Long-term hyperuricemia impact on atrial fibrillation outcomes.

BACKGROUND: No studies have been conducted to analyze the impact of serum uric acid (UA) levels on the outcome of atrial fibrillation (AF) patients. We aimed to evaluate the effect of hyperuricemia (HU) on the prognosis of AF. METHODS AND RESULTS: Consecutive patients who consulted our emergency room for an episode of AF, already known or newly diagnosed, between January 1, 2010, and December 31, 2015 (n=2017) were enrolled. After applying exclusion criteria, 1772 patients were included. Serum UA levels in the 6 months before or after the date of the episode were recorded and classified into quartiles: Q1 (n=443) serum UA levels <4.6 mg/dL; Q2 (n=430) 4.6-5.6 mg/dL; Q3 (n=435) 5.7-6.9 mg/dL; and Q4 (n=464) ≥7 mg/dL. Two groups were differentiated: patients without HU (Q1-Q3) and those with HU (Q4). The mean follow-up was 3.7 ± 1.4 years. The primary endpoint was all-cause mortality during follow-up. Mortality during follow-up in the bivariate analysis was higher (p < 0.001) in patients with HU (52.1 %) compared to those without it (35.3 %), confirming multivariate Cox analysis of HU as an independent risk factor for death [hazard ratio 1.89 (1.59-2.25)]. Kaplan-Meier survival analysis showed a shorter survival time in patients with HU (log-rank test, p<0.001). Cox analysis confirmed significant differences in the risk of heart failure (30 % vs. 22 %) in patients with HU. CONCLUSIONS: HU is independently associated with an increased risk for all-cause mortality and hospitalization for heart failure in patients with AF.

Implicaciones pronósticas del daño miocárdico en pacientes con y sin diagnóstico confirmado de COVID-19 atendidos en un hospital universitario / Prognostic implications of myocardial injury in patients with and without COVID-19 infection treated in a university hospital

INTRODUCCIÓN Y OBJETIVOS: La elevación de la troponina cardiaca como marcador de daño miocárdico es un predictor pronóstico en pacientes con COVID-19. Sin embargo, se desconoce su rendimiento en pacientes coetáneos con sospecha de COVID-19 pero con prueba de reacción en cadena de la polimerasa negativa. MÉTODOS: Estudio de cohortes retrospectivo que incluyó a todos los pacientes consecutivos atendidos en un hospital universitario con sospecha de COVID-19, confirmada o descartada mediante prueba de reacción en cadena de la polimerasa, todos ellos con determinaciones de troponina cardiaca I. Se analizó el impacto de la positividad de la troponina cardiaca I en la mortalidad a 30 días. RESULTADOS: Un total de 433 pacientes quedaron distribuidos en los siguientes grupos: COVID-19 confirmada (n=186), el 22% de ellos con daño miocárdico (n=41), y COVID-19 descartada (n=247), el 21,5% de ellos con daño miocárdico (n=52). Los grupos de COVID-19 confirmada y descartada tuvieron similares edad, sexo y antecedentes cardiovasculares. La mortalidad en el grupo de COVID-19 confirmada frente al de descartada fue significativamente superior (el 19,9 frente al 5,3%; p <0,001). En ambos grupos, el daño miocárdico fue predictor de mortalidad en el análisis multivariado de regresión de Cox (grupo de COVID-19 confirmada, HR=3,54; IC95%, 1,70-7,34; p = 0,001; grupo de COVID-19 descartada, HR=5,57; IC95%, 1,70-18,20; p = 0,004). El modelo predictivo analizado por curvas ROC fue similar en ambos grupos: COVID-19 confirmada, AUC=0,808 (0,750-0,865); COVID-19 descartada, AUC=0,812 (0,760-0,864) (p = 0,701). CONCLUSIONES: Se detecta daño miocárdico en 1 de cada 5 pacientes con infección por COVID-19 confirmada o descartada. En ambas circunstancias, el daño miocárdico es predictor de mortalidad a 30 días en similar grado

INTRODUCTION AND OBJECTIVES: Cardiac troponin, a marker of myocardial injury, is frequently observed in patients with COVID-19 infection. Our objective was to analyze myocardial injury and its prognostic implications in patients with and without COVID-19 infection treated in the same period of time. METHODS: The present study included patients treated in a university hospital with cardiac troponin I measurements and with suspected COVID-19 infection, confirmed or ruled out by polymerase chain reaction analysis. The impact was analyzed of cardiac troponin I positivity on 30-day mortality. RESULTS: In total, 433 patients were distributed among the following groups: confirmed COVID-19 (n=186), 22% with myocardial injury (n=41); and ruled out COVID-19 (n=247), 21.5% with myocardial injury (n=52). The confirmed and ruled out COVID-19 groups had a similar age, sex, and cardiovascular history. Mortality was significantly higher in the confirmed COVID-19 group than in the ruled out group (19.9% vs 5.3%, P <.001). In Cox multivariate regression analysis, cardiac troponin I was a predictor of mortality in both groups (confirmed COVID-19 group: HR, 3.54; 95%CI, 1.70-7.34; P=.001; ruled out COVID-19 group: HR, 5.57; 95%CI, 1.70-18.20; P=.004). The predictive model analyzed by ROC curves was similar in the 2 groups (P=.701), with AUCs of 0.808 in the confirmed COVID-19 group (0.750-0.865) and 0.812 in the ruled out COVID-19 group (0.760-0.864). CONCLUSIONS: Myocardial injury is detected in 1 in every 5 patients with confirmed or ruled out COVID-19 and predicts 30-day mortality to a similar extent in both circumstances