Background Acute complete occlusion of a coronary artery results in progressive ischemia, moving from the endocardium to the epicardium (ie, wavefront). Dependent on time to reperfusion and collateral flow, myocardial infarction ( MI ) will manifest, with transmural MI portending poor prognosis. Late gadolinium enhancement cardiac magnetic resonance imaging can detect MI with  high diagnostic accuracy. Primary percutaneous coronary intervention is the preferred reperfusion strategy in patients with ST ‐segment–elevation MI with <12 hours of symptom onset. We sought to visualize time‐dependent necrosis in a population with ST ‐segment–elevation MI by using late gadolinium enhancement cardiac magnetic resonance imaging (STEMI‐SCAR project). Methods and Results ST ‐segment–elevation MI patients with single‐vessel disease, complete occlusion with TIMI (Thrombolysis in Myocardial Infarction) score 0, absence of collateral flow (Rentrop score 0), and symptom onset <12 hours were consecutively enrolled. Using late gadolinium enhancement cardiac magnetic resonance imaging, the area at risk and infarct size, myocardial salvage index, transmurality index, and transmurality grade (0–50%, 51–75%, 76–100%) were determined. In total, 164 patients (aged 54±11 years, 80% male) were included. A receiver operating characteristic curve (area under the curve: 0.81) indicating transmural necrosis revealed the best diagnostic cutoff for a symptom‐to‐balloon time of 121 minutes: patients with >121 minutes demonstrated increased infarct size, transmurality index, and transmurality grade (all P <0.01) and decreased myocardial salvage index ( P <0.001) versus patients with symptom‐to‐balloon times ≤121 minutes. Conclusions In MI with no residual antegrade and no collateral flow, immediate reperfusion is vital. A symptom‐to‐balloon time of >121 minutes causes a high grade of transmural necrosis. In this pure ST ‐segment–elevation MI population, time to reperfusion to salvage myocardium was less than suggested by current guidelines.

BackgroundThe diagnostic performance of adenosine stress cardiovascular magnetic resonance (CMR) in patients with arrhythmias presenting for work-up of suspected or known CAD is largely unknown, since most CMR studies currently available exclude arrhythmic patients from analysis fearing gating problems, or other artifacts will impair image quality. The primary aim of our study was to evaluate the diagnostic performance of adenosine stress CMR for detection of significant coronary stenosis in patients with arrhythmia presenting for 1) work-up of suspected coronary artery disease (CAD), or 2) work-up of ischemia in known CAD.MethodsPatients with arrhythmia referred for work-up of suspected CAD or work-up of ischemia in known CAD undergoing adenosine stress CMR were included if they had coronary angiography within four weeks of CMR.ResultsOne hundred fifty-nine patients were included (n = 64 atrial fibrillation, n = 87 frequent ventricular extrasystoles, n = 8 frequent supraventricular extrasystoles). Of these, n = 72 had suspected CAD, and n = 87 had known CAD. Diagnostic accuracy of the adenosine stress CMR for detection of significant CAD was 73 % for the entire population (sensitivity 72 %, specificity 76 %). Diagnostic accuracy was 75 % (sensitivity 80 %, specificity 74 %) in patients with suspected CAD, and 74 % (sensitivity 71 %, specificity 79 %) in the group with known CAD. For different types of arrhythmia, diagnostic accuracy of CMR was 70 % in the atrial fibrillation group, and 79 % in patients with ventricular extrasystoles. On a per coronary territory analysis, diagnostic accuracy of CMR was 77 % for stenosis of the left and 82 % for stenosis of the right coronary artery.ConclusionThe present data demonstrates good diagnostic performance of adenosine stress CMR for detection of significant coronary stenosis in patients with arrhythmia presenting for work-up of suspected CAD, or work-up of ischemia in known CAD. This holds true for a per patient, as well as for a per coronary territory analysis.

BackgroundAdenosine stress cardiovascular magnetic resonance (CMR) can detect significant coronary artery stenoses with high diagnostic accuracy. Caffeine is a nonselective competitive inhibitor of adenosine2A-receptors, which might hamper the vasodilator effect of adenosine stress, potentially yielding false-negative results. Much controversy exists about the influence of caffeine on adenosine myocardial perfusion imaging. Our study sought to investigate the effects of caffeine on ischemia detection in patients with suspected or known coronary artery disease (CAD) undergoing adenosine stress CMR.MethodsThirty patients with evidence of myocardial ischemia on caffeine-naïve adenosine stress CMR were prospectively enrolled and underwent repeat adenosine stress CMR after intake of 200 mg caffeine. Both CMR exams were then compared for evaluation of ischemic burden.ResultsDespite intake of caffeine, no conversion of a positive to a negative stress study occurred on a per patient basis. Although we found significant lower ischemic burden in CMR exams with caffeine compared to caffeine-naïve CMR exams, absolute differences varied only slightly (1 segment based on a 16-segment model, 3 segments on a 60-segment model, and 1 ml in total ischemic myocardial volume, p < 0.001 each). Moreover, no relevant ischemia (≥2 segments in a 16-segment model) was missed by prior ingestion of caffeine.ConclusionsAlthough differences were small and no relevant myocardial ischemia had been missed, prior consumption of caffeine led to significant reduction of ischemic burden, and might lower the high diagnostic and prognostic value of adenosine stress CMR. Therefore, we suggest that patients should still refrain from caffeine prior adenosine stress CMR tests.

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Background: Increased cardiac fat has been identified as a risk factor for coronary artery disease. Metabolic syndrome is associated with increased cardiac fat deposition. Steroids are known to imitate some effects of metabolic syndrome and are frequently used in patients with rheumatic disorders. Primary aim was to evaluate the impact of long-term steroid use on cardiac fat deposition in patients with rheumatic disorders. In addition, we sought to investigate if this effect might be dose-dependent. Methods:Patients were enrolled as follows: (1) rheumatic disorder; and (2) long-term steroid therapy, and (3) underwent cardiovascular magnetic resonance (CMR) imaging. Patients were stratified in a high-dose (>7.5 mg prednisone equivalent/day for at least 6 months) and a low-dose steroid group (<7.5 mg prednisone equivalent/day) and compared to steroid-naïve controls without rheumatic disorders.Results: 122 patients were included (n = 61 steroid patients, n = 61 controls). N = 36 were classified as high-dose, n = 25 as low-dose steroid group. Steroid patients showed larger epicardial 5. , p < 0.05, and patients in the low-dose steroid group (p < 0.01, p < 0.001, respectively). Conclusion:The present data suggest increased cardiac fat deposition in steroid-treated patients with rheumatic disorders. Furthermore, this accumulation of cardiac fat seems to be dose-dependent, pointing towards a cumulative effect of steroids.