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Diffusion-weighted imaging (DWI) has been confirmed to be associated with late gadolinium enhancement (LGE) in hypertrophic cardiomyopathy (HCM). In this context, we aimed to study whether DWI could reflect the active tissue injury and edema information of HCM which were usually indicated by T2 weighted images. Forty HCM patients were examined using a 3.0 T magnetic resonance scanner. Cine, T2-weighted short tau inversion recovery (T2-STIR), DWI and LGE sequences were acquired. T1 mapping was also included to quantify the focal and diffuse fibrosis. Cardiac troponin I (cTnI) was tested to assess the recently myocardial injury. Student's t-test, Mann-Whitney U test, One-way analysis, Kruskal-Wallis analysis, the Spearman correlation analysis, and multivariable regression were used in this study. The apparent diffusion coefficient (ADC) was significantly elevated in the cTnI positive group (P = 0.01) and correlated with LGE (ρ = 0.312, P = 0.049) and HighT2 extent (ρ = 0.443, P = 0.004) in the global level. In the segmental analysis, the ADC significantly differentiated the segments with and without HighT2/LGE presence (P = 0.00). The average ADC values were higher in segments with HighT2 and LGE coexistence than in those with only LGE presence (P < 0.05). Multivariable regression indicated that segmental HighT2 and LGE were both contributing factors to the ADC values. In this study of HCM, we confirmed that ADC as a molecular diffusion parameter reflects the replacement fibrosis of myocardium. Moreover, it also reveals edema extent and its association with serum cTnI.

Aims: The aim of this study was to investigate the occurrence of myocardial injury and cardiac dysfunction after an endurance race by biomarkers and cardiac magnetic resonance in triathletes with and without myocardial fibrosis., Methods and Results: Thirty asymptomatic male triathletes (45 ± 10 years) with over 10 training hours per week and 55 ± 8 ml/kg per minute maximal oxygen uptake during exercise testing were studied before (baseline) and 2.4 ± 1.1 hours post-race. Baseline cardiac magnetic resonance included cine, T1/T2, late gadolinium enhancement (LGE) and extracellular volume imaging. Post-race non-contrast cardiac magnetic resonance included cine and T1/T2 mapping. Non-ischaemic myocardial fibrosis was present in 10 triathletes (LGE+) whereas 20 had no fibrosis (LGE-). At baseline, LGE + triathletes had higher peak exercise systolic blood pressure with 222 ± 21 mmHg compared to LGE- triathletes (192 ± 30 mmHg, P  < 0.01). Post-race troponin T and creatine kinase MB were similarly increased in both groups, but there was no change in T2 and T1 from baseline to post-race with 54 ± 3 ms versus 53 ± 3 ms ( P  = 0.797) and 989 ± 21 ms versus 989 ± 28 ms ( P  = 0.926), respectively. However, post-race left atrial ejection fraction was significantly lower in LGE + triathletes compared to LGE- triathletes (53 ± 6% vs. 59 ± 6%, P  < 0.05). Furthermore, baseline atrial peak filling rates were lower in LGE -  triathletes (121 ± 30 ml/s/m 2 ) compared to LGE + triathletes (161 ± 34 ml/s/m 2 , P  < 0.01). Post-race atrial peak filling rates increased in LGE- triathletes to 163 ± 46 ml/s/m 2 , P  < 0.001), but not in LGE + triathletes (169 ± 50ml/s/m 2 , P  = 0.747)., Conclusion: Despite post-race troponin T release, we did not find detectable myocardial oedema by cardiac magnetic resonance. However, the unfavourable blood pressure response during exercise testing seemed to be associated with post-race cardiac dysfunction, which could explain the occurrence of myocardial fibrosis in triathletes.

Background: Fast noninvasive identification of ischemic territories at rest (before tissue-specific changes) and assessment of functional status can be valuable in the management of severe coronary artery disease. This study investigated the use of cardiac phase-resolved blood oxygen level-dependent (CP-BOLD) cardiovascular magnetic resonance in detecting myocardial ischemia at rest secondary to severe coronary artery stenosis., Methods and Results: CP-BOLD, standard cine, and T2-weighted images were acquired in canines (n=11) at baseline and within 20 minutes of ischemia induction (severe left anterior descending stenosis) at rest. After 3 hours of ischemia, left anterior descending stenosis was removed, and T2-weighted and late-gadolinium-enhancement images were acquired. From standard cine and CP-BOLD images, end-systolic and end-diastolic myocardium was segmented. Affected and remote sections of the myocardium were identified from postreperfusion late-gadolinium-enhancement images. Systolic-to-diastolic ratio (S/D), quotient of mean end-systolic and end-diastolic signal intensities (on CP-BOLD and standard cine), was computed for affected and remote segments at baseline and ischemia. Ejection fraction and segmental wall thickening were derived from CP-BOLD images at baseline and ischemia. On CP-BOLD images, S/D was >1 (remote and affected territories) at baseline; S/D was diminished only in affected territories during ischemia, and the findings were statistically significant (ANOVA, post hoc P<0.01). The dependence of S/D on ischemia was not observed in standard cine images. Computer simulations confirmed the experimental findings. Receiver-operating characteristic analysis showed that S/D identifies affected regions with performance (area under the curve, 0.87) similar to ejection fraction (area under the curve, 0.89) and segmental wall thickening (area under the curve, 0.75)., Conclusions: Preclinical studies and computer simulations showed that CP-BOLD cardiovascular magnetic resonance could be useful in detecting myocardial ischemia at rest. Patient studies are needed for clinical translation.

In patients with acute myocarditis, viral genome can be detected in plasma and peripheral leukocytes. Its relationship with active myocardial inflammation, however, is not well understood. Myocardial edema as a feature of inflammation and myocardial necrosis or fibrosis can be frequently observed in patients with acute myocarditis by cardiovascular magnetic resonance (CMR). We assessed the association of viral genome presence in peripheral blood samples with myocardial edema and irreversible injury. We examined consecutive patients with clinically suspected myocarditis after an episode of viral illness. State-of-the-art methods were used for detecting myocardial edema and irreversible injury using CMR and viral genome applying reverse transcribed, nested polymerase chain reaction in peripheral blood samples. The specificity of viral amplification products was confirmed by automatic DNA sequencing. Of a total of 55 patients (53.5 ± 15.6 years), 21 were positive for viral genome in peripheral leukocytes. Interestingly, 18 (86%) of these patients also showed global myocardial edema, as compared to only 7/34 (21%) without PCR evidence for viral genome. The overall agreement between CMR criteria for edema and viral PCR was 84%. In contrast, there was no significant relationship of viral genome presence with myocardial necrosis or scars. In patients with clinically suspected myocarditis, myocardial edema but not irreversible myocardial injury is associated with the presence of viral genome in peripheral blood.