Early subcortical ischemic infarction and delayed leucoencephalopathy after carbon monoxide poisoning

Controversy still exists about uric acid as a potential prognosticrisk factor for outcomes in patients with acute myocardial infarction. We prospectively assessed, in 856 patients with ST-elevation myocardial infarction (STMI) consecutively admitted to our Intensive Cardiac Care Unit after primary percutaneous coronary intervention (PCI) whether uric acid (UA) levels are associated with in-hospital mortality and complications. Killip classes III-–IV were more frequent in the 3° UA tertile that was associated with the highest values of peak Tn I (p = 0.005), NT-proBNP (p < 0.001), and fibrinogen (p = 0.036). Uric acid was associated with mortality (crude OR: 1.24; 95% CI 1.03–1.51; p = 0.025), but, when adjusted for Tn I and renal failure (as inferred by eGFR <60 ml/min/1.73 m²), uric acid lost its statistical significance, while Tn I (100 pg/ml step OR: 1.002; 95% CI 1.000–1.003; p = 0.007) and renal failure (OR 9.16; 95% CI 3.60–23.32; p < 0.001) were independent predictors for in-ICCU mortality. Uric acid remained as independent predictor for in-ICCU complications (1 mg/dl step OR: 1.11; 95% CI 1.01–1.21; p = 0.030) together with admission glycemia (1 g/dl step OR: 1.50; 95% CI 1.19–1.91; p < 0.001) and renal failure (OR: 1.46; 95% CI 0.99–2.16; p < 0.001). In STEMI patients submitted to PCI, increased uric acid levels identify a subgroup more prone to in-ICCU complications, probably because hyperuricemia stems from several complex mechanisms ranging from pre-existing risk factors to the degree of myocardial ischemia (as indicated by Killip class, ejection fraction) and to the acute metabolic response (as inferred by glucose levels). Hyperuricemia is not independently associated with early mortality when adjusted for renal function and the degree of myocardial damage.