1989
DOI: 10.1016/0022-0736(89)90086-1
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Electrocardiographic and hemodynamic effects of intravenous cocaine in awake and anesthetized dogs

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Cited by 68 publications
(27 citation statements)
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“…38 Cocaine prolongs the PR, QRS, and QT intervals. 39,40 Cocaine is associated with coronary atherosclerosis even in young users with relatively few cardiac risk factors. 41,42 …”
Section: Clinicalmentioning
confidence: 99%
“…38 Cocaine prolongs the PR, QRS, and QT intervals. 39,40 Cocaine is associated with coronary atherosclerosis even in young users with relatively few cardiac risk factors. 41,42 …”
Section: Clinicalmentioning
confidence: 99%
“…Several examples best illustrate this point. First, in anaesthetized animals the heart rate remains largely unchanged and the arrhythmic effects of small (sub-lethal) doses of cocaine are minimized [18]. In contrast massive doses of cocaine in humans occasionally result from rupture of smuggled drug packets.…”
Section: Sodium Channel Blockadementioning
confidence: 99%
“…However, it has also been proposed that cocaine-related deaths of cardiac origin may occur in the absence of myocardial infarction, presumably because of direct adverse effects on cardiac electrophysiology. [11][12][13][14][15] Cocaine is a local anesthetic, and its blockade of Na+ channels1617 may produce conduction disturbances in the heart. Such conduction disturbances could contribute to the generation of reentrant arrhythmias, and previous investigators have emphasized this concept of cocaine arrhythmogenesis"~- 15; however, it has also been shown that cocaine prolongs repolarization.…”
mentioning
confidence: 99%