Colchicine has emerged as a promising anti-inflammatory option for secondary prevention in coronary artery disease, but its role in routine practice remains uncertain. Evidence from randomised trials suggests a more consistent benefit in chronic coronary syndromes and selected post-myocardial infarction populations. In contrast, results in acute coronary syndromes and PCI-related settings have been less convincing. This review summarises the main limitations and unresolved challenges of colchicine use in coronary artery disease, including heterogeneity across trials, lack of biomarker-guided patient selection, uncertainty regarding timing and duration of therapy, and concerns about tolerability, safety, and drug interactions. Current data suggest that colchicine may be useful in selected patients rather than as a universal treatment strategy. Further studies are needed to define its optimal clinical use better and to support a more personalised anti-inflammatory approach.

Idiopathic and recurrent pericarditis are increasingly recognised as autoinflammatory conditions driven by the NLRP3 inflammasome and interleukin-1 signalling. Despite this shift in understanding, the misuse of high-dose corticosteroids has often led to a 'massacre of the innocents', transforming acute events into chronic, steroid-dependent diseases. This narrative review analyses the evolution of corticosteroid use in pericarditis, emphasising the transition from aggressive loading doses to the low-dose, 'rheumatological' strategies codified in the 2025 European Society of Cardiology (ESC) guidelines.Evidence confirms that medium-dose prednisone (0.2-0.5 mg/kg/day), when integrated into triple therapy with non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine, reduces recurrence rates and iatrogenic toxicity compared to traditional high-dose regimens (1.0 mg/kg/day). A critical challenge remains the tapering process; rapid withdrawal triggers inflammatory rebounds, necessitating meticulous, long-lasting (months-years), C-reactive protein (CRP)-guided reductions as small as 5 to 1.25 mg every two to six weeks, similar to the tapering used in polymyalgia rheumatica. Chronic maintenance with low-dose prednisone (≤5 mg/day) may be considered in selected cases, with a good risk-benefit balance. The elderly usually require medium dosages (e.g. prednisone 12.5-25 mg), pregnant women no more than 10 mg, while children should avoid chronic corticosteroid therapy. CRP-negative cases may benefit from low doses (5 mg). Given the long-term duration of therapy, bone protection therapy is essential yet underutilised, while protonpump inhibitors should be used only for concomitant NSAIDs therapy. Corticosteroids are generally ineffective in chronic idiopathic pericardial effusions with normal CRP.In conclusion, modern management redefines corticosteroids as a precision tool rather than a blunt anti-inflammatory agent.

Inflammation is now recognised as a central mechanism in atherosclerosis and its clinical complications, shifting coronary heart disease management beyond exclusive lipid lowering and antithrombotic therapy. In this setting, colchicine is a potential low-cost antiinflammatory candidate for cardiovascular prevention. While the CANTOS trial provided proof of principle that targeting inflammation can reduce recurrent cardiovascular events independently of lipid lowering, randomised colchicine trials such as COLCOT and LoDoCo2 showed reductions in major adverse cardiovascular events in patients with recent myocardial infarction and chronic coronary disease, respectively. Later meta-analyses generally confirmed benefit for major adverse cardiovascular events, myocardial infarction, stroke, and coronary revascularisation, although without a consistent mortality reduction and with gastrointestinal intolerance as the most common adverse effect. This review summarises the biological rationale, clinical trial evidence, safety profile, practical use, limitations, and current place of colchicine in coronary heart disease highlighting that colchicine is a real available cheap option for secondary prevention at least in chronic coronary syndromes.

Atherosclerosis as an inflammatory process has been a Leitmotiv in cardiology for the past 30 years, and the hypothesis of a causal role has now been tested in several clinical trials aimed at demonstrating that drugs that primarily target inflammation can reduce cardiovascular events. Inflammation indeed drives all phases of atherosclerosis, from inception, through progression, and ultimately acute thrombotic complications triggered by plaque rupture and plaque erosion. Since atherothrombosis causes most acute myocardial ischaemic syndromes, appropriate anti-inflammatory treatments should limit the occurrence of such events and, consequently, of cardiovascular death. Such treatments might also reduce the propensity to thrombosis once the trigger (plaque rupture or erosion) has occurred. This brief review will summarise the main concepts, initial results and current expectations in this rapidly evolving area of cardiology, borrowing concepts and drugs from immunology and rheumatology. This is an extremely attractive, but still incomplete story, with still many challenges and shadows.

Colchicine is an ancient drug that remains a cornerstone in the management of crystal-induced inflammatory diseases, particularly gout and calcium pyrophosphate crystal disease (CPPD). Its clinical use is supported by well-established pharmacological and mechanistic evidences, mainly derived from experimental studies. Colchicine interferes with microtubule-dependent cellular functions, inhibits neutrophil activation, and modulates NLRP3 inflammasome signalling, resulting in reduced interleukin-1β production. In addition, colchicine exerts pleiotropic anti-inflammatory effects that extend beyond crystal synovitis, including modulation of platelet-leukocyte interactions and vascular inflammation. Owing to its narrow therapeutic index, low-dose regimens and careful attention to drug-drug interactions are essential. This narrative review summarises the pharmacology, mechanisms of action, and clinical applications of colchicine in rheumatic disorders, particularly gout and CPPD, and its expanding use in cardiovascular diseases, dermatology, and other inflammatory disorders.