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Cardiovascular Research 2003 59(4):805-806; doi:10.1016/S0008-6363(03)00532-7
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

The cardiac cocaine connection

Christian Grohé*

c.grohe@uni-bonn.de

The first 10% of the full text of this article appears below.

See article by Moritz et al. [9] (pages 834–843) in this issue.

Cocaine (benzoylmethylecgonine) is increasingly used as an illegal stimulatory and hallucinogenic drug. This abuse is associated with a large array of clinically relevant cardiovascular side effects that after long-term use may lead from myocardial hypertrophy and necrosis to progressive left ventricular dysfunction [1]. To further dissect the underlying mechanisms, two pathophysiological entities have to be taken into account and deserve further attention: the acute effects and the biochemical and cellular changes in the myocardium after chronic abuse.

Cocaine was introduced as the first local anaesthetic agent at the end of the 19th century. Its local anaesthetic effect originates in from a blockade of voltage-gated Na+ . . . [Full Text of this Article]


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