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Effects of a β-blocker on the cardiovascular response to MDMA (Ecstasy)
  1. C M Hysek1,
  2. F X Vollenweider2,
  3. M E Liechti1
  1. 1Division of Clinical Pharmacology and Toxicology and Department of Biomedicine, University Hospital and University of Basel, Switzerland
  2. 2Heffter Research Center, University Hospital of Psychiatry, Zurich, Switzerland
  1. Correspondence to Matthias Liechti, Division of Clinical Pharmacology and Toxicology, Department of Internal Medicine, University Hospital Basel, Hebelstasse 2, CH-4031 Basel, Switzerland; mliechti{at}


Background MDMA (3,4-methylenedioxymethamphetamine, ‘Ecstasy’) produces tachycardia and hypertension and is rarely associated with cardiovascular and cerebrovascular complications. In clinical practice, β-blockers are often withheld in patients with stimulant intoxication because they may increase hypertension and coronary artery vasospasm due to loss of β2-mediated vasodilation and unopposed α-receptor activation. However, it is unknown whether β-blockers affect the cardiovascular response to MDMA.

Methods The effects of the non-selective β-blocker pindolol (20 mg) on the cardiovascular effects of MDMA (1.6 mg/kg) were investigated in a double-blind placebo-controlled crossover study in 16 healthy subjects.

Results Pindolol prevented MDMA-induced increases in heart rate. Peak values (mean±SD) for heart rate were 84±13 beats/min after MDMA vs 69±7 beats/min after pindolol-MDMA. In contrast, pindolol pretreatment had no effect on increases in mean arterial blood pressure (MAP) after MDMA. Peak MAP values were 115±11 mm Hg after MDMA vs 114±11 mm Hg after pindolol-MDMA. Pindolol did not change adverse effects of MDMA.

Conclusion The results of this study indicate that β-blockers may prevent increases in heart rate but not hypertensive and adverse effects of MDMA.

  • MDMA
  • 3,4-methylenedioxymethamphetamine
  • ecstasy
  • norepinephrine
  • pindolol
  • β-adreneric receptor
  • β-blocker
  • cardiovascular effects
  • mental health
  • drug abuse
  • toxicology

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  • Funding This study was supported by the Heffter Research Institute, Santa Fe, New Mexico, USA, the Swiss Federal Office of Public Health, Berne, Switzerland (Nr 00.001683) and the Swiss National Foundation (Nr 323230_126231/1).

  • Competing interests None.

  • Ethics approval This study was conducted with the approval of the ethics committee of the University Hospital of Zurich.

  • Provenance and peer review Not commissioned; externally peer reviewed.