Clinical phenotypes, aetiologies, management, and mortality in acute heart failure: a single-institution study in Latin-America.

AIMS: Little is known regarding acute heart failure (AHF) clinical characteristics and its hospital outcome in Latin America. This study sought to assess the prevalence of, and identify differences among, in-hospital outcomes in patients hospitalized for AHF who were stratified by clinical phenotype at a hospital in Latin America. METHODS AND RESULTS: This is a retrospective cohort study of patients with AHF who were hospitalized in the coronary care unit of a Latin American teaching hospital from January 2006 to December 2018. Cox regression analysis was used to identify predictors of mortality. Of 21 042 patients admitted, 7759 (36.6%) had AHF. Their median age was 62 years, and 35% were women. De novo heart failure was seen in 39.4% of patients. Most common was AHF-associated acute coronary syndromes (ACS-HF) in 43.0%, decompensated heart failure (DHF) in 33.7%, hypertensive heart failure (HT-HF) in 11.8%, and cardiogenic shock (CS) in 5.2%. Pulmonary oedema (PO) (3.3%) and right heart failure (RHF) (3.0%) were least frequent. Coronary artery disease was the most frequent aetiology in 56.5% of patients, valvular heart disease in 22.4%, and cardiomyopathies in 12.3%. Other less frequent aetiology included adult congenital heart disease (2.5%), lung diseases (2.1%), acute aortic syndromes (1.4%), pericardial diseases (0.8%), and intracardiac tumours (0.3%). Aetiology could not be established in 1.6% of patients. Before admission, patients with worsening chronic heart failure and reduced ejection fraction were treated with renin-angiotensin system blockers (60.4%), beta-blockers (42.5%), or spironolactone (34.4%). The percentages of patients given in-hospital management with intravenous diuretics, vasodilators, inotropes, and vasopressors were 81.2%, 33.4%, 18.9%, and 20.4%, respectively. The overall in-hospital mortality was 17.9% (71.3%, 43.9%, 23.8%, 14.9%, 13.6%, and 10.1% for CS, PO, RHF, DHF, ACS-HF, and HT-HF, respectively; P < 0.0001). Multivariate analysis revealed that PO (hazard ratio [HR] 2.68, 95% confidence interval [CI] 1.73-4.14, P < 0.0001) and CS (HR 3.37, 95% CI 2.12-5.35, P < 0.0001) were independent predictors of in-hospital mortality. Use of intravenous diuretics was linked to reduction of in-hospital mortality (HR 0.70, 95% CI 0.59-0.59, P < 0.0001). By contrast, increased in-hospital mortality was associated with the use of intravenous inotrope or vasopressor (HR 1.49, 95% CI 1.27-1.76 and HR 2.91, 95% CI 2.41-3.51, P < 0.0001, respectively). CONCLUSIONS: Real-world evidence from a university hospital in Latin America shows that the high mortality among patients with AHF may depend, among other factors, on patients' AHF clinical phenotypes. The clinical characteristics and aetiologies of AHF appear to differ between these data from Mexico and those from European and US registries.

Derivation and validation of a simple inflammation-based risk score system for predicting in-hospital mortality in acute coronary syndrome patients.

BACKGROUND: Accurate assessment of inflammatory status of patients during acute coronary syndrome (ACS) has become of great importance in their risk classification and in the research of new anti-inflammatory therapies. METHOD: The study cohort included 7396 patients with ACS. We sought to derive and internally validate an inflammation-based score that included high-sensitivity C-reactive protein, white blood cell count, and serum albumin level at admission to evaluate the predictive role of systemic inflammation in the clinical outcome of these patients. We randomly assigned patients into derivation (66.6%) and validation (33.4%) cohorts. A total of four categories of systemic inflammation were defined. RESULTS: Assessed individually, the three biomarkers were associated with a higher rate of in-hospital mortality. When we combined them into an inflammation score, in-hospital mortality was significantly different across the four categories of inflammation in the derivation cohort (1.8%, 2.8%, 4.1%, and 13.8% for without, mild, moderate, and severe inflammation, respectively; p<0.0001, C-statistic, 0.71). These results were similar in the validation cohort (1.1%, 2.9%, 5.2%, and 12.6%, respectively; p<0.0001, C-statistic, 0.71). After multivariate adjustment, only the category of severe systemic inflammation was associated with a threefold increased risk of in-hospital mortality (odds ratios 3.02, p<0.0001) and was the most powerful predictor of mortality. In the whole cohort, after subsetting patients based on GRACE risk score, the severe inflammation category was associated with a significant increase of in-hospital mortality across all sub-groups, mainly in patients with higher GRACE risk score. The inflammation-based risk score reclassified 25.3% of the population. The net reclassification index was 8.2% (p=0.001). CONCLUSION: A risk score system based on biomarkers of inflammation readily available at admission in patients with ACS, could better assess the inflammatory status and predict in-hospital mortality, as well as severe systemic inflammation that contributes to a worse outcome independently of clinical risk factors.