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Lipoprotein(a) Is Associated With Onset of Aortic Valve Calcification
Quick Takes
- Lp(a) is associated with baseline and new-onset aortic valve calcium (AVC), but not with AVC progression.
- Lp(a)-lowering interventions may effectively prevent AVC onset but are less likely to attenuate AVC progression in individuals with established AVC.
- Studies of Lp(a)-lowering treatment in the pre-calcific stages of aortic valve disease are indicated to assess potential benefits.
Study Questions:
Are high serum levels of lipoprotein(a) [Lp(a)] associated with aortic valve calcium (AVC) incidence and progression?
Methods:
The investigators enrolled a total of 922 individuals from the population-based Rotterdam Study (mean age 66.0 ± 4.2 years, 47.7% men), whose Lp(a) measurements were available. The subjects underwent non–enhanced cardiac computed tomography imaging at baseline and after a median follow-up of 14.0 (interquartile range [IQR], 13.9–14.2) years. New-onset AVC was defined as an AVC score >0 on the follow-up scan in the absence of AVC on the first scan. Progression was defined as the absolute difference in AVC score between the baseline and follow-up scan. Logistic and linear regression analyses were performed to evaluate the relationship of Lp(a) with baseline, new onset, and progression of AVC. All analyses were corrected for age, sex, body mass index, smoking, hypertension, dyslipidemia, and creatinine. AVC progression was analyzed conditional on baseline AVC score expressed as restricted cubic splines.
Results:
Of the 702 individuals without AVC at baseline, 415 (59.1%) developed new-onset AVC on the follow-up scan. In those with baseline AVC, median annual progression was 13.5 (IQR, 5.2–37.8) Agatston units (AU). Lp(a) concentration was independently associated with baseline AVC (odds ratio [OR], 1.43 for each 50 mg/dL higher Lp[a]; 95% confidence interval [CI], 1.15–1.79) and new-onset AVC (OR, 1.30 for each 50 mg/dL higher Lp[a]; 95% CI, 1.02–1.65), but not with AVC progression (β: −71 AU for each 50 mg/dL higher Lp[a]; 95% CI, −117 to 35). Only baseline AVC score was significantly associated with AVC progression (p < 0.001).
Conclusions:
The authors reported that Lp(a) is robustly associated with baseline and new-onset AVC but not with AVC progression.
Perspective:
This study reports that Lp(a) is associated with baseline and new-onset AVC, but not with AVC progression. Furthermore, among individuals with AVC at baseline, the AVC score was the only determinant of further progression. These data suggest that Lp(a)-lowering interventions may effectively prevent AVC onset but are less likely to attenuate AVC progression in individuals with established AVC. Studies of Lp(a)-lowering treatment in the pre-calcific stages of aortic valve disease are indicated to assess potential benefits.
Clinical Topics: Cardiac Surgery, Dyslipidemia, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Prevention, Valvular Heart Disease, Aortic Surgery, Cardiac Surgery and Arrhythmias, Cardiac Surgery and VHD, Advanced Lipid Testing, Lipid Metabolism, Interventions and Imaging, Interventions and Structural Heart Disease, Computed Tomography, Nuclear Imaging
Keywords: Aortic Valve Disease, Aortic Valve Stenosis, Calcium, Cardiac Surgical Procedures, Diagnostic Imaging, Heart Valve Diseases, Lipoprotein(a), Secondary Prevention, Tomography, X-Ray Computed, Vascular Calcification
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