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Drug Treatment of Orthostatic Hypotension Because of Autonomic Failure or Neurocardiogenic Syncope

  • Therapy in Practice
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Abstract

Orthostatic hypotension either because of autonomic failure or neurocardiogenic syncope can be very incapacitating and should be treated accordingly. Drug therapy is frequently needed to alleviate orthostatic symptoms. The physiopathological basis of neurocardiogenic syncope and of autonomic failure is completely different and their treatment should be distinct.

In the past 5 years, many randomized, placebo-controlled trials have shed light on the efficacy of specific pressor drugs. In patients with orthostatic hypotension because of autonomic failure, α-adrenoceptor agonists, and midodrine in particular, have been shown to increase standing blood pressure and decrease orthostatic symptoms. Other drugs such as octreotide, indomethacin or ergotamine have also been shown to elevate standing blood pressure and/or orthostatic tolerance. Fludrocortisone is a well known and frequently used pressor drug but randomized controlled studies are needed to measure its efficacy. In patients with orthostatic hypotension associated with neurocardiogenic syncope, clinical trials have demonstrated that β-blockers, especially β1-selective agents without intrinsic sympathomimetic activity such as atenolol, midodrine and paroxetine can decrease recurrence of syncope.

Treatment algorithms, such as those presented in this review, should always be interpreted in the light of individual patient characteristics. Many of the drugs used for orthostatic hypotension have multiple indications and contraindications that should influence therapeutic decisions. Little is known about the effectiveness and tolerability of specific combinations of pressor drugs. Consequently, sound clinical judgment and close follow-up of patients should always guide combination therapy.

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    Maxime Lamarre-Cliche

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Lamarre-Cliche, M. Drug Treatment of Orthostatic Hypotension Because of Autonomic Failure or Neurocardiogenic Syncope. Am J Cardiovasc Drugs 2, 23–35 (2002). https://doi.org/10.2165/00129784-200202010-00004

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