P110 - CARDIAC ORIGINS OF CEREBRAL HYPOPERFUSION: IMPLICATIONS FOR POSTURAL TACHYCARDIA USING A CONTROLLED HEART RATE MODEL

Background: Postural Orthostatic Tachycardia Syndrome (POTS) is characterized by excessive heart rate (HR) increase upon standing and is often accompanied by presyncope symptoms (e.g., light-headedness, blurred vision). These symptoms are thought to result from impaired regulation of brain circulation. Previous studies in POTS patients have shown that reductions in stroke volume (SV) correlate strongly with diminished cerebral perfusion. To better understand the physiological relationship between HR and brain hemodynamics, we investigated this link using controlled pacing conditions in patients with a structurally normal heart going for a supraventricular tachycardia ablation.

METHODS AND RESULTS: Eighteen patients (mean age 41 ± 17 years; 13 females; height: 171 ± 10 cm; weight: 82 ± 17 kg; BMI: 27.8 ± 4.6 kg/m²) with preserved left ventricular function (LVEF ≥50%) underwent incremental right atrial pacing (100, 120, 150, and 171 bpm). HR, SV, cardiac output (CO), blood pressures, and middle cerebral artery velocity (MCAv) were continuously monitored using non-invasive hemodynamic assessment and transcranial Doppler ultrasound.
Baseline heart rate was 81 ± 11 bpm. All patients had intact atrioventricular nodal conduction at all pacing rates. Increased heart rate resulted in a significant HR-dependent decrease in SV (100 bpm: -9 ± 7 mL, 120 bpm: -17 ± 11 mL, 150 bpm: -29 ± 14 mL, 171 bpm: -29± 15 mL; p< 0.001) and pulse pressure (100 bpm: -1.6 ± 7 mmHg, 120 bpm: -7 ± 5 mmHg, 150 bpm: -12 ± 7 mmHg, 171 bpm: -18 ± 8 mmHg; p< 0.001) Most notably, MCAv pulsatility index (a surrogate for perfusion) also declined progressively with increasing HR (100 bpm: -0.04 ± 0.06, 120 bpm: -0.12 ± 0.06, 150 bpm: -0.12 ± 0.08, 171 bpm: -0.21 ± 0.05; p< 0.001). CO (p=0.01) remained relatively stable across conditions, as the increase in HR and decrease in SV cancelled each other to some extent.

Conclusion: Controlled increases in HR induced by atrial pacing led to progressive significant reductions in SV, pulse pressure, and MCAv PI. These findings provide new evidence linking tachycardia-induced reductions in stroke volume to impaired cerebral perfusion dynamics, supporting a mechanistic pathway that has been hypothesized but not previously demonstrated under controlled conditions.