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Background Right ventricular-pulmonary circulation coupling (RVPAC), which can be measured by the relation between tricuspid annular plane systolic excursion (TAPSE) and systolic pulmonary artery pressure (SPAP) by echocardiography, has been postulated as an independent prognostic factor of hospitalizations and mortality in heart failure (HF) patients. Purpose Our aim was to know the predictors of RVPAC improvement in a chronic HF cohort. Methods Retrospective analysis of a prospectively studied cohort of HF outpatients of different aetiologies attended in a multidisciplinary HF Unit. Prospectively scheduled echo-Doppler studies were performed at first visit and 1 year. A TAPSE/SPAP ratio Results From August 2001 to July 2017, 554 patients with TAPSE and SPAP data in the initial visit were included. Mean follow-up time was 4.6±3.7 years. At first visit 252 (45.5%) patients had RVPAC Conclusions Atrial fibrillation/flutter, increasing SPAP and female gender hamper RVPAC improvement at 1 year in HF patients with baseline TAPSE/SPAP ratio Funding Acknowledgement Type of funding sources: None. Multivariate regression analysis

Rationale The use of sodium-glucose co-transporter 2 inhibitors (SGLT2i) to treat heart failure with preserved ejection fraction (HFpEF) is under investigation in ongoing clinical trials, but the exact mechanism of action is unclear. Here we aimed to use artificial intelligence (AI) to characterize the mechanism of action of empagliflozin in HFpEF at the molecular level. Methods We retrieved information regarding HFpEF pathophysiological motifs and differentially expressed genes/proteins, together with empagliflozin target information and bioflags, from specialized publicly available databases. Artificial neural networks and deep learning AI were used to model the molecular effects of empagliflozin in HFpEF. Results The model predicted that empagliflozin could reverse 59% of the protein alterations found in HFpEF. The effects of empagliflozin in HFpEF appeared to be predominantly mediated by inhibition of NHE1 (Na+/H+ exchanger 1), with SGLT2 playing a less prominent role. The elucidated molecular mechanism of action had an accuracy of 94%. Empagliflozin's pharmacological action mainly affected cardiomyocyte oxidative stress modulation, and greatly influenced cardiomyocyte stiffness, myocardial extracellular matrix remodelling, heart concentric hypertrophy, and systemic inflammation. Validation of these in silico data was performed in vivo in patients with HFpEF by measuring the declining plasma concentrations of NOS2, the NLPR3 inflammasome, and TGF-β1 during 12 months of empagliflozin treatment. Conclusion Using AI modelling, we identified that the main effect of empagliflozin in HFpEF treatment is exerted via NHE1 and is focused on cardiomyocyte oxidative stress modulation. These results support the potential use of empagliflozin in HFpEF. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Instituto de Salud Carlos IIICentro de investigaciόn biomédica en red cardiovascular (CIBERCV) Summary figureTable 1

Altres ajuts: acords transformatius de la UAB Aims: Several heart failure (HF) web-based risk scores are currently used in clinical practice. Currently, we lack head-to-head comparison of the accuracy of risk scores. This study aimed to assess correlation and mortality prediction performance of Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC-HF) risk score, which includes clinical variables + medications; Seattle Heart Failure Model (SHFM), which includes clinical variables + treatments + analytes; PARADIGM Risk of Events and Death in the Contemporary Treatment of Heart Failure (PREDICT-HF) and Barcelona Bio-Heart Failure (BCN-Bio-HF) risk calculator, which also include biomarkers, like N-terminal pro B-type natriuretic peptide (NT-proBNP). Methods and results: A total of 1166 consecutive patients with HF from different aetiologies that had NT-proBNP measurement at first visit were included. Discrimination for all-cause mortality was compared by Harrell's C-statistic from 1 to 5 years, when possible. Calibration was assessed by calibration plots and Hosmer-Lemeshow test and global performance by Nagelkerke's R. Correlation between scores was assessed by Spearman rank test. Correlation between the scores was relatively poor (rho value from 0.66 to 0.79). Discrimination analyses showed better results for 1-year mortality than for longer follow-up (SHFM 0.817, MAGGIC-HF 0.801, PREDICT-HF 0.799, BCN-Bio-HF 0.830). MAGGIC-HF showed the best calibration, BCN-Bio-HF overestimated risk while SHFM and PREDICT-HF underestimated it. BCN-Bio-HF provided the best discrimination and overall performance at every time-point. Conclusions: None of the contemporary risk scores examined showed a clear superiority over the rest. BCN-Bio-HF calculator provided the best discrimination and overall performance with overestimation of risk. MAGGIC-HF showed the best calibration, and SHFM and PREDICT-HF tended to underestimate risk. Regular updating and recalibration of online web calculators seems necessary to improve their accuracy as HF management evolves at unprecedented pace.

Sudden cardiac death (SCD) is one of the main modes of death in heart failure (HF) patients and its prediction remains a real challenge. Our aim was to assess the incidence of SCD at 5 years HF contemporary managed outpatients, and to find a simple prediction model for SCD.SCD was considered any unexpected death, witnessed or not, occurring in a previously stable patient with no evidence of worsening HF or any other cause of death. A competing risk strategy was adopted using the Fine-Gray method of Cox regressions analyses that considered other causes of death as the competing event.The derivation cohort included 744 consecutive outpatients (72% men, age 67.9 ± 12.2 years, left ventricular ejection fraction [LVEF] 36% ± 14). During follow-up, 312 deaths occurred, 40 SCDs (5.4%). Age, haemoglobin, eGFR, HF duration, high-sensitivity troponin T, NTproBNP, and ST2 were associated with SCD in univariate analyses; HF duration (p = 0.006), eGFR (p 0.001), LVEF45% (p = 0.03), and ST2 (p = 0.006) remained in multivariable analysis. A predictive score (ST2-SCD) including dichotomous variables (ST2 45, LVEF45%, HF duration3 years, eGFR 55, age ≥ 60 years and male sex) provided a Harrell's C-statistic of 0.82 (0.76-0.89)), reaching 0.87 (0.80-0.95) in the validation cohort (n = 149).In contemporary managed HF, SCD occurred in 5.4% of outpatients, accounting for 12.8% of all deaths at 5 years. Of the 3 studied biomarkers, only ST2 remained independently associated with SCD. A model containing age, sex, ST2, eGFR, LVEF, and HF duration reasonably predicted 5-years risk of SCD.

BACKGROUND This study aimed to examine the prevalence of atrial tricuspid regurgitation (ATR) and atrial mitral regurgitation (AMR) in the setting of atrial fibrillation (AFib) and identify variables related to the severity of both types of regurgitation. METHODS Cross-sectional study evaluating data from transthoracic echocardiograms performed during 2019. We included patients with AFib during the examination, and without primary valve disease or other significant heart disease. RESULTS Four-hundred and thirty-two patients fulfilled the inclusion criteria (mean age 77.5±9.2 years, 49.1% women). We observed significant ATR in 14.8%, and significant AMR in 1.4% of patients. ATR and AMR severities were equal in 49.3% of patients, and 41% displayed greater ATR severity. ATR prevalence was significantly greater among women (23.1% vs 6.8%, p

The use of sodium-glucose co-transporter 2 inhibitors to treat heart failure with preserved ejection fraction (HFpEF) is under investigation in ongoing clinical trials, but the exact mechanism of action is unclear. Here we aimed to use artificial intelligence (AI) to characterize the mechanism of action of empagliflozin in HFpEF at the molecular level. We retrieved information regarding HFpEF pathophysiological motifs and differentially expressed genes/proteins, together with empagliflozin target information and bioflags, from specialized publicly available databases. Artificial neural networks and deep learning AI were used to model the molecular effects of empagliflozin in HFpEF. The model predicted that empagliflozin could reverse 59% of the protein alterations found in HFpEF. The effects of empagliflozin in HFpEF appeared to be predominantly mediated by inhibition of NHE1 (Na+/H+ exchanger 1), with SGLT2 playing a less prominent role. The elucidated molecular mechanism of action had an accuracy of 94%. Empagliflozin's pharmacological action mainly affected cardiomyocyte oxidative stress modulation, and greatly influenced cardiomyocyte stiffness, myocardial extracellular matrix remodelling, heart concentric hypertrophy, and systemic inflammation. Validation of these in silico data was performed in vivo in patients with HFpEF by measuring the declining plasma concentrations of NOS2, the NLPR3 inflammasome, and TGF-beta1 during 12months of empagliflozin treatment. Using AI modelling, we identified that the main effect of empagliflozin in HFpEF treatment is exerted via NHE1 and is focused on cardiomyocyte oxidative stress modulation. These results support the potential use of empagliflozin in HFpEF.

BackgroundCirculating Neprilysin (sNEP) has emerged as a potential prognostic biomarker in heart failure (HF). In PARAGON-HF benefit of sacubitril/valsartan was only observed in patients with left ventricular ejection fraction (LVEF) ≤57%. We aimed to assess the prognostic value of sNEP in outpatients with HF and LVEF >57%, in comparison with patients with LVEF ≤57%.MethodsConsecutive HF outpatients were included from May-2006 to February-2016. The primary endpoint was the composite of all-cause death or HF hospitalization and the main secondary endpoint was the composite of cardiovascular death or HF hospitalization. For the later competing risk methods were used.ResultssNEP was measured in 1428 patients (age 67.7±12.7, 70.3% men, LVEF 35.8% ±14), 144 of which had a LVEF >57%. sNEP levels did not significantly differ between LVEF groups (p = 0.31). During a mean follow-up of 6±3.9 years, the primary endpoint occurred in 979 patients and the secondary composite endpoint in 714 (in 111 and 84 of the 144 patients with LVEF >57%, respectively). sNEP was significantly associated with both composite endpoints. Age- and sex- adjusted Cox regression analyses showed higher hazard ratios for sNEP in patients with LVEF >57%, both for the primary (HR 1.37 [1.16–1.61] vs. 1.04 [0.97–1.11]) and the secondary (HR 1.38 [1.21–1.55] vs. 1.11 [1.04–1.18]) composite endpoints.ConclusionssNEP prognostic value in patients with HF and LVEF >57% outperforms that observed in patients with lower LVEF. Precision medicine using sNEP may identify HF patients with preserved LVEF that may benefit from treatment with sacubitril/valsartan.

Inflammation plays an important role in atherosclerosis. Acute coronary syndromes (ACS), and particularly myocardial infarction (MI), are associated with a systemic inflammatory response that may accelerate coronary atherosclerotic processes, leading to plaque destabilization and increased risk of further cardiovascular events. These considerations provide a conceptual framework for the use of anti-inflammatory therapies in patients with chronic coronary syndrome or ACS. Following the diverging results of trials on canakinumab and methotrexate, the Colchicine Cardiovascular Outcomes Trial (COLCOT) and the Low-Dose Colchicine trial-2 (LoDoCo2) have sparked new interest in the perspective of an anti-inflammatory therapy for CAD by showing that colchicine confers a prognostic benefit in patients with a recent MI or CCS, respectively. Colchicine blocks multiple steps of the inflammatory cascade and modulates also platelet function and endothelial activation. It has a better safety profile than canakinumab and is a very inexpensive drug throughout the world. We deemed it useful to reappraise the available literature on colchicine and coronary artery disease to assess the likelihood that it might become part of the therapeutic armamentarium of this condition.

Evidence regarding any association of HDL-particle (HDL-P) derangements and HDL-cholesterol content with cardiovascular (CV) death in chronic heart failure (HF) is lacking. To investigate the prognostic value of HDL-P size (HDL-Sz) and the number of cholesterol molecules per HDL-P for CV death in HF patients. Outpatient chronic HF patients were enrolled. Baseline HDL-P number, subfractions and HDL-Sz were measured using 1H-NMR spectroscopy. The HDL-C/P ratio was calculated as HDL-cholesterol over HDL-P. Endpoint was CV death, with non-CV death as the competing event. 422 patients were included and followed-up during a median of 4.1 (0–8) years. CV death occurred in 120 (30.5%) patients. Mean HDL-Sz was higher in CV dead as compared with survivors (8.39 nm vs. 8.31 nm, p

Background: Sutureless-surgical aortic valve replacement (SU-SAVR) has been proposed as a surgical alternative for treating aortic stenosis, which facilitates a minimally invasive approach. While some studies have compared the early outcomes of SU-SAVR versus transcatheter aortic valve replacement (TAVR), most data were obtained in high-risk patients and/or limited to in-hospital outcomes. This study aimed to compare in-hospital and midterm clinical outcomes following SU-SAVR and TAVR in low-risk patients with aortic stenosis. Methods: A total of 806 consecutive low-risk (EuroSCORE II Results: Baseline characteristics were well balanced between groups, with a median EuroSCORE II of 1.9% (1.3%–2.5%) in both SU-SAVR and TAVR groups ( P =0.85). There were no statistically significant differences regarding in-hospital mortality (SU-SAVR: 4.1%, TAVR: 1.8%, P =0.199) and stroke (SU-SAVR: 2.3%, TAVR: 2.9%, P =0.736), but SU-SAVR recipients exhibited higher rates of bleeding and new-onset atrial fibrillation, higher residual transvalvular gradients ( P P =0.011). After a median follow-up of 2 (1–3) years, there were no differences between groups in all-cause mortality (hazard ratio, 0.97 [95% CI, 0.52–1.82], P =0.936) and stroke (hazard ratio, 0.83 [95% CI, 0.32–2.15], P =0.708), but SU-SAVR was associated with a higher risk of heart failure hospitalization (hazard ratio, 5.38 [95% CI, 1.88–15.38], P =0.002). Conclusions: In low-risk patients with aortic stenosis, TAVR was associated with improved in-hospital outcomes (except for conduction disturbances) and valve hemodynamics, compared with SU-SAVR. Although similar mortality and stroke rates were observed at 2-year follow-up, the risk of heart failure hospitalization was higher among SU-SAVR patients. These results may contribute to reinforce TAVR over SU-SAVR for the majority of such patients. Graphic Abstract: A graphic abstract is available for this article.

To assess mortality trends at 1 and 3 years from 2001 to 2018 in a real-life cohort of HF outpatients from different etiologies with depressed and preserved LVEF. A total of 2368 consecutive patients with HF (mean age 66.4 ± 12.9 years, 71% men, 15.4% with preserved LVEF) admitted to a HF clinic from August 2001 to September 2018 were included in the study. Patients were divided into five quintiles (Q) according to the period of admission. Trends for all-cause and cardiovascular mortality from Q1 to Q5 were assessed by linear regression. Patients with LVEF

Background Anthracycline-based cancer chemotherapy (ACC) has been related to myocardial interstitial fibrosis (MIF), a lesion contributing to left ventricular dysfunction (LVD). We investigated whether biomarker-assessed MIF was associated with LVD in patients with breast cancer receiving ACC and in patients with ACC-induced heart failure (ACC-HF). Moreover, chemotherapy agent’s pro-fibrotic activity was evaluated in human cardiac fibroblasts (HCFs). Methods Echocardiography, serum biomarkers of collagen deposition (procollagen type-I C-terminal-propeptide [PICP]) and crosslinking (collagen type-I C-terminal-telopeptide/matrix metalloproteinase-1 ratio), and biomarkers of myocardial and vascular stress (galectin-3, sST2, amino-terminal pro-brain natriuretic peptide [NT-proBNP], hs-troponin-T and vascular cell adhesion molecule-1 [VCAM-1]) were assessed in 70 breast cancer patients at baseline, and during ACC at 3 and 6 months. Subclinical cardiotoxicity was defined as a global longitudinal strain (GLS) relative reduction>15%. In addition, PICP and NT-proBNP were determined in 347 patients with different HF etiologies, 37 with ACC-HF of whom 33 had 12-month-follow-up LVEF assessment. HCF activation was examined after incubation with chemotherapy agents for 24 hours. Results In breast cancer patients, six-months-ACC reduced GLS and upregulated PICP, hs-troponin-T, NT-proBNP and VCAM-1 (PP for interactionPrd tertile) but improved in the remaining patients (PConclusion These results indicate that increased levels of PICP, a biomarker related to MIF, are associated with early LVD in ACC-treated patients with breast cancer and with established LVD in ACC-HF patients, hindering LV functional improvement after 12 months. Chemotherapy can directly activate collagen metabolism and increase PICP extracellular presence in HCFs. Therefore, PICP emerges as a promising biomarker of ACC-induced cardiotoxicity.

Background Anthracycline-based cancer chemotherapy (ACC) has been related to myocardial interstitial fibrosis (MIF), a lesion contributing to left ventricular dysfunction (LVD). We investigated whether biomarker-assessed MIF was associated with LVD in patients with breast cancer receiving ACC and in patients with ACC-induced heart failure (ACC-HF). Moreover, chemotherapy agent’s pro-fibrotic activity was evaluated in human cardiac fibroblasts (HCFs). Methods Echocardiography, serum biomarkers of collagen deposition (procollagen type-I C-terminal-propeptide [PICP]) and crosslinking (collagen type-I C-terminal-telopeptide/matrix metalloproteinase-1 ratio), and biomarkers of myocardial and vascular stress (galectin-3, sST2, amino-terminal pro-brain natriuretic peptide [NT-proBNP], hs-troponin-T and vascular cell adhesion molecule-1 [VCAM-1]) were assessed in 70 breast cancer patients at baseline, and during ACC at 3 and 6 months. Subclinical cardiotoxicity was defined as global longitudinal strain (GLS) relative reduction>15%. In addition, PICP and NT-proBNP were determined in 347 patients with different HF etiologies, 37 with ACC-HF (of whom 65% had been diagnosed with breast cancer) and 12-month-follow-up LVEF assessment. HCFs activation was examined after incubation with doxorubicin, cyclophosphamide, paclitaxel and trastuzumab for 24 hours. Results In patients with breast cancer, six-months-ACC reduced GLS and upregulated PICP, hs-troponin-T, NT-proBNP and VCAM-1 (PP for interactionPrd tertile) but improved in the remaining patients (PConclusion These results indicate that biomarker-assessed MIF associates with early LVD in ACC-treated patients with breast cancer. In addition, these findings suggest that MIF may be associated with established LVD in ACC-HF patients, hindering LV functional improvement after 12 months. Finally, chemotherapy can directly activate collagen metabolism in HCFs.

Background Growth differentiation factor 15 (GDF-15) in ST-elevation myocardial infarction (STEMI) is prognostic in first-generation radioimmunoassays. We examined GDF-15 temporal dynamics in STEMI and its predictive value using a first fully automated GDF-15 electrochemiluminescence assay. Methods In this prospective study, circulating GDF-15 concentration was measured at admission (0 h), 12 h and 24 h in 1026 consecutive STEMI patients treated between February 2011 and May 2016 with primary percutaneous coronary intervention. GDF-15 dynamics (0 h, 12 h, 24 h) and predictive value (30 days and 3 years) were examined. Results Median GDF-15 concentration was 1443 pg/mL at 0 h, 1731 pg/mL at 12 h and 1510 pg/mL at 24 h (p Conclusions GDF-15 peaked at 12 h and remained elevated at 24 h in STEMI. GDF-15 measurement during the first 24 h in STEMI is valuable for predicting especially short- but also long-term outcomes, and may be a useful addition to risk stratification.

OBJECTIVES: Dietary marine omega-3 eicosapentaenoic acid (EPA) is readily incorporated into cardiac cell membranes, partially replacing the omega-6 arachidonic acid (AA). Blood omega-3 is an objective marker of their intake over the last days. Increasing blood EPA at the time of a ST-segment elevation myocardial infarction (STEMI) relates to a smaller infarct size and preserved long-term left ventricular ejection fraction. We explored whether blood EPA at the time of STEMI also relates to a lower incidence of hard clinical endpoints. We also explored whether blood alpha-linolenic acid (ALA, the vegetable omega-3) modulates such association. METHODS: We prospectively included 944 consecutive patients treated with primary percutaneous coronary intervention in a single tertiary referral hospital. We determined fatty acids in serum phosphatidylcholine (PC) at 12 hours of evolution. The primary outcomes were cardiovascular disease-related hospital readmission and all-cause mortality after 3 years of follow-up. We constructed multivariable Cox proportional hazards models, calculating risk estimates as hazard ratios (HR). RESULTS: The mean age of the cohort was 61 years and 209 (22.1%) were women. During follow-up, 130 patients (13.8%) were readmitted for cardiovascular disease, and 108 (11.4%) died. After adjustment for known clinical predictors, multivariate analysis showed that EPA in serum PC at the time of STEMI inversely related to incident hospital readmission (HR, 0.74; 95% CI, 0.56–0.96; P = 0.024, for a 1 SD increase). Further adjustment for serum PC AA and ALA did not change the association. EPA in serum PC was found to be unrelated to 3-y total mortality. However, after including serum PC proportions of AA and ALA into the model, we observed a significantly decreased risk of mortality for ALA (HR, 0.65; 95% CI, 0.44–0.96; P = 0.030, for a 1 SD increase). CONCLUSIONS: Increasing proportions of EPA and ALA in serum PC at the time of STEMI inversely relate to 3-y cardiovascular disease-hospital readmission and all-cause mortality, respectively. Dietary EPA and ALA act synergistically and are partners rather than competitors in improving prognosis in case of a STEMI. FUNDING SOURCES: Instituto de Salud Carlos III, Spain; California Walnut Commission.

The role of lung ultrasound (LUS) in acute heart failure (HF) has been widely studied, but little is known about its usefulness in chronic HF. This study assessed the prognostic value of LUS in a cohort of chronic HF stable ambulatory patients.We included consecutive outpatients who attended a scheduled follow-up visit in a HF clinic. LUS was performed in situ. The operators were blinded to clinical data and examined 8 thoracic areas. The sum of B-lines across all lung zones and the quartiles of this addition were used for the analyses. Linear regression and Cox regression analyses were performed. The main clinical outcomes were a composite of all-cause death or hospitalization for HF and mortality from any cause.A total of 577 individuals were included (72% men; 69± 12 years). The mean number of B-lines was 5±6. During a mean follow-up of 31±7 months, 157 patients experienced the main clinical outcome and 111 died. Having ≥ 8 B-lines (Q4) doubled the risk of experiencing the composite primary event (P.001) and increased the risk of death from any cause by 2.6-fold (P.001). On multivariate analysis, the total sum of B-lines remained independent predictive factor of the composite endpoint (HR, 1.04; 95%CI, 1.02-1.06; P=.002) and of all-cause death (HR, 1.04; 95%CI, 1.02-1.07; P=.001), independently of whether or not N-terminal pro-B-type natriuretic peptide (NT-proBNP) was included in the model (P=.01 and P=.008, respectively), with a 3% to 4% increased risk for each 1-line addition.LUS identified patients with stable chronic HF at high risk of death or HF hospitalization.

Advanced interatrial block (IAB) is characterized by a prolonged (≥120 ms) and bimodal P wave in the inferior leads. The association between advanced IAB and atrial fibrillation (AF) is known as “Bayes' Syndrome”, and there is scarce information about it in heart failure (HF). We examined the prevalence of IAB and whether advanced IAB could predict new-onset AF and/or stroke in HF patients. Methods and results: The prospective observational “Bayes' Syndrome-HF” study included consecutive outpatients with chronic HF. The primary endpoints were new-onset AF, ischemic stroke, and the composite of both. A secondary endpoint included all-cause death alone or in combination with the primary endpoint. Comprehensive multivariable Cox regression analyses were performed. Among 1050 consecutive patients, 536 (51.0%) were in sinus rhythm, 464 with a measurable P wave are the focus of this study. Two-hundred and sixty patients (56.0%) had normal atrial conduction, 95 (20.5%) partial IAB, and 109 (23.5%) advanced IAB. During a mean follow-up of 4.5 ± 2.1 years, 235 patients experienced all-cause death, new-onset AF, or stroke. In multivariable comprehensive Cox regression analyses, advanced IAB was associated with new-onset AF (HR 2.71 [1.61–4.56], P

Background The use of β-blocker therapy in the setting of acute coronary syndrome (ACS) associated with cocaine consumption (ACS-ACC) is discouraged due to the risk of coronary vasoconstriction. We examined the prognostic value of β-blocker therapy in a contemporary ACS cohort. Methods and results Prospective, single-center study conducted between January 2001 and December 2014 that examined cocaine use among young (≤50-year-old) consecutive patients admitted with an ACS. During the study period, 1002 patients were admitted; of these, 57 (5.7%) had a positive cocaine urine test We collected data on clinical characteristics and major adverse cardiovascular events (MACE) during follow-up. Among ACS-ACC patients, 33 (57.9%) received β-blocker therapy during hospital admission and after discharge. During a median follow-up of 4.0 (IQR: 2.4–6.5) years after the index event, 2 (6.1%) patients treated with β-blocker therapy died and 6 (18.2%) experienced hospital re-admission for myocardial infarction (MI); in contrast, there were 5 (20.8%) deaths and 5 (20.8%) readmissions due to MI in patients without β-blocker therapy. Lower rates of MACE were observed in patients treated with β-blocker therapy (30.3%) than those without β-blocker therapy (41.7%). The 90-day survival was higher in patients treated with β-blocker therapy (87.5% vs. 100%; Log rank test p = 0.035). Conclusions In patients with ACS-ACC, β-blocker treatment was associated with a significantly better clinical outcome, with lower rates of death and MI. Our findings support the evidence for long-term β-blocker administration in high-risk patients and highlight the need for large prospective multicenter studies of β-blocker treatment in ACS-ACC.

Introduction: There are inconclusive data about the potential delay of procedure time in emergent percutaneous coronary intervention (PCI) by radial compared with femoral approach in patients with ST-segment elevation myocardial infarction (STEMI). Aims: The purpose of the current study is to conduct a comprehensive meta-analysis of controlled randomized trials (CRTs) comparing the procedure time in STEMI patients undergoing emergent PCI with radial versus femoral access. Methods: Formal search of CRTs through electronic databases (Medline and PubMed) was performed from January 1990 to October 2014 without language restrictions. Mean difference (MD) of procedure time was evaluated as overall effect. Results: Twelve studies were included with 2052 and 2121 patients in radial and femoral group, respectively. Variability in the definition of procedure time was found with unavailability of a precise definition in 41.6% of studies. When all studies were included, no significant longer procedure time in radial approach was detected (MD [95% confidence interval [CI] = 1.6 min [−0.10, 3.3], P = 0.07, P het = 0.56). After deleting RIVAL trial, procedure time was significantly longer in radial group (MD [95% CI] = 1.5 min [0.71, 2.3], P < 0.001, P het = 0.20). Meta-analysis of three studies with similar definition of procedure time showed (MD [95% CI] = 1.26 min [−0.43, 2.95], P = 0.14, P het = 0.85). Conclusions: Although the procedure time in STEMI patients undergoing emergent PCI by radial access is generally comparable with femoral approach, there is an absence of uniformity in its definition, which leads to divergent results. A standardized definition of procedure time is required to elucidate this relevant matter.

Patients with cardiovascular risk factors or established cardiovascular disease have an increased risk of developing coronavirus disease 19 and have a worse outcome when infected, but translating this notion into effective action is challenging. At present it is unclear whether cardiovascular therapies may reduce the likelihood of infection, or improve the survival of infected patients. Given the crucial importance of this issue for clinical cardiologists and all specialists dealing with coronavirus disease 19, we tried to recapitulate the current evidence and provide some practical recommendations.

Purpose:The aim of our study was to analyse the long-term prognostic value of soluble urokinase plasminogen activator receptor (suPAR) in the setting of an acute coronary syndrome (ACS). Methods:We included 340 patients with an ACS who underwent coronary angiography and plasma suPAR concentration was measured. Patients were classified into low suPAR concentrations (= 2.6 ng/mL) and long-term events were evaluated. suPAR prognostic value was assessed beyond a clinical model that included age, GRACE score, estimated glomerular filtration rate, cardiac troponin-I peak and left ventricular ejection fraction Results:Higher suPAR concentrations were associated with an increased prevalence of cardiovascular risk factors. After multivariate adjustment, suPAR >= 2.6 ng/mL were independently associated with an increased risk of all-cause death (HR 2.3; 95%CI 1.2-4.4;p = .017), major adverse cardiovascular events (MACE) (HR 1.7; 95%CI 1.1-2.5;p = .020) and heart failure (HR 4.1; 95%CI 1.3-12.6;p = .015), but not with myocardial infarction. For long-term all-cause death significant improvement of reclassification and discrimination were seen after addition of suPAR to a clinical model. Conclusions:In the setting of an ACS, suPAR is associated with long-term all-cause death, heart failure and MACE, and provides incremental prognostic value beyond traditional risks factors.

Altres ajuts: This work was supported in part by Fundació La Marató de TV3 (201516-10, 201502-30), Societat Catalana de Cardiologia, "la Caixa" Banking Foundation. Altres ajuts: PERIS/SLT002-16-00234 Sacubitril/valsartan is a first-in-class angiotensin receptor-neprilysin inhibitor developed for the treatment of heart failure with reduced ejection fraction. Its benefits are achieved through the inhibition of neprilysin (NEP) and the specific blockade of the angiotensin receptor AT1. The many peptides metabolized by NEP suggest multifaceted potential consequences of its inhibition. We sought to evaluate the short-term changes in serum endorphin (EP) values and their relation with patients' physical functioning after initiation of sacubitril/valsartan treatment. A total of 105 patients with heart failure with reduced ejection fraction, who were candidates for sacubitril/valsartan treatment, were included in this prospective, observational, multicentre, and international study. In a first visit, and in agreement with current guidelines, treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blocker was replaced by sacubitril/valsartan because of clinical indication by the responsible physician. By protocol, patients were reevaluated at 30 days after the start of sacubitril/valsartan. Serum levels of α- (α-EP), γ-Endorphin (γ-EP), and soluble NEP (sNEP) were measured using enzyme-linked immunoassays. New York Heart Association (NYHA) functional class was used as an indicator of patient's functional status. Baseline median levels of circulating α-EP, γ-EP, and sNEP were 582 (160-772), 101 (37-287), and 222 pg/mL (124-820), respectively. There was not a significant increase in α-EP nor γ-EP serum values after sacubitril/valsartan treatment (P value = 0.194 and 0.102, respectively). There were no significant differences in sNEP values between 30 days and baseline (P value = 0.103). Medians (IQR) of Δα-EP, Δγ-EP, and ΔsNEP between 30 days and baseline were 9.3 (−34 − 44), −3.0 (−46.0 − 18.9), and 0 units (−16.4 − 157.0), respectively. In a pre-post sacubitril/valsartan treatment comparison, there was a significant improvement in NYHA class, with 36 (34.3%) patients experiencing improvement by at least one NYHA class category. Δα-EP and ΔsNEP showed to be significantly associated with NYHA class after 30 days of treatment (P = 0.014 and P < 0.001, respectively). Δα-EP was linear and significantly associated with NYHA class improvement after 30 days of sacubitril/valsartan treatment. These preliminary data suggest that beyond the haemodynamic benefits achieved with sacubitril/valsartan, the altered cleavage of endorphin peptides by NEP inhibition may participate in patients' symptoms improvement.

Heart failure (HF) is a major public health problem and a leading cause of hospitalization in western countries. Over the past decades, the goal has been to find the best method for monitoring congestive symptoms to prevent hospitalizations. Addressing this task through regular physician visits, blood tests, and imaging has proven insufficient for optimal control and has not decreased enough HF-related hospitalization rates. In recent years, new devices have been developed for this reason and CardioMEMS is one of the therapeutic monitoring options. CardioMEMS has shown to be effective in preventing and reducing HF hospitalizations in patients both with HF with reduced ejection fraction and HF with preserved ejection fraction. CardioMEMS’ versatility has made it a great option for pulmonary artery pressure monitoring, both during the coronavirus disease-19 (COVID-19) pandemic and when the clinic visits have (partially) resumed. CardioMEMS is the remote haemodynamic monitoring system with the most evidence-driven efficacy, and COVID-19 has put it in the spot as a centre-stage technology for HF monitoring. In a few months of the COVID-19 epidemic, CardioMEMS has grown to maturity, making it the new normal for high-quality, high-value remote HF care.

Background CHA2DS2-VASc score has been used as a surrogate marker for predicting outcomes beyond thromboembolic risk in patients with atrial fibrillation (AF). Likewise, cardiac troponin I (cTnI) is a predictor of mortality in AF. Purpose This study aimed to investigate the association of cTnI and CHA2DS2-VASc score with long-term prognosis in patients admitted to the emergency department with AF. Methods A retrospective cohort study conducted between January 2012 and December 2013, enrolling patients admitted to the emergency department with AF and having documented cTnI measurements. CHA2DS2-VASc score was estimated. Primary endpoint was 5-year all-cause mortality, readmission for heart failure (HF), readmission for myocardial infarction (MI) and the composite end point of major adverse cardiac events defined as death, readmission for HF or readmission for MI (MACE). Results A total of 578 patients with AF were studied, of whom 252 patients had elevated levels of cTnI (43.6%) and 334 patients had CHA2DS2-VASc score >3 (57.8%). Patients with elevated cTnI tended to be oldercompared with those who did not have cTnI elevation and were more frequently comorbid and of higher ischemic risk, including hypertension, prior MI, prior HF, chronic renal failure and peripheral artery disease. The overall median CHA2DS2-VASc score was higher in those with cTnI elevation compared to those patients elevated cTnI levels (4.2 vs 3.3 points, p Conclusions cTnI is independently associated with long-term all-cause mortality in patients attending the emergency department with AF. cTnI compared to CHA2DS2-VASc score is thus a biomarker with predictive capacity for mortality in late follow-up, conferring utility in the risk stratification of patients with atrial fibrillation.

Background Cardiogenic shock (CS) is an ominous complication of ST elevation myocardial infarction (STEMI). However, the widespread use of reperfusion therapies and invasive management could have reduced the prevalence of CS and improved the prognosis of these patients in the last decades. Purpose The aim is to analyze the changes over last three decades in the prevalence, management and acute phase prognosis and 1-year mortality of STEMI patients complicated with CS. Method Between February 1989 and December 2017, 7,589 STEMI patients were consecutively admitted in the Coronary Care Unit of a University Hospital and were included in a prospective registry. Depending on the year of admission, patients were classified in five groups: 1989–1994: n=1,337, period 1; 1995–1999: n=960, period 2; 2000–2004: n=1,059, period 3; 2005–2009: n=1,535, period 4 and 2010–2015: n=2,698, period 5). We analyze the trend in prevalence of CS, management and 28-day and 1-year mortality over these five periods. Results The global prevalence of CS was 6.1% (466 patients), mean age was 67.7 (SD 11.7) years and 68.7% were men. Prevalence of CS in STEMI decreased from period 1 to 5 (7.3%, 6.4%, 5.5%, 5.8%, 6.0%, p Kaplan-Meier curves, 1-year mortality Conclusions Cardiogenic shock development in STEMI patients has been reduced from 7.3% to 6.1% in the last three decades. The whole improvement in management of these patients achieves a 37% of reduction in 28-day case fatality and 1-year all-cause mortality. Despite this improvement, acute phase (28-day) case fatality of STEMI complicated with CS remains over 57% in the primary angioplasty era.

AIMS Better management of heart failure (HF) over the past two decades has improved survival, mainly by reducing the incidence of death due to cardiovascular (CV) causes. Deaths due to non-CV causes, particularly cancer, may be increasing. This study explored the modes of death of consecutive patients who attended a HF clinic over 17 years. METHODS AND RESULTS A total of 935 deaths were ascertained from 2002 to 2018 among 1876 patients (mean age 65.8 ± 12.5 years, 75% men, left ventricular ejection fraction

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.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.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, p0.001 and 4.3%, HR: 0.22 95% CI 0.12 to 0.41, p0.001), 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.

Background: The use of cocaine as a recreational drug has increased over recent years. In this study, we aimed to analyze the prevalence, and in-hospital and long-term outcomes of acute coronary syndrome (ACS) associated with cocaine consumption (ACS-ACC). Methods: A prospective observational registry of young patients hospitalised with ACS from 2001 through 2015, we analysed ACS-ACC temporal trends, clinical characteristics, and major adverse cardiovascular events (MACE) during long-term follow-up. Results: There were 8153 admissions with ACS, of whom 864 patients were

Background: In asymptomatic severe aortic stenosis (ASAS), treatment decisions are made on an individual basis, and case management presents a clinical conundrum.Methods: We prospectively phenotyped consecutive patients with ASAS using echocardiography, exercise echocardiography, cardiac MRI and biomarkers (NT-proBNP, high-sensitivity troponin T (hs-TnT) and ST2) (n=58). The primary endpoint was a composite of cardiovascular death, new-onset symptoms, cardiac hospitalization, guideline-driven indication for valve replacement and cardiovascular death at 12months.Results: During the first year, 46.6% patients met primary endpoint. In multivariable analysis, aortic regurgitation 2 (p=0.01) and hs-TnT (p=0.007) were the only independent predictors of the primary endpoint. The best cutoff value was identified as hs-TnT >10ng/L, which was associated with a approximate to 10-fold greater risk of the primary endpoint (HR, 9.62; 95% CI, 2.27-40.8; p=0.002). A baseline predictive model including age, sex and variables showing p10ng/L was associated with high risk of events within 12months. Including hs-TnT in routine ASAS management markedly improved prediction metrics.

Aim: To explore long-term prognostic value of SDF-1 in acute coronary syndrome (ACS). Materials & methods: We included 254 patients with ACS. Plasma SDF-1 was measured and patients were classified into tertiles of SDF-1. Results: Multivariate analysis showed third tertile of SDF-1 as an independent predictor of all-cause death (HR: 2.5; 95% CI: 1.2–5.2; p = 0.011) and the composite of major adverse cardiovascular and cerebrovascular events (HR: 1.8; 95% CI: 1.1–3.1; p = 0.031). SDF-1 added to a clinical model can improve all-cause death prediction (net reclassification improvement 0.362; 95% CI: 0.423–0.681; p = 0.027). Conclusion: SDF-1 is an independent predictor of all-cause mortality and major adverse cardiovascular and cerebrovascular events in long-term follow-up of patients with ACS and adds prognostic information beyond traditional cardiovascular risks factors.

BACKGROUND: Despite adverse prognoses of type 2 myocardial infarction and myocardial injury, an effective, practical risk stratification method remains an unmet clinical need. We sought to develop an efficient clinical bedside tool for estimating the risk of major adverse cardiovascular events at 180 days for this patient population. METHODS: The derivation cohort included patients with type 2 myocardial infarction or myocardial injury admitted to a tertiary hospital between 2012 and 2013 (n = 611). The primary outcome was a major adverse cardiovascular event (death or readmission for heart failure or myocardial infarction). The score included clinical variables significantly associated with the outcome. External validation was conducted using the UTROPIA cohort (n = 401). RESULTS: The TARRACO Score included cardiac troponin (cTn) concentrations and 5 independent clinical predictors of adverse cardiovascular events: age, hypertension, absence of chest pain, dyspnea, and anemia. The score exhibited good discriminative accuracy (area under the curve = 0.74; 95% CI, 0.700.79). Patients were classified into low-risk (score 0-6) and high-risk (score >= 7) categories. Major adverse cardiovascular events rates were 5 times more likely in high-risk patients compared with those at low risk (78.9 vs 15.4 events/100 patient-years, respectively; logrank P < .001). The external validation showed equivalent prognostic capacity (area under the curve=0.71, 0.65-0.78). CONCLUSION: A novel risk score based on bedside clinical variables and cTn concentrations allows risk stratification for death and cardiac-related rehospitalizations in patients with type 2 myocardial infarctions and myocardial injury. This score identifies patients at the highest risk of adverse events, a subset of patients who may benefit from close observation, medical intensification, or both. (C) 2018 Elsevier Inc. All rights reserved.

BACKGROUND: This study aimed to investigate the clinical features and prognosis of acute and chronic myocardial injury without clinical evidence of myocardial infarction inpatients admitted to the emergency department. METHODS: We analyzed the clinical data of all consecutive patients admitted to the emergency department during the years 2012 and 2013 who had at least 2 determinations of troponin I (TnI Ultra Siemens, Advia Centaur) and without a diagnosis of myocardial infarction. Clinical events were evaluated in a 3-year follow-up. RESULTS: A total of 1201 patients met the study's inclusion criteria and were included in the analysis (833 with cTnI below the 99th percentile, 261 with acute myocardial injury, and 107 with chronic myocardial injury). During a median follow-up of more than 36 months, mortality and rehospitalization for heart failure were significantly higher in patients with acute or chronic myocardial injury compared with patients without myocardial injury. No differences were observed in overall mortality between patients with acute and chronic myocardial injury, or in the rate of readmission due to acute coronary syndrome. However, the risk of readmission due to heart failure (adjusted HR 2.17; 95% confidence interval, 1.26-3.75; P = .005) was higher in patients with chronic myocardial injury. CONCLUSIONS: Mortality in long-term follow-up is high and similar in acute and chronic myocardial injury; however, the risk of readmission due to heart failure is higher in patients with chronic myocardial injury compared with patients with acute myocardial injury. (C) 2018 Elsevier Inc. All rights reserved.

Aims Cardiogenic shock (CS) is associated with high short-term mortality and a precise CS risk stratification could guide interventions to improve patient outcome. Here, we developed a circulating protein-based score to predict short-term mortality risk among patients with CS. Methods and results Mass spectrometry analysis of 2654 proteins was used for screening in the Barcelona discovery cohort (n = 48). Targeted quantitative proteomics analyses (n = 51 proteins) were used in the independent CardShock cohort (n = 97) to derive and cross-validate the protein classifier. The combination of four circulating proteins (Cardiogenic Shock 4 proteins—CS4P), discriminated patients with low and high 90-day risk of mortality. CS4P comprises the abundances of liver-type fatty acid-binding protein, beta-2-microglobulin, fructose-bisphosphate aldolase B, and SerpinG1. Within the CardShock cohort used for internal validation, the C-statistic was 0.78 for the CardShock risk score, 0.83 for the CS4P model, and 0.84 (P = 0.033 vs. CardShock risk score) for the combination of CardShock risk score with the CS4P model. The CardShock risk score with the CS4P model showed a marked benefit in patient reclassification, with a net reclassification improvement (NRI) of 0.49 (P = 0.020) compared with CardShock risk score. Similar reclassification metrics were observed in the IABP-SHOCK II risk score combined with CS4P (NRI =0.57; P = 0.032). The CS4P patient classification power was confirmed by enzyme-linked immunosorbent assay (ELISA). Conclusion A new protein-based CS patient classifier, the CS4P, was developed for short-term mortality risk stratification. CS4P improved predictive metrics in combination with contemporary risk scores, which may guide clinicians in selecting patients for advanced therapies.

Objective: To assess the effects of comorbidities, fragility, and quality of life (QOL) on long-term prognosis in ambulatory patients with heart failure (HF) with midrange left ventricular ejection fraction (HFmrEF), an unexplored area. Patients and Methods: Consecutive patients prospectively evaluated at an HF clinic between August 1, 2001, and December 31, 2015, were retrospectively analyzed on the basis of left ventricular ejection fraction category. We compared patients with HFmrEF (n=185) to those with reduced (HFrEF; n=1058) and preserved (HFpEF; n=162) ejection fraction. Fragility was defined as 1 or more abnormal evaluations on 4 standardized geriatric scales (Barthel Index, Older Americans Resources and Services scale, Pfeiffer Test, and abbreviated-Geriatric Depression Scale). The QOL was assessed with the Minnesota Living with Heart Failure Questionnaire. A comorbidity score (0-7) was constructed. All-cause death, HF-related hospitalization, and the composite end point of both were assessed. Results: Comorbidities and QOL scores were similar in HFmrEF (2.41±1.5 and 30.1±18.3, respectively) and HFrEF (2.30±1.4 and 30.8±18.5, respectively) and were higher in HFpEF (3.02±1.5, P

Background: Primary ventricular fibrillation is an ominous complication of ST-segment elevation myocardial infarction, and proper biomarkers for risk prediction are lacking. Growth differentiation factor-15 is a marker of inflammation, oxidative stress and hypoxia with well-established prognostic value in ST-segment elevation myocardial infarction patients. We explored the predictive value of growth differentiation factor-15 in a subgroup of ST-segment elevation myocardial infarction patients with primary ventricular fibrillation. Methods: Prospective registry of ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention from February 2011–August 2015. Growth differentiation factor-15 concentrations were measured on admission. Logistic regression and Cox proportional regression analyses were used. Results: A total of 1165 ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention (men 78.5%, age 62.3±13.1 years) and 72 patients with primary ventricular fibrillation (6.2%) were included. Compared to patients without primary ventricular fibrillation, median growth differentiation factor-15 concentration was two-fold higher in ST-segment elevation myocardial infarction patients with primary ventricular fibrillation (2655 vs 1367 pg/ml, p Conclusions: Growth differentiation factor-15 is a robust independent predictor of 30-day mortality in ST-segment elevation myocardial infarction patients with primary ventricular fibrillation.

To analyze the prognostic implications of the absence of chest pain in emergency department patients with elevated troponin I levels.Observational retrospective study of patients for whom troponin I level was analyzed at least once between January 2012 and December 2013. Patient characteristics were recorded and survival was modeled.A total of 3629 patients were distributed in 4 groups according to troponin I level and chest pain as follows: chest pain without troponin I elevation (n = 1379), no chest pain and no troponin I elevation (n = 1196), chest pain with troponin I elevation (n = 517), and troponin I elevation but no chest pain (n = 537). The patients with troponin I elevation but no chest pain were older and had more chronic conditions as well as more alternative diagnoses to consider other than acute coronary syndrome. Mortality was also higher at 12 months (log rank test0.001) in these patients. Multivariate analysis showed that absence of chest pain accompanying troponin I elevation was an independent predictor of mortality (hazard ratio, 5.130; 95% CI, 3.291-7.996; P.001) vs patients with chest pain but no troponin I elevation.The absence of chest pain in the presence of troponin I elevation identifies a heterogeneous group of patients with a worse 12-month prognosis.Analizar la implicación en el pronóstico de la ausencia de dolor torácico en pacientes con troponina elevada atendidos en urgencias.Estudio observacional de cohortes retrospectivo realizado en un servicio de urgencias entre enero 2012 y diciembre de 2013, que incluyó a todos los pacientes a los que se les había solicitado al menos una determinación de troponina I. Se recogieron las características clínicas de los pacientes y se realizó un modelo de supervivencia.Un total de 3.629 pacientes quedaron distribuidos en 4 grupos: dolor torácico y troponina I no elevada (n = 1.379), ausencia de dolor torácico y troponina I no elevada (n = 1.196), dolor torácico y troponina I elevada (n = 517) y ausencia de dolor torácico y troponina I elevada (n = 537). Los pacientes con ausencia de dolor torácico y troponina I elevada fueron de mayor edad y tuvieron mayor carga de comorbilidad, así como otros diagnósticos alternativos al de síndrome coronario agudo con respecto a los otros grupos estudiados. En el análisis de supervivencia a los 12 meses tuvieron mayor mortalidad (log rank test0,001). En el análisis multivariado la ausencia de dolor torácico con elevación de troponina I demostró ser factor independiente de exceso de mortalidad con respecto a los otros grupos diagnósticos (hazard ratio con respecto al grupo dolor torácico con troponina no elevada = 5,130; intervalo de confianza del 95% 3,291-7,996; p0,001).La ausencia de dolor torácico y troponina I elevada identifica a un grupo heterogéneo de pacientes con un pronóstico al año adverso.

ntroduccion y objetivos Las troponinas son biomarcadores especificos de dano miocardico y tienen implicacion en el diagnostico y el pronostico de pacientes con sindrome coronario agudo. El objetivo es determinar las caracteristicas clinicas y el pronostico en pacientes con elevacion de troponina no diagnosticados de sindrome coronario agudo. Metodos Se estudio retrospectivamente a 1.032 pacientes con determinacion de troponinas en un servicio de urgencias, que quedaron distribuidos en tres grupos: 681 pacientes sin elevacion de troponina y sin sindrome coronario agudo, 139 con sindrome coronario agudo y 212 con troponina elevada sin diagnostico de sindrome coronario agudo. Se compararon las caracteristicas clinicas de estos tres grupos y su mortalidad hospitalaria y a los 12 meses de seguimiento. Full English text available from: www.revespcardiol.org/en Conclusiones La troponina elevada es un importante predictor de mortalidad, independientemente del diagnostico definitivo del paciente. Patients with troponin elevation not diagnosed with acute coronary syndrome were older and had greater comorbidity than patients with acute coronary syndrome or no troponin elevation. The 12-month mortality was 30.2%, compared with 15.1% and 4.7% in the other groups (log rank test, P < .001). In the Cox logistic regression model adjusted for confounding variables, patients with troponin elevation and no diagnosis of acute coronary syndrome had higher mortality compared with patients with negative troponin without acute coronary syndrome (hazard ratio = 3.99; 95% confidence interval, 2.36-6.75; P < .001) and similar prognosis as patients with acute coronary syndrome.