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Altered peripheral haemodynamics, decreased cardiac output, decreased blood volume and increased AngII (angiotensin II) have been reported in POTS (postural tachycardia syndrome). Recent findings indicate that BMI (body mass index) may be reduced. In the present study, we investigated the hypothesis that reduced BMI is associated with haemodynamic abnormalities in POTS and that this is related to AngII. We studied 52 patients with POTS, aged 14-29 years, compared with 36 control subjects, aged 14-27 years. BMI was not significantly reduced on average in the POTS patients, but was reduced in patients with decreased peripheral blood flow. POTS patients were then subdivided on the basis of BMI, and supine haemodynamics were measured. There was no difference in blood volume or cardiac output once BMI or body mass were accounted for. When POTS patients with BMI &lt;50th percentile were compared with controls, calf blood flow [1.63+/-0.31 compared with 3.58+/-0.67 ml(-1).min(-1).(100 ml of tissue)(-1)] and maximum venous capacity (3.87+/-0.32 compared with 4.98+/-0.36 ml/100 ml of tissue) were decreased, whereas arterial resistance [56+/-0.5 compared with 30+/-4 mmHg.ml(-1).min(-1).(100 ml of tissue)(-1)] and venous resistance [1.23+/-0.17 compared with 0.79+/-0.11 mmHg.ml(-1).min(-1).(100 ml of tissue)(-1)] were increased. Similar findings were also observed when POTS patients with BMI &lt;50th percentile were compared with POTS patients with BMI &gt;50th percentile. There was no relationship between blood flow, resistance or maximum venous capacity with BMI in control subjects. BMI was inversely related to plasma AngII concentrations in those POTS patients with decreased peripheral blood flow, consistent with cachectic properties of the octapeptide. Patients with low-flow POTS had decreased body mass, but decreased body mass alone cannot account for findings of peripheral vasoconstriction. In conclusion, the findings suggest that reduced body mass relates to increased plasma AngII.

Reduced body mass index is associated with increased angiotensin II in young women with postural tachycardia syndrome