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      A High Association of Aortic Valve Sclerosis Detected by Transthoracic Echocardiography with Coronary Arteriosclerosis

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          Objective: To examine whether aortic valve sclerosis (AVS) detected by transthoracic echocardiography (TTE) has a high association with coronary arteriosclerosis. Methods: Clinical and angiographic features and TTE findings were retrospectively analyzed in a blinded fashion for 138 consecutive patients, of whom 58 had AVS and 80 had non-AVS diseases. Both histological and immunohistochemical studies were performed on frozen aortic valve sections obtained at autopsy from 7 AVS and 3 non-AVS patients. Results: AVS and coronary artery disease (CAD) had similar clinical risk factors. The AVS group had a higher positive rate of coronary angiography and a higher incidence rate of multivessel CAD than the non-AVS group. The sensitivity, specificity, positive predictive value and negative predictive value of AVS in diagnosing CAD were 63.8, 71.3, 61.7 and 73.1%, respectively. Early lesions of AVS were characterized by accumulation of lipid and infiltration of macrophages and T lymphocytes as indicated by immunohistochemical staining. Late lesions were characterized by formation of calcific plaques, proliferation of fibrous connective tissue and immunohistochemical staining identifying a few macrophages or T lymphocytes and little lipid accumulation on the surface of aortic valve leaflets. Late lesions in the basement of aortic valve leaflets were characterized by hyperplastic granulation tissues. Three aortic valve leaflets from the non-AVS group were characterized by nonspecific thickened tips, increased collagen, no calcification, no lipid accumulation and no inflammatory cells. Conclusions: There were significant similarities in clinical risk factors, histopathological alterations of AVS and coronary atherosclerosis. AVS detected by TTE had a high association with coronary arteriosclerosis.

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          Most cited references 19

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          Clinical Factors Associated With Calcific Aortic Valve Disease fn1fn1This study was supported in part by Contracts NO1-HC85079 through HC-850086 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.

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            Effect of hydroxymethylglutaryl coenzyme a reductase inhibitors on the progression of calcific aortic stenosis.

            Recent studies have supported the hypothesis that calcific aortic stenosis is the product of an active inflammatory process, with similarities to atherosclerosis. We sought to determine whether therapy with hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) might slow the progression of aortic stenosis. A retrospective study of 174 patients (mean age 68+/-12 years) with mild to moderate calcific aortic stenosis was conducted. Patients required normal left ventricular function, /=2 echocardiograms performed at least 12 months apart. Fifty-seven patients (33%) received treatment with a statin; the remaining 117 (67%) did not. The statin group was older and had a higher prevalence of hypertension, diabetes mellitus, and coronary disease. During a mean follow-up of 21 months, patients treated with statin had a smaller increase in peak and mean gradient and a smaller decrease in aortic valve area. When annualized, the decrease in aortic valve area for the nonstatin group was 0.11+/-0.18 cm(2) compared with 0.06+/-0.16 cm(2) for those treated with a statin (P=0.03). In multivariate analysis, statin usage was a significant independent predictor of a smaller decrease in valve area (P=0.01) and a lesser increase in peak gradient (P=0.02). Statin-treated patients, despite a higher risk profile for progression, had reduced aortic stenosis progression compared with those not treated with a statin. These data provide justification for a prospective randomized trial to substantiate whether statin therapy slows the progression of aortic stenosis.
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              Association of coronary risk factors and use of statins with progression of mild valvular aortic stenosis in older persons.


                Author and article information

                S. Karger AG
                November 2007
                12 February 2007
                : 108
                : 4
                : 322-330
                Departments of aCardiology and bPathology, Second Hospital of Shandong University, and cKey Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Shandong University Qi Lu Hospital, Jinan, China
                99103 Cardiology 2007;108:322–330
                © 2007 S. Karger AG, Basel

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                Figures: 3, Tables: 7, References: 28, Pages: 9
                Original Research


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