Lipoprotein(a) and Aortic Valve Calcification
- Using data from MESA, among people without known CVD, Lp(a) was associated with aortic valve calcification (AVC) prevalence, incidence, and progression.
- Lp(a) measurement might help identify individuals at risk of progressive aortic stenosis, and the finding of AVC on CT could be useful to prompt Lp(a) testing as part of cardiovascular risk assessment.
Among individuals without known cardiovascular disease (CVD), are there associations between lipoprotein(a) (Lp[a]) levels and incident and/or progressive aortic valve calcification (AVC) on serial computed tomography (CT)?
Data were used from the MESA (Multi-Ethnic Study of Atherosclerosis), a prospective study of people without known CVD. CT scans for AVC were performed in all participants at baseline, and in half of participants between 2002-2004 and half between 2004-2005; a second follow-up CT scan was performed in a subset between 2010-2011. Lp(a) quartile was evaluated for associations with prevalent AVC, incident AVC, and AVC progression.
Prevalence data were available for 6,699 participants; 5,063 had AVC = 0 at baseline (for incidence analysis), and 583 had AVC >0 at baseline and first follow-up and 297 had AVC >0 baseline and second follow-up (for progression analysis). The prevalence of AVC >0 was greater in the fourth Lp(a) quartile (>40.6 mg/dL) compared to the first quartile (2.0-7.5 mg/dL, 4.4 vs. 3.3%, p < 0.001). The highest Lp(a) quartile was significantly associated with prevalent AVC (odds risk [OR], 1.75; 95% confidence interval [CI], 1.39-2.21). Among participants without baseline AVC, the highest Lp(a) quartile was associated with incident AVC at first follow-up CT (OR, 2.49; 95% CI, 1.59-3.88) and the second follow-up (OR, 1.72; 95% CI, 1.17-2.54). Among those with AVC at the first follow-up, the fourth Lp(a) quartile was associated with greater annual AVC progression (ß 21.24, standard error [SE] 9.20, p = 0.021) at a median follow-up of 2.68 (interquartile range [IQR], 1.56-3.10) years; however, among those with AVC at the second follow-up, Lp(a) was not associated with AVC progression from baseline to second follow-up (fourth Lp[a] quartile ß –0.51, SE 5.25, p = 0.923) at a median follow-up of 9.42 (IQR, 9.18-9.80) years.
In individuals without baseline CVD, Lp(a) was associated with AVC prevalence, incidence, and progression. The authors conclude that assessment of AVC might be a useful clinical tool for patients with elevated Lp(a), especially in the context of future therapy for lowering Lp(a).
Lp(a) is associated with AVC and the development and progression of aortic stenosis. In this study, data from MESA were used to show associations between higher Lp(a) levels and the prevalence, incidence, and progression of AVC among people without known CVD. The study was limited by a relatively small sample size and possible selection bias, possibly explaining a demonstrated association between Lp(a) and AVC progression at a median of 2.7 years but not at 9.4 years. The demonstrated associations between Lp(a) and AVC suggest that Lp(a) measurement might help identify individuals at risk of progressive aortic stenosis, and that the presence of AVC on CT could be useful to prompt Lp(a) testing as part of cardiovascular risk assessment.
Clinical Topics: Diabetes and Cardiometabolic Disease, Dyslipidemia, Noninvasive Imaging, Prevention, Valvular Heart Disease, Advanced Lipid Testing, Lipid Metabolism, Computed Tomography, Nuclear Imaging
Keywords: Aortic Valve Stenosis, Atherosclerosis, Calcinosis, Cardiovascular Diseases, Diagnostic Imaging, Dyslipidemias, Heart Valve Diseases, Lipoprotein(a), Risk Factors, Secondary Prevention, Tomography, X-Ray Computed, Vascular Calcification
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