科研之友
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摘要
POTS (postural tachycardia syndrome) is a chronic form of OI (orthostatic intolerance). Neuropathic POTS is characterized by decreased adrenergic vasoconstriction, whereas hyperadrenergic POTS exhibits increased adrenergic vasoconstriction. We hypothesized that midodrine, an alpha(1)-adrenergic receptor agonist, would increase CVR (calf vascular resistance), decrease C-v (calf venous capacitance) and decrease orthostatic tachycardia in neuropathic POTS, but not alter haennodynannics in hyperadrenergic POTS. A total of 20 POTS patients (12 neuropathic and eight hyperadrenergic), ages 12-20 years, participated in this randomized placebo-controlled double-blind cross-over study. Of these subjects, 15 were female. POTS subjects received 2 weeks of treatment with midodrine or placebo, with increased dosing from 2.5 to 10 mg three times daily. Following a 7-day drug-washout period, subjects received the cross-over treatment. HR (heart rate), MAP (mean arterial pressure), Q (calf) (calf blood flow) and CVR were measured supine and during 35 degrees HUT (head-up tilt). C-v was measured supine. In neuropathic POTS, midodrine decreased supine HR, Q (calf) and C-v, while increasing MAP and CVR compared with placebo. During HUT, in neuropathic POTS, midodrine decreased HR, Q (calf) and C-v, while increasing MAP and CVR. In hyperadrenergic POTS, placebo and nnidodrine both decreased upright HR and increased supine CVR. Placebo also increased supine C-v, compared with midodrine in hyperadrenergic POTS. Therefore midodrine improved postural tachycardia in neuropathic POTS by increasing CVR and decreasing Q (calf) and C-v, whereas these effects were not seen in hyperadrenergic POTS patients who experienced a placebo effect. This suggests that midodrine is probably an effective treatment for neuropathic POTS, but not for hyperadrenergic POTS.
- 出版日期2014-2
