No abstract

Background-In patients with sarcoidosis, sudden death is a leading cause of mortality, which may represent unrecognized cardiac involvement. Delayed-enhancement cardiovascular magnetic resonance (DE-CMR) can detect minute amounts of myocardial damage. We sought to compare DE-CMR with standard clinical evaluation for the identification of cardiac involvement. Methods and Results-Eighty-one consecutive patients with biopsy-proven extracardiac sarcoidosis were prospectively recruited for a parallel and masked comparison of cardiac involvement between (1) DE-CMR and (2) standard clinical evaluation with the use of consensus criteria (modified Japanese Ministry of Health [JMH] guidelines). Standard evaluation included 12-lead ECG and at least 1 dedicated non-CMR cardiac study (echocardiography, radionuclide scintigraphy, or cardiac catheterization). Patients were followed for 21Ϯ8 months for major adverse events (death, defibrillator shock, or pacemaker requirement). Patients were predominantly middle-aged (46Ϯ11 years), female (62%), and black (73%) and had chronic sarcoidosis (median, 7 years) and preserved left ventricular ejection fraction (median, 56%). DE-CMR identified cardiac involvement in 21 patients (26%) and JMH criteria in 10 (12%, 8 overlapping), a Ͼ2-fold higher rate for DE-CMR (Pϭ0.005). All patients with myocardial damage on DE-CMR had coronary disease excluded by x-ray angiography. Pathology evaluation in 15 patients (19%) identified 4 with cardiac sarcoidosis; all 4 were positive by DE-CMR, whereas 2 were JMH positive. On follow-up, 8 had adverse events, including 5 cardiac deaths. Patients with myocardial damage on DE-CMR had a 9-fold higher rate of adverse events and an 11.5-fold higher rate of cardiac death than patients without damage. Conclusions-In patients with sarcoidosis, DE-CMR is more than twice as sensitive for cardiac involvement as current consensus criteria. Myocardial damage detected by DE-CMR appears to be associated with future adverse events including cardiac death, but events were few, and this needs confirmation in a larger

Myocardial scarring is common in asymptomatic or mildly symptomatic HCM patients who have not suffered sudden death. When present, scarring occurs in hypertrophied regions, is consistently localized to the junctions of the septum and RV free wall, and correlates positively with regional hypertrophy and inversely with regional contraction.

A combined perfusion and infarction CMR examination with a visual interpretation algorithm can accurately diagnose CAD in the clinical setting. The combination is superior to perfusion-CMR alone.

Background-The reproducibility of contrast-enhanced MRI has not been established. We compared MRI reproducibility for infarct size determination with that of 99m Tc-sestamibi (MIBI) single photon emission computed tomography (SPECT). Methods and Results-Patients with chronic myocardial infarction defined by enzymes (peak creatine kinase-MB 173Ϯ119 U/L) were scanned twice by MRI (MRI I and MRI II, nϭ20) and twice by SPECT (SPECT I and SPECT II, nϭ15) on the same day. The MRI contrast agent was injected during MRI I but not MRI II to test the effect of imaging time after contrast. Resting Tc-MIBI SPECT images were acquired and infarct size was determined with commercial software. Infarct size in patients scanned by MRI and SPECT was 14Ϯ6% of left ventricular mass (%LV) by MRI (range 4%LV to 27%LV) and 14Ϯ7%LV by SPECT (range 4%LV to 26%LV). MRI I and II scans were performed 10Ϯ2 and 27Ϯ3 minutes after contrast, respectively. For MRI, the difference in infarct size between scans I and II (bias) was Ϫ0.1%LV, and the coefficient of repeatability was Ϯ2.4%LV. For SPECT, bias was Ϫ1.3%LV, and the coefficient of repeatability was Ϯ4.0%LV. Within individual patients, no systematic differences in infarct size were detected when the 2 MRI scans were compared, the 2 SPECT scans were compared, or MRI was compared to SPECT. Conclusion-The size of healed infarcts measured by contrast-enhanced MRI does not change between 10 and 30 minutes after contrast. The clinical reproducibility of contrast-enhanced MRI for infarct size determination compares favorably with that of routine clinical SPECT.

Background-The identification and assessment of myocardial infarction (MI) are important for therapeutic and prognostic purposes, yet current recommended diagnostic strategies have significant limitations. We prospectively tested the performance of delayed-enhancement magnetic resonance imaging (MRI) with gadolinium-based contrast for the detection of MI in an international, multicenter trial. Methods and Results-Patients with their first MI were enrolled in an acute (Յ16 days after MI; nϭ282) or chronic (17 days to 6 months; nϭ284) arm and then randomized to 1 of 4 doses of gadoversetamide: 0.05, 0.1, 0.2, or 0.3 mmol/kg. Standard delayed-enhancement MRI was performed before contrast (control) and 10 and 30 minutes after gadoversetamide. For blinded analysis, precontrast and postcontrast MRIs were randomized and then scored for enhanced regions by 3 independent readers not associated with the study. The infarct-related artery perfusion territory was scored from x-ray angiograms separately. In total, 566 scans were performed in 26 centers using commercially available scanners from all major US/European vendors. All scans were included in the analysis. The sensitivity of MRI for detecting MI increased with rising dose of gadoversetamide (PϽ0.0001), reaching 99% (acute) and 94% (chronic) after contrast compared with 11% before contrast. Likewise, the accuracy of MRI for identifying MI location (compared with infarct-related artery perfusion territory) increased with rising dose of gadoversetamide (PϽ0.0001), reaching 99% (acute) and 91% (chronic) after contrast compared with 9% before contrast. For gadoversetamide doses Ն0.2 mmol/kg, 10-and 30-minute images provided equal performance, and peak creatine kinase-MB levels correlated with MRI infarct size (PϽ0.0001). Conclusions-Gadoversetamide-enhanced MRI using doses of Ն0.2 mmol/kg is effective in the detection and assessment of both acute and chronic MI. This study represents the first multicenter trial designed to evaluate an imaging approach for detecting MI. (Circulation. 2008;117:629-637.)

As our understanding of the complications of coronavirus disease–2019 (COVID-19) evolve, sub-clinical cardiac pathology such as myocarditis, pericarditis and right ventricular dysfunction in the absence of significant clinical symptoms represents a concern. The potential implications of these findings in athletes are significant given the concern that exercise, during the acute phase of viral myocarditis, may exacerbate myocardial injury and precipitate malignant ventricular arrhythmias. Such concerns have led to the development and publication of expert consensus documents aimed at providing guidance for the evaluation of athletes after contracting COVID-19 in order to permit safe return-to-play. Cardiac imaging is at the center of these evaluations. This review seeks to evaluate the current evidence regarding COVID-19associated cardiovascular disease and how multi-modality imaging may be useful in the screening and clinical evaluation of athletes with suspected cardiovascular complications of infection. Guidance is provided with diagnostic “red flags” that raise the suspicion of pathology. Specific emphasis is placed on the unique challenges posed in distinguishing athletic cardiac remodeling from sub-clinical cardiac disease. The strengths and limitations of different imaging modalities are discussed and an approach to return-to-play decision making for athletes’ post COVID-19, as informed by multi-modality imaging, is provided.

Background-An ultrafast, delayed contrast-enhancement cardiovascular magnetic resonance technique that can acquire subsecond, "snapshot" images during free breathing (subsecond) is becoming widely available. This technique provides myocardial infarction (MI) imaging with complete left ventricular coverage in Ͻ30 seconds. However, the accuracy of this technique is unknown. Methods and Results-We prospectively compared subsecond imaging with routine breath-hold delayed contrastenhancement cardiovascular magnetic resonance (standard) in consecutive patients. Two cohorts with unambiguous standards of truth were prespecified: (1) patients with documented prior MI (nϭ135) and (2)