Journal of hypertension · 2025
Haemodynamic determinants of supine hypertension in patients with classical orthostatic hypotension.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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van der Stam Amber H, Gagaouzova Boriana S, Kerkhof Fabian I, van Rossum Ineke A, Shmuely Sharon, Reijntjes Robert H, van Houwelingen Marc J, Thijs Roland D, van Dijk J Gert
Аннотация
OBJECTIVE: The relation between classical orthostatic hypotension (cOH) and supine hypertension is largely unknown. We investigated the relative contributions of heart rate (HR), stroke volume (SV) and total peripheral resistance (TPR) to supine and upright blood pressure (BP).
METHODS: In this retrospective study, tilt tests were divided in four groups: 19 normotensive and 61 hypertensive controls, 50 cOH patients with SH (cOH/SH+) and 30 without (cOH/SH-). Hypertension was defined as supine SBP at least 140 mmHg. We used linear regression to relate cOH severity to supine SBP, and the logratio method to analyse relative contributions of HR, SV and TPR. P values less than 0.003 were considered significant.
RESULTS: High supine SBP was associated with high TPR in patients and controls. Orthostatic SBP decrease in cOH was larger in those with higher supine SBP. The main parameter explaining this effect was a high supine TPR that did not increase after tilt in cOH/SH+ compared to cOH/SH- (logratio difference, P < 0.002). SV logratio decreased more in cOH/SH- than in cOH/SH+ ( P < 0.003), and HR logratio contributed similarly to orthostatic SBP in both cOH groups ( P = 0.028).
CONCLUSION: While high supine TPR explained SH, a failure to further increase upright TPR explained the orthostatic SBP fall in patients. Autonomic failure can explain the SBP fall but not directly the high supine TPR that causes SH. We assume that slow-acting humoral vasoconstrictors are triggered in the upright position and continue to act after tilting back, causing high TPR and SH.
METHODS: In this retrospective study, tilt tests were divided in four groups: 19 normotensive and 61 hypertensive controls, 50 cOH patients with SH (cOH/SH+) and 30 without (cOH/SH-). Hypertension was defined as supine SBP at least 140 mmHg. We used linear regression to relate cOH severity to supine SBP, and the logratio method to analyse relative contributions of HR, SV and TPR. P values less than 0.003 were considered significant.
RESULTS: High supine SBP was associated with high TPR in patients and controls. Orthostatic SBP decrease in cOH was larger in those with higher supine SBP. The main parameter explaining this effect was a high supine TPR that did not increase after tilt in cOH/SH+ compared to cOH/SH- (logratio difference, P < 0.002). SV logratio decreased more in cOH/SH- than in cOH/SH+ ( P < 0.003), and HR logratio contributed similarly to orthostatic SBP in both cOH groups ( P = 0.028).
CONCLUSION: While high supine TPR explained SH, a failure to further increase upright TPR explained the orthostatic SBP fall in patients. Autonomic failure can explain the SBP fall but not directly the high supine TPR that causes SH. We assume that slow-acting humoral vasoconstrictors are triggered in the upright position and continue to act after tilting back, causing high TPR and SH.