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Published on: February 4, 2021
Association between Aortic Valve Calcification Progression and Coronary Atherosclerotic Plaque Volume Progression in
Sang-Eun Lee1, Ji Min Sung1, Daniele Andreini1
1From the Division of Cardiology, Department of Internal Medicine, Ewha Womans University Seoul Hospital, Ewha Womans University College of Medicine, Seoul, South Korea (S.E.L.); Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea (S.E.L., J.M.S., H.J.C.); Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, South Korea (J.M.S., S.S., H.J.C.); Centro Cardiologico Monzino, IRCCS, Milan, Italy (D.A., E.C., G.P.); Houston Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital, Houston, Tex (M.H.A.); Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, Calif (M.J.B.); Cardiovascular Imaging Unit, SDN IRCCS, Naples, Italy (F.C.); Department of Cardiology, William Beaumont Hospital, Royal Oak, Mich (K.C.); Pusan University Hospital, Busan, South Korea (J.H.C.); Seoul National University Bundang Hospital, Seongnam, South Korea (E.J.C.); Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil (I.G.); Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany (M.H.); Department of Internal Medicine, Seoul National University College of Medicine, Cardiovascular Center, Seoul National University Hospital, Seoul, South Korea (Y.J.K.); Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea (B.K.L.); Department of Medicine and Radiology, University of British Columbia, Vancouver, Canada (J.A.L.); Department of Radiology, Area Vasta 1/ASUR Marche, Urbino, Italy (E.M.); UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisbon, Portugal (H.M., P.d.A.G.); Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, Mass (P.H.S.); Division of Cardiology, Emory University School of Medicine, Atlanta, Ga (H.S.); Department of Pathology, CVPath Institute, Gaithersburg, Md (R.V.); Icahn School of Medicine at Mount Sinai, New York, NY (J.N.); Department of Imaging and Medicine, Cedars-Sinai Medical Center, Los Angeles, Calif (D.S.B.); Department of Radiology, New York-Presbyterian Hospital and Weill Cornell Medicine, New York, NY (L.J.S., F.Y.L., J.K.M.); Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands (J.J.B.).
Insights
Aortic valve calcification (AVC) progression is linked to increased calcified plaque in coronary arteries, but not noncalcified plaque. This finding may refine treatment strategies for patients with aortic stenosis and coronary artery disease.
Area of Science:
- Cardiovascular Imaging
- Atherosclerosis Research
- Cardiac CT Angiography
Background:
- Aortic valve calcification (AVC) is a marker for aortic stenosis, a condition often co-occurring with coronary artery disease.
- Understanding the relationship between AVC progression and coronary atherosclerosis can improve patient management.
- Coronary CT angiography (CCTA) provides detailed insights into both conditions.
Purpose of the Study:
- To investigate the association between the progression of AVC and changes in coronary plaque volume and composition.
- To analyze serial CCTA data from a large, multicenter registry to quantify these relationships.
Main Methods:
- Utilized data from the PARADIGM registry, including serial CCTA examinations over at least two years.
- Quantitatively assessed AVC scores and normalized total, calcified, and noncalcified plaque volumes at baseline and follow-up.
- Employed multivariable linear mixed-effects models to analyze associations, adjusting for clinical factors.
Main Results:
- In 594 participants, baseline AVC was associated with total, calcified, and noncalcified plaque volumes.
- Progression of AVC was significantly associated with the progression of total plaque volume.
- This association was driven by an increase in calcified plaque volume, not noncalcified plaque volume.
Conclusions:
- Baseline coronary atherosclerosis burden is associated with AVC.
- Progression of AVC specifically correlates with the progression of calcified coronary plaque, not noncalcified plaque.
- These findings highlight distinct pathways in the progression of calcification in the aorta and coronary arteries.
Abstract:
Background Aortic valve calcification (AVC) is a key feature of aortic stenosis, and patients with aortic stenosis often have coronary -artery disease. Therefore, proving the association between the progression of AVC and coronary atherosclerosis could improve follow-up and treatment strategies. Purpose To explore the association between the progression of AVC and the progression of total and plaque volume composition from a large multicenter registry of serial coronary CT angiographic examinations. Materials and Methods A prospective multinational registry (PARADIGM) of consecutive participants who underwent serial coronary CT angiography at intervals of every 2 years or more was performed (January 2003-December 2015). AVC and the total and plaque volume composition at baseline and follow-up angiography were quantitatively analyzed. Plaque volumes were normalized by using the mean total analyzed vessel length of the study population. Multivariable linear mixed-effects models were constructed. Results Overall, 594 participants (mean age ± standard deviation, 62 years ± 10; 330 men) were included (mean interval between baseline and follow-up angiography, 3.9 years ± 1.5). At baseline, the AVC score was 31 Agatston units ± 117, and the normalized total plaque volume at baseline was 122 mm3 ± 219. After adjustment for age, sex, clinical risk factors, and medication use, AVC was independently associated with total plaque volume (standardized β = 0.24; 95% CI: 0.16, 0.32; P < .001) and both calcified (β = 0.26; 95% CI: 0.18, 0.34; P < .001) and noncalcified (β = 0.17; 95% CI: 0.08, 0.25; P < .001) plaque volumes at baseline. The progression of AVC was associated with the progression of total plaque volume (β = 0.13; 95% CI: 0.03, 0.22; P = .01), driven solely by calcified plaque volume (β = 0.24; 95% CI: 0.14, 0.34; P < .001) but not noncalcified plaque volumes (β = -0.06; 95% CI: -0.14, 0.03; P = .17). Conclusion The overall burden of coronary atherosclerosis was associated with aortic valve calcification at baseline. However, the progression of aortic valve calcification was associated with only the progression of calcified plaque volume but not with the -progression of noncalcified plaque volume. Clinical trial registration no. NCT02803411 © RSNA, 2021 See also the editorial by Sinitsyn in this issue.
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