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Published on: February 4, 2021
Adverse outcome in aortic sclerosis is associated with coronary artery disease and inflammation
Harish R Chandra1, James A Goldstein, Nivedita Choudhary
1Division of Cardiology, Department of Internal Medicine, William Beaumont Hospital, Royal Oak, Michigan 48073, USA.
Insights
Aortic sclerosis is linked to cardiovascular events, but coronary artery disease and inflammation are the true predictors, not the valve condition itself. This finding impacts understanding of heart disease risk factors.
Area of Science:
- Cardiology
- Vascular Biology
- Inflammation Research
Background:
- Aortic sclerosis, a nonobstructive valve lesion, is recognized as a risk factor for adverse cardiovascular outcomes.
- The precise mechanisms linking aortic sclerosis to increased cardiovascular risk remain incompletely understood.
Purpose of the Study:
- To investigate the association between aortic sclerosis, inflammatory markers, and cardiovascular events.
- To determine if aortic sclerosis independently predicts adverse cardiovascular outcomes.
Main Methods:
- Echocardiography and serologic testing, including C-reactive protein (CRP), were performed on 425 emergency room patients presenting with chest pain.
- Aortic valve sclerosis was graded, and cardiovascular outcomes (cardiac death, myocardial infarction) were tracked for one year.
- Multivariable analysis was used to identify independent predictors of cardiovascular events.
Main Results:
- Aortic sclerosis was present in 49% of patients and was associated with a higher incidence of cardiovascular events on univariate analysis.
- However, multivariable analysis revealed that aortic sclerosis was not an independent predictor of cardiac death or myocardial infarction.
- Independent predictors included coronary artery disease, prior myocardial infarction, elevated CRP levels, congestive heart failure, and age.
Conclusions:
- The elevated risk of cardiovascular events in patients with aortic sclerosis is primarily attributed to coexisting coronary artery disease and systemic inflammation.
- Aortic sclerosis itself does not appear to be an independent driver of adverse cardiovascular outcomes.
Objectives:
The present study was designed to evaluate the relationship between the presence of aortic sclerosis, serologic markers of inflammation, and adverse cardiovascular outcomes.
Background:
Aortic sclerosis is associated with adverse cardiovascular outcomes. However, the mechanism by which such nonobstructive valve lesions impart excess cardiovascular risk has not been delineated.
Method:
In 425 patients (mean age 68 +/- 15 years, 54% men) presenting to the emergency room with chest pain, we studied the relationship among aortic sclerosis, the presence and acuity of coronary artery disease, serologic markers of inflammation, and cardiovascular outcomes. Patients underwent echocardiography and serologic testing including C-reactive protein (CRP). Aortic valves were graded for the degree of sclerosis, and cardiovascular outcomes including cardiac death and nonfatal myocardial infarction (MI) were analyzed over one year.
Results:
Aortic sclerosis was identified in 203 patients (49%), whereas 212 (51%) had normal aortic valves. On univariate analysis at one year, patients with aortic sclerosis had a higher incidence of cardiovascular events (16.8% vs. 7.1%, p = 0.002) and worse event-free survival (normal valves = 93%, mild aortic sclerosis = 85%, and moderate to severe aortic sclerosis = 77%, p = 0.002). However, by multivariable analysis aortic sclerosis was not independently associated with adverse cardiovascular outcomes; the only independent predictors of cardiac death or MI at one year were coronary artery disease (hazard ratio [HR] 3.23, p = 0.003), MI at index admission (HR 2.77, p = 0.008), ascending tertiles of CRP (HR 2.2, p = 0.001), congestive heart failure (HR 2.15, p = 0.02) and age (HR 1.03, p = 0.04).
Conclusions:
The increased incidence of adverse cardiovascular events in patients with aortic sclerosis is associated with coronary artery disease and inflammation, not a result of the effects of valvular heart disease per se.
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