Does Aortic Valve Calcification Predict Cardiovascular Events?
Does Aortic Valve Calcification Predict Cardiovascular Events?
Abstract & Commentary
By Harold L. Karpman, MD, FACC, FACP
Clinical Professor of Medicine, UCLA School of Medicine
Dr. Karpman reports no financial relationships relevant to this field of study.
Synopsis: The presence of aortic valve calcification (AVC) predicts cardiovascular and coronary event risk independent of traditional risk factors and inflammatory biomarkers, likely due to the strong correlation between AVC and subclinical atherosclerosis.
Source: Owens DS, et al. Aortic valve calcium independently predicts coronary and cardiovascular events in a primary prevention population. J Am Coll Cardiol Img 2012;5:619-625.
CALCIFIC AORTIC VALVE DISEASE (CAVD) IS COMMON IN older adults with an estimated prevalence of 25% in individuals older than 65 years of age.1 It is caused by biological processes that share both epidemiological2,3 and histopathological4 similarities to coronary atherosclerosis.
The presence of aortic valve calcification (AVC) without obstruction has been found to be associated with a 50% increase in the risk of cardiovascular events.5 Owens and his colleagues sought to determine whether the presence of aortic valve calcium detected on computed tomography (CT) scans predicts cardiovascular events in a younger cohort by performing a prospective analysis6 of the subjects in the Multi-Ethnic Study of Atherosclerosis (MESA).7 In the MESA study, all subjects who were 45 to 84 years old and free of clinical cardiovascular disease at baseline underwent CT for evaluation of AVC and coronary artery calcium (CAC) scoring. AVC was found to predict cardiovascular and coronary event risk independent of traditional risk factors and inflammatory biomarkers, likely due to the strong correlation between AVC and subclinical atherosclerosis.
Commentary
The MESA study is a National Heart, Lung, and Blood Institute-sponsored, population-based investigation of subclinical cardiovascular disease and its progression.7 In addition to a comprehensive baseline examination including a clinic visit, baseline testing, evaluation of cardiovascular risk factors, and blood analyses, baseline CT scans were obtained and analyzed for both coronary artery and aortic valve calcium content. The aortic valve was considered to be calcified if calcific lesions resided solely within the aortic valve leaflets (i.e., exclusive of the aortic annulus and/or coronary arteries) and found to contain at least three contiguous pixels ≥ 130 Hounsfield units of brightness. Participants with baseline AVC had a higher prevalence of CAC compared to those subjects without AVC (87.1% vs 45.1%) with skewing of the distribution of CAC scores toward those subjects with more severe CAC.
CAVD appears to begin in midlife as a clinically latent but progressive disorder that is detected most often incidentally, following the performance of routine CT examinations. Even in this latent preobstructive phase, the presence of AVC appears to be a marker of increased cardiovascular risk. Echocardiographically detected aortic sclerosis in adults over the age of 65 has previously been demonstrated to be associated with a 50% increased risk of cardiovascular mortality and a 42% increased risk of myocardial infarction.5 The results of this study appear to extend these previously reported findings into a younger, healthier, multiethnic population group and seem to offer at least a partial explanation for the observed association between aortic calcification and coronary events.
In summary, AVC appears to be an independent predictor of cardiovascular mortality after adjustment for traditional risk factors and CAC severity, even though the presence of CAC may be unrelated to progressive valve disease. These risk associations were attenuated after adjustment for CAC, but not for inflammatory markers, suggesting that AVC may actually be a marker of subclinical atherosclerosis severity. Even after adjustment for any risk factors that may be present, such as inflammation and/or subclinical atherosclerosis, it remains unclear how determination of AVC adds to cardiovascular risk prediction in a predictably significant way. In any case, clinicians should be aware that this easily determined marker may eventually prove to be very helpful to them in both primary and secondary cardiovascular disease prevention.
References
1. Stewart BF, et al. Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. J Am Coll Cardiol 1997;29:630-634.
2. Agmon Y, et al. Aortic valve sclerosis and aortic atherosclerosis: Different manifestations of the same disease? Insights from a population-based study. J Am Coll Cardiol 2001;38:827-834.
3. Owens DS, et al. Incidence and progression of aortic valve calcium in the Multi-Ethnic Study of Atherosclerosis (MESA). Am J Cardiol 2010;105:701-708.
4. O’Brien KD. Pathogenesis of calcific aortic valve disease: A disease process comes of age (and a good deal more). Arterioscler Thromb Vasc Biol 2006;26:1721-1728.
5. Otto CM, et al. Association of aortic valve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl J Med 1999;341:142-147.
6. Owens DS, et al. Aortic valve calcium independently predicts coronary and cardiovascular events in a primary prevention population. J Am Coll Cardiol Img 2012;5:619-625.
7. Bild DE, et al. Multi-ethnic study of atherosclerosis: Objectives and design. Am J Epidemiol 2002;156:871-881.
The presence of aortic valve calcification (AVC) predicts cardiovascular and coronary event risk independent of traditional risk factors and inflammatory biomarkers, likely due to the strong correlation between AVC and subclinical atherosclerosis.Subscribe Now for Access
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