Key result
Tilt syncope in POTS links to reduced cardiac output from splanchnic pooling, unlike in healthy controls.
Why the study?
Upright tilt table testing can produce false positives in healthy volunteers and POTS patients without a history of syncope, but whether the mechanisms of hypotensive susceptibility differ between these groups is unclear.
Does the mechanism of hypotensive susceptibility during upright tilt differ between healthy volunteers and POTS patients who experience tilt-induced fainting?
Observational (n=34)
Does the mechanism of hypotensive susceptibility during upright tilt differ between healthy volunteers and POTS patients who experience tilt-induced fainting?
The mechanisms of tilt-induced syncope differ between healthy volunteers (decreased systemic vascular resistance) and POTS patients (decreased cardiac output from splanchnic pooling), highlighting distinct pathophysiological pathways for false-positive tilt tests.
Answers are grounded in this paper and cite their sources.
May refine tilt-test interpretation in POTS; hypothesis-generating for mechanism-specific interventions.
Upright tilt table testing has been used to test for vasovagal syncope (VVS) but can result in "false positives" in which tilt-induced fainting (tilt+) occurs in the absence of real-world fainting. Tilt+ occurs in healthy volunteers and in patients with postural tachycardia syndrome (POTS) and show enhanced susceptibility to orthostatic hypotension. We hypothesized that the mechanisms for hypotensive susceptibility differs between tilt+ healthy volunteers (Control-Faint (N = 12)), tilt+ POTS patients (POTS-Faint (N = 12)) and a non-fainter control group of (Control-noFaint) (N = 10). Subjects were studied supine and during 70° upright tilt while blood pressure (BP), cardiac output (CO), and systemic vascular resistance (SVR), were measured continuously. Impedance plethysmography estimated regional blood volumes, flows, and vascular resistance. Heart rate was increased while central blood volume was decreased in both Faint groups. CO increased in Control-Faint because of reduced splanchnic vascular resistance; splanchnic pooling was similar to Control-noFaint. Splanchnic blood flow in POTS-Faint decreased and resistance increased similar to Control-noFaint but splanchnic blood volume was markedly increased. Decreased SVR and splanchnic arterial vasoconstriction is the mechanism for faint in Control-Faint. Decreased CO caused by enhanced splanchnic pooling is the mechanism for faint in POTS-Faint. We propose that intrahepatic resistance is increased in POTS-Faint resulting in pooling and that both intrahepatic resistance and splanchnic arterial vasoconstriction are reduced in Control-Faint resulting in increased splanchnic blood flow and reduced splanchnic resistance.
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Stewart et al. (2019) conducted an observational in Vasovagal syncope and postural tachycardia syndrome (n=34). 70° upright tilt table testing vs. Control-noFaint group was evaluated on Hemodynamic mechanisms of tilt-induced syncope (blood pressure, cardiac output, systemic vascular resistance). Tilt-induced fainting in healthy volunteers is driven by decreased systemic vascular resistance, whereas in POTS patients it is caused by decreased cardiac output from enhanced splanchnic pooling.
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