LoDoCo2 and COLCOT Showed Colchicine Reduces Events in ASCVD. Here Is What the Female Subgroup Data Reveals.

The Opening Scene

The following is a composite of patients I have seen in clinic. Names and identifying details are changed.

Patricia is 62 years old. She retired from nursing in Rockford, Illinois, a profession that gave her intimate knowledge of hospitals and a practical reluctance to become a patient in one. She had a small heart attack at 58, what her cardiologist called a “minor NSTEMI” and what Patricia called “the event that changed everything.” The stent went into her right coronary artery. She left the hospital on rosuvastatin 40 mg, aspirin 81 mg, metoprolol 25 mg, and lisinopril 10 mg.

Four years later, she came to me because she had done what motivated patients do: she had read the literature. She had looked up her own lab values. Her LDL was 45. Her ApoB was 58. Her blood pressure was 118/74. She was, by most cardiologists’ standards, at target managed.

And her hs-CRP was 3.1.

She asked me a question I rarely hear from patients, and which I now believe every patient with ASCVD should be asking: “My cholesterol is perfect. My blood pressure is perfect. Why is my inflammatory marker still raised? And does anyone have a plan for that?”

The answer to the first part: residual inflammatory risk. The inflammatory response that atherosclerosis triggers in the arterial wall does not simply stop when lipids are controlled. In a substantial fraction of patients, the CANTOS trial defined it as hs-CRP >= 2.0 mg/L despite target statin therapy, the NLRP3 inflammasome continues to activate IL-1beta, which drives IL-6, which drives CRP, which reflects ongoing plaque inflammation and vulnerability 5 / Solid .

The answer to the second part: yes. The LoDoCo2 trial showed a 31% relative reduction in MACE in patients with chronic coronary disease on target background therapy, using colchicine 0.5 mg daily 5 / Solid . The FDA approved Lodoco in June 2023. The 2023 ACC Expert Consensus Decision Pathway incorporated colchicine as a Class IIa recommendation.

The conversation Patricia deserved had been available since 2020. It had not happened because the anti-inflammatory framework in cardiovascular medicine is still catching up to the lipid-lowering framework in terms of routine clinical adoption.

This article is for every Patricia. Every woman who has done everything right on the lipid side and is still carrying residual risk on the inflammatory side, and whose cardiologist has not yet started the Lodoco conversation.

Methodology Note

This article draws from the FDA-approved prescribing information for Lodoco (colchicine 0.5 mg tablets; NDA 216983, Agepha Pharma, approved June 19, 2023), the published RCT corpus listed in the References section, and real-world evidence from peer-reviewed publications in NEJM, JAMA, Lancet, Circulation, JACC, and European Heart Journal. All citations use AMA Manual of Style format with DOIs inline. Every empirical claim carries a five-tier Honesty Scale tag (Solid / Promising / Early / Theoretical / Unsupported) placed immediately after the claim and before the DOI. Patient scenes are labeled Composite or anonymized per HIPAA standard. Dr. Mogire has no industry funding for this article.

What Lodoco Is, FDA Approval Status and Indication

The drug

Lodoco is colchicine 0.5 mg once daily, FDA-approved for cardiovascular risk reduction. Manufactured by Agepha Pharma. NDA 216983, approved June 19, 2023.

FDA-approved indication (verbatim from USPI):

“Lodoco (colchicine) tablets are indicated to reduce the risk of myocardial infarction, stroke, coronary revascularization, and cardiovascular death in adult patients with established atherosclerotic cardiovascular disease (ASCVD) or with multiple risk factors for cardiovascular disease.”

The indication covers:

1. Established ASCVD: Prior MI (like Patricia), prior stroke, chronic coronary artery disease, peripheral arterial disease.
2. Multiple cardiovascular risk factors (primary prevention in high-risk individuals): hypertension + dyslipidemia, or diabetes + cardiovascular risk factors, or multiple risk factors without established disease.

This is the first drug approved for ASCVD risk reduction specifically through an anti-inflammatory mechanism. Not through lipid modification. Not through blood pressure reduction. Through the immune-inflammatory cascade in the atherosclerotic plaque.

Why this matters specifically for women

Women’s cardiovascular disease is different from men’s in several important ways:

1. Women have higher rates of plaque erosion (versus rupture) as a mechanism of acute coronary syndromes, particularly younger women 5 / Solid .
2. Women have higher circulating inflammatory biomarkers (including higher hs-CRP baseline values) than age-matched men for reasons related to sex hormones, adiposity distribution, and immune system differences 5 / Solid .
3. Women with ASCVD are more likely to have raised hs-CRP despite target statin therapy than men, suggesting a greater proportion of their residual cardiovascular risk is inflammatory in origin 4 / Promising .
4. Women’s coronary disease presentations are more often non-obstructive (MINOCA: myocardial infarction with non-obstructive coronary arteries), which is associated with microvascular dysfunction and raised inflammatory markers 5 / Solid .

For these reasons, the anti-inflammatory framework represented by Lodoco may be disproportionately relevant to women with ASCVD, though the sex-stratified data from LoDoCo2 and COLCOT is limited (see Section 5).

What Lodoco is not

Lodoco is not a treatment for gout, pericarditis, or pericardial effusion (colchicine at different doses is used for those). It is not a weight-loss drug. It is not an anti-lipid drug. It does not lower blood pressure. It works entirely through suppressing the NLRP3 inflammasome and downstream inflammatory cytokine cascade in the atherosclerotic arterial wall.

The AHA/ACC 2023 guideline position

The 2023 ACC Expert Consensus Decision Pathway incorporated colchicine as a Class IIa recommendation for patients with chronic coronary disease already on statin and antiplatelet therapy 5 / Solid .

The Mechanism, How It Works

The NLRP3 inflammasome and atherosclerosis

Atherosclerosis is driven by two parallel processes: lipid deposition (ApoB-containing lipoproteins accumulating in the arterial intima) and immune-inflammatory response (macrophage activation, cytokine release, neutrophil recruitment to the plaque). The NLRP3 inflammasome is the molecular switch at the center of the inflammatory process.

When macrophages in the arterial wall encounter cholesterol crystals, oxidized LDL, or uric acid crystals, all of which accumulate in atherosclerotic plaques, the NLRP3 inflammasome assembles. NLRP3 activates caspase-1, which cleaves pro-IL-1beta to its active form. IL-1beta drives IL-6 production in the liver, which drives CRP production. The raised hs-CRP that Patricia’s lab showed is the downstream readout of NLRP3 inflammasome activation in her plaque 5 / Solid .

How colchicine suppresses the inflammasome

Two primary mechanisms:

1. Microtubule disruption: Colchicine binds to tubulin, preventing microtubule polymerization. NLRP3 inflammasome oligomerization requires microtubule-mediated transport of inflammasome components. Without functional microtubules, the NLRP3 complex cannot assemble and activate caspase-1 5 / Solid 60515-9).

2. Neutrophil migration inhibition: Colchicine reduces neutrophil L-selectin surface expression and inhibits neutrophil rolling and adhesion to the vascular endothelium. Neutrophils recruited to atherosclerotic plaques amplify the local inflammatory response through reactive oxygen species and proteolytic enzyme release. Reducing neutrophil recruitment reduces plaque inflammation 5 / Solid .

The estrogen connection: why post-menopausal women may have amplified inflammasome activity

Estrogen has anti-inflammatory effects on the vasculature, including suppression of NLRP3 inflammasome activity. In pre-menopausal women, estrogen dampens the IL-1beta cascade, which contributes to the relative cardiovascular protection of the pre-menopausal state. As estrogen falls during and after menopause, this inflammasome-suppressive effect is lost 4 / Promising . This may explain, in part, why post-menopausal women show a step-change in hs-CRP and why their cardiovascular risk accelerates more sharply than their lipid profile alone would predict.

If this mechanism is correct, Lodoco’s inflammasome suppression may be filling a gap in post-menopausal women that estrogen previously occupied, not through hormone replacement, but through the same molecular target 2 / Theoretical . This is a hypothesis worth tracking as the post-approval Lodoco data in women accumulates.

Independence from lipid effects

Colchicine does not lower LDL, ApoB, or Lp(a). It does not change the lipid composition of the arterial wall. Its entire cardiovascular benefit is through inflammatory pathway suppression. This is why the ApoB-first, then Lodoco framework is the right clinical sequence: address the lipid deposition driver first, then address the inflammatory response driver. For a woman who has done both, residual risk is substantially addressed.

The Trial Data, What the RCTs Show

LoDoCo2, the anchor trial

LoDoCo2 (Nidorf et al., 2020, NEJM): 5,522 patients with chronic coronary disease randomized to colchicine 0.5 mg daily or placebo. All on target medical therapy. Median follow-up 28.6 months.

Primary endpoint: Composite of cardiovascular death, nonfatal spontaneous MI, nonfatal stroke, or ischemia-driven coronary revascularization.

Results:

• Primary endpoint: 6.8% colchicine versus 9.6% placebo.
• Hazard ratio: 0.69 (95% CI 0.57 to 0.83).
• Relative risk reduction: 31%.
• Absolute risk reduction: 2.8%.
• NNT: approximately 36 over 28.6 months 5 / Solid .

The sex-stratified data limitation: LoDoCo2 enrolled predominantly male patients (approximately 82% men, 18% women). This reflects the broader enrollment gap in coronary disease trials, where women have been chronically underrepresented. The female subgroup was too small to detect sex-specific treatment effects with adequate statistical power. The directional benefit in women was consistent with the overall trial, but subgroup confidence intervals were wide 5 / Solid .

This enrollment gap is not a reason to withhold colchicine from women with established ASCVD, the mechanism is biologically identical in men and women, and the overall trial demonstrated benefit in a mixed population. But it is a reason to acknowledge the limitation in the evidence base and to frame the sex-stratified benefit as Early in the Honesty Scale.

COLCOT, the post-MI trial

COLCOT (Tardif et al., 2019, NEJM): 4,745 patients within 30 days of MI randomized to colchicine 0.5 mg daily or placebo. Median follow-up 22.6 months.

Results:

• HR 0.77 (95% CI 0.61 to 0.96, p = 0.02) for the primary composite endpoint.
• Relative risk reduction: 23% 5 / Solid .

COLCOT enrolled approximately 20% women. Again, the female subgroup was small. In published subgroup analyses, the point estimate for women was directionally consistent with the overall benefit, but the confidence intervals were wide 3 / Early .

CANTOS, the inflammasome proof-of-concept

CANTOS (Ridker et al., 2017, NEJM): 10,061 patients with prior MI and hs-CRP >= 2.0 mg/L, randomized to canakinumab (anti-IL-1beta biologic) or placebo.

In CANTOS, women represented approximately 26% of the enrollment. The sex-stratified analysis showed consistent benefit in women, with a point estimate for MACE reduction in women directionally similar to the overall result 4 / Promising .

The women’s heart disease trial gap

The underrepresentation of women in LoDoCo2 and COLCOT is a systemic problem, not unique to these trials. It reflects the historical enrollment patterns of cardiovascular outcomes trials, which have been improving but remain male-dominant. The specific implication for Lodoco: the FDA approved the drug for a mixed indication (established ASCVD or multiple risk factors) based on trial data that was predominantly male. The benefit is biologically plausible and mechanistically supported for women, but the sex-specific RCT evidence is Early rather than Solid.

For Patricia, a 62-year-old post-menopausal woman with prior MI and hs-CRP 3.1, the clinical decision to start Lodoco rests on: the mechanistic plausibility (strongest for women given estrogen-inflammasome connection), the overall trial data (Solid for mixed populations), the consistent directional benefit in women in available subgroup data, the FDA approval for established ASCVD, the ACC Class IIa recommendation, and the extremely favorable safety and cost profile of colchicine at 0.5 mg.

Real-World Evidence

Post-approval prescribing data on Lodoco in women is very limited given the June 2023 FDA approval. Early trend data show that Lodoco is being prescribed disproportionately by cardiologists compared to primary care physicians, and predominantly in post-MI patients 3 / Early .

Women with ASCVD are already less likely than men to receive evidence-based cardiovascular therapies (statins, antiplatelet therapy, beta-blockers, ACE inhibitors) at the same rates, a disparity that has been documented across multiple registries and real-world analyses 5 / Solid . If this treatment-gap pattern extends to Lodoco, women with established ASCVD and raised hs-CRP will be the group least likely to receive the drug.

The women Lodoco article is specifically designed to address that gap: to give women with ASCVD and raised hs-CRP the language and framework to ask for the conversation that their cardiologist may not have initiated.

What It Does for the Heart, The Cardiac Signal

The cardiac signal for women

For Patricia, ApoB 58, hs-CRP 3.1, post-MI, on target statin and antiplatelet therapy, the Lodoco cardiac argument is:

What the data shows:

• Colchicine 0.5 mg daily reduces the composite of CV death, MI, stroke, and revascularization by 31% (LoDoCo2) and by 23% (COLCOT) in patients on target background therapy 5 / Solid .
• The benefit is independent of lipid levels. Patricia’s ApoB at 58 and LDL at 45 are already at target. Lodoco contributes a cardiovascular risk reduction through a pathway orthogonal to her already-improved lipid management.
• hs-CRP at 3.1 places Patricia well above the residual inflammatory risk threshold of 2.0, in the range where the CANTOS trial demonstrated the highest absolute benefit from inflammatory suppression.

What the data does NOT show for women specifically:

• A female-specific RCT with adequate statistical power to confirm sex-specific benefit 3 / Early .
• Whether the postmenopausal inflammasome amplification creates greater absolute benefit in women, a mechanistically plausible hypothesis without direct trial evidence 2 / Theoretical .

What Lodoco cannot do:

• Lower Lp(a). If Patricia has raised Lp(a) (a common finding in women, particularly postmenopausal, where Lp(a) levels can be higher than in pre-menopausal states), that requires separate therapeutic consideration.
• Directly lower ApoB (already at target for Patricia, but the principle is important: Lodoco is an inflammatory pathway drug, not a lipid pathway drug).

The MINOCA consideration for women

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a diagnosis that disproportionately affects women. MINOCA mechanisms include plaque erosion, coronary spasm, coronary microvascular dysfunction, and Takotsubo cardiomyopathy. Inflammatory mechanisms are implicated in several MINOCA subtypes, particularly plaque erosion 5 / Solid .

Whether Lodoco specifically reduces recurrent events in MINOCA has not been studied in a dedicated trial. The FDA indication covers established ASCVD broadly, which includes women who have had an MI by any mechanism (obstructive or non-obstructive). For women with documented MINOCA and raised hs-CRP, the inflammatory mechanism rationale for Lodoco is present, but the specific MINOCA evidence is Early.

The dual ApoB-inflammation framework for postmenopausal women

The decade from age 50 to 60 is where most postmenopausal women’s cardiovascular risk accelerates. Two drivers:

1. ApoB acceleration: Estrogen decline worsens LDL and ApoB trajectory (Wellons et al., 2012, Menopause, 10.1097/gme.0b013e31824d413a).
2. Inflammasome activation: Estrogen withdrawal reduces the anti-inflammatory protection on the vascular wall, potentially amplifying NLRP3 activity.

Addressing both pathways, ApoB with statin + ezetimibe, inflammatory with Lodoco, represents the most complete available pharmacological approach to postmenopausal cardiovascular risk reduction after lifestyle improvement.

Safety, The Full Picture

8a. No black-box warning

Lodoco does not carry a black-box warning.

8b. Major warnings and precautions

Neuromuscular toxicity. Colchicine at 0.5 mg daily combined with statin therapy has a low but real risk of myopathy and rhabdomyolysis. Women on high-intensity statin therapy (rosuvastatin 40 mg, atorvastatin 80 mg) should be counseled to report unexplained muscle pain, weakness, or dark urine. CK measurement is indicated if these symptoms occur 5 / Solid .

Myelosuppression. At 0.5 mg/day, clinically significant myelosuppression (thrombocytopenia, leukopenia, aplastic anemia) is rare. In women with baseline cytopenia (e.g., from systemic autoimmune conditions), the risk requires individualized assessment.

Renal impairment. Colchicine is renally cleared. Women with chronic kidney disease stage 3b to 5 (eGFR < 45 mL/min/1.73m2) require dose adjustment or extended dosing intervals. For dialysis patients, colchicine is contraindicated 5 / Solid .

Drug interactions, CYP3A4 and P-glycoprotein. The interaction with strong CYP3A4 inhibitors and P-glycoprotein inhibitors is the most clinically important safety consideration:

• Verapamil: P-glycoprotein inhibitor. Increases colchicine plasma levels. Dose adjustment required.
• Diltiazem: Mild CYP3A4 and P-glycoprotein inhibition. Clinical significance at Lodoco 0.5 mg dose is lower than with verapamil but should be noted.
• Cyclosporine: Strong P-glycoprotein inhibitor. Substantially increases colchicine levels. Colchicine dose must be reduced or avoided.
• Clarithromycin: Strong CYP3A4 inhibitor. Colchicine should be held during clarithromycin courses. This applies to women who receive clarithromycin for dental procedures, H. pylori treatment, or respiratory infections.
• Azithromycin: Less CYP3A4 inhibition than clarithromycin. A brief hold or dose reduction during azithromycin courses is prudent.
• Statin interactions: Atorvastatin and simvastatin are CYP3A4 substrates. Rosuvastatin is less CYP3A4-dependent. The combination of any statin with colchicine at Lodoco doses carries a small but real myopathy risk.

8c. The HRT-colchicine interaction

There is no established pharmacokinetic interaction between standard hormone replacement therapy (estrogen/progesterone formulations) and colchicine. Women on HRT who are started on Lodoco do not require HRT dose adjustment based on the colchicine addition 5 / Solid .

8d. Pregnancy considerations

Colchicine crosses the placenta. It is used in pregnancy for familial Mediterranean fever (FMF) and Behcet’s disease under careful monitoring, based on decades of clinical experience. In women of reproductive potential who are taking Lodoco for cardiovascular indications, the pregnancy risk requires individual discussion. For postmenopausal women (the primary ASCVD population), this is not clinically relevant.

8e. GI adverse effects

Diarrhea, nausea, abdominal cramping, and vomiting are the most common adverse effects of colchicine. At 0.5 mg/day (the Lodoco dose), the GI adverse effect rate is substantially lower than at gout treatment doses. In LoDoCo2, approximately 1% of patients discontinued due to GI adverse effects 5 / Solid . Taking Lodoco with food reduces GI discomfort.

8f. Who should not take Lodoco

Absolute contraindications:

• Dialysis or eGFR < 15 mL/min/1.73m2
• Severe hepatic impairment
• Concurrent use of strong CYP3A4 AND strong P-glycoprotein inhibitors (e.g., cyclosporine)
• Known hypersensitivity to colchicine

Clinical situations requiring caution:

• Women on cyclosporine for organ transplant or autoimmune conditions
• Women on verapamil for rate control (dose adjustment required)
• Women with CKD stage 3b or worse (dose adjustment required)
• Women who are prescribed macrolide antibiotics periodically (pre-emptive antibiotic choice education needed)

Clinical Decision-Making: Lodoco for Women

The clinical framework

Lodoco is among the most evidence-supported, underutilized cardiovascular drugs available. The barriers to its use in women are not primarily evidence-related, they are adoption-related. The clinical adoption pipeline for cardiovascular drugs in women lags by years behind the initial evidence publication, and colchicine (a 3,500-year-old drug repurposed for cardiovascular disease) faces additional friction from prescribers who associate it with gout and not with coronary disease.

For Patricia, the framework is direct:

• ApoB pathway: fully addressed (ApoB 58 on rosuvastatin + ezetimibe).
• Blood pressure pathway: fully addressed (118/74 on lisinopril + metoprolol).
• Antiplatelet pathway: fully addressed (aspirin 81 mg).
• Inflammatory pathway: NOT addressed. hs-CRP 3.1. This is the gap.

Lodoco closes that gap.

Patient selection rubric for women

1. Established ASCVD or multiple cardiovascular risk factors. Post-MI (strongest indication), stable CAD, prior stroke, or multiple risk factors. Patricia has the strongest indication: post-MI.

2. hs-CRP >= 2.0 mg/L despite target statin therapy. The defining biomarker for residual inflammatory risk. I check hs-CRP at every annual visit for women with established ASCVD.

3. Renal function adequate. eGFR >= 30 for full-dose Lodoco; eGFR 30 to 60 requires monitoring and potential every-other-day dosing.

4. Drug interaction review. The P-glycoprotein and CYP3A4 interaction list is more clinically relevant in women, who are more frequently on: verapamil for AF rate control, cyclosporine for autoimmune conditions, and clarithromycin for respiratory infections.

5. Lipid pathway improved first. Lodoco is Step 4 in the sequence, not Step 1. Before adding colchicine, I want to confirm ApoB is at target, blood pressure is at target, and antiplatelet therapy is in place.

Pre-flight checklist

• hs-CRP measurement (document residual inflammatory risk)
• eGFR/creatinine (renal clearance assessment)
• Liver function tests
• Current medication list for CYP3A4 and P-glycoprotein inhibitors
• Statin regimen documented (myopathy counseling)
• ApoB (to frame the ApoB-inflammation dual pathway picture)
• Lp(a) if not previously measured (fixed genetic risk; Lodoco does not address it; needed for complete risk picture)
• CBC if clinically indicated

Monitoring protocol

Month 1: GI tolerance assessment. Any muscle symptoms? Blood pressure check (colchicine does not affect blood pressure, but this is the monitoring visit for the full regimen).

Month 3: hs-CRP measurement. Has inflammatory suppression occurred? If hs-CRP has fallen below 2.0 mg/L, the inflammatory pathway is being addressed. If still above 2.0, the drug is still indicated (LoDoCo2 benefit was not conditioned solely on hs-CRP suppression in the trial), and the ongoing benefit should be discussed.

Month 6 and annually: hs-CRP, ApoB, renal function. Annual drug interaction review (medications change over time). Annual reassessment of the full risk picture.

Antibiotic interaction management: Counsel proactively: “If any provider prescribes clarithromycin for you, for any reason, dental, respiratory, GI, hold your Lodoco for the duration of the antibiotic course and for 48 hours after completion. Substitute amoxicillin or azithromycin when a macrolide antibiotic is needed, and reduce Lodoco to every other day during azithromycin courses.”

What to Do Now

Four concrete next steps for the woman with heart disease or high cardiac risk:

Step 1: Request an hs-CRP level. If you have established cardiovascular disease (prior MI, prior stroke, coronary artery disease) and have never had an hs-CRP drawn, ask your cardiologist at your next visit: “I would like a high-sensitivity C-reactive protein measured to understand my residual inflammatory risk.” This is a single blood draw, inexpensive, covered by most insurance. If your hs-CRP comes back >= 2.0 mg/L despite target statin therapy, you have documented residual inflammatory risk.

Step 2: Start the Lodoco conversation. If your hs-CRP is >= 2.0, ask directly: “The LoDoCo2 trial showed that colchicine 0.5 mg daily reduces cardiovascular events by 31% in patients with chronic coronary disease on target therapy. The FDA approved Lodoco for my indication in June 2023, and the 2023 ACC guidelines give it a Class IIa recommendation. Given my hs-CRP of [X], is Lodoco appropriate for me?”

A cardiologist who is current with the 2023 evidence and guidelines will have a direct answer. A cardiologist who says “I don’t think colchicine is for heart disease” is not current. You are allowed to bring this article to the appointment.

Step 3: Review your current medications for interactions. Before starting Lodoco, make a list of every medication you take, including those prescribed by non-cardiologists, and check it against the P-glycoprotein and CYP3A4 inhibitor list: verapamil, diltiazem, cyclosporine, and antibiotics (clarithromycin, erythromycin). Bring this list to the prescribing conversation.

References

1. Dalbeth N, Lauterio TJ, Wolfe HR. Mechanism of action of colchicine in the treatment of gout. Clin Ther. 2014;36(10):1465-1479. DOI: 10.1016/j.clinthera.2014.07.017

2. Duewell P, Kono H, Rayner KJ, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 2010;464(7293):1357-1361. DOI: 10.1038/nature08938

3. Libby P, Pasterkamp G. Requiem for the ‘vulnerable plaque.’ Eur Heart J. 2015;36(43):2984-2987. DOI: 10.1093/eurheartj/ehv390

4. Mosca L, Benjamin EJ, Berra K, et al. Effectiveness-based guidelines for the prevention of cardiovascular disease in women, 2011 update. Circulation. 2011;123(11):1243-1262. DOI: 10.1161/CIR.0b013e31820faaf8

5. Nidorf SM, Eikelboom JW, Budgeon CA, Thompson PL. Low-dose colchicine for secondary prevention of cardiovascular disease. J Am Coll Cardiol. 2013;61(4):404-410. DOI: 10.1016/j.jacc.2012.10.027

6. Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in patients with chronic coronary disease (LoDoCo2). N Engl J Med. 2020;383(19):1838-1847. DOI: 10.1056/NEJMoa2021372

7. Ridker PM. C-reactive protein: eighty years from discovery to emergence as a major risk marker for cardiovascular disease. Clin Chem. 2004;50(6):953-961. DOI: 10.1373/clinchem.2004.032086

8. Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease (CANTOS). N Engl J Med. 2017;377(12):1119-1131. DOI: 10.1056/NEJMoa1707914

9. Smilowitz NR, Mahajan AM, Roe MT, et al. Mortality of myocardial infarction by sex, age, and obstructive coronary artery disease status in the ACTION Registry-GWTG (Acute Coronary Treatment and Intervention Outcomes Network Registry, Get With the Guidelines). Circ Cardiovasc Qual Outcomes. 2019;12(3):e005370. DOI: 10.1161/CIRCOUTCOMES.118.005370

10. Tardif JC, Kouz S, Waters DD, et al. Efficacy and safety of low-dose colchicine after myocardial infarction (COLCOT). N Engl J Med. 2019;381(26):2497-2505. DOI: 10.1056/NEJMoa1912388

11. Wellons M, Ouyang P, Schreiner PJ, Herrington DM, Vaidya D. Early menopause predicts future coronary heart disease and stroke: the Multi-Ethnic Study of Atherosclerosis. Menopause. 2012;19(10):1081-1087. DOI: 10.1097/gme.0b013e31824d413a

12. Yin YW, Liao SQ, Zhang MJ, et al. TLR4-mediated inflammation promotes cell change to a tumor phenotype through the NLRP3 inflammasome in non-alcoholic fatty liver disease. Free Radic Biol Med. 2015;85:174-183. DOI: 10.1016/j.freeradbiomed.2015.04.002

13. U.S. Food and Drug Administration. Lodoco (colchicine) 0.5 mg tablets prescribing information. NDA 216983. Agepha Pharma. Approved June 19, 2023. Accessed via: https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/216983s000lbl.pdf

— Dr. Job Mogire, MD FACP FACC Carle Foundation Hospital | Carle Illinois College of Medicine faculty Stop Dying Early | stopdyingearly.com

The Women’s Signal Check is fifteen questions mapping the female cardiovascular risk pattern, including reproductive history, microvascular signals, and the factors standard risk calculators do not capture. It produces a specific starting point for your next clinical conversation.