We have located links that may give you full text access.
Evaluation of Carotid Plaque Neovascularization in Patients With Coronary Heart Disease on Contrast-Enhanced Ultrasonography.
OBJECTIVES: To examine the repeatability of quantitative time-intensity curve analysis of neovascularization within carotid plaques with contrast-enhanced ultrasonography (US) and to investigate carotid plaque neovascularization in patients with coronary heart disease using contrast-enhanced US and the correlation between risk factors and acute coronary syndrome (ACS).
METHODS: Sixty patients with ACS and 60 with stable coronary artery disease (CAD) underwent conventional carotid and contrast-enhanced US, and plaque enhancement was observed and analyzed quantitatively. Carotid contrast-enhanced US was performed within 1 month of ACS occurrence. Interobserver and intraobserver variability of the measurements was assessed. The peak signal intensity was the maximum number of contrast microbubbles that local tissues could accumulate, reflecting the local microvascular density and representing the capillary volume.
RESULTS: The ACS group had higher low-density lipoprotein cholesterol (mean ± SD, 3.21 ± 0.75 versus 2.53 ± 0.71 mmol/L; P < .01) and high-sensitivity C-reactive protein (CRP; 3.76 ± 0.19 versus 2. 93 ± 0.15 mg/L; P < .01) levels than the stable CAD group. The proportion of soft plaques in the ACS group (81%) was higher than in the stable CAD group (53%). The proportion of plaque enhancement, peak signal intensity, and plaque-to-carotid lumen enhancement intensity ratio were higher in the ACS group than the stable CAD group. The peak signal intensity was correlated with the high-sensitivity CRP value. Logistic regression analyses indicated that age (65-74 years), high-sensitivity CRP, and enhancement intensity were correlated with the occurrence of ACS. The sensitivity and specificity of the peak signal intensity in carotid plaques were 80.0% and 88.3%, respectively (cutoff value, 9.97 dB; area under the receiver operating characteristic curve, 0.865). The time-intensity curve measurements had good repeatability.
CONCLUSIONS: Carotid plaque enhancement is a potential independent risk factor for ACS occurrence. These results illustrate the correlation of carotid plaque vulnerability with the coronary artery symptomatic state according to the common pathogenetic mechanism of atherosclerosis.
METHODS: Sixty patients with ACS and 60 with stable coronary artery disease (CAD) underwent conventional carotid and contrast-enhanced US, and plaque enhancement was observed and analyzed quantitatively. Carotid contrast-enhanced US was performed within 1 month of ACS occurrence. Interobserver and intraobserver variability of the measurements was assessed. The peak signal intensity was the maximum number of contrast microbubbles that local tissues could accumulate, reflecting the local microvascular density and representing the capillary volume.
RESULTS: The ACS group had higher low-density lipoprotein cholesterol (mean ± SD, 3.21 ± 0.75 versus 2.53 ± 0.71 mmol/L; P < .01) and high-sensitivity C-reactive protein (CRP; 3.76 ± 0.19 versus 2. 93 ± 0.15 mg/L; P < .01) levels than the stable CAD group. The proportion of soft plaques in the ACS group (81%) was higher than in the stable CAD group (53%). The proportion of plaque enhancement, peak signal intensity, and plaque-to-carotid lumen enhancement intensity ratio were higher in the ACS group than the stable CAD group. The peak signal intensity was correlated with the high-sensitivity CRP value. Logistic regression analyses indicated that age (65-74 years), high-sensitivity CRP, and enhancement intensity were correlated with the occurrence of ACS. The sensitivity and specificity of the peak signal intensity in carotid plaques were 80.0% and 88.3%, respectively (cutoff value, 9.97 dB; area under the receiver operating characteristic curve, 0.865). The time-intensity curve measurements had good repeatability.
CONCLUSIONS: Carotid plaque enhancement is a potential independent risk factor for ACS occurrence. These results illustrate the correlation of carotid plaque vulnerability with the coronary artery symptomatic state according to the common pathogenetic mechanism of atherosclerosis.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association.Circulation 2024 April 19
Essential thrombocythaemia: A contemporary approach with new drugs on the horizon.British Journal of Haematology 2024 April 9
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app