engleski

Higher serum uric acid on admission is associated with higher short-term mortality and poorer long-term survival after myocardial infarction: Retrospective prognostic study

Aim was to assess serum uric acid (SUA) levels determined on admission as a potential predictor of short-term mortality and long-term survival in acute myocardial infarction (AMI) patients. Data for this retrospective prognostic study were drawn from the patient database of the Varaždin County General Hospital in Varaždin, Croatia. We included consecutive patients with verified AMI admitted within 48 hours since the symptom onset during the period between 1 January 1996 and 31 December 2001. Long-term survival/ mortality data were collected through direct contacts with patients and search of the community death registries. Relative risks (RR) and hazard ratios (HR) by 10 μmol/ L increase in SUA were determined using modified Poisson regression with robust error variance and proportional hazard regression, respectively. A total of 621 patients (age 27-90 years, 64.7% men, 77.5% AMI with ST elevation, SUA 63-993 μmol/L) were included. Higher SUA on admission was independently associated with higher in-hospital mortality (RR, 1.016 ; 95% confidence interval [CI], 1.001-1.031, P = 0.043) and higher thirty-day mortality (RR, 1.016 ; 95% CI, 1.003-1.029, P = 0.018). Considered covariates were demographics, preindex event cardiovascular morbidity and treatment, onadmission serum creatinine, total cholesterol and triglycerides, AMI characteristics, and peak creatine phosphokinase. Higher SUA on admission was also independently associated with poorer long-term survival (ie, higher all-cause mortality) (HR, 1.105 ; 95% CI, 1.020-1.195, P = 0.010). Considered covariates were demographics, laboratory variables on admission, AMI characteristics, peak creatine phosphokinase, acute complications, and treatment at discharge. Higher serum uric acid determined on admission is associated with higher in-hospital mortality and thirty- day mortality and poorer long-term survival after AMI. In humans, uric acid (UA) is the end product of purine catabolism (1). Its serum levels (SUA), governed by the production (liver) and elimination (mainly the kidney) rates, are influenced by genetically determined factors (eg, activity of synthesizing enzymes or renal transporter systems), racial and demographic characteristics (eg, sex, gonadal function in women, obesity), diet (eg, purine-rich foods, fructose, alcohol), habits (eg, SUA is lower in smokers and increases after quitting), morbidity (eg, heart or renal failure, malignancies), and medications (eg, diuretics, cytotoxic agents) (1-4). The role of SUA in cardiovascular and renal diseases has been intensively investigated, although not without controversy (5). On the molecular and cellular level, UA exerts a number of effects of potential interest: it is one of the most important antioxidants in plasma, but at high concentrations it may promote oxidative stress ; it may induce endothelial dysfunction and vascular smooth muscle cell proliferation in vitro, platelet aggregation, and microinflammation ; increased UA causes tubulointerstitial inflammation, morphological and functional changes in the glomeruli and renal arteriole and increased salt sensitivity (3, 5). There is now sufficient evidence to consider increased SUA as an etiological factor in "hyperuricemic hypertension" or "salt-sensitive kindey-dependent hypertension" (3, 5). Clinical and epidemiological studies have linked increased SUA to occurrence and outcomes of diabetes mellitus, metabolic syndrome, and chronic renal failure (3, 5, 6). It has also been suggested as a risk factor for occurrence and a predictor of poorer outcomes in acute stroke (7-9) and a risk factor for occurrence/outcomes in various aspects of cardiovascular morbidity (3, 5, 6). However, there are also views that SUA is not relevant in the pathophysiology of cardiovascular diseases and that it should be viewed as a secondary side-marker of etiologically relevant processes (3, 5). Acute myocardial infarction (AMI) is the most dramatic manifestation of the coronary artery disease (CAD) (10). High SUA has been indicated as a risk factor for CAD (10) and as an independent prognostic factor of poorer outcomes (occurrence of AMI, fatal AMI, sudden death, allcause mortality) in patients with verified CAD (11, 12). Less is known about SUA as a potential prognostic/risk factor for outcomes in patients affected specifically by AMI. A recent retrospective analysis from Japan (13) observed a univariate association between higher SUA on admission (within 48 hours since the symptom onset) and higher thirty-day mortality (fourth vs first quartile SUA values) in AMI patients. It also reported an independent association between higher SUA and poorer long-term survival (13). Having in mind potential ethnic/racial specificities and cultural differences (eg, diet, alcohol consumption), we aimed to investigate SUA levels determined on admission as a potential predictor of short-term mortality (while accounting for relevant covariates) and long-term survival in a sample of patients of European descent (Caucasians) with verified AMI.

serum uric acid; acute myocardial infarction; mortality; all-cause mortality

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