[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to demonstrate the feasibility of providing spatially matched, 3-dimensional (3D) myocardial scar and coronary imaging for the purpose of fused volumetric image display in patients undergoing cardiac resynchronization therapy (CRT) or coronary artery revascularization (CAR).
Clinical success in coronary vascular-based interventions is mitigated by the presence of scar in related myocardium. Pre-procedural fused volumetric imaging of both myocardial scar and coronary vasculature may benefit pre-procedural planning and patient selection in populations referred for CRT or CAR.
A total of 55 studies were performed in patients referred for either CRT (n = 42) or CAR (n = 13). Coronary-enhanced and scar-enhanced imaging was performed on a 3-T cardiac magnetic resonance scanner using the same cardiac-gated, 3D, free-breathing cardiac magnetic resonance technique during and 20 minutes following slow gadolinium infusion. Matched image datasets were fused and volume-rendered to simultaneously display coronary anatomy and myocardial scar. Visual scoring of coronary artery, coronary vein, and myocardial scar image quality (score 0 to 4) was performed. The clinical impact of imaging was also scored using a physician survey.
Mean age was 57 ± 14 years. Combined 3D coronary and scar imaging was successful in 49 studies (89%). A quality score ≥ 2 was obtained for 97% of proximal- and mid-coronary artery and vein segments. The mean quality score of 3D scar imaging was 2.8 ± 1.0 and was scored as ≥ 2 in 86% of patients with myocardial scar. All patients with a scar quality score ≥ 2 achieved successful image fusion. Transmural scar was present below ≥ 1 planned target vessel in 9 patients (39%) planned for CRT and 8 patients (62%) planned for CAR. Physician surveys demonstrated incremental clinical impact in 67% of patients.
Three-dimensional myocardial scar and coronary imaging with fused volumetric display is clinically feasible and may be valuable for the planning of vascular-based interventions when regional myocardial scar is pertinent to therapeutic success.
[Show abstract][Hide abstract] ABSTRACT: Background: Reduced myocardial perfusion has been speculated as a potential mechanism for the development and/or propagation of myocardial fibrosis in hypertrophic cardiomyopathy (HCM). This study aims to evaluate the prevalence, distribution and extent of stress-induced perfusion abnormalities and their relationship to underlying fibrosis in patients with HCM using magnetic resonance imaging.Methods: 15 patients with echocardiographically diagnosed HCM have been enrolled. Cine imaging, first-pass stress perfusion imaging using vasodilator stress (Dipyridamole), and delayed gadolinium enhancement imaging were performed. Stress hypoperfusion and delayed enhancement images were assessed both quantitatively and visually using a 16-segment model. Conversion of segmental visual scoring to % of LV by volume was achieved for both hypoperfusion (HP) and late enhancement (LE) using a standardized scoring system. For quantitative assessment prospectively defined cut-offs for LE and HP were used.Results: Maximal wall thickness ranged from 13 to 22 mm (mean 17 ± 2.6 mm). Non-ischemic pattern LE was present in 70% of patients. Perfusion abnormalities were identified on stress perfusion images in 80% of patients using visual analysis and 87% of patients using quantitative analysis. Perfusion abnormalities were predominantly subendocardial, and were regionally associated with segments containing LE (p < 0.01). Mean percent HP and mean percent LE were 17 ± 8.4% and 10 ± 9.3%, respectively by visual estimation and 20.0 ± 12.1% and 14.0 ± 7.4%, respectively by quantitative assessment. Figure 1.Conclusion: These preliminary results suggest that patients with HCM have a high prevalence of stress-induced myocardial hypoperfusion as represented by reduced first-pass gadolinium enhancement during vasodilator stress. This hypoperfusion appears to extend beyond regions of established LE suggesting a potential contribution of ischemia in the development and/or propagation of myocardial fibrosis in patients with HCM.
Journal of Cardiovascular Magnetic Resonance 01/2009; DOI:10.1186/1532-429X-11-S1-P55 · 4.56 Impact Factor