Key result
In patients with classical orthostatic hypotension, those with supine hypertension failed to increase total peripheral resistance upon upright tilt compared to those without supine hypertension (median TPR logratio -0.002 vs 0.055; P=0.0025).
Why the study?
The relation between classical orthostatic hypotension and supine hypertension was largely unknown.
What are the haemodynamic determinants (HR, SV, TPR) of supine hypertension and orthostatic blood pressure drops in patients with classical orthostatic hypotension?
Observational (n=160)
No
What are the haemodynamic determinants (HR, SV, TPR) of supine hypertension and orthostatic blood pressure drops in patients with classical orthostatic hypotension?
In patients with classical orthostatic hypotension, supine hypertension is driven by elevated supine total peripheral resistance, but their orthostatic blood pressure fall is due to an autonomic failure to further increase resistance upon assuming the upright position.
Impaired TPR response may underlie greater orthostatic BP falls in cOH with supine hypertension; extends mechanistic insights but leaves open therapeutic implications.
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.
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Stam et al. (2025) conducted an observational in Classical orthostatic hypotension and supine hypertension (n=160). Supine hypertension in classical orthostatic hypotension (cOH/SH+) vs. Classical orthostatic hypotension without supine hypertension (cOH/SH-) was evaluated on Total peripheral resistance logratio (TPR LR) in the fourth minute of 70-degree tilt (p=0.0025). In patients with classical orthostatic hypotension, those with supine hypertension failed to increase total peripheral resistance upon upright tilt compared to those without supine hypertension (median TPR logratio -0.002 vs 0.055; P=0.0025).
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