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Intracardiac Calcification Is a Marker of Generalized Atherosclerosis

First Department of Internal Medicine, St Imre Teaching Hospital, nemcsikjanos{at}yahoo.com

Katalin Farkas, MD, PhD

First Department of Internal Medicine, St Imre Teaching Hospital

Endre Kolossváry, MD

First Department of Internal Medicine, St Imre Teaching Hospital, School of PhD Studies, Semmelweis University

Zoltán Járai, MD, PhD

First Department of Internal Medicine Semmelweis Univ.

József Egresits, MD

School of PhD Studies, Semmelweis University

Gábor Borgulya, MD, MSc

School of PhD Studies, Semmelweis University

István Kiss, MD, PhD

First Department of Internal Medicine, St Imre Teaching Hospital

Mária Lengyel, MD, PhD, DSc

First Department of Internal Medicine, St Imre Teaching Hospital, Gottsegen Gyorgy National Institute of Cardiology, Budapest, Hungary

Aortic valve calcification (AVC) and carotid artery calcification (CAC) are considered to be markers of generalized atherosclerosis. However, the role of intracardiac calcification (ICC) (valvular and perivalvular calcification) is unclear. The objective of this retrospective study was to analyze the relationship between ICC and CAC, risk factors, and clinical atherosclerotic disease. Risk factors included age, sex, diabetes mellitus, hypercholesterolemia, and hypertension; clinical atherosclerosis comprised stroke, coronary artery disease, and peripheral artery disease. Between January 1, 2001, and January 1, 2004, all consecutive patients were enrolled into the study who underwent both carotid ultrasonography and transthoracic echocardiography examinations within 2 months. Patients with renal failure, substantial aortic stenosis, and carotid artery occlusion were excluded. There were 320 patients (104 men; mean ± SEM age, 66.6 ± 0.76 years). Positive results on carotid ultrasonography are defined as any CAC. Patients were categorized as having mild, moderate, or severe CAC. Positive results on transthoracic echocardiography were defined as any ICC; AVC was defined as mitral anulus calcification (MAC) or both. Intracardiac calcification was found in 181 patients, AVC in 51 patients, MAC in 48 patients, and calcification of both structures in 82 patients. Using multiple logistic regression analysis, ICC (odds ratio, 1.9), age (10-year periods) (odds ratio, 2.0), and the presence of peripheral artery disease (odds ratio, 1.7) were independent predictors of CAC. Carotid ultrasonography results were positive in 227 patients. For CAC, the sensitivities of AVC, MAC, both, and any ICC were 52.4%, 52.0%, 33.5%, and 71.2%, respectively, and the specificities were 84.9%, 87.1%, 92.5%, and 78.5%, respectively. The extension of ICC as 0, 1 location (AVC or MAC) , or 2 locations (AVC and MAC) was associated with the severity of CAC (P < .001, = 0.42). There was no difference between patients with AVC vs patients with MAC in the presence of different stages of CAC (P = .62). Intracardiac calcification (MAC or AVC) is an independent predictor of CAC as a marker of atherosclerosis, although the lack of ICC does not rule out atherosclerosis. Intracardiac calcification is related to CAC, with high specificity. The extension of ICC is related to the severity of atherosclerosis. Based on our results, antiatherothrombotic therapy should be considered in patients with ICC even before obtaining a positive carotid ultrasonography result.

Angiology, Vol. 58, No. 4, 413-419 (2007)
DOI: 10.1177/0003319706291112


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