Performance of native and contrast-enhanced T1 mapping to detect myocardial damage in patients with suspected myocarditis: a head-to-head comparison of different cardiovascular magnetic resonance techniques.

Myocardial T1 mapping is a novel technique that has proven to be superior to standard imaging for differentiation between healthy individuals in acute myocarditis. Aim of this study was comparison of T1 mapping with a clinical biomarker. We retrospectively investigated 171 patients undergoing cardiovascular magnetic resonance (CMR) examination with suspected myocarditis by performing native and contrast enhanced T1-mapping. Additionally, T2w and T1w images and late gadolinium enhancement sequences (LGE) were utilized for myocardial evaluation; Lake Louise Criteria comprise T1w, T2w and LGE imaging in a score. Reference for positive myocarditis diagnosis was a ten-fold increase of troponin level above normal (0.14 ng/ml). Native T1 and extracellular volume (ECV) showed good association with relevant troponin elevations. Area under the curve (AUC) was 81% (p = 0.0001) for native T1 with an optimal threshold of 979 ms and 86% (p < 0.0001) for ECV with an optimal cutoff of 32.4%. AUC for T2w imaging (T2-signal intensity ratio to skeletal muscle) was 77% (p = 0.0003). AUC for T2w imaging (T2-signal intensity compared to remote myocardium) was 69% (p = 0.012). Additionally, we found positive correlation for native T1 and ECV with the Lake Louise Criteria (r = 0.44, p = 0.0001 for native T1 and r = 0.45, p = 0.0001 for ECV). Correlated to troponin as biomarker, ECV and native T1 mapping perform at least equally well in comparison to established CMR-techniques LGE, T2w imaging and the combined Lake Louise Criteria in detecting acute myocardial damage. Normal ECV values rule out myocardial damage with very high certainty. T1 mapping qualifies for further prospective evaluations to evolve as a separate biomarker.

Prognostic value of T1-mapping in TAVR patients: extra-cellular volume as a possible predictor for peri- and post-TAVR adverse events.

The benefit of a transcatheter aortic valve replacement (TAVR) can differ in patients, and therapy bears severe risks. High-degree aortic stenosis can lead to cardiac damage such as diffuse myocardial fibrosis, evaluable by extra-cellular volume (ECV) in CMR. Therefore, fibrosis might be a possible risk factor for unfavorable outcome after TAVR. We sought to assess the prognostic value of T1-mapping and ECV to predict adverse events during and after TAVR. The study population consisted of patients undergoing clinically indicated TAVR by performing additional CMR with native and contrast-enhanced T1-mapping sequences for additional evaluation of ECV. Study endpoints were congestive heart failure (CHF) and TAVR-associated conduction abnormalities defined as new onset of left bundle branch block (LBBB), AV-Block or implantation of a pacemaker. 94 patients were examined and followed. Median follow up time was 187 days (IQR 79-357 days). ECV was increased (>30 %) in 38 patients (40 %). There was no significant correlation between ECV and death, Hazard ratio (HR) 0.847 (95 % CI 0.335; 2.14), p = 0.72. ECV in patients with subsequent CHF was higher than in those without an event (33.5 ± 4.6 and 29.1 ± 4.1 %, respectively), but the difference just did not reach the level of significance HR 2.16 (95 % CI 0.969; 4.84), p = 0.06. Patients with post-TAVR conduction abnormality (LBBB, AV-block or pacemaker implantation) had statistically relevant lower ECV values compared to those without an event. Patients with an event had a mean ECV of 28.1 ± 3.16 %; patients without an event had a mean ECV of 29.8 ± 4.53, HR 0.56 (95 % CI 0.32; 0.96), p = 0.036. In this study, elevated myocardial ECV is a predictor of CHF by trend; CMR may be helpful in identifying patients with a high risk for post-TAVR cardiac decompensation benefitting from an intensified post-interventional surveillance. Patients with post-TAVR conductions abnormalities have a significantly decreased ECV. Nevertheless, it remains unclear which precise molecular tissue alteration is the protective factor or risk factor in this case.