Meta-analysis of the effect of colchicine on C-reactive protein in patients with acute and chronic coronary syndromes

Objective The anti-inflammatory drug colchicine has recently shown benefits in the prevention of major adverse cardiovascular events (MACE) in patients with the acute coronary syndrome (ACS) and chronic coronary syndromes (CCS). This meta-analysis focuses on understanding Colchicine’s effects on the high-sensitivity C-reactive protein (hs-CRP) to provide mechanistic insight to explain its clinical event reduction.Methods A computerized search of MEDLINE was conducted to retrieve journal articles with studies performed on humans from 1 January 2005 to 1 January 2022, using keywords: ‘Colchicine AND Coronary’, ‘Colchicine AND CRP’, and ‘Colchicine AND Coronary Artery Disease’. Studies were included if they measured hs-CRP changes from baseline, and colchicine or placebo were given to patients with ACS or CCS.Results Thirteen studies with a biomarker subgroup population of 1636 patients were included in the hs-CRP meta-analysis. Of those 13 studies, 8 studies with a total population of 6016 reported clinical events defined as myocardial infarction (MI), stroke, cardiovascular death, periprocedural MI, repeat angina after PCI and repeat revascularization. Multivariate analysis revealed a weak negative correlation of −0.1056 (P = 0.805) between change in CRP and clinical events. Overall, colchicine treatment resulted in a greater reduction in hs-CRP levels compared with placebo (Mean Difference: -1.59; 95% Confidence Interval, −2.40 to −0.79, P = 0.0001) and clinical events (Odds Ratio: 0.78; 95% Confidence Interval 0.64 to 0.95, P = 0.01)Conclusion Colchicine therapy is associated with a reduction in hs-CRP and clinical events in patients with ACS and CCS. This finding supports colchicine’s anti-inflammatory efficacy via CRP reduction to explain its clinical benefit

Chronic Stress Impairs Collateral Blood Flow Recovery in Aged Mice

Chronic stress is associated with increased risk of cardiovascular diseases. Aging is also associated with vascular dysfunction. We hypothesize that chronic stress accelerates collateral dysfunction in old mice. Mice were subjected to either chronic social defeat (CSD) or chronic cold stress (CCS). The CSD mice were housed in a box inside an aggressor’s cage and exposed to the aggressor. The CCS group was placed in iced water. After chronic stress, mice underwent femoral artery ligation (FAL) and flow recovery was measured. For the CSD group, appearance and use scores of the foot and a behavioral test were performed. CSD impaired collateral flow recovery after FAL. Further, stressed mice had greater ischemic damage, impaired foot function, and altered behavior. The CCS mice also showed impaired collateral flow recovery. Chronic stress causes hind limb collateral dysfunction in old mice, a conclusion reinforced by the fact that two types of stress produced similar changes