Objective To identify patients with type 2 myocardial infarction (MI) and patients with non-ischaemic myocardial injury (NIMI) and to compare their prognosis with those of patients with type 1 MI. Methods A retrospective observational study was performed in 1010 patients admitted to the emergency department of a university hospital with at least one troponin I test between 2012 and 2013. Participants were identified using laboratory records and divided into three groups: type 1 MI (rupture of atheromatous plaque), type 2 MI (imbalance between myocardial oxygen supply and/or demand) and NIMI (patients who did not meet diagnostic criteria for type 1 or type 2 MI). Clinical characteristics and 2-year outcomes were analysed. Results Patients with type 2 MI and NIMI were older, with higher proportion of women and more comorbidities than patients with type 1 MI. Absolute mortality and the adjusted risk for all-cause mortality in both groups were significantly higher than that of patients with type 1 MI (39.7%, HR: 1.41 95% CI 1.02 to 1.94, p=0.038 and 40.0%, HR: 1.54 95% CI 1.16 to 2.04, p=0.002, respectively). Patients with type 2 MI and NIMI tended to present more readmissions due to heart failure (16.5%, HR: 1.55 95% CI 0.87 to 2.76, p=0.133 and 12.3%, HR: 1.15 95% CI 0.70 to 1.90, p=0.580) and less readmission rates due to acute coronary syndrome (ACS) than patients with type 1 MI (2.1%, HR: 0.11 95% CI 0.04 to 0.31, p<0.001 and 4.3%, HR: 0.22 95% CI 0.12 to 0.41, p<0.001), Conclusions Patients diagnosed with type 2 MI and NIMI have higher rates of mortality and lower readmission rates for ACS compared with patients with type 1 MI.

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous disorder developing from multiple aetiologies with overlapping pathophysiological mechanisms. HFpEF diagnosis may be challenging, as neither cardiac imaging nor physical examination are sensitive in this situation. Here, we review biomarkers of HFpEF, of which the best supported are related to myocardial stretch and injury, including natriuretic peptides and cardiac troponins. An overview of biomarkers of inflammation, extracellular matrix derangements and fibrosis, senescence, vascular dysfunction, anaemia/iron deficiency and obesity is also provided. Finally, novel biomarkers from -omics technologies, including plasma metabolites and circulating microRNAs, are outlined briefly. A cardiac-centred approach to HFpEF diagnosis using natriuretic peptides seems reasonable at present in clinical practice. A holistic approach including biomarkers that provide information on the non-cardiac components of the HFpEF syndrome may enrich our understanding of the disease and may be useful in classifying HFpEF phenotypes or endotypes that may guide patient selection in HFpEF trials.

Heart failure (HF) is associated with a high rate of readmissions within 30 days post-discharge and in the following year, especially in frail elderly patients. Biomarker data are scarce in this high-risk population. This study assessed the value of early post-discharge circulating levels of ST2, NT-proBNP, CA125, and hs-TnI for predicting 30-day and 1-year outcomes in comorbid frail elderly patients with HF with mainly preserved ejection fraction (HFpEF). Blood samples were obtained at the first visit shortly after discharge (4.9 ± 2 days). The primary endpoint was the composite of all-cause mortality or HF-related rehospitalization at 30 days and at 1 year. All-cause mortality alone at one year was also a major endpoint. HF-related rehospitalizations alone were secondary end-points. From February 2014 to November 2016, 522 consecutive patients attending the STOP-HF Clinic were included (57.1% women, age 82 ± 8.7 years, mean Barthel index 70 ± 25, mean Charlson comorbidity index 5.6 ± 2.2). The composite endpoint occurred in 8.6% patients at 30 days and in 38.5% at 1 year. In multivariable analysis, ST2 [hazard ratio (HR) 1.53; 95% CI 1.19–1.97; p = 0.001] was the only predictive biomarker at 30 days; at 1 year, both ST2 (HR 1.34; 95% CI 1.15–1.56; p < 0.001) and NT-proBNP (HR 1.19; 95% CI 1.02–1.40; p = 0.03) remained significant. The addition of ST2 and NT-proBNP into a clinical predictive model increased the AUC from 0.70 to 0.75 at 30 days (p = 0.02) and from 0.71 to 0.74 at 1 year (p < 0.05). For all-cause death at 1 year, ST2 (HR 1.50; 95% CI 1.26–1.80; p < 0.001), and CA125 (HR 1.41; 95% CI 1.21–1.63; p < 0.001) remained independent predictors in multivariable analysis. The addition of ST2 and CA125 into a clinical predictive model increased the AUC from 0.74 to 0.78 (p = 0.03). For HF-related hospitalizations, ST2 was the only predictive biomarker in multivariable analyses, both at 30 days and at 1 year. In a comorbid frail elderly population with HFpEF, ST2 outperformed NT-proBNP for predicting the risk of all-cause mortality or HF-related rehospitalization. ST2, a surrogate marker of inflammation and fibrosis, may be a better predictive marker in high-risk HFpEF.

Aims: To investigate the distribution of left atrioventricular coupling index (LACI) among patients with heart failure and left ventricular ejection fraction (LVEF) < 50% and to explore its association with the combined endpoint of all-cause death or HF hospitalization at long-term follow-up. Methods and results: Patients with HF and LVEF < 50% undergoing cardiac magnetic resonance were evaluated. Patients with atrial fibrillation or flutter were excluded. Left atrioventricular coupling index was measured as the ratio between the left atrial (LA) and the LV end-diastolic volumes. Patient population was divided according to LACI tertiles and followed up. Total of 478 patients (mean age 62 ± 12 years, 78% male) were included. The median value of LACI was 27.1% (interquartile range 19.9–34.5). Patients within the worst LACI tertile (≥30.9%) showed smaller LV volumes and larger LA volumes as compared with patients in the first or second tertile (LACI 6.2–22.2 and LACI 22.3–30.9, respectively). Left atrioventricular coupling index was significantly associated with the combined endpoint [hazard ratio (HR) 1.87, P = 0.01]. After adjusting for sex, age, ischaemic HF aetiology, LVEF, LA reservoir strain, diabetes mellitus, LV scar, mitral regurgitation, and LVEDVi, LACI remained significantly associated with the combined endpoint (HR 1.77, P = 0.02). Patients with the highest LACI values had worse outcomes compared with patients in first and second tertiles (HR 1.69, P = 0.02 and HR 1.77, P = 0.02, respectively). Conclusion: In patients with HF and LVEF <50%, LACI is independently associated with adverse events. Patients with most impaired left atrioventricular coupling have the worst clinical outcomes.

Background: Coronary artery disease remains a major cause of death despite better outcomes of ST‐segment–elevation myocardial infarction (STEMI). We aimed to analyze data from the Ruti‐STEMI registry of in‐hospital, 28‐day, and 1‐year events in patients with STEMI over the past 3 decades in Catalonia, Spain, to assess trends in STEMI prognosis. Methods and Results: Between February 1989 and December 2017, a total of 7589 patients with STEMI were admitted consecutively. Patients were grouped into 5 periods: 1989 to 1994 (period 1), 1995 to 1999 (period 2), 2000 to 2004 (period 3), 2005 to 2009 (period 4), and 2010 to 2017 (period 5). We used Cox regression to compare 28‐day and 1‐year STEMI mortality and in‐hospital complication trends across these periods. Mean patient age was 61.6±12.6 years, and 79.3% were men. The 28‐day all‐cause mortality declined from period 1 to period 5 (10.4% versus 6.0%; P <0.001), with a 40% reduction after multivariable adjustment (hazard ratio [HR], 0.6; 95% CI, 0.46–0.80; P <0.001). One‐year all‐cause mortality declined from period 1 to period 5 (11.7% versus 9.0%; P =0.001), with a 24% reduction after multivariable adjustment (HR, 0.76; 95% CI, 0.60–0.98; P =0.036). A significant temporal reduction was observed for in‐hospital complications including postinfarct angina (−78%), ventricular tachycardia (−57%), right ventricular dysfunction (−48%), atrioventricular block (−45%), pericarditis (−63%), and free wall rupture (−53%). Primary ventricular fibrillation showed no significant downslope trend. Conclusions: In‐hospital STEMI complications and 28‐day and 1‐year mortality rates have dropped markedly in the past 30 years. Reducing ischemia‐driven primary ventricular fibrillation remains a major challenge.