In patients with classical orthostatic hypotension, high supine total peripheral resistance explained supine hypertension, and a failure to increase upright TPR explained the orthostatic SBP fall.
Observational (n=160)
In patients with classical orthostatic hypotension, supine hypertension is driven by high supine total peripheral resistance, and the subsequent orthostatic blood pressure fall is due to a failure to further increase upright resistance.
p-value: p=<0.002
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.
Stam et al. (Thu,) conducted a observational in Classical orthostatic hypotension and supine hypertension (n=160). Classical orthostatic hypotension with supine hypertension vs. Classical orthostatic hypotension without supine hypertension and controls was evaluated on Relative contributions of heart rate, stroke volume, and total peripheral resistance to supine and upright blood pressure (p=<0.002). In patients with classical orthostatic hypotension, high supine total peripheral resistance explained supine hypertension, and a failure to increase upright TPR explained the orthostatic SBP fall.