Biomarkers of Calcific Aortic Valve Disease

Abstract

Calcific Aortic Valve Disease (CAVD) is a highly prevalent cardiovascular disorder accounting for a rising economic and social burden on aging populations. In spite of continuing study on the pathophysiology of disease, there remain no medical therapies to prevent the progression of CAVD. The discovery of biomarkers represents a potentially complementary approach in stratifying risk and timing of intervention in CAVD, and has the advantage of providing insight into causal factors for the disease. Biomarkers have been studied extensively in atherosclerotic cardiovascular disease, with success as additive for clinical and scientific purposes. Similar research in CAVD is less robust, however, the available studies of biomarkers in CAVD show promise for enhanced clinical decision-making and identification of causal factors for the disease. This comprehensive review summarizes available established and novel biomarkers in CAVD, their contributions toward an understanding of pathophysiology, their potential clinical utility, and provides an outline to direct future research in the field.

Bacterial infiltration in structural heart valve disease

“…9 Investigations of various bacteria have identified different mechanisms that promote calcification of tissues. 5,7 Molecular biological studies of the heart valve tissue of patients with sVHD have confirmed the detection of bacteria. 8,10 The literature reveals positive evidence for streptococci, 8 staphylococci, and Propionibacterium, 10 Chlamydophila, and Mycoplasma 11 on the basis of polymerase chain reaction studies.…”

“…[2][3][4] For years, it has been suggested that classical cardiovascular risk factors such as diabetes, hyperlipidemia, arterial hypertension, smoking, and familial predisposition promote the pathogenesis of calcific aortic valve stenosis. 5,6 In addition to a disturbed calcium metabolism and immunological influences, 7 in particular subacute or acute endocarditis is responsible for the development of sVHD. 8 In 2004 Cohen and colleagues 9 confirmed a link between subclinical bacterial endocarditis and calcification of the aortic valve in an animal model.…”

Urea level is an independent predictor of mortality in patients with severe aortic valve stenosis

“…Recently, a large amount of data is also gathered on the role of biomarkers in aortic stenosis. [35][36][37] NT-proBNP levels correlate with AS severity and echocardiographic markers of higher risk for adverse outcomes in AS. [38] ST2 has shown to correlate with AS severity, symptoms and prognosis.…”

Association of aortic valve calcification with carotid artery lesions and peripheral artery disease in patients with chronic kidney disease: a cross-sectional study

“…Nevertheless, whether an association of AVC with carotid artery lesions and PAD exists in predialysis patients remains unknown. Furthermore, especially in patients with CKD, in addition to traditional CV risk factors, nontraditional CV risk factors such as renal dysfunction itself and deranged mineral metabolism [e.g., hyperphosphatemia, elevated parathyroid hormone (PTH) or fibroblast growth factor 23 (FGF23)] associated with CKD are also associated with AVC [28][29][30][31][32]. However, in predialysis patients, the association of AVC with carotid artery lesions and PAD beyond both traditional and nontraditional CV risk factors remains uncertain.…”