Review

Low-dose colchicine for management of coronary artery disease

Abhayjit Singh, MD, Vikas Sunder, MD and Leslie Cho, MD
Cleveland Clinic Journal of Medicine October 2025, 92 (10) 609-618; DOI: https://doi.org/10.3949/ccjm.92a.25005

ABSTRACT

Cardiovascular disease remains a leading cause of morbidity and mortality worldwide. Though inflammation plays an important role in atherogenesis, treatments directly targeting inflammatory pathways have had mixed results on improving clinical outcomes. Low-dose colchicine has been studied recently for the management of atherosclerotic cardiovascular disease. We explore the history of colchicine as an anti-inflammatory agent, review clinical trial data of colchicine for atherosclerotic cardiovascular disease, and discuss practical considerations for adding low-dose colchicine in this setting.

KEY POINTS

  • Inflammation plays an important role in the pathogenesis of atherosclerosis and contributes to residual risk of cardiovascular events despite optimal treatment of traditional cardiovascular risk factors.

  • Colchicine, an anti-inflammatory agent long used for the prevention and treatment of gout, was recently approved by the US Food and Drug Administration for the reduction of cardiovascular events in adults with established atherosclerotic disease or with multiple risk factors for atherosclerotic cardiovascular disease.

  • Contemporary clinical trials examining the use of low-dose colchicine in patients with stable coronary artery disease or following an acute coronary syndrome have produced somewhat conflicting results.

The past half century has seen significant progress in the prevention and treatment of coronary artery disease. Increased understanding of the pathophysiology of atherosclerosis, advancements in drug therapy for cardiovascular risk factors, and evolving treatment paradigms for acute and chronic coronary syndromes have collectively decreased the mortality rate from premature heart disease. Despite this progress, atherosclerotic cardiovascular disease remains the leading cause of death in the United States, with mortality rates largely having plateaued since 2010.1

At a societal level, this is likely due to continued high rates of uncontrolled hypertension and the increasing prevalence of diabetes and obesity, all of which are firmly established risk factors for cardiovascular disease.2 At an individual level, however, many patients continue to experience cardiovascular events despite aggressive treatment. This so-called “residual risk” may stem from inflammatory, thrombotic, and metabolic pathways that remain suboptimally controlled even with guideline-directed medical therapy.3

Clinical trial data suggest that a large proportion of patients treated with statins and other lipid-lowering therapies have residual inflammatory risk.4 In addition, both historical and contemporary data support the notion that inflammation may be as strong a predictor of cardiovascular risk as low-density lipoprotein cholesterol.5 These observations have fueled significant interest in developing novel cardiovascular drugs that can target residual inflammatory risk.

Here, we review data from clinical trials of the anti-inflammatory agent colchicine as a therapy for atherosclerotic cardiovascular disease, and discuss practical considerations for adding low-dose colchicine to standard medical therapy for coronary artery disease.

INFLAMMATION IN ATHEROSCLEROTIC CARDIOVASCULAR DISEASE

The role of inflammation in atherogenesis was initially recognized in the 19th century, when Rudolph Virchow noted inflammatory changes in histological preparations of coronary arteries.6 Since that time, inflammation has emerged as an increasingly important risk factor for the development of cardiovascular disease.

The pathobiological role that inflammation plays in the atherosclerotic cascade—including plaque initiation, maturation, destabilization, and ultimately rupture—has been known for decades.7 It is well-established that patients with autoimmune inflammatory conditions are at increased risk for coronary atherosclerosis, endothelial dysfunction, and ultimately cardiovascular events.8 In studies of patients without autoimmune disease followed in the Physicians’ Health Study9 and Women’s Health Study,10 inflammatory markers such as C-reactive protein, interleukin 6, and interleukin 1beta were highly associated with incident atherosclerotic cardiovascular disease.

In 1950, the first semiquantitative test for measuring C-reactive protein was developed, and around the start of the 21st century, more sensitive assays capable of detecting chronic low-grade inflammation became commercially available.11 Today, the presence of autoinflammatory comorbidities is recognized as an important risk enhancer for atherosclerotic cardiovascular disease, and current guidelines support the assessment of systemic inflammation by measuring serum high-sensitivity C-reactive protein (hsCRP) concentrations to better discriminate cardiovascular risk in patients with an intermediate 10-year risk score.12,13

TARGETING INFLAMMATION TO LOWER ATHEROSCLEROTIC RISK

Despite the abundance of data, it was unclear whether atherosclerotic cardiovascular disease risk can be attenuated by reducing inflammation. In the early 2000s, Nissen et al14 used intravascular ultrasonography to demonstrate that the magnitude of reduction in serum C-reactive protein and low-density lipoprotein cholesterol levels with statin therapy were each independent predictors of plaque regression.

The landmark JUPITER (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin) trial,15 published in 2008, showed that in patients taking rosuvastatin for primary prevention who had a low-density lipoprotein cholesterol of 130 mg/dL or lower and an hsCRP greater than 2.0 mg/L, treatment with rosuvastatin lowered serum hsCRP levels by 37% and significantly lowered the risk of major adverse cardiovascular events. Nevertheless, we didn’t know whether the benefit of statin therapy was mediated by reduced systemic inflammation or lower atherogenic lipoprotein levels.

In 2017, results from CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcome Study)16 strongly supported the notion that inflammation plays a critical role in atherosclerotic events. In this trial, Ridker et al16 showed that treatment with canakinumab, a therapeutic monoclonal antibody targeting interleukin 1beta, resulted in significantly fewer adverse cardiovascular events than placebo in patients with previous myocardial infarction with optimally treated low-density lipoprotein cholesterol but elevated hsCRP. Importantly, this effect appeared to be independent of lipid-level lowering, as there was no significant treatment effect on low-density lipoprotein cholesterol levels.

A prespecified secondary analysis further showed that trial participants randomized to canakinumab whose hsCRP concentrations were reduced below 2.0 mg/L had a 25% reduction in major adverse cardiovascular events, while no significant benefit was observed in patients whose on-treatment hsCRP concentrations remained above 2.0 mg/L.17 However, the US Food and Drug Administration (FDA) did not approve canakinumab for the secondary prevention of atherosclerotic cardiovascular disease, citing concerns that the drug provided only modest cardiovascular benefits with a concurrent increase in the risk of fatal infection.

Although canakinumab failed to gain FDA approval as a cardiovascular therapy, CANTOS16 provided an important proof of concept that it was possible to lower atherosclerotic risk by targeting inflammation. This concept was further explored in CIRT (Cardiovascular Inflammation Reduction Trial),18 a study in which patients with established cardiovascular disease were treated with low-dose methotrexate. CIRT was stopped early due to futility, as methotrexate did not result in fewer cardiovascular events compared with placebo. In this trial, methotrexate treatment did not lower inflammatory biomarkers such as C-reactive protein, interleukin 1beta, or interleukin 6, suggesting that its failure to improve cardiovascular outcomes may have been due in part to its inability to meaningfully suppress systemic inflammation.

Similarly, in the 2014 phase 3 STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Therapy) trial,19 darapladib (a selective oral inhibitor of proinflammatory lipoprotein-associated phospholipase A2) failed to reduce cardiovascular events in patients with stable coronary heart disease.

Despite these setbacks for anti-inflammatory drug therapy in coronary artery disease, evidence of a causal role of inflammation in the development and progression of atherosclerotic cardiovascular disease continued to grow. Attention subsequently turned to a much older anti-inflammatory therapy: colchicine.

MECHANISMS OF COLCHICINE’S ANTI-INFLAMMATORY EFFECTS

Colchicine exerts its anti-inflammatory effects through multiple mechanisms. Microtubules play a key role in the inflammatory cascade, including cytokine and chemokine secretion, cell division, cytoskeletal rearrangement, and intracellular signaling.20 By binding to tubulin, colchicine blocks microtubule assembly and polymerization, which prevents the chemotaxis, adhesion, mobilization, and superoxide anion production of inflammatory cells (primarily neutrophils).

Colchicine also impairs mitosis, inhibiting the growth of vascular smooth muscle cells and fibroblasts, and intracellular signaling, inhibiting assembly of the macromolecular NLRP3 inflammasome complex that mediates the release of interleukin 1beta and other interleukins.21

Finally, colchicine blunts the platelet-leukocyte interaction and activation of macrophages by tumor necrosis factor alpha.

HISTORY OF COLCHICINE AS AN ANTI-INFLAMMATORY AGENT

The earliest known use of colchicine dates back to 1550 bce, when it was extracted from the autumn crocus plant (Colchicum autumnale) by the ancient Egyptians for the treatment of pain and swelling.22 More than 3,300 years later, Nicolas Husson developed Eau Medicinale, a commercial preparation for the treatment of gout in which colchicine was the main ingredient.23 Benjamin Franklin is credited with introducing colchicine in the United States later in the 18th century, and the purified active ingredient was finally developed by Philipp Lorenz Geiger in 1833.23,24

Despite colchicine’s long history, it was not until 1961 that it was approved in the United States, where it is commonly used for the prophylaxis and treatment of acute gout flares. A half century later, in 2009, the FDA approved a new formulation of colchicine for the prevention of gout flares and the treatment of familial Mediterranean fever.25

Although colchicine is approved for only a few indications, its potent anti-inflammatory effects have led to frequent off-label use for the management of pericarditis, BehÇet syndrome, pseudogout, and other inflammatory conditions.

Subsequent clinical data further suggested that colchicine could be useful in patients with coronary artery disease:

  • Nidorf and Thompson26 in 2007 showed that low-dose colchicine significantly decreased hsCRP levels in patients with stable coronary artery disease and a baseline hsCRP level of 2 mg/L or greater.

  • Multiple retrospective analyses showed an association between colchicine and a lower incidence of cardiovascular events in patients with gout.27,28

  • More recent imaging studies using coronary computed tomography angiography29 and optical coherence tomography30 suggested that the anti-inflammatory and immunomodulatory properties of colchicine may favorably modify and stabilize atherosclerotic coronary plaque.

CLINICAL TRIALS OF COLCHICINE IN CORONARY ARTERY DISEASE

The preclinical and retrospective data discussed above set the stage for conducting prospective randomized clinical trials to evaluate the role of colchicine in patients with coronary artery disease. Five trials (summarized in Table 1)31–38 that enrolled more than 18,500 patients have provided most of the randomized trial data for colchicine as a therapy in atherosclerotic cardiovascular disease.

View this table:
TABLE 1

Summary of seminal clinical trials studying the use of low-dose colchicine

Prevention in stable coronary artery disease

The LoDoCo (Low-Dose Colchicine) trial,31 published in 2013, was the first among these trials that studied colchicine in coronary artery disease. It enrolled about 500 patients with stable coronary artery disease and randomized them to 0.5 mg colchicine daily or no colchicine. After a median follow-up of 3 years, treatment with colchicine reduced the incidence of the primary end point (composite of acute coronary syndrome, cardiac arrest, noncardioembolic stroke) by 10.7% (5.3% vs 16%). Most patients in this trial were on antiplatelet (93%) and statin (95%) therapy. LoDoCo, although relatively small, was the first randomized controlled trial to suggest that adding low-dose colchicine to standard medical therapy could prevent cardiovascular events in patients with stable coronary artery disease.

LoDoCo2,32 a larger trial, confirmed the findings of LoDoCo. Published in 2020, this randomized, controlled, double-blind trial assigned over 5,500 patients with stable coronary artery disease to 0.5 mg colchicine daily or placebo. After 28.6 months of follow-up, the primary composite end point of major adverse cardiovascular events occurred in 6.8% of patients in the colchicine group vs 9.6% of patients in the placebo group. A total of 451 primary outcome events were reported, and colchicine was associated with a 31% lower relative risk of the primary end point (hazard ratio [HR] 0.69, 95% confidence interval [CI] 0.57–0.83). The benefits of colchicine on the primary end point were consistent in subgroup analyses defined by sex, age, renal function, and presence of hypertension or diabetes.

Interestingly, LoDoCo232 showed a numerically higher incidence of noncardiovascular death (HR 1.51, 95% CI 0.99–2.31) and all-cause death (HR 1.21, 95% CI 0.86–1.71) in patients who received colchicine vs those receiving placebo.

Neither LoDoCo31 or LoDoCo232 routinely measured C-reactive protein, so the effects of treatment according to inflammatory state at baseline could not be examined. Nevertheless, these trials provided robust evidence that in patients with stable chronic coronary disease, treatment with daily low-dose colchicine significantly reduced the incidence of cardiovascular events.

After an acute coronary syndrome

Unlike low-dose colchicine in stable coronary artery disease, the clinical trials that looked at the potential benefit of low-dose colchicine in patients after a recent acute coronary syndrome produced conflicting data. Two trials specifically evaluated the effectiveness of colchicine in preventing major adverse cardiovascular events in the post–myocardial infarction setting.

COPS (Colchicine in Patients With Acute Coronary Syndromes)34 was a trial conducted in Australia that randomized 795 patients who presented with acute coronary syndrome to receive either colchicine or placebo. Although there was a numeric trend toward reduction of the primary major adverse cardiovascular events end point, the COPS trial34 was unable to demonstrate a statistically significant reduction in coronary events with colchicine treatment after 12 months (HR 0.65, 95% CI 0.38–1.09), which may have been related, in part, to difficulty recruiting the required number of patients. However, a subsequent analysis at the 24-month mark did show a significant reduction in the primary composite outcome (8.1% vs 13.5%, P = .02).35

Of note, 8 deaths occurred in the colchicine arm of the COPS trial34,35 compared with 1 death in the placebo arm.

COLCOT (Colchicine Cardiovascular Outcomes Trial)33,37 randomized 4,745 patients who had a myocardial infarction to either colchicine 0.5 mg daily or placebo within 30 days of the event. After a median follow-up of 22.6 months, the incidence of major adverse cardiovascular events was statistically significantly lower in the colchicine arm (5.5%) than in the placebo arm (7.1%), a 23% relative reduction (HR 0.77, 95% CI 0.61–0.96).

Both COPS and COLCOT were published around the same time as LoDoCo2 and overall supported the notion that colchicine may be a useful adjunct in patients with atherosclerotic cardiovascular disease.

CLEAR-Synergy (Colchicine and Spironolactone in Patients With Myocardial Infarction/Synergy Stent Registry),36 the most recent colchicine trial, however, tells a different story. This 2 × 2 factorial study evaluated both low-dose colchicine and spironolactone in more than 7,000 patients who presented with acute coronary syndrome and were treated with percutaneous coronary intervention. Initially, colchicine dosing was weight based and patients weighing 70 kg or more were given colchicine 0.5 mg or placebo twice daily, although due to increased rates of discontinuation, the steering committee changed the dosing to daily during the trial.

At a median 3 years of follow-up, the incidence of major adverse cardiovascular events in the colchicine arm was 9.1% vs 9.3% in the placebo arm (HR 0.99, 95% CI 0.85–1.16). No cardiovascular benefit was seen, despite a significantly greater reduction in C-reactive protein levels (measured in a subset of the trial population) in patients receiving colchicine.

CLEAR-Synergy36 represents the largest randomized assessment of colchicine in patients who have had a myocardial infarction and failed to demonstrate the same benefit that was shown in COLCOT.

DIVERGENT FINDINGS AFTER ACUTE CORONARY SYNDROME

The reason for the divergent outcomes in CLEAR-Synergy and COLCOT is not immediately apparent, but similarities and differences between the trials and missing details from each can be considered when interpreting these data.

Type of acute coronary syndrome. Initially, CLEAR-Synergy36 enrolled only patients with ST-segment elevation myocardial infarction, and later expanded enrollment criteria to include patients with large, high-risk non–ST-segment elevation myocardial infarction. Ultimately, 95.1% of patients in this trial had a ST-segment elevation myocardial infarction and 4.9% had non–ST-segment elevation myocardial infarction, whereas the type of acute coronary syndrome was not reported in COLCOT.33,37

Interventions and concurrent therapy. In both trials, most patients (> 90%) underwent percutaneous coronary intervention. Rates of concurrent therapy with aspirin, P2Y12 inhibitors (eg, clopidogrel), and statins were also similar, but use of nonstatin therapies and low-density lipoprotein cholesterol levels were not reported in either trial.

Timing of colchicine initiation. In COLCOT,33 all patients underwent randomization within 30 days (mean 13.5 days) of their acute myocardial infarction. A secondary analysis found that patients who received colchicine within 3 days of myocardial infarction derived greater benefit than those treated later.37 Other data suggested that administration of colchicine before percutaneous coronary intervention resulted in lower vascular inflammation biomarkers after the procedure.39 The benefits of early colchicine therapy were not reproduced in CLEAR-Synergy,36 however, which did not show similar benefits despite patients being randomized within 48 hours of percutaneous coronary intervention.

Number of primary events. While COLCOT33,37 had 377 primary outcome events, CLEAR-Synergy36 was a larger trial and had 649 events. As discussed by the authors, earlier data have shown that trials with more than 600 outcome events rarely produce results disproven by subsequent trials.40

COVID-19 pandemic effects. It is notable that much of the CLEAR-Synergy36 enrollment and follow-up period coincided with the COVID-19 pandemic. Interestingly, there was a 22% reduction in the incidence of that trial’s primary end point event with colchicine before the pandemic that was subsequently lost during the pandemic.41 Post hoc analyses of other cardiovascular outcomes trials conducted during the pandemic have shown similar findings.

FDA APPROVAL

When the results of the published clinical trials are evaluated in their entirety, the data for patients with stable atherosclerotic cardiovascular disease or subclinical atherosclerosis—determined by invasive angiography, computed tomography angiography, or coronary calcium scoring—overall support the use of low-dose colchicine for reducing the risk of future cardiovascular events. Despite the reduction in major adverse cardiovascular events, trials have not shown a reduction in all-cause mortality with low-dose colchicine. On the contrary, LoDoCo232 and COPS34,35 found numerically higher rates of all-cause death in patients treated with colchicine, and a 2021 meta-analysis found that colchicine was associated with a nominal increase in death from noncardiovascular causes, counterbalanced by a lower incidence of cardiovascular death.42 Reassuringly, neither COLCOT (HR 0.98, 95% CI 0.64–1.49)33,37 nor CLEAR-Synergy (HR 0.90, 95% CI 0.73–1.12)36 found an increase in all-cause mortality, and no such trend is observed in retrospective analyses of patients receiving colchicine therapy for gout.28

Reflecting this evidence, the FDA in June 2023 approved colchicine 0.5 mg daily for reducing the risk of myocardial infarction, stroke, coronary revascularization, and cardiovascular death in adults with established atherosclerotic cardiovascular disease or with multiple risk factors for it. Notably, this approval came before the CLEAR-Synergy trial36 data were published.

This landmark decision marked the first FDA approval for a pure anti-inflammatory therapy for atherosclerotic cardiovascular disease risk reduction. Shortly after regulatory approval was granted, both the American43 and European44 multisociety guidelines for chronic coronary disease endorsed the use of colchicine in patients with coronary artery disease.

COLCHICINE NOT YET WIDELY ADOPTED IN ROUTINE PRACTICE

Despite recent FDA approval, low-dose colchicine (0.5 mg daily) added to optimal medical therapy for patients with coronary artery disease has not yet been adopted in routine clinical practice. A recent analysis of the National Prescription Audit found a very modest increase in monthly colchicine prescriptions since 2020, with less than 4% prescribed by cardiologists.45

This relative underutilization likely stems, at least in part, from the divergent trial data presented above, ie, the data suggest that colchicine confers cardiovascular benefit in patients with chronic coronary artery disease, but its benefit during the stable phase after an acute coronary syndrome event remains uncertain. However, LoDoCo2,32 the largest clinical trial of colchicine in patients with chronic coronary disease, showed that 35 patients needed to be treated with low-dose colchicine for just under 2.5 years to prevent 1 major adverse cardiovascular event, a number needed to treat comparable to that of aspirin, statins, and antihypertensive therapy in secondary prevention.46

PRACTICAL CONSIDERATIONS

Measure biomarkers of inflammation before starting colchicine?

In theory, the benefit of colchicine may be greatest in patients with the highest residual inflammatory risk, but none of the aforementioned clinical trials required an elevated C-reactive protein for enrollment, and the trials did not systematically measure hsCRP or other biomarkers of inflammation. Multisociety guidelines and the FDA label similarly do not stipulate that hsCRP should be measured before colchicine therapy is started.

In CLEAR-Synergy,36 C-reactive protein was measured at baseline and at 3 months in about 40% of the trial population, and treatment with colchicine resulted in a placebo-adjusted difference in C-reactive protein levels of –1.28 mg/L. Despite this reduction, the least-squares mean hsCRP remained elevated at 2.98 mg/L (95% CI 2.6–3.5) in the colchicine arm, suggesting potentially inadequate control of residual inflammation. Though treatment with colchicine did not reduce the primary end point in this trial, data are not yet available about whether patients who had significant decreases in inflammatory biomarkers may have derived clinical benefit.

Post hoc analyses of the LoDoCo2 and COLCOT trials, along with a recent meta-analysis, similarly showed reductions in C-reactive protein levels with colchicine treatment.47,48 Though the data may not necessarily support the use of inflammatory markers to discern which patients may derive the greatest benefit from colchicine therapy, some experts advocate measuring hsCRP concentrations to document residual inflammation before starting colchicine.49

Balancing risk and benefit

When considering colchicine therapy, clinicians must take into account other medications, relative contraindications, and tolerability of treatment. Colchicine has many drug-drug interactions, and while many of these may not be clinically significant, special attention should be paid to cytochrome P450 and P-glycoprotein inhibitors.50 Similarly, in patients with blood dyscrasias or significant renal or hepatic impairment, the risks, benefits, and necessary dosing adjustments of colchicine therapy should be carefully considered.

Also, it is important to counsel patients about potential adverse effects. In colchicine clinical trials, the most commonly reported side effect was diarrhea (placebo-adjusted rates of 5%–15%), while other gastrointestinal effects (nausea, abdominal pain) and myalgias were reported less often.31–37,46 However, most clinical trials have a run-in period, which may result in underestimation of side effects. In LoDoCo2,32 for example, 43% of patients who started the run-in period but did not undergo randomization reported gastrointestinal upset. Other observed adverse effects occurred at similar rates in patients receiving colchicine and those receiving placebo.

Though colchicine reduces leukocyte-platelet interaction, it does not appear to meaningfully impact platelet function or increase the risk of clinically significant bleeding or cytopenias.51

OUR RECOMMENDATIONS

Low-dose colchicine appears to confer cardiovascular benefit in patients with stable ischemic heart disease, but benefits remain more uncertain for patients with a recent acute coronary syndrome. When caring for aging populations with increasingly more comorbidities, it is important to weigh the relative clinical benefits, adverse effect profiles, and potential costs of multiple therapies. In doing so, clinicians should explore whether patients might derive a meaningful clinical benefit from low-dose colchicine using the trial data that were the basis for both its FDA approval and the American43 and European44 guideline recommendations. For patients in whom the benefits of colchicine are likely to outweigh the harms, clinicians should formulate individualized, patient-centric care strategies and consider the use of colchicine on a case-by-case basis.

Figure 131–37 shows a potential algorithm for considering the addition of low-dose colchicine to guideline-directed medical therapy for coronary artery disease.

Figure 1
Figure 1

Proposed algorithm for considering the initiation of low-dose colchicine based on findings from large randomized controlled trials.31–37

aSubclinical atherosclerosis: calcium score of at least 400 Agatston units on a coronary artery calcium scan or evidence of coronary artery disease on invasive coronary angiography or computed tomography angiography.

bCytochrome P450 and P-glycoprotein inhibitors share metabolism pathways with colchicine.

cColchicine dose studied in most clinical trials was 0.5 mg daily.

CLEAR = Colchicine and Spironolactone in Patients With Myocardial Infarction/Synergy Stent Registry; COLCOT = Colchicine Cardiovascular Outcomes Trial; COPS = Colchicine in Patients With Acute Coronary Syndromes; LoDoCO = Low-Dose Colchicine

FUTURE DIRECTIONS

It is abundantly clear that patients have residual cardiovascular risk despite optimal control of traditional risk factors, and inflammation is increasingly recognized as a causal risk factor in the development of coronary artery disease. Future research of anti-inflammatory therapies to reduce cardiovascular risk may further elucidate the link between inflammation and atherogenesis and help clarify which patients may benefit most from immunomodulating therapies.

Divergent data from clinical trials of colchicine, canakinumab, methotrexate, and darapladib also underscore the need for further studies looking at whether modifying inflammatory pathways can achieve cardiovascular benefit. To this end, 2 ongoing trials are evaluating the impact of ziltivekimab (a monoclonal antibody targeting interleukin 6) on cardiovascular outcomes in patients with atherosclerotic cardiovascular disease who have had a recent myocardial infarction (ARTEMIS [Effects of Ziltivekimab Versus Placebo on Cardiovascular Outcomes in Patients With Acute Myocardial Infarction]) and those who have not had a recent myocardial infarction (ZEUS [Effects of Ziltivekimab Versus Placebo on Cardiovascular Outcomes in Participants With Established Atherosclerotic Cardiovascular Disease, Chronic Kidney Disease and Systemic Inflammation]).

Although the treatment of inflammation in cardiovascular disease requires further study, landmark clinical trials and recent FDA approval of low-dose colchicine have added this drug to the armamentarium of therapies for coronary artery disease.

DISCLOSURES

Dr. Cho has disclosed consulting for AstraZeneca Pharmaceuticals and Esperion; serving as a research principal investigator for AstraZeneca Pharmaceuticals and Novartis Pharmaceuticals; serving as research study chair for Eli Lilly; and serving on the steering committee for CLEAR outcomes for Esperion. The other authors report no relevant financial relationships which, in the context of their contributions, could be perceived as a potential conflict of interest.

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