RESUMEN
BACKGROUND: Allopurinol, a xanthine inhibitor that lowers uric acid concentration, has been proven to reduce inflammation and oxidative stress in patients with cardiovascular disease. However, it is unknown whether these beneficial effects translate into favorable plaque modiï¬cation in acute coronary syndromes (ACS). This study aimed to investigate whether allopurinol could improve coronary plaque stabilization using coronary computed tomography angiography (CCTA). METHODS: This was a prospective, single-center, randomized, double-blind clinical trial began in March 2019. A total of 162 ACS patients aged 18-80 years with a blood level of high-sensitivity C-reactive protein (hsCRP) â> â2 âmg/L were included. The subjects were randomly assigned in a 1:1 ratio to receive either allopurinol sustained-release capsules (at a dose of 0.25 âg once daily) or placebo for 12 months. The plaque analysis was performed at CCTA. The primary efficacy endpoint was the change in low-attenuation plaque volume (LAPV) from baseline to the 12-month follow-up. RESULTS: Among 162 patients, 54 in allopurinol group and 51 in placebo group completed the study. The median follow-up duration was 14 months in both groups. Compared with placebo, allopurinol therapy did not signiï¬cantly alter LAPV (-13.4 â± â3.7 â% vs. -17.8 â± â3.6 â%, p â= â0.390), intermediate attenuation plaque volume (-16.1 â± â3.0 â% vs. -16.2 â± â2.9 â%, p â= â0.992), dense calciï¬ed plaque volume (12.2 â± â13.7 â% vs. 9.7 â± â13.0 â%, p â= â0.894), total atheroma volume (-15.2 â± â3.2 â% vs. -16.4 â± â3.1 â%, p â= â0.785), remodeling index (2.0 â± â3.9 â% vs. 5.4 â± â3.8 â%, p â= â0.536) or hsCRP levels (-73.6 [-91.6-17.9] % vs. -81.2 [-95.4-47.7] %, p â= â0.286). CONCLUSIONS: Our ï¬ndings suggest that allopurinol does not improve atherosclerotic plaque stability or inï¬ammation in ACS.