To investigate the prognostic impact of left-ventricular (LV) cardiac magnetic resonance (CMR) deformation imaging in patients with non-ischaemic dilated cardiomyopathy (DCM) compared with late-gadolinium enhancement (LGE) quantification and LV ejection fraction (EF). A total of 210 subjects with DCM were examined prospectively with standard CMR including measurement of LGE for quantification of myocardial fibrosis and feature tracking strain imaging for assessment of LV deformation. The predefined primary endpoint, a combination of cardiac death, heart transplantation, and aborted sudden cardiac death, occurred in 26 subjects during the median follow-up period of 5.3 years. LV radial, circumferential, and longitudinal strains were significantly associated with outcome. Using separate multivariate analysis models, global longitudinal strain (average of peak negative strain values) and mean longitudinal strain (negative peak of the mean curve of all segments) were independent prognostic parameters surpassing the value of global and mean LV radial and circumferential strain, as well as NT-proBNP, EF, and LGE mass. A global longitudinal strain greater than −12.5% predicted outcome even in patients with EF < 35% (P < 0.01) and in those with presence of LGE (P < 0.001). Mean longitudinal strain was further investigated using a clinical model with predefined cut-offs (EF < 35%, presence of LGE, NYHA class, mean longitudinal strain greater than −10%). Mean longitudinal strain exhibited an independent prognostic value surpassing that provided by NYHA, EF, and LGE (HR = 5.4, P < 0.01). LV longitudinal strain assessed with CMR is an independent predictor of survival in DCM and offers incremental information for risk stratification beyond clinical parameters, biomarker, and standard CMR.

Objective To understand the determinants of troponin release in patients with stable coronary artery disease (CAD) by comparing high sensitive troponin T (hsTnT) levels with computed tomography angiography (CTA) characteristics of atherosclerotic plaque. Methods hsTnT was determined in 124 consecutive patients with stable angina, who underwent clinically indicated 256-slice CTA for suspected CAD. CTA was used to assess (1) coronary calcification; (2) stenosis severity; (3) non-calcified plaque volume; (4) plaque composition (soft or mixed, described as ‘non-calcified’ versus calcified) and (5) the presence of vascular remodeling in areas of non-calcified plaque. Results All CT scans were performed without adverse events, and diagnostic image quality was achieved in 1830/1848 available coronary segments (99.0%). In 29/124 patients, hsTnT was ≥14 pg/ml (range 14.0–34.4). Weak, albeit significant, correlations were found between hsTnT and calcium scoring (r=0.45, p<0.001), while a stronger correlation was found between hsTnT and the total non-calcified plaque burden (r=0.79, p<0.001). Patients with non-calcified plaque (n=44) yielded significantly higher hsTnT values than those with normal vessels (n=46) or those with only calcified lesions (n=26), (12.6±5.2 vs 8.3±2.6 and 8.8±3.0 pg/ml, respectively, p<0.001). Furthermore, those with remodeled non-calcified plaque (n=8) showed even higher hsTnT values of 26.3±6.5 pg/ml than all other groups (p<0.001). This allowed the identification of patients with remodeled non-calcified plaque by hsTnT with high accuracy (area under the curve=0.90, SE=0.07, 95% CI 0.84 to 0.95). Conclusions Chronic clinically silent rupture of non-calcified plaque with subsequent microembolisation may be a potential source of troponin elevation. In light of recent imaging studies, in which patients with positively remodeled non-calcified plaque were shown to be at high risk for developing acute coronary syndromes, hsTnT may serve as a biomarker for such ‘vulnerable’ coronary lesions even in presumably stable CAD.

Purpose: To study myocardial perfusion reserve and myocellular metabolic alterations indicated by triglyceride content as possible causes of diastolic dysfunction in patients with type 2 diabetes mellitus, preserved systolic function, and without clinically evident coronary artery disease.Materials and Methods: Patients with type 2 diabetes mellitus (n = 42) underwent cardiac magnetic resonance (CMR) for quantification of 1) myocardial contractility by strain‐encoded MR (SENC); 2) myocardial triglyceride content by proton magnetic resonance spectroscopy (¹H‐MRS); and 3) myocardial perfusion reserve during pharmacologic hyperemia. Age‐matched healthy volunteers (n = 16) also underwent CMR to acquire normal values for myocardial strain and perfusion reserve.Results: Stress CMR procedures were successfully performed in all subjects, and no regional inducible perfusion defects were observed in type 2 diabetes mellitus patients. Diastolic strain rate and myocardial perfusion reserve were significantly impaired in patients with type 2 diabetes mellitus compared to control subjects (P < 0.001 for both). Interestingly, impaired diastolic function in type 2 diabetes mellitus was not associated with impaired myocardial perfusion reserve (r = 0.12, P = NS). Conversely a significant association was observed between diastolic dysfunction and myocardial triglyceride content (r = −0.71, P < 0.001), which proved to be independent of age, gender, diabetes duration, blood pressure, and fasting blood glucose.Conclusion: Myocardial steatosis may represent an early marker of diabetic heart disease, triggering subclinical myocardial dysfunction irrespective of myocardial perfusion reserve. J. Magn. Reson. Imaging 2012;35:804–811.

Background: Our goal was to evaluate the ability of cardiovascular magnetic resonance for detecting and predicting cardiac dysfunction in patients receiving cancer therapy. Left ventricular ejection fraction, global and regional strain utilizing fast-strain-encoded, T1 and T2 mapping, and cardiac biomarkers (troponin and BNP [brain natriuretic peptide]) were analyzed. Methods: Sixty-one patients (47 with breast cancer, 11 with non-Hodgkin lymphoma, and 3 with Hodgkin lymphoma) underwent cardiovascular magnetic resonance scans at baseline and at regular intervals during 2 years of follow-up. The percentage of all left ventricular myocardial segments with strain ≤−17% (normal myocardium [%]) was analyzed. Clinical cardiotoxicity (CTX) and sub-CTX were defined according to standard measures. Results: Nine (15%) patients developed CTX, 26 (43%) had sub-CTX. Of the 35 patients with CTX or sub-CTX, 24 (69%) were treated with cardioprotective medications and showed recovery of cardiac function. The amount of normal myocardium (%) exhibited markedly higher accuracy for the detection of CTX and sub-CTX compared with left ventricular ejection fraction, T1, and T2 mapping as well as troponin I (Δareas under the curve=0.20, 0.24, and 0.46 for normal myocardium (%) versus left ventricular ejection fraction, troponin I, and T1 mapping, P <0.001 for all). In addition, normal myocardium (%) at baseline accurately identified patients with subsequent CTX ( P <0.001), which was not achieved by any other markers. Conclusions: Normal myocardium (%) derived by fast-strain-encoded cardiovascular magnetic resonance, is an accurate and sensitive tool that can establish cardiac safety in patients with cancer undergoing cardiotoxic chemotherapy not only for the early detection but also for the prediction of those at risk of developing CTX. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03543228.