0289 : Correlation of higher serum uric acid and severity of congestive heart failure in myocardial infarction: prospective study

Abstract

Serum uric acid (SUA) reflects xanthine oxidase activity's level and oxidative stress’ production. Hyperuricemia has been identified as a marker of poor prognosis in patients with congestive heart failure (CHF) after acute myocardial infarction (AMI). To assess SUA levels determined on admission as a potential predictor of severity of the CHF in AMI patients. Data for this prospective observational study were collected from the ACS database register created on January 2015. We included consecutive patients with verified AMI admitted within 48 hours since the symptom onset during the period between January and November 2015. Clinical, biological and echocardiographic data were collected through direct contacts with patients during their hospitalization. The study was conducted on two groups: Fifty four patients (42.1%) with high level of SUA on admission were allocated to the group I and were compared to patients of group II (n=74, 57.9%) with normal SUA. Group I patients had less previous history of hypertension, dyslipidemia and smoking (37.8% vs 45.3%; 10.8% vs 17.6% and 51.3% vs 58.8% respectively) but more history of stroke 5.4% vs 1.96%. On admission, mean HR was higher in group 1 than in group 2 (83,73 +/– 17,19 vs 78,37+/–14,64 bpm). Mean SBP was lower in group 1 than in group 2. The mean LVEF was significantly lower in group 1 (40%+/–9,675 vs 45,67%+/–7,528 ; p= 0.03). This observational cohort identified a close relationship between SUA and Killip classification. Patients who developed short-term CHF had higher concentrations of SUA; the severity of the congestion was proportional to the value of SUA (Killip III-IV: 27.02% vs 7.8%; p =0.04). Our results suggest that hyperuricemia after myocardial infarction is associated with the severity of CHF. The serum level of uric acid is a suitable marker to predict adverse events related to myocardial infarction. The author hereby declares no conflict of interest