Open Access

ARTICLE

Risk factors for hyperuricemia in congenital heart disease patients and its relation to cardiovascular death

Juan Lizandro Rodríguez‐Hernández¹, Fayna Rodríguez‐González², Marta Riaño‐Ruiz³, Efrén Martínez‐Quintana^1,4

1 Cardiology Service, Insular‐Materno Infantil University Hospital, Las Palmas de Gran Canaria, Spain
2 Ophthalmology Service, Dr. Negrín University Hospital of Gran Canaria, Las Palmas de Gran Canaria, Spain
3 Department of Biochemistry and Clinical Analyses, Insular-Materno Infantil University Hospital, Las Palmas de Gran Canaria, Spain
4 Medical and Surgical Sciences Department, Faculty of Health Sciences, University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Spain

* Corresponding Author: Efrén Martínez‐Quintana, Servicio de Cardiología, Complejo Hospitalario Universitario Insular Materno Infantil, Avd. Marítima del Sur s/n. 35016 Las Palmas de Gran Canaria, Spain. Email:

Congenital Heart Disease 2018, 13(5), 655-662. https://doi.org/10.1111/chd.12620

Abstract

Introduction: Hyperuricemia has been associated with cardiovascular risk factors but it remains controversial if uric acid is an independent predictor of cardiac mortality.
Methods: A total of 503 CHD patients (457 nonhypoxemic and 46 hypoxemic) and 772 control patients fulfilled inclusion criteria. Demographic, clinical, and analytical data [serum uric acid and 24h urine uric acid levels, N‐terminal pro‐B‐type natriuretic peptide (NT‐pro‐BNP), and C‐reactive‐protein (CRP) concentrations] were studied. Survivals curves to determine cardiac death and arterial thrombosis in CHD patients were also examined.
Results: Noncyanotic and cyanotic CHD patients had significant higher serum uric acid concentration (5.2 ± 1.5 vs 4.9 ± 1.3mg/dL, P = .007 and 6.7 ± 2.1 vs 4.9 ± 1.3mg/ dL, P < .001, respectively) and gout (1% vs 0%, P = .003 and 4% vs 0%, P < .01, respec‐ tively) than the control population. Among CHD patients, hyperuricemic patients were significant older and with overweight, used more diuretics, were more cyanotic and had higher serum creatinine, NT‐pro‐BNP and CRP concentrations than nonhy‐ peruricemic. In the multivariable analysis, the body mass index (BMI) (OR 1.09; 95% CI 1.01–1.18), cyanosis (OR 6.2; 95 CI 1.5–24.6), serum creatinine concentration (OR 49; 95% CI 44–538), and being under diuretic treatment (OR 4.5; 95% CI 1.4–14.5) proved to be risk factors for hyperuricemia in CHD patients. The Kaplan–Meier events free survival curves, during a 5.2 ± 2.7 years follow‐up of up time, showed that hyperuricemic CHD patients had significant higher cardiovascular death (P = .002). However, after applying the Cox regression analysis uric acid levels lost its statistical significance. No significant differences were seen in relation to thrombotic events between CHD patients with and without hyperuricemia.
Conclusions: CHD patients, noncyanotic and cyanotic, have higher serum uric acid levels and gout than patients in the general population. BMI, renal insufficiency, cya‐ nosis, and the use of diuretics were risk factor for hyperuricemia among CHD patients.

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