Purpose: The present study was designed to examine the relative impact of arterial stiffness on presence and/or severity of MR in patients with hypertension. Methods: 141 hypertensive patients (mean age 56.6+11.5 years) were prospectically enrolled: 94 with chronic MR and 47 without MR. Causes of secondary hypertension were excluded. Patients were ineligible if they had concomitant other heart valve disease, ischemic cardiomyopathy (with or without ischemic MR), severe renal insufficiency, diabetes mellitus or other systemic diseases. As measure of arterial stiffness, pulsewave velocity (PWV)was determinedby applanation tonometry.Acomprehensive echocardiographic examination was performed. All measurements of LV dimensions and function were obtained from both M-mode and two-dimensional acquisitions. Assessment of the severity of MR was obtained through the calculation of the effective regurgitant orifice area (ERO) (cm2), vena contracta (mm) and regurgitant volume (RV, ml). Results: There was a significant increase in arterial stiffness according to the presence and severity of MR (PWV= 7.3+1.1 m/sec vs.7.9+1.3 m/sec vs. 9.0+1.7 m/sec vs.13.3+4.1 m/sec, p,0.001, in patients without MR and with mild, moderate or severe MR, respectively). Onlinear Pearson’s correlations,PWVwas positively correlated with age (p,0.001), systolic blood pressure (BP) (p=0.02) fasting glucose (p=0.01), creatinine (p=0.006) and negatively correlated with ejection fraction (EF) (p=0.003); EROA was positively correlated with age (p=0.004), fasting glucose (p=0.003), creatinine (p=0.02), PWV (p,0.001) and negatively correlated with EF (p=0.002) and heart rate (HR) (p=0.03). On multivariate logistic regression analysis, independent predictors ofPWV were: age (p,0.001), EF (p=0.046), systolic BP (p=0.012) and creatinine (p=0.02); independent predictors of the presence of MR were HR (OR 0.94, 95% CI 0.891-0.993, p=0.02) and PWV (OR 2.87 95% CI 1.750-4.738, p,0.001). Receiver Operating Curves (ROC) showed that a cut-off of 9 m/sec for PWV provided the best sensitivity and specificity for predicting the presence (sensitivity 73%; specificity 87%, area under curve (AUC)=0.86, p,0.001) and the severity of MR (sensitivity 100%; specificity 81%, AUC=0.95, p,0.001). Conclusions: A reduced aortic compliance, indicated by elevated PWV, may be an important marker for the presence and/or severity of MR. Thus, the adverse consequences of abnormal ventricular–vascular interaction in hypertension deserve attention also for their important implications on mitral valve competency.
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