myocardial inversion time at the null point was shorter in patients with dilated cardiomyopathy than in patients with hypertrophic cardiomyopathy (337.0 +/- 29.6 vs 358.6 +/- 17.1 milliseconds, p = 0.02). In the dilated cardiomyopathy group, contrast-enhanced myocardial inversion time at the null point was significantly related to the left ventricular ejection fraction (r = 0.52; p = 0.01). However, in the hypertrophic cardiomyopathy group, contrast-enhanced myocardial inversion time at the null point had only a small positive correlation with the left ventricular ejection fraction (r = 0.27; p = 0.41).
Conclusion: Contrast-enhanced myocardial inversion time at the null point is shorter with myocardial fibrosis in patients with dilated cardiomyopathy and hypertrophic cardiomyopathy. In dilated cardiomyopathy, contrast-enhanced myocardial inversion time at the null point is inversely related to the severity of dilated cardiomyopathy.
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