Simon W Rabkin1. 1. Department of Medicine (Cardiology), University of British Columbia, Vancouver, Canada. rabkin@interchange.ubc.ca
Abstract
BACKGROUND: Aortic valve sclerosis (AVS), a condition of thickening and calcification of the normal trileaflet aortic valve without the obstruction to left ventricular outflow, is likely the initial stage in the development of aortic stenosis and is associated with an increased incidence of cardiovascular events. The objective of this study is to critically review the data on the association of blood pressure and hypertension with AVS. METHODS: A systematic search of MEDLINE and EMBASE (to June 2004) was conducted using the keywords hypertension and aortic valve. All English language papers were examined if they dealt with hypertension and AVS. All studies were included for analysis if they had a control group. RESULTS: Three population-based, cross-sectional studies with a total sample size of 6450 individuals showed a consistent and significant relationship between hypertension and AVS with an odds ratio (OR) ranging from 1.23 to 1.74. Smaller case-control studies with a total sample size of 1609 individuals did not show consistent results but the OR ranged from 1.75 to 2.38. Only one small study (n = 188) showed fewer cases with hypertension and AVS than in the control group. Hypertension was a significant factor remaining in multivariate analysis after consideration of age and other risk factors in several cross-sectional studies. In contrast, other studies with blood pressure measurements consistently showed no increased blood pressures in the presence of AVS. However, these studies did not examine the prevalence of AVS within age-adjusted blood pressure levels. CONCLUSIONS: Cross-sectional population-based studies present evidence of an association between hypertension and AVS with an OR between 1.23 and 1.74. The major limitation in establishing a causal relationship is the failure to demonstrate a gradient of risk between increasing blood pressure and increasing incidence of AVS. In addition, the literature is confounded by the wide variety of definitions for AVS as well as hypertension. At this time, further data is required to conclude that there is a causal relationship between AVS and elevated blood pressure.
BACKGROUND:Aortic valve sclerosis (AVS), a condition of thickening and calcification of the normal trileaflet aortic valve without the obstruction to left ventricular outflow, is likely the initial stage in the development of aortic stenosis and is associated with an increased incidence of cardiovascular events. The objective of this study is to critically review the data on the association of blood pressure and hypertension with AVS. METHODS: A systematic search of MEDLINE and EMBASE (to June 2004) was conducted using the keywords hypertension and aortic valve. All English language papers were examined if they dealt with hypertension and AVS. All studies were included for analysis if they had a control group. RESULTS: Three population-based, cross-sectional studies with a total sample size of 6450 individuals showed a consistent and significant relationship between hypertension and AVS with an odds ratio (OR) ranging from 1.23 to 1.74. Smaller case-control studies with a total sample size of 1609 individuals did not show consistent results but the OR ranged from 1.75 to 2.38. Only one small study (n = 188) showed fewer cases with hypertension and AVS than in the control group. Hypertension was a significant factor remaining in multivariate analysis after consideration of age and other risk factors in several cross-sectional studies. In contrast, other studies with blood pressure measurements consistently showed no increased blood pressures in the presence of AVS. However, these studies did not examine the prevalence of AVS within age-adjusted blood pressure levels. CONCLUSIONS: Cross-sectional population-based studies present evidence of an association between hypertension and AVS with an OR between 1.23 and 1.74. The major limitation in establishing a causal relationship is the failure to demonstrate a gradient of risk between increasing blood pressure and increasing incidence of AVS. In addition, the literature is confounded by the wide variety of definitions for AVS as well as hypertension. At this time, further data is required to conclude that there is a causal relationship between AVS and elevated blood pressure.
Authors: Jason Linefsky; Ronit Katz; Matthew Budoff; Jeffrey Probstfield; David Owens; Junichiro Takasu; David Shavelle; Pamela Ouyang; Bruce Psaty; Kevin D O'Brien Journal: Am J Cardiol Date: 2011-01 Impact factor: 2.778