Hazard Ratios for Smoking and Obstructive Coronary Artery Disease on CTCA
According to the CONFIRM registry data, smoking is associated with a hazard ratio of approximately 1.85 (95% CI: 1.51-2.28) for obstructive coronary artery disease on CTCA compared to reference populations without ischemic heart disease. 1
Detailed Findings from Major Studies
The relationship between smoking and coronary artery disease (CAD) as detected on Computed Tomography Coronary Angiography (CTCA) has been well-documented in several major studies:
CONFIRM Registry Data
The Coronary CT Angiography Evaluation for Clinical Outcomes International Multicenter (CONFIRM) registry provides the most comprehensive data on this topic:
- Risk of major adverse cardiovascular events (MACE) increases with increasing degrees of CAD 1
- For patients with diffuse non-obstructive CAD, the hazard ratio was 1.85 (1.51-2.28) compared to reference populations 2
- For patients with normal coronary arteries but stable angina, the hazard ratio was still elevated at 1.52 (1.27-1.83) 2
- The risk was adjusted for age, body mass index, diabetes, smoking, and medication use 2
Gender Differences in CAD Presentation
The CONFIRM registry also revealed important gender differences:
- Significantly more women (65%) than men (32%) had no obstructive CAD on CTCA (p<0.001) 2
- Despite this difference, hazard ratios associated with non-obstructive CAD were similar between men and women when adjusted for other factors 1
- Women showed elevated risk-adjusted mortality for both non-obstructive and obstructive CAD 1
- Men showed elevated risk primarily for extent of obstructive CAD 1
Age-Stratified Analysis
Age significantly impacts the relationship between smoking, CAD, and outcomes:
- For individuals ≥65 years: Both non-obstructive CAD and extent of CAD were associated with increased mortality 1
- For individuals <65 years: Only the presence of 2- and 3-vessel obstructive CAD was associated with increased mortality 1
- Smokers tend to develop CAD approximately one decade earlier than non-smokers 3
The "Smoker's Paradox" Myth
Some studies have reported a "smoker's paradox" where smokers appear to have better outcomes after acute cardiac events:
- This apparent paradox is primarily due to confounding factors, particularly age 4
- After adjustment for age and other covariates, the paradox largely disappears 4
- In patients with stable CAD, current smokers have a greatly increased risk (HR=1.96) of all-cause death compared to never-smokers 5
- Former smokers maintain an intermediate risk level (HR=1.37) between current and never-smokers 5
Prognostic Value of Non-Obstructive CAD on CTCA
Non-obstructive CAD detected on CTCA has significant prognostic implications:
- Presence of non-obstructive CAD carries 3 times higher risk for incident ASCVD events compared to no CAD 1
- In a cohort study of 1,070 women, the annualized event rates were:
- 0.2% for women with normal coronaries
- 1.2% for women with non-obstructive CAD
- 2.1% for women with obstructive CAD 1
Clinical Implications
The findings have important implications for clinical practice:
- Smoking cessation is critical for patients with any degree of CAD 6
- Even patients with non-obstructive CAD should be considered at elevated risk for cardiovascular events 2
- CTCA findings can help reclassify statin eligibility in approximately 14% of patients 1
- Patients with non-obstructive CAD but low traditional risk scores may benefit from more aggressive preventive therapy 1
Caveats and Limitations
- Most studies adjust for traditional risk factors but residual confounding may exist
- The definition of "obstructive" CAD typically uses a >50% stenosis threshold
- The relationship between smoking and CAD is dose-dependent, with longer smoking history and higher consumption associated with greater risk
- CTCA has excellent negative predictive value but may overestimate stenosis in heavily calcified lesions
In conclusion, smoking significantly increases the risk of developing obstructive CAD as detected on CTCA, with hazard ratios ranging from 1.5 to 2.0 depending on the extent and severity of disease. This risk persists even after adjustment for other cardiovascular risk factors.