Contrasting neurovascular findings in chronic orthostatic intolerance and neurocardiogenic syncope.

Simple faint (neurocardiogenic syncope) and postural tachycardia syndrome (POTS) characterize acute and chronic orthostatic intolerance respectively. We explored the hypothesis that vascular function is similar in the two conditions. We studied 29 patients with POTS and compared them with 20 patients with neurocardiogenic syncope who were otherwise well, and with 15 healthy control subjects. We measured continuous heart rate, respiration and blood pressure, and used venous occlusion strain gauge plethysmography to measure calf and forearm blood flow, peripheral arterial resistance, peripheral venous resistance and venous pressure ( P (v)). Upright tilt was performed to 70 degrees for 10 min, during which calf blood flow and volume were measured. Calf P (v) was increased (to 27.2+/-2.0 mmHg) in a subgroup of POTS patients, who also had increased arterial resistance (57+/-6 mmHg.ml(-1).min(-1).100 ml(-1) tissue), increased venous resistance (2.4+/-0.3 mmHg.ml(-1).min(-1).100 ml(-1) tissue), and decreased peripheral flow (1.0+/-0.2 ml.min(-1).100 ml(-1) tissue) in the calf; other POTS patients with a normal P (v) had decreased arterial resistance (18+/-2 mmHg.ml(-1).min(-1).100 ml(-1) tissue) and increased blood flow (3.8+/-0.3 ml.min(-1).100 ml(-1) tissue). Syncope patients were not different from controls ( P (v)=11.4+/-0.5 mmHg; calf flow=3.1+/-0.2 ml.min(-1).100 ml(-1) tissue; arterial resistance=27+/-2 mmHg.ml(-1).min(-1).100 ml(-1) tissue; venous resistance=1.2+/-0.3 mmHg.ml(-1).min(-1).100 ml(-1) tissue). When upright, syncope patients and control subjects had similar increases in heart rate and calf volume, stable blood pressure, and decreases in blood flow. POTS patients had markedly increased heart rate and calf blood flow, unstable blood pressure, and pooling in the lower extremities, regardless of subgroup. We conclude that peripheral vascular physiology in patients with POTS is abnormal, in contrast with normal peripheral vascular physiology in neurocardiogenic syncope.