BackgroundCardiac magnetic resonance (CMR) can detect inflammatory myocardial alterations in patients suspected of having acute myocarditis. There is limited information regarding the degree of normalization of CMR parameters during the course of the disease and the time window during which quantitative CMR should be most reasonably implemented for diagnostic work‐up.Methods and ResultsTwenty‐four patients with suspected acute myocarditis and 45 control subjects underwent CMR. Initial CMR was performed 2.6±1.9 days after admission. Myocarditis patients underwent CMR follow‐up after 2.4±0.6, 5.5±1.3, and 16.2±9.9 weeks. The CMR protocol included assessment of standard Lake Louise criteria, T1 relaxation times, extracellular volume fraction, and T2 relaxation times. Group differences between myocarditis patients and control subjects were highest in the acute stage of the disease (P<0.001 for all parameters). There was a significant and consistent decrease in all inflammatory CMR parameters over the course of the disease (P<0.01 for all parameters). Myocardial T1 and T2 relaxation times—indicative of myocardial edema—were the only single parameters showing significant differences between myocarditis patients and control subjects on 5.5±1.3‐week follow‐up (T1: 986.5±44.4 ms versus 965.1±28.1 ms, P=0.022; T2: 55.5±3.2 ms versus 52.6±2.6 ms; P=0.001).ConclusionsIn patients with acute myocarditis, CMR markers of myocardial inflammation demonstrated a rapid and continuous decrease over several follow‐up examinations. CMR diagnosis of myocarditis should therefore be attempted at an early stage of the disease. Myocardial T1 and T2 relaxation times were the only parameters of active inflammation/edema that could discriminate between myocarditis patients and control subjects even at a convalescent stage of the disease.

• Myocardial strain measures are considerably reduced in patients with suspected myocarditis. • Myocardial strain measures can sufficiently discriminate between diseased and healthy patients. • Myocardial strain measures show basic associations with the extent of myocardial oedema/inflammation.

Diagnosis of cardiac sarcoidosis is often challenging. Whereas cardiac magnetic resonance imaging (CMR) and positron emission tomography/computed tomography (PET/CT) with 18F-fluorodeoxyglucose (FDG) are most commonly used to evaluate patients, PET/CT using radiolabeled somatostatin receptor (SSTR) ligands for visualization of inflammation might represent a more specific alternative. This study aimed to investigate the feasibility of SSTR–PET/CT for detecting cardiac sarcoidosis in comparison to CMR.15 patients (6 males, 9 females) with sarcoidosis and suspicion on cardiac involvement underwent SSTR-PET/CT imaging and CMR. Images were visually scored. The AHA 17-segment model of the left myocardium was used for localization and comparison of inflamed myocardium for both imaging modalities. In semi-quantitative analysis, mean (SUVmean) and maximum standardized uptake values (SUVmax) of affected myocardium were calculated and compared with both remote myocardium and left ventricular (LV) cavity.SSTR-PET was positive in 7/15, CMR in 10/15 patients. Of the 3 CMR+/PET− subjects, one patient with minor involvement (<25% of wall thickness in CMR) was missed by PET. The remaining two CMR+/PET− patients displayed no adverse cardiac events during follow-up.In the 17-segment model, PET/CT yielded 27 and CMR 29 positive segments. Overall concordance of the 2 modalities was 96.1% (245/255 segments analyzed). SUVmean and SUVmax in inflamed areas were 2.0±1.2 and 2.6±1.2, respectively. The lesion-to-remote myocardium and lesion-to-LV cavity ratios were 1.8±0.2 and 1.9±0.2 for SUVmean and 2.0±0.3 and 1.7±0.3 for SUVmax, respectively.Detection of cardiac sarcoidosis by SSTR-PET/CT is feasible. Our data warrant further analysis in larger prospective series.

Background The phenomenon of exercise‐induced hypoalgesia and concomitant mood changes is well‐established. How exercise‐induced hypoalgesia and affective responses are shaped by the intensity of an acute exercise bout and individual fitness levels is as yet not well‐understood. This study investigates whether heat pain threshold (PTh), pain tolerance (PTol) and affective parameters are modulated by the intensity of an acute exercise bout and/or individuals’ fitness level. Stronger analgesic responses are hypothesized after high‐intensity exercise in physically fitter subjects, possibly in sync with concomitant mood changes. Methods Thirty‐three healthy men were recruited (sedentary: N = 17 or recreational: N = 14; mean age: 25.3 ± 4.4 years). After a fitness assessment on a cycle ergometer, subjects underwent three experimental conditions on separate days: high (20 min exercise 20% above lactate threshold), low (20 min exercise 20% below lactate threshold) and control (seated rest). Before and after each intervention Positive and Negative Affect Schedule, PTh and PTol (cold water emersion test) were assessed. Results Results indicate an increase of the Positive Affect Scale (high: 26.7 ± 9.0 vs. 32.9 ± 7.1, p < .001; low: 26.3 ± 7.2 vs. 32.0 ± 7.0, p < .001) and PTh (high: 45.1 ± 3.1°C vs. 46.0 ± 2.6°C, p = .003; low: 45.4 ± 2.7°C vs. 45.9 ± 2.6°C, p = .012) after both exercise conditions. In an exploratory analysis, PTol significantly increased only after the high exercise condition (51.2 ± 33.7 s vs. 72.4 ± 64.0 s, p = .045). Fitness level was positively correlated with the increase in PTol from pre to post high‐intensity exercise (r = .59, p (one‐tailed) = .002). Conclusion Exercise‐induced hypoalgesia depends on exercise intensity and appears to be influenced by individual fitness status, independent of mood responses. Significance Antinociceptive effects can be elicited by physical exercise and have been extensively investigated in the literature. However, the relation between exercise intensity, fitness status, and the degree of antinociception is not well‐understood. This randomized intervention provides novel evidence that antinociceptive effects indeed depend on exercise intensity, but also on general fitness status. Data extend the existing literature by highlighting aspects of exercise behaviour that promote antinociception. Effects do not simply mirror positive affective responses induced by exercise, hence, indicating partially distinct underlying mechanisms.

Background Cardiac magnetic resonance (CMR) may detect early signs of cardiomyopathy. Purpose The purpose of this CMR study was to evaluate epicardial fat volume (EFV), T1-relaxation times (T1), and left ventricular (LV) strain in non-obese (<30 kg/m2) and obese (>30 kg/m2) individuals with no other cardiovascular risk factor and with a normal LV ejection fraction (LVEF) to detect early changes of obesity cardiomyopathy. Material and Methods Seventy-five individuals (38 men) without additional cardiovascular risk factors were examined at 1.5 T. EFV was assessed by a 3D-Dixon sequence. A 3(3)3(3)5 MOLLI scheme was used to assess T1 (ms). Myocardial strain (%) was evaluated by longitudinal (LS) and circumferential strain (CS) analysis. Results Obese individuals (n = 34; age = 55.6 ± 13.8 years; BMI = 33.4 ± 2.9 kg/m2) had higher EFVs (70.2 ± 27.9 vs. 56.1 ± 25.2 mL/m2; P < 0.05) and T1 values (991.0 ± 38.6 vs. 974.6 ± 32.0; P = 0.061) as well as worse LS and CS values (LS = −21.0 ± 4.8 vs. −23.2 ± 3.7; CS = −23.8 ± 5.7 vs. −27.7 ± 4.2; P < 0.05, for all) compared to non-obese individuals (n = 41; age = 57.2 ± 15.5 years; BMI = 25.1 ± 2.3 kg/m2). Individuals with severe obesity (BMI > 35 kg/m2) had a significantly higher T1 compared to non-obese (1010.5 ± 39.9 vs. 974.6 ± 32.0 ms; P < 0.05). There were no significant differences regarding age or gender. Conclusion Obesity is associated with an increased EFV and a disturbed LV contractility despite a normal LVEF. Myocardial fibrosis as well as metabolic and inflammatory mechanisms of increased epicardial fat may play role. Multi-parametric CMR may be a valuable tool for the detection of such early signs of an obesity cardiomyopathy.