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Warfarin Use Is Associated With Progressive Coronary Arterial Calcification: Insights From Serial Intravascular
Jordan Andrews1, Peter J Psaltis1, Ozgur Bayturan2
1Vascular Research Centre, Heart Health Theme, South Australian Health and Medical Research Institute and School of Medicine, University of Adelaide, Adelaide, Australia.
Insights
Warfarin treatment in patients with coronary artery disease did not alter atheroma volume but was associated with increased coronary artery calcification. Further research is needed to understand the impact on plaque stability and cardiovascular outcomes.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Pharmacology
Background:
- Warfarin inhibits matrix Gla protein, a key regulator of arterial calcification.
- The in vivo effect of warfarin on coronary artery calcification progression in humans remains largely unknown.
Purpose of the Study:
- To compare serial changes in coronary percent atheroma volume (PAV) and calcium index (CaI) in patients with coronary artery disease treated with and without warfarin.
Main Methods:
- A post hoc analysis of 8 prospective randomized trials involving serial coronary intravascular ultrasound examinations.
- Compared changes in PAV and CaI in matched arterial segments in patients with and without warfarin over 18-24 months.
Main Results:
- Warfarin treatment was not associated with significant differences in annualized changes in PAV.
- Warfarin-treated patients showed a significantly greater annualized increase in CaI compared to non-warfarin-treated patients.
- Warfarin was independently associated with increasing CaI in a multivariate model.
Conclusions:
- Warfarin therapy is linked to progressive coronary artery calcification, independent of changes in atheroma volume.
- The clinical implications of warfarin-associated calcification on plaque stability and cardiovascular outcomes warrant further investigation.
Objectives:
This study compared serial changes in coronary percent atheroma volume (PAV) and calcium index (CaI) in patients with coronary artery disease who were treated with and without warfarin.
Background:
Warfarin blocks the synthesis and activity of matrix Gla protein, a vitamin K-dependent inhibitor of arterial calcification. The longitudinal impact of warfarin on serial coronary artery calcification in vivo in humans is unknown.
Methods:
In a post hoc patient-level analysis of 8 prospective randomized trials using serial coronary intravascular ultrasound examinations, this study compared changes in PAV and CaI in matched arterial segments in patients with coronary artery disease who were treated with (n = 171) and without (n = 4,129) warfarin during an 18- to 24-month period.
Results:
Patients (mean age 57.9 ± 9.2 years; male 73%; prior and concomitant 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statin) use, 73% and 97%, respectively) demonstrated overall increases in PAV of 0.41 ± 0.07% (p = 0.001 compared with baseline) and in CaI (median) of 0.04 (interquartile range [IQR]: 0.00 to 0.11; p < 0.001 compared with baseline). Following propensity-weighted adjustment for clinical trial and a range of clinical, ultrasonic, and laboratory parameters, there was no significant difference in the annualized change in PAV in the presence and absence of warfarin treatment (0.33 ± 0.05% vs. 0.25 ± 0.05%; p = 0.17). A significantly greater annualized increase in CaI was observed in warfarin-treated compared with non-warfarin-treated patients (median 0.03; IQR: 0.0 to 0.08 vs. median 0.02; IQR: 0.0 to 0.06; p < 0.001). In a sensitivity analysis evaluating a 1:1 matched cohort (n = 164 per group), significantly greater annualized changes in CaI were also observed in warfarin-treated compared with non-warfarin-treated patients. In a multivariate model, warfarin was independently associated with an increasing CaI (odds ratio: 1.16; 95% confidence interval: 1.05 to 1.28; p = 0.003).
Conclusions:
Warfarin therapy is associated with progressive coronary atheroma calcification independent of changes in atheroma volume. The impact of these changes on plaque stability and cardiovascular outcomes requires further investigation.
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