Decreased upright cerebral blood flow and cerebral autoregulation in normocapnic postural tachycardia syndrome

Abstract

Postural tachycardia syndrome (POTS), a chronic form of orthostatic intolerance, has signs and symptoms of lightheadedness, loss of vision, headache, fatigue, and neurocognitive deficits consistent with reductions in cerebrovascular perfusion. We hypothesized that young, normocapnic POTS patients exhibit abnormal cerebral autoregulation (CA) that results in decreased static and dynamic cerebral blood flow (CBF) autoregulation. All subjects had continuous recordings of mean arterial pressure (MAP) and CBF velocity (CBFV) using transcranial Doppler sonography in both the supine supine position and during a 70 degrees head-up tilt. During tilt, POTS patients (n = 9) demonstrated a higher heart rate than controls (n = 7) (109 +/- 6 vs. 80 +/- 2 beats/min, P < 0.05), whereas controls demonstrated a higher MAP than POTS (87 +/- 2 vs. 77 +/- 3 mmHg, P < 0.05). Also during tilt, mean CBFV decreased 19.5 +/- 2.6% in POTS patients versus 10.3 +/- 2.0% in controls (P < 0.05). We then used a transfer function analysis of MAP and CFBV in the frequency domain to quantify these changes. The low-frequency (LF; 0.04-0.15 Hz) component of CBFV variability increased during tilt in POTS patients (supine: 3 +/- 0.9 vs. tilt: 9 +/- 2, P < 0.02). In POTS patients, there was an increase in LF and high-frequency coherence between MAP and CBFV, an increase in LF gain, and a lack of significant change in phase. Static CA may be less effective in POTS patients compared with controls, since immediately after tilt CBFV decreased more in POTS patients and was highly oscillatory and autoregulation did not restore CBFV to baseline values until the subjects became supine. Dynamic CA may be less effective in POTS patients because MAP and CBFV during tilt became almost perfectly synchronous. We conclude that dynamic and static autoregulation of CBF are less effective in POTS patients compared with control subjects during orthostatic challenge.

Respiration drives phase synchronization between blood pressure and RR interval following loss of cardiovagal baroreflex during vasovagal syncope

“…Young fainting subjects exhibit varying temporal patterns during HUT. We have previously used intervals to describe physiologically related events that vary in time (25,26,41). For both groups, we defined our baseline interval as the 5-min supine period before HUT.…”

Sympathetic Nervous System Moves Toward Center Stage in Cardiovascular Medicine

“…32,34,35,45,46 Neurally mediated cerebral vasoconstriction with reduction of cerebral blood flow seems to be common and is the cause of syncope. 47 Postural hypotension is usually absent. The research of my group implicates augmentation of the postural sympathetic neural signal as a result of severe deficiency of the noradrenaline transporter protein 35 as a mechanism of the postural tachycardia and excessive postural fall in cerebral blood flow.…”

Blunted cerebral blood flow velocity in response to a nitric oxide donor in postural tachycardia syndrome

“…*P Ͻ 0.05 compared with the control group. When present, systemic circulatory abnormalities are also found in the brain (34,55) and may account for impaired CBF autoregulation in the upright POTS patient (34). Impairment of cerebral autoregulation is associated with a reduction in neurovascular coupling (52) as well as cognition (33).…”

“…Postural orthostatic tachycardia syndrome (POTS) is the most common form of chronic OI (2), defined by the symptoms of OI with concomitant excessive upright tachycardia. We have previously demonstrated impaired cerebral blood flow (CBF) in POTS (34).…”