The role of cardiac troponins as diagnostic biomarkers of myocardial injury in the context of acute coronary syndrome (ACS) is well established. Since the initial 1st-generation assays, 5th-generation high-sensitivity cardiac troponin (hs-cTn) assays have been developed, and are now widely used. However, its clinical adoption preceded guidelines and even best practice evidence. This review summarizes the history of cardiac biomarkers with particular emphasis on hs-cTn. We aim to provide insights into using hs-cTn as a quantitative marker of cardiomyocyte injury to help in the differential diagnosis of coronary versus non-coronary cardiac diseases. We also review the recent evidence and guidelines of using hs-cTn in suspected ACS.

Word count: 4478words (including figures legends and references)Running title: Prognostic role of CMR and conventional risk factors in MINOCA Abstract: Objective: Assess the prognostic impact of Cardiovascular Magnetic Resonance (CMR) and conventional risk factors in patients with Myocardial infarction with non-obstructed coronaries (MINOCA). Background: MINOCA represents a diagnostic dilemma and the prognostic markers have not been clarified. Methods: 388 consecutive MINOCA patients undergoing CMR assessment were identified retrospectively from registry database and prospectively followed up for a primary clinical endpoint of all-cause mortality. 1.5T CMR was performed using a comprehensive protocol (cines, T2-weighted, and late gadolinium enhancement sequences). Patients were grouped into 4 categories based on their CMR findings: myocardial infarction (MI) (embolic/spontaneous recanalization), myocarditis, cardiomyopathy and normal CMR. Results: CMR(performed at a median of 37days from presentation) was able to identify the cause for the troponin rise in 74% of the patients (25% myocarditis, 25% MI and 25% cardiomyopathy), whilst a normal CMR was identified in 26%. Over a median follow-up of 1262days(3.5years), 5.7% patients died. Cardiomyopathy group had the worst prognosis (mortality 15%, log rank 19.9 p<0.001), MI had 4% mortality, and 2% in both myocarditis and normal CMR. In a multivariable cox regression model (including clinical and CMR parameters), CMR diagnosis of cardiomyopathy and ST-segment elevation on presentation ECG remained the only 2 significant predictors of mortality. Using presentation with ECG ST-elevation and CMR diagnosis of cardiomyopathy as risk markers, the mortality risk rates were 2%, 11% and 21% for presence of 0, 1 and 2 factor respectively(p<0.0001). Conclusion: In a large cohort of MINOCA, CMR(median 37days from presentation) identified a final diagnosis in 74% of patients. Cardiomyopathy had the highest mortality, followed by MI. The strongest predictors of mortality were a CMR diagnosis of cardiomyopathy and ST-elevation on presentation ECG.

ObjectiveMyocardial intracellular/extracellular structure and aortic function were assessed among hypertensive left ventricular (LV) phenotypes using cardiovascular magnetic resonance (CMR).MethodsAn observational study from consecutive tertiary hypertension clinic patients referred for CMR (1.5 T) was performed. Four LV phenotypes were defined: (1) normal with normal indexed LV mass (LVM) and LVM to volume ratio (M/V), (2) concentric remodelling with normal LVM but elevated M/V, (3) concentric LV hypertrophy (LVH) with elevated LVM but normal indexed end-diastolic volume (EDV) or (4) eccentric LVH with elevated LVM and EDV. Extracellular volume fraction was measured using T1-mapping. Circumferential strain was calculated by voxel-tracking. Aortic distensibility was derived from high-resolution aortic cines and contemporaneous blood pressure measurements.Results88 hypertensive patients (49±14 years, 57% men, systolic blood pressure (SBP): 167±30 mm Hg, diastolic blood pressure (DBP): 96±14 mm Hg) were compared with 29 age-matched/sex-matched controls (47±14 years, 59% men, SBP: 128±12 mm Hg, DBP: 79±10 mm Hg). LVH resulted from increased myocardial cell volume (eccentric LVH: 78±19 mL/m2 vs concentric LVH: 73±15 mL/m2 vs concentric remodelling: 55±9 mL/m2, p<0.05, respectively) and interstitial fibrosis (eccentric LVH: 33±10 mL/m2 vs concentric LVH: 30±10 mL/m2 vs concentricremodelling: 19±2 mL/m2, p<0.05, respectively). LVH had worst circumferential impairment (eccentric LVH: −12.8±4.6% vs concentric LVH: −15.5±3.1% vs concentric remodelling: –17.1±3.2%, p<0.05, respectively). Concentric remodelling was associated with reduced aortic distensibility, but not with large intracellular/interstitial expansion or myocardial dysfunction versus controls.ConclusionsMyocardial interstitial fibrosis varies across hypertensive LV phenotypes with functional consequences. Eccentric LVH has the most fibrosis and systolic impairment. Concentric remodelling is only associated with abnormal aortic function. Understanding these differences may help tailor future antihypertensive treatments.