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Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
Published on: October 15, 2010
Coronary endothelial dysfunction is associated with increased risk of venous thromboembolism
Megha Prasad1, Robert McBane1, Martin Reriani1
1Division of Cardiovascular Disease, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Insights
Coronary endothelial dysfunction (CED) predicts venous thromboembolism (VTE) in patients with coronary atherosclerosis. This suggests endothelial injury may disrupt vascular hemostasis, increasing VTE risk.
Area of Science:
- Cardiovascular Medicine
- Vascular Biology
- Thrombosis Research
Background:
- Normal endothelial function is crucial for natural anticoagulation.
- Endothelial dysfunction is a potential risk factor for venous thromboembolism (VTE).
- Coronary atherosclerosis patients without critical stenoses may have underlying endothelial dysfunction.
Purpose of the Study:
- To determine if coronary endothelial dysfunction (CED) predicts the development of VTE.
- To investigate the association between CED and VTE incidence in patients with coronary atherosclerosis.
Main Methods:
- Evaluated coronary microvascular function in 502 patients with coronary atherosclerosis using intracoronary acetylcholine.
- Defined coronary microvascular endothelial dysfunction as ≤50% increase in coronary blood flow.
- Assessed VTE development via questionnaire after a median follow-up of 6.3 years.
Main Results:
- Coronary endothelial dysfunction (CED) was present in 56% of patients.
- Nine VTE events occurred in patients with CED, versus none in the control group (P=0.01).
- Common risk factors included hypertension, diabetes, and hyperlipidemia.
Conclusions:
- Coronary endothelial dysfunction (CED) is significantly associated with the future development of VTE.
- Endothelial injury may contribute to VTE by disrupting vascular hemostasis.
- CED could serve as a predictive marker for VTE in specific patient populations.
Background:
Normal endothelial function is central to physiologic anticoagulation mechanisms. Endothelial dysfunction may predispose to venous thromboembolism (VTE). We aimed to investigate if coronary endothelial dysfunction (CED) predicts development of VTE in patients presenting with coronary atherosclerosis without critical stenoses.
Methods:
Coronary microvascular function was evaluated in 502 patients with coronary atherosclerosis without critical stenoses by administration of intracoronary acetylcholine at the time of diagnostic study. After a median follow-up of 6.3years, patients were assessed for the development of VTE by administration of a questionnaire. Coronary microvascular endothelial dysfunction was defined as ≤50% increase in coronary blood flow from baseline in response to maximal dose of acetylcholine.
Results:
The median age was 53years (IQR: 45, 62) 68% were female and CED occurred in 279 (56%) patients. Hypertension (40.8%), diabetes (8.4%), and hyperlipidemia (58.3%) were common risk factors. There were no differences in baseline characteristics between those with and without CED. There were 9 VTE events (6 unprovoked) among patients with CED compared to no events in the control group (P=0.01).
Discussion:
CED was associated with the development of VTE. Endothelial injury by causing disruption of vascular hemostasis may play a role in predisposing patients to VTE.
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