Lp(a) linked to aortic valve calcium in people without aortic stenosis
Lipoprotein(a) was associated with prevalent and incident aortic valve calcification and calcium progression in participants without aortic stenosis, researchers reported.
“Lp(a) may represent a therapeutic target for aortic stenosis, and clinical tools are needed to guide such future therapy,” Harpreet S. Bhatia, MD, MAS, cardiologist and assistant professor of medicine at UC San Diego Health, and colleagues wrote. “We aimed to evaluate the associations between baseline Lp(a) levels in individuals without known CVD with incident aortic valve calcium and aortic valve calcium progression on serial CT examinations, which have not previously been studied.”
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To assess the associations between Lp(a) quartile and prevalent and incident aortic valve calcium and calcium progression, researchers used data from 6,699 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort study without aortic stenosis at baseline.
Lp(a) was measured by using turbidimetric immunoassay (Denka Seiken) and all participants underwent cardiac CT at baseline.
Half of the cohort was followed up from 2002 to 2004, and half from 2004 to 2005, according to the study. In addition, a second follow-up was performed in a subgroup from 2010 to 2011.
Participants were stratified into quartiles according to Lp(a) levels (quartile 1, 2-7.5 mg/dL; quartile 2, 7.6-17.3 mg/dL; quartile 3, 17.4-40.6 mg/dL; quartile 4, > 40.6 mg/dL).
Researchers noted that baseline aortic valve calcium score and follow-up time were not significantly different across the quartiles of Lp(a).
Lp(a) and aortic valve calcium
Prevalence of aortic valve calcium score of more than 0 was greater among participants in the fourth quartile of Lp(a) compared with the first quartile (4.4% vs. 3.2%; P < .001) and was significantly associated with prevalent aortic valve calcium (OR = 1.75; 95% CI, 1.39-2.21).
Among participants without aortic valve calcium at baseline, the fourth quartile of Lp(a) was associated with incident aortic valve calcium at first follow-up (OR = 2.49; 95% CI, 1.59-3.88) and second follow-up (OR = 1.72; 95% CI, 1.17-2.54) compared with the first quartile.
Researchers reported that the fourth quartile of Lp(a) in participants with incident aortic valve calcium at baseline was associated with greater annual calcium progression at first follow-up (median, 2.68 years) compared with the first quartile (P = .021). However, among those with aortic valve calcium at second follow-up, Lp(a) was not significantly associated with calcium progression from baseline to second follow-up (median, 9.42 years; P = .923), according to the researchers.
Guideline defined elevated Lp(a)
Bhatia and colleagues noted that in their analysis, prevalent aortic valve calcium and calcium progression were observed at Lp(a) levels as low as 40.6 mg/dL, and incident aortic valve calcium at Lp(a) levels as low as 17.4 mg/dL, whereas current joint guidelines define elevated Lp(a) as 50 mg/dL or more.
“In individuals without baseline CVD, Lp(a) was associated with aortic valve calcification prevalence, incidence and progression,” the researchers wrote. “This provides further evidence for calcification as the mechanism linking Lp(a) to aortic stenosis, and Lp(a) measurement may identify individuals at risk for development and progression of aortic valve calcium. Aortic valve calcium may also prompt Lp(a) testing for cardiovascular risk assessment. This is the first study, to our knowledge, to describe the association between Lp(a) and aortic valve calcium incidence and progression in individuals without aortic stenosis.”
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