Combined dyssynchrony and scar imaging with cardiac magnetic resonance imaging predicts clinical response and long-term prognosis following cardiac resynchronization therapy.

AIMS: Cardiac resynchronization therapy (CRT) is advocated in advanced heart failure; however, patient selection remains challenging. We examined the utility of multi-sequential cardiac magnetic resonance imaging (CMR) in predicting outcome after CRT. METHODS AND RESULTS: We performed multi-sequential CMR on 40 subjects with cardiomyopathy and advanced heart failure, despite optimized medical therapy. All patients had been recommended for CRT according to accepted clinical guidelines. Patients were defined by CMR as likely responders if they had significant mechanical dyssynchrony (> or =65 ms delay between septal and posterolateral wall contraction on cine imaging), and no transmural scarring of the anteroseptal or posterolateral wall on delayed contrast-enhanced imaging. Clinical composite score was recorded at baseline and 6 months post-CRT. Long-term follow-up (transplant-free survival) was 497 +/- 55 days post-CRT. A clinical response was achieved in 19/26 (73%) of the CMR-predicted responders and 2/12 (17%) of the CMR-predicted non-responders (P < 0.01, chi(2)). The sensitivity of CMR for prediction of clinical response to CRT was 90%, with a specificity of 59%. Transplant-free survival post-CRT was achieved in 88% of the CMR-predicted responders and 58% of the CMR-predicted non-responders (P < 0.05, Kaplan-Meier survival analysis). CONCLUSION: Multi-sequential CMR identifies patients with severe cardiomyopathy who will respond to CRT with a favourable long-term prognosis.

Utility of myocardial fibrosis and fatty infiltration detected by cardiac magnetic resonance imaging in the diagnosis of arrhythmogenic right ventricular dysplasia--a single centre experience.

INTRODUCTION: Cardiac magnetic resonance imaging (CMR) has evolved as a major diagnostic tool to evaluate arrhythmogenic right ventricular dysplasia (ARVD). However, there is a lack of consensus in the interpretation of findings such as fatty infiltration or myocardial fibrosis. We examined the diagnostic utility of these two features in the diagnosis of ARVD. METHODS: We performed fast imaging employing steady-state acquisition cine imaging, T(1)-weighted black blood imaging with and without fat suppression and post-contrast delayed enhancement on a 1.5-T scanner to evaluate ventricular function and morphology, fatty infiltration and regional myocardial fibrosis in 52 subjects with suspected ARVD. RESULTS: Eight subjects met the international diagnostic criteria for ARVD. Right ventricle (RV) delayed hyper-enhancement was found in 7 of 8 (88%) ARVD subjects compared to 6 of 44 (14%) subjects without ARVD (p<0.001). Fatty infiltration was only identified in 1 ARVD patient, and 1 non-ARVD patient. On multiple logistic regression analysis RV enhancement remained an independent predictor for the diagnosis of ARVD (p<0.05). CONCLUSION: RV delayed enhancement is common in patients with ARVD, whereas detection of fatty infiltration of the right ventricle was rare in our patient population. The inclusion of RV fibrosis on CMR as a feature of ARVD may improve the diagnostic accuracy of this condition.

Diagnostic performance of multisequential cardiac magnetic resonance imaging in acute cardiac allograft rejection.

AIMS: We evaluated cardiac magnetic resonance imaging (CMR) as a non-invasive test for cardiac allograft rejection. METHODS AND RESULTS: We performed CMR on 50 heart-transplant recipients. Acute rejection was confirmed in 11 cases by endomyocardial biopsy (EMB) and presumed in 8 cases with a recent fall in left-ventricular ejection fraction (LVEF) not attributable to coronary allograft vasculopathy. Control patients had both normal LVEF and no significant rejection on EMB. Cardiac magnetic resonance imaging evaluated myocardial function, oedema, and early and late post-Gadolinium-DTPA contrast enhancement. Patients with confirmed rejection demonstrated elevated early relative myocardial contrast enhancement (4.1 +/- 0.3 vs. 2.8 +/- 0.2, P < 0.001) and a trend to higher oedema suggested by higher relative myocardial intensity on T(2)-weighted imaging compared to controls (2.1 +/- 0.1 vs. 1.7 +/- 0.1, P = 0.1). With rejection defined as increased early contrast enhancement or myocardial oedema, the sensitivity and specificity of CMR compared with EMB were 100 and 73%, respectively. Eight patients with presumed rejection also had elevated early myocardial contrast enhancement compared with controls, (8.7 +/- 1.9 vs. 2.8 +/- 0.2, P < 0.05), which reduced following increased immunosuppression (8.7 +/- 1.9 vs. 4.6 +/- 1.2, P < 0.05). In these patients LVEF improved following increased immunosuppression (32 +/- 5 vs. 46 +/- 5%, P < 0.05). CONCLUSION: Cardiac magnetic resonance imaging is a promising modality for non-invasive detection of cardiac allograft rejection.

Evaluation of diffuse myocardial fibrosis in heart failure with cardiac magnetic resonance contrast-enhanced T1 mapping.

OBJECTIVES: The purpose of this study was to investigate a noninvasive method for quantifying diffuse myocardial fibrosis with cardiac magnetic resonance imaging (CMRI). BACKGROUND: Diffuse myocardial fibrosis is a fundamental process in pathologic remodeling in cardiomyopathy and is postulated to cause increased cardiac stiffness and poor clinical outcomes. Although regional fibrosis is easily imaged with cardiac magnetic resonance, there is currently no noninvasive method for quantifying diffuse myocardial fibrosis. METHODS: We performed CMRI on 45 subjects (25 patients with heart failure, 20 control patients), on a clinical 1.5-T CMRI scanner. A prototype T(1) mapping sequence was used to calculate the post-contrast myocardial T(1) time as an index of diffuse fibrosis; regional fibrosis was identified by delayed contrast enhancement. Regional and global systolic function was assessed by cine CMRI in standard short- and long-axis planes, with echocardiography used to evaluate diastology. An additional 9 subjects underwent CMRI and endomyocardial biopsy for histologic correlation. RESULTS: Post-contrast myocardial T(1) times correlated histologically with fibrosis (R = -0.7, p = 0.03) and were shorter in heart failure subjects than controls (383 +/- 17 ms vs. 564 +/- 23 ms, p < 0.0001). The T(1) time of heart failure myocardium was shorter than that in controls even when excluding areas of regional fibrosis (429 +/- 22 ms vs. 564 +/- 23 ms, p < 0.0001). The post-contrast myocardial T(1) time shortened as diastolic function worsened (562 +/- 24 ms in normal diastolic function vs. 423 +/- 33 ms in impaired diastolic function vs. 368 +/- 20 ms in restrictive function, p < 0.001). CONCLUSIONS: Contrast-enhanced CMRI T(1) mapping identifies changes in myocardial T(1) times in heart failure, which appear to reflect diffuse fibrosis.