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      Left Ventricular Hypertrophy Induced by Reduced Aortic Compliance

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          Aim: It was the aim of this study to investigate the long- term effects of reduced aortic compliance on cardiovascular hemodynamics and cardiac remodeling. Method: Sixteen swine, divided into 2 groups, a control and a banding group, were instrumented for pressure and flow measurement in the ascending aorta. Teflon prosthesis was wrapped around the aortic arch in order to limit wall compliance in the banding group. Hemodynamic parameters were recorded throughout a 60-day period. After sacrifice, the mean cell surface of the left ventricle was documented. Results: Banding decreased aortic compliance by 49 ± 9, 44 ± 16 and 42 ± 7% on the 2nd, 30th and 60th postoperative day, respectively (p < 0.05), while systolic pressure increased by 41 ± 11, 30 ± 11 and 35 ± 12% (p < 0.05), and pulse pressure by 86 ± 27, 76 ± 21 and 88 ± 23%, respectively (p < 0.01). Aortic characteristic impedance increased significantly in the banding group. Diastolic pressure, cardiac output and peripheral resistance remained unaltered. The mean left ventricular cell surface area increased significantly in the banding group. Conclusions: Acute reduction in aortic compliance results in a significant increase in characteristic and input impedance, a significant decrease in systemic arterial compliance and a subsequent increase in systolic and pulse pressures leading to left ventricular hypertrophy.

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          Most cited references 10

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          Steady and pulsatile energy losses in the systemic circulation under normal conditions and in simulated arterial disease.

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            Cardiovascular remodeling is greater in isolated systolic hypertension than in diastolic hypertension in older adults: the Insufficienza Cardiaca negli Anziani Residenti (ICARE) a Dicomano Study.

            We investigated cardiac and vascular remodeling in an unselected older population with either diastolic hypertension (HTN) or isolated systolic hypertension (ISH). Isolated systolic hypertension accounts for a substantial proportion of hypertension in individuals older than 65 years and is strongly associated with an increased risk of cardiac and cerebrovascular events. The exact mechanisms underlying the increased risk associated with ISH and elevated pulse pressure (PP), in comparison with HTN, have not been extensively investigated. Community-dwelling residents age >/=65 years in a small town in Italy (Dicomano) were enrolled. Untreated subjects considered in this study included 173 normotensive subjects (blood pressure [BP] /=90 mm Hg), and 43 subjects with ISH (BP >/=160/<90 mm Hg). All subjects underwent extensive clinical examination, echocardiography, carotid ultrasonography, and carotid applanation tonometry. Subjects with ISH had higher left ventricular (LV) mass, which was independently related to PP but not to systolic or mean pressures. Both carotid wall cross-sectional area and vascular stiffness were greater in ISH patients than in HTN and normal subjects and were independently related to PP but not to systolic BP. In addition, ISH was associated with a higher prevalence of carotid plaque and more extensive carotid atherosclerosis. In our community-based elderly population, individuals with ISH had higher prevalences of LV hypertrophy and carotid atherosclerosis than subjects with HTN despite lower mean BP. These findings provide potential pathophysiologic mechanisms underlying the associations of ISH and PP with increased risk of cardiovascular morbidity and mortality.
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              Compliance mismatch may promote graft–artery intimal hyperplasia by altering suture-line stresses


                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                August 2009
                21 January 2009
                : 46
                : 5
                : 417-425
                aDivision of Vascular Surgery, University Hospital of Heraklion, University of Crete Medical School, and bTechnological Educational Institute of Crete, Heraklion, Greece; cLaboratory of Hemodynamics and Cardiovascular Technology, Swiss Federal Institute of Technology, Lausanne, dDivision of Anesthesiological Investigations, and eDepartment of Cardiovascular Surgery, University Hospital of Geneva, Geneva, Switzerland; fLaboratory for Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands
                194272 J Vasc Res 2009;46:417–425
                © 2009 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 34, Pages: 9
                Research Paper


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