Low coenzyme Q10 levels in patients with acute cardiovascular disease are associated with long-term mortality
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ORIGINAL ARTICLE
Low coenzyme Q10 levels in patients with acute cardiovascular disease are associated with long‑term mortality Megumi Shimizu1 · Tetsuro Miyazaki1 · Atsutoshi Takagi1 · Yurina Sugita1 · Shohei Ouchi1 · Tatsuro Aikawa1 · Tomoyuki Shiozawa1 · Masaru Hiki1 · Shuhei Takahashi1 · Makoto Hiki1 · Kazunori Shimada1 · Hiroyuki Daida1 Received: 6 January 2020 / Accepted: 4 September 2020 © Springer Japan KK, part of Springer Nature 2020
Abstract Coenzyme Q10 (CoQ10) plays a potential role in the prevention and treatment of cardiovascular disease through improved cellular bioenergetics. Critical illness in the intensive care unit has been reported to be associated with decreased circulating CoQ10 levels, and we previously demonstrated the association of low CoQ10 levels with in-hospital mortality. However, the association of CoQ10 with the acute phase of cardiovascular disease and long-term mortality remains unclear. We enrolled 242 consecutive patients with cardiovascular disease admitted to the coronary care unit of Juntendo University Hospital to investigate the association between long-term mortality and serum CoQ10 levels. During a mean follow-up of 3.2 years, 58 patients died. The mean serum CoQ10 levels were significantly lower in the non-survivors than in the survivors (0.48 ± 0.27 vs. 0.58 ± 0.38 mg/L; p = 0.035). Compared with the patients with above-median CoQ10 levels (0.46 mg/L), the cumulative incidence of all-cause mortality was significantly higher in those with lower CoQ10 levels (p = 0.025). Multivariate Cox regression analysis further demonstrated that lower CoQ10 levels were associated with poor prognosis. Low serum CoQ10 levels during the acute phase of cardiovascular diseases were associated with long-term mortality in patients, suggesting the utility of low serum CoQ10 levels as a predictor and potential therapeutic target. Keywords Coenzyme Q10 · Long-term mortality · Acute cardiovascular disease · Inflammation · Malnutrition
Introduction Supplementation with coenzyme Q10 (CoQ10), a mitochondrial coenzyme essential for the production of adenosine triphosphate [1, 2], has been shown to prevent cardiovascular disease in several clinical trials [3, 4]. CoQ10 has numerous demonstrated benefits, such as improved endothelial dysfunction, reduced inflammatory response, and antioxidant effect [5–8]. Furthermore, CoQ10 can potentially contribute to the prevention and treatment of heart failure through improved cellular bioenergetics [9–12]. CoQ10 supplementation has been shown to improve mitochondrial and endothelial function in patients with ischemic left ventricular systolic dysfunction [13], who may also benefit from the
antioxidant, free radical scavenging, and vasodilatory effects of CoQ10 [14–16]. Plasma CoQ10 concentrations have also been shown to be an independent predictor of mortality in patients with chronic heart failure [17]. The beneficial effects of CoQ10 supplementation have also been reported in congestive heart failure [18, 19]. We recently reported that a low serum CoQ10
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