The Society for Cardiovascular Magnetic Resonance Registry at 150,000.

OBJECTIVES: To summarize the status of the SCMR Registry at 150,000 exams. BACKGROUND: Cardiovascular magnetic resonance (CMR) is increasingly utilized to evaluate expanding cardiovascular conditions. The SCMR Registry is a central repository for real-world clinical data to support cardiovascular research, including those relating to outcomes, quality improvement, and machine learning. The SCMR Registry is built on a regulatory-compliant, cloud-based infrastructure that houses searchable content and Digital Imaging and Communications in Medicine (DICOM) images. METHODS: The processes for data security, data submission, and research access are outlined. We interrogated the Registry and present a summary of its contents. RESULTS: Data were compiled from 154,458 CMR scans across 20 United States sites, containing 299,622,066 total images (~100 terabytes of storage). The human subjects had an average age of 58 years (range 1 month to >90 years old), were 44% female, 72% Caucasian, and had a mortality rate of 8%. The most common indication was cardiomyopathy (27%), and most frequently used current procedural terminology (CPT) code was 75561 (35%). Macrocyclic gadolinium-based contrast agents represented 89% of contrast utilization after 2015. Short-axis cines were performed in 99% of scans, short-axis LGE in 66%, and stress perfusion sequences in 30%. Mortality data demonstrated increased mortality in patients with left ventricular ejection fraction (LVEF) < 35%, the presence of wall motion abnormalities, stress perfusion defects, and infarct late gadolinium enhancement (LGE), compared to those without these markers. There were 456,678 patient-years of all-cause mortality follow-up, with a median follow-up time of 3.6 years. CONCLUSIONS: The vision of the SCMR Registry is to promote evidence-based utilization of CMR through a collaborative effort by providing a web mechanism for centers to securely upload de-identified data and images for research, education, and quality control. The Registry quantifies changing practice over time and supports large-scale real-world multicenter observational studies of prognostic utility. CONDENSED ABSTRACT: The SCMR Registry is a central regulatory-compliant cloud-based repository for real-world clinical data and DICOM images for multicenter cardiovascular research, including outcomes-based data. The Registry contains 299,622,066 DICOM images and 456,678 patient-years follow-up. Data compiled from 154,458 CMR scans across 20 US sites demonstrated cardiomyopathy as the most common indication and 89% macrocyclic gadolinium contrast utilization after 2015. There was an overall mortality rate of 8%, with higher rates in those with LVEF<35%, abnormal wall motion, ischemia presence, or infarct LGE. The Registry aims to promote evidence-based CMR utilization through a collaborative effort to positively impact cardiovascular outcomes.

Relationship of T2-Weighted MRI Myocardial Hyperintensity and the Ischemic Area-At-Risk.

RATIONALE: After acute myocardial infarction (MI), delineating the area-at-risk (AAR) is crucial for measuring how much, if any, ischemic myocardium has been salvaged. T2-weighted MRI is promoted as an excellent method to delineate the AAR. However, the evidence supporting the validity of this method to measure the AAR is indirect, and it has never been validated with direct anatomic measurements. OBJECTIVE: To determine whether T2-weighted MRI delineates the AAR. METHODS AND RESULTS: Twenty-one canines and 24 patients with acute MI were studied. We compared bright-blood and black-blood T2-weighted MRI with images of the AAR and MI by histopathology in canines and with MI by in vivo delayed-enhancement MRI in canines and patients. Abnormal regions on MRI and pathology were compared by (a) quantitative measurement of the transmural-extent of the abnormality and (b) picture matching of contours. We found no relationship between the transmural-extent of T2-hyperintense regions and that of the AAR (bright-blood-T2: r=0.06, P=0.69; black-blood-T2: r=0.01, P=0.97). Instead, there was a strong correlation with that of infarction (bright-blood-T2: r=0.94, P<0.0001; black-blood-T2: r=0.95, P<0.0001). Additionally, contour analysis demonstrated a fingerprint match of T2-hyperintense regions with the intricate contour of infarcted regions by delayed-enhancement MRI. Similarly, in patients there was a close correspondence between contours of T2-hyperintense and infarcted regions, and the transmural-extent of these regions were highly correlated (bright-blood-T2: r=0.82, P<0.0001; black-blood-T2: r=0.83, P<0.0001). CONCLUSION: T2-weighted MRI does not depict the AAR. Accordingly, T2-weighted MRI should not be used to measure myocardial salvage, either to inform patient management decisions or to evaluate novel therapies for acute MI.

Reproducible porcine model of thoracic aortic aneurysm.

BACKGROUND: Thoracic aortic aneurysms (TAAs) develop secondary to abnormal aortic extracellular matrix remodeling, resulting in a weakened and dilated aortic wall that progressed to rupture if left unattended. Currently, no diagnostic/prognostic tests are available for the detection of TAA disease. This is largely driven by the lack of a large animal model, which would permit longitudinal/mechanistic studies. Accordingly, the objective of the present study was to establish a reproducible porcine model of aortic dilatation, which recapitulates the structural and biochemical changes observed during human TAA development. METHODS AND RESULTS: Descending TAAs were induced in Yorkshire pigs (20-25 kg; n=7) through intra-adventitial injections of collagenase (5 mL, 0.35 mg/mL) and periadventitial application of crystalline CaCl2 (0.5 g). Three weeks after TAA induction, aortas were harvested and tissue was collected for biochemical and histological measurements. A subset of animals underwent MRI preoperatively and at terminal surgery. Results were compared with sham-operated controls (n=6). Three weeks after TAA induction, aortic luminal area increased by 38 ± 13% (P=0.018 versus control). Aortic structural changes included elastic lamellar degradation and decreased collagen content. The protein abundance of matrix metalloproteinases 3, 8, 9, and 12 increased in TAA tissue homogenates, whereas tissue inhibitors of metalloproteinases 1 and 4 decreased. CONCLUSIONS: These data demonstrate aortic dilatation, aortic medial degeneration, and alterations in matrix metalloproteinase/tissue inhibitors of metalloproteinase abundance, consistent with TAA formation. This study establishes for the first time a large animal model of TAA that recapitulates the hallmarks of human disease and provides a reproducible test bed for examining diagnostic, prognostic, and therapeutic strategies.