AFRICA CARDIOVASCULAR JOURNAL OF AFRICA • SAHS Biennial Congress 16-18 September 2022 36 Submission ID: 1375 Introduction Although renal mechanisms are well-established causes of hypertension, this has only recently been recognized as causing sustained volume-dependent, primary hypertension. This observation was documented in the SOWETO community. Although no current antihypertensive agent can produce sustained volume reduction, targeting pressures has generally been accepted as sufficient therapy. However, whether volume overload causes cardiovascular damage beyond pressure effects is uncertain. Methods In 734 participants of African descent randomly selected from SOWETO, we aimed to determine whether volume effects in primary hypertension cause vascular damage beyond BP. Haemodynamics were determined from central pressure, aortic velocity and diameter measurements (outflow tract)(echocardiography) and arterial structure and function from several end-organ measures. Results Independent of age, sex, conventional risk factors and both mean arterial pressure and central arterial pulse pressure or systolic BP, several indices of volume overload were associated with aortic pulse wave velocity (PWV) and index of aortic stiffness. These included aortic stroke volume (SV) (p<0.0001), peak aortic flow (p<0.0001), the volume ejected from the left ventricle in late systole (p<0.0001), and left ventricular end diastolic volume (p<0.001). These associations were explained by an increase in aortic diameter (p<0.0001) which increases aortic wall stress. Independent of confounders, SV was also independently associated with markers of endothelial function including V-CAM-1 and I-CAM1 (p<0.05). However, no independent relations were noted between indices of volume overload and carotid intima-media thickness. Conclusion Independent of confounders, and BP load, volume overload in sustained volume-dependent primary hypertension, is strongly associated with aortic stiffness. These effects may be explained by increases in wall stress and consequently endothelial dysfunction. These data indicate that beyond BP changes, reductions in volume overload in volume-dependent primary hypertension are essential for risk reduction. Name: Presenting Author Information Article Category Abstract Title Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. oluwatosin.tade@wits.ac.za English Abstract Basic Sciences Independent Relationship Between Volume Overload and Aortic Stiffness in a Community with Prevalent Volume-Dependent Primary Hypertension Author Affiliation: Email: Grace Tade Authors Name & Surname Title Expertise Affiliation Email Country Grace Tade Dr Cardiovascular pathophysiology Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg Oluwatosin.Tade@wits.ac.za South Africa Vernice R Peterson Dr Cardiovascular pathophysiology Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg vernice.peterson@wits.ac.za South Africa Manishka Reddy Ms Cardiovascular pathophysiology Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg manishka.r99@gmail.com South Africa ORAL PRESENTATION
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