Safety and efficacy of anti-inflammatory therapy in patients with coronary artery disease: a systematic review and meta-analysis

Abstract

Background The inflammation hypothesis of atherosclerosis has been put forward for more than 20 years. Although many animal experiments have suggested that anti-inflammatory therapy can inhibit the atherosclerotic process, the efficacy of anti-inflammatory therapy for patients with coronary artery disease (CAD) is still controversial. Therefore, this study aims to evaluate the safety and efficacy of anti-inflammatory drugs in patients with CAD. Method We conducted this systematic review and meta-analysis of randomized controlled trials by searching PubMed, EMBASE, web of science, and Cochrane Library database. The primary outcome was a composite outcome of cardiovascular death, myocardial infarction (MI), or stroke. The secondary outcomes included individual MI, coronary revascularization, cardiovascular death, all-cause death, and stroke. The relative risk (RR) and 95% confidence intervals (CI) for outcome events were calculated by the fixed effects model, and trial sequential analysis was applied to assess the results. Result A total of ten randomized controlled trials and 60,782 patients with CAD was included. Compared with patients receiving placebo, anti-inflammatory therapy significantly reduced the incidence of the primary outcome in patients with CAD (RR 0.93, 0.89–0.98, P = 0.007). In addition, the anti-inflammatory therapy can also reduce the risk of MI (RR 0.90, 0.84–0.96, P = 0.002) and coronary revascularization (RR 0.74, 0.66–0.84, P < 0.00001) remarkably. However, there was no significant difference in the incidence of cardiovascular death (RR 0.94, 0.86–1.02, P = 0.14), all-cause death (RR 1.00, 0.94–1.07, P = 0.98) and stroke (RR 0.96, 0.85–1.09, P = 0.51) between two groups. Conclusions Anti-inflammatory therapy can reduce the incidence of the primary outcome in patients with CAD, especially the risk of MI and coronary revascularization. However, anti-inflammatory therapy increases the risk of infection. (Registered by PROSPERO, CRD 420212291032).

The Role of Inflammation in Cardiovascular Disease

“…Overall, the meta-analyses of the randomized trials indicate that anti-inflammatory interventions in patients with coronary artery disease, who were already on statin therapy, reduce the risk of myocardial infarction and stroke [ 39 , 227 , 228 ]. However, their potential use is limited by the increased incidence of infections and non-CV death.…”

“…In the last few years, the inflammatory biology of atherosclerosis has been translated into therapeutic strategies. Recent clinical trials indicated that targeting inflammation results in a lower incidence of CAD and stroke [ 39 , 40 , 41 ]. This review summarizes the current knowledge about the role of inflammation and the immune system in the development of atherosclerosis, the progression to stable and vulnerable plaque, the relationship between the central nervous system and arterial inflammatory response, the role of ageing in promoting atherosclerosis beyond a prolonged exposure to the traditional risk factors, and new therapeutic opportunities targeting inflammation to reduce the CVD burden.…”

Lesion-specific suppression of YAP/TAZ by biomimetic nanodrug ameliorates atherosclerosis development

“…Recent clinical trials have demonstrated the feasibility of antiinflammatory agents in reducing secondary cardiovascular events, positioning them as potential future therapeutic options for atherosclerosis, alongside statin treatments [3,4]. Despite the success, the impact of systemic cytokine neutralization on plaque characteristics, as well as issues associated with impaired host defense and infections, remain to be addressed [5,6]. In comparison to systemic treatments, local delivery of therapeutics that directly target specific inflammatory pathways in diseased blood vessels would be a more preferable approach to treat plaque progression, potentially improving effectiveness and safety.…”

KLF9 deficiency protects the heart from inflammatory injury triggered by myocardial infarction

“…However, DAMPs and ischemia triggered an excessive inflammatory response of infiltrative inflammatory cells, leading to increased myocardial damage. Anti-inflammatory therapy has been shown to reduce the extent of infarction and prevent cardiac remodeling in the treatment of MI [ 19 ]. Macrophages are one of the most abundant cardiac inflammatory cell clusters and are responsible for the predominant role in the inflammatory response of the heart after MI [ 20 ].…”