Hyperuricemia: risk factor for thromboembolism in hypertrophic cardiomyopathy patients
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Hyperuricemia: risk factor for thromboembolism in hypertrophic cardiomyopathy patients Ziqiong Wang1 · Hang Liao1 · Xiaoping Chen1 · Sen He1 Received: 28 August 2019 / Accepted: 8 January 2020 © Società Italiana di Medicina Interna (SIMI) 2020
Abstract Hyperuricemia has been regarded as a risk factor for various cardiovascular diseases. However, few studies have evaluated its influence on thromboembolism in hypertrophic cardiomyopathy (HCM) patients. The purpose of the present study is to investigate the association between hyperuricemia and thromboembolism in a retrospective HCM cohort. A total of 447 adult HCM patients were enrolled in this study from December 2008 to May 2016. Uric acid levels were measured at baseline. Hyperuricemia was defined as blood uric acid level > 360 µmol/L for female patients and > 420 µmol/L for male patients, respectively. The association between hyperuricemia and thromboembolism was analyzed. During the follow-up period of 1786.8 person-years, 31 patients (6.9%) developed thromboembolic events. There was a higher thromboembolism incidence in patients with hyperuricemia than those with normouricemia (8.9% vs. 5.6%; unadjusted HR 2.35, 95% CI 1.16–4.78, P = 0.018). The association slightly increased after adjusting for potential confounders (HR 2.67, 95% CI 1.24–5.76, P = 0.013). Atrial fibrillation (AF) and left ventricular outflow tract obstruction played an interactive role in the relationship between hyperuricemia and thromboembolism with P for interaction of 0.011 and 0.007, respectively. Adjusted HRs of hyperuricemia were 8.99 (95% CI 2.23–36.29, P = 0.002) for thromboembolism in HCM patients with AF and 6.89 (95% CI 2.23–21.24, P = 0.001) in non-obstructive HCM patients. The association lost statistical significance among patients without AF and obstructive ones. Hyperuricemia significantly predicts future thromboembolism in HCM patients, especially in HCM patients with AF and non-obstructive HCM patients. Future studies are warranted for further evaluation. Keywords Hyperuricemia · Hypertrophic cardiomyopathy · Thromboembolism · Atrial fibrillation
Introduction Hypertrophic cardiomyopathy (HCM) is a genetic disorder caused by mutations in cardiac sarcomere protein genes and inherited as an autosomal dominant trait [1, 2]. Thromboembolism, including cerebral stroke and systemic embolism, is a common complication for HCM patients with an incidence rate around 1.0% per year [3–5], which was higher than that of general population [6–9]. To reduce the disease burden, it would be helpful if we can identify individuals who are at high risk to develop thromboembolism, and thus relevantly
therapeutic interventions could be taken. As the end-product of purine metabolism, uric acid has been reported to be significantly associated with stroke in several large studies, including the Rotterdam study [6], the Atherosclerosis Risk in Communities (ARIC) Study [7], the Apolipoprotein MOrtality RISk (AMORIS) study [8] and the Tromsø Study [9]. However, participants of these l
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