CARDIOVASCULAR JOURNAL OF AFRICA • SAHS Biennial Congress 16-18 September 2022 21 AFRICA Submission ID: 1362 Authors Name & Surname Title Expertise Affiliation Email Country Angela J Woodiwiss Prof Cardiovascular Physiology Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg Angela.Woodiwiss@wits.ac.za South Africa Nonhlanhla Mthembu Ms Cardiovascular Physiology Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg nonhlanhla.mthembu@yahoo.com South Africa Vernice R Peterson Dr Cardiovascular Physiology 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 Ravi Naran Dr Cardiovascular Physiology Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg naran.ravi1@gmail.com South Africa Introduction Heart rate (HR) lowering agents such β-adrenoreceptor blockers used for the management of hypertension in patients with cardiac conditions, increase central arterial (PPc), but not brachial pulse pressure (PP). However, the mechanisms of this effect are uncertain. A lower heart rate (HR) increases left ventricular (LV) ejection volume and hence systemic flow. Whether this contributes to the adverse effects of HR on central pulse pressure (PPc) through reservoir volume effects, is unknown. Methods Using non-invasive central pressure, aortic velocity and diameter measurements in the outflow tract (echocardiography), we assessed the role of LV ejection volume as a determinant of HR relations with PPc in 824 community participants. Results A lower HR was independently associated with both stroke volume (SV) (p<0.001) and a shift in ejection volume from early (until the first systolic shoulder) to late (from first systolic shoulder to peak PP) systole (p<0.05 to p<0.005). Adjustments for LV end diastolic volume (EDV) markedly diminished HR relations with SV and indexes of the shift in ejection volume to late systole. A lower HR was also independently associated with increases in both forward travelling pressure waves (Pf) and PPc (p<0.0001). However, adjustments for neither SV, nor indexes of a shift in ejection volume to late systole modified HR-Pf or PPc relations. This was despite relationships between indexes of a shift in left ventricular ejection volume to late systole and both Pf and PPc (p<0.0001). In contrast, adjustments for the increases in re-reflected and backward travelling wave pressures with a lower HR, eliminated HR-Pf and PPc relations. Conclusion In contrast to current thought, a lower HR is not associated with increases in PPc through an impact of increases in late systolic ejection volume on aortic reservoir volume, but rather through increases in backward wave pressures. These data suggest that increases in systemic flow, which may have beneficial effects in cardiac disease, are not responsible for increases in PPc with HR reduction. In contrast, increases in impedance to flow, which have deleterious effects in cardiac disease, are responsible for HR-associated increases in PPc. 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 angela.woodiwiss@wits.ac.za English Abstract Population Sciences Contribution of Increases in Late Systolic Ejection Volume to the Impact of Heart Rate on Central Arterial Pulse Pressure in a Community Sample Author Affiliation: Email: Angela J Woodiwiss ORAL PRESENTATION
RkJQdWJsaXNoZXIy NDIzNzc=