Hyperuricemia predicts increased cardiovascular events in patients with chronic coronary syndrome after percutaneous coronary intervention: A nationwide cohort study from Japan

• Published in: Frontiers in cardiovascular medicine Vol. 9; p. 1062894
• Main Authors: Akashi, Naoyuki, Kuwabara, Masanari, Matoba, Tetsuya, Kohro, Takahide, Oba, Yusuke, Kabutoya, Tomoyuki, Imai, Yasushi, Kario, Kazuomi, Kiyosue, Arihiro, Mizuno, Yoshiko, Nochioka, Kotaro, Nakayama, Masaharu, Iwai, Takamasa, Nakao, Yoko, Iwanaga, Yoshitaka, Miyamoto, Yoshihiro, Ishii, Masanobu, Nakamura, Taishi, Tsujita, Kenichi, Sato, Hisahiko, Fujita, Hideo, Nagai, Ryozo
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 10.01.2023
• Subjects: Cardiovascular Medicine; chronic coronary syndrome; hyperuricemia; percutaneous coronary intervention; real-world database; serum uric acid; hyperuricemia; percutaneous coronary intervention; serum uric acid; real-world database; chronic coronary syndrome
• ISSN: 2297-055X; 2297-055X
• DOI: 10.3389/fcvm.2022.1062894

The causal relationship between hyperuricemia and cardiovascular diseases is still unknown. We hypothesized that hyperuricemic patients after percutaneous coronary intervention (PCI) had a higher risk of major adverse cardiovascular events (MACE). This was a large-scale multicenter cohort study. We enrolled patients with chronic coronary syndrome (CCS) after PCI between April 2013 and March 2019 using the database from the Clinical Deep Data Accumulation System (CLIDAS), and compared the incidence of MACE, defined as a composite of cardiovascular death, myocardial infarction, and hospitalization for heart failure, between hyperuricemia and non-hyperuricemia groups. In total, 9,936 patients underwent PCI during the study period. Of these, 5,138 patients with CCS after PCI were divided into two group (1,724 and 3,414 in the hyperuricemia and non-hyperuricemia groups, respectively). The hyperuricemia group had a higher prevalence of hypertension, atrial fibrillation, history of previous hospitalization for heart failure, and baseline creatinine, and a lower prevalence of diabetes than the non-hyperuricemia group, but the proportion of men and age were similar between the two groups. The incidence of MACE in the hyperuricemia group was significantly higher than that in the non-hyperuricemia group (13.1 vs. 6.4%, log-rank < 0.001). Multivariable Cox regression analyses revealed that hyperuricemia was significantly associated with increased MACE [hazard ratio (HR), 1.52; 95% confidential interval (CI), 1.23-1.86] after multiple adjustments for age, sex, body mass index, estimated glomerular filtration rate, left main disease or three-vessel disease, hypertension, diabetes mellitus, dyslipidemia, history of myocardial infarction, and history of hospitalization for heart failure. Moreover, hyperuricemia was independently associated with increased hospitalization for heart failure (HR, 2.19; 95% CI, 1.69-2.83), but not cardiovascular death or myocardial infarction after multiple adjustments. Sensitive analyses by sex and diuretic use, B-type natriuretic peptide level, and left ventricular ejection fraction showed similar results. CLIDAS revealed that hyperuricemia was associated with increased MACE in patients with CCS after PCI. Further clinical trials are needed whether treating hyperuricemia could reduce cardiovascular events or not.