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Drug-induced fibrotic valvular heart disease.
Lancet
August 2009
Valvular Heart Disease Clinic, Department of Cardiology, Royal Free Hospital, London, UK.
The initial association between the development of valvular heart disease and drugs stems from observations made during the use of methysergide and ergotamine for migraine prophylaxis in the 1960s. Since then, the appetite suppressants fenfluramine and dexfenfluramine, the dopamine agonists pergolide and cabergoline, and more recently, the recreational drug ecstasy (3,4 methylenedioxymethamphetamine; MDMA) have been implicated. Results from clinical trials show that drug dose and treatment duration affect both the risk of developing the disease and its severity.
View Article and Find Full Text PDFHeart failure induced by non-cardiac drugs.
Drug Saf
December 2006
Department of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.
Although heart failure is predominantly caused by cardiovascular conditions such as hypertension, coronary heart disease and valvular heart disease, it can also be an adverse reaction induced by drug therapy. In addition, some drugs have the propensity to adversely affect haemodynamic mechanisms in patients with an already existing heart condition. In this article, non-cardiac drugs known to be associated with the development or worsening of heart failure are reviewed.
View Article and Find Full Text PDFSevere multivalvular heart disease: a new complication of the ergot derivative dopamine agonists.
Mov Disord
June 2004
Department of Neurology, University Hospital, Geneva, Switzerland.
We report on 4 new cases of valvular heart disease in Parkinson's disease patients treated with the ergot derivative dopamine agonists pergolide and cabergoline. Noninflammatory fibrotic degeneration of cardiac valves has been reported to occur in patients with carcinoid syndrome and to occasionally complicate therapies with the anti-migraine ergot alkaloid ergotamine and methysergide and with the appetite suppressants fenfluramine and dexfenfluramine. In these cases, the pathogenesis is suspected to involve serotonin-mediated abnormal fibrogenesis by means of the 5-HT2B receptors, which are expressed in the fibroblasts of heart valves.
View Article and Find Full Text PDFPossible role of valvular serotonin 5-HT(2B) receptors in the cardiopathy associated with fenfluramine.
Mol Pharmacol
January 2000
CNS Diseases Research, The DuPont Pharmaceuticals Research Laboratories, Experimental Station, Wilmington, Delaware, USA.
Dexfenfluramine was approved in the United States for long-term use as an appetite suppressant until it was reported to be associated with valvular heart disease. The valvular changes (myofibroblast proliferation) are histopathologically indistinguishable from those observed in carcinoid disease or after long-term exposure to 5-hydroxytryptamine (5-HT)(2)-preferring ergot drugs (ergotamine, methysergide). 5-HT(2) receptor stimulation is known to cause fibroblast mitogenesis, which could contribute to this lesion.
View Article and Find Full Text PDFCharacterization of 5-hydroxytryptamine1A properties of flesinoxan: in vivo electrophysiology and hypothermia study.
Neuropharmacology
October 1995
Department of Psychiatry, McGill University, Montréal, Québec, Canada.
Article Synopsis
- Flesinoxan is a selective 5-HT1A ligand that does not produce the antagonistic effects seen with other drugs in its class, potentially contributing to its antidepressant properties.
- In experiments, flesinoxan was more effective than gepirone in suppressing neuron activity, acting as a partial agonist on postsynaptic and full agonist on presynaptic 5-HT1A receptors in the rat brain.
- Although both intravenous and subcutaneous doses of flesinoxan induced hypothermia, more of the drug was needed compared to 8-OH-DPAT, and the hypothermic effects were reduced by prior administration of certain 5-HT antagonists.
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