Methamphetamine-Related Deaths in San Francisco: Demographic, Pathologic, and Toxicologic Profiles

Karch, Steven B.; Stephens, Boyd G.; Ho, Chih-Hsiang

doi:10.1520/jfs14464j

Cited by 224 publications

(124 citation statements)

References 28 publications

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“…Coronary heart disease appears to occur more frequently and at a younger age among methamphetamine users than others [75]. Methamphetamine users have a 3.7-fold increased risk for cardiomyopathy, and the associated left ventricular dysfunction is more severe compared with other patients with cardiomyopathy [76].…”

Section: Cardiovascular Complicationsmentioning

confidence: 98%

A review of the clinical pharmacology of methamphetamine

2009

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Aims To examine the literature regarding clinical pharmacokinetics, direct effects and adverse clinical outcomes associated with methamphetamine use. Methods Relevant literature was identified through a PubMed search. Additional literature was obtained from relevant books and monographs. Findings and conclusions The mean elimination half-life for methamphetamine is approximately 10 hours, with considerable inter-individual variability in pharmacokinetics. Direct effects at low-to-moderate methamphetamine doses (5-30 mg) include arousal, positive mood, cardiac stimulation and acute improvement in cognitive domains such as attention and psychomotor coordination. At higher doses used typically by illicit users (Ն50 mg), methamphetamine can produce psychosis. Its hypertensive effect can produce a number of acute and chronic cardiovascular complications. Repeated use may induce neurotoxicity, associated with prolonged psychiatric symptoms, cognitive impairment and an increased risk of developing Parkinson's disease. Abrupt cessation of repeated methamphetamine use leads to a withdrawal syndrome consisting of depressed mood, anxiety and sleep disturbance. Acute withdrawal lasts typically for 7-10 days, and residual symptoms associated with neurotoxicity may persist for several months.

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Section: Cardiovascular Complicationsmentioning

confidence: 98%

A review of the clinical pharmacology of methamphetamine

2009

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“…Similar types of cardiac toxicity have been reported in animals after acute and chronic administration of METH (Islam et al, 1995;He et al, 1996). A growing clinical literature has also linked METH use/abuse with cardiac toxicity and death in humans (Hong et al, 1991;Chan et al, 1994;Karch et al, 1999). However, the toxic effects of METH in these clinical reports are often difficult to evaluate due to the polydrug use and a lack of data regarding quantity and frequency of METH administration.…”

Section: Cardiovascular and Reflex Responses To Methamphetaminementioning

confidence: 99%

“…The illicit use of methamphetamine (METH) has dramatically increased during the past several years, as has the number of clinical reports detailing serious and sometimes fatal cardiovascular toxicity associated with the use of this drug (Hong et al, 1991;Karch et al, 1999). Despite the potential dangers posed by METH, the cardiovascular effects of this drug have not been well characterized.…”

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confidence: 99%

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Cardiovascular Responses Elicited by the “Binge” Administration of Methamphetamine

Varner

Ogden²,

Delcarpio³

et al. 2002

J Pharmacol Exp Ther

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Methamphetamine (METH) abuse is often characterized by a repeated pattern of frequent drug administrations (binge) followed by a period of abstinence. The effect of this pattern of METH use on cardiovascular function has not been characterized. Radiotelemetry was used to record the cardiovascular responses elicited during three successive METH binges (3 mg/kg, b.i.d. for 4 days) in conscious rats. Each binge was followed by a 10-day METH-free period. The effects of METH administration on vascular reactivity, Bezold-Jarisch reflex function, and cardiac morphology were also evaluated. The pressor responses elicited by the first three doses of METH in the second and third binges were significantly larger than those elicited by the corresponding doses in the first binge. The heart rate (HR) responses elicited by METH were similar within and among the three binges. Ten days after the last binge, the depressor responses elicited by the i.v. injection of sodium nitroprusside, isoproterenol, and acetylcholine were significantly smaller than those elicited before each binge. The arterial pressure and HR responses elicited by phenylephrine were unchanged. Bezold-Jarisch reflex function evoked by i.v. serotonin (10 g/kg) was significantly altered. The hearts from treated rats showed focal inflammatory infiltrates with abundant monocytes and occasional necrotic foci. These results indicate that this binge pattern of METH administration can significantly alter cardiovascular function and cardiovascular reflex function and produce serious cardiac pathology.

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“…The concentration of methamphetamine in blood and tissue samples in fatalities associated with methamphetamine is highly variable, with levels ranging from less than 1 mg/l to over 14 mg/l (Carvey and Reed, 1970;Kojima et al, 1983;Matoba et al, 1985;Moore et al, 1996). In addition, there does not appear to be a close correlation between the blood levels of methamphetamine or amphetamine and survival (Karch et al, 1999). Often, low levels of amphetamines are thought to be incidental findings, but very low concentrations of methamphetamine (0.7 mg/l) have been observed in patients dying of what is often described as 'classic stimulant toxicity' with agitation, hypertension, tachycardia and hyperthermia (Fukunaga et al, 1987;Moore et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Chloroephedrine: contaminant of methamphetamine synthesis with cardiovascular activity

Varner¹,

Hein²,

Ogden³

et al. 2001

Drug and Alcohol Dependence

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Chloroephedrine is an intermediate and possible contaminant formed when methamphetamine is manufactured using ephedrine or pseudoephedrine as precursors. The purpose of this study was to determine whether this contaminant has biological activity and might contribute to methamphetamine-induced cardiovascular toxicity. In conscious rats, the ( − ) and ( + ) isomers of chloroephedrine (0.1 and 1.0 mg/kg, i.v.) dose-dependently increased mean arterial pressure (MAP) and heart rate (HR). The potency of the pressor effects of ( −) and (+)-chloroephedrine was between that of ephedrine and pseudoephedrine. The increases in HR elicited by the four stimulants were similar except that the tachycardia elicited by all doses of ephedrine and pseudoephedrine were preceded by a brief decrease in HR. The i.v. administration of 10 mg/kg of (+ ) or (− )-chloroephedrine produced biphasic (decrease followed by increase) the MAP and HR responses. Ephedrine and pseudoephedrine did not decrease MAP at any dose tested. The initial decrease in HR elicited by ( − )-chloroephedrine was significantly reduced and the hypotensive response abolished by atropine, indicating that these components of the MAP and HR responses resulted from vagal activation. The secondary pressor response elicited by ( − )-chloroephedrine was significantly reduced and the tachycardia significantly increased by pretreatment with phentolamine (3 mg/kg, i.v.). The increase in HR was reversed by propranolol. These results indicate that ( − ) and (+)-chloroephedrine have sympathomimetic properties similar to other known sympathomimetic stimulants. In addition, larger doses of chloroephedrine can activate the vagus nerve. The combination of ( +)-methamphetamine and ( −)-chloroephedrine did not markedly alter the magnitude of the MAP and HR responses of ( + )-methamphetamine alone except at high doses of ( −)-chloroephedrine (10 mg/kg). Contamination of illicit methamphetamine with chloroephedrine may have toxic consequences.

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Methamphetamine-Related Deaths in San Francisco: Demographic, Pathologic, and Toxicologic Profiles

Cited by 224 publications

References 28 publications

A review of the clinical pharmacology of methamphetamine

A review of the clinical pharmacology of methamphetamine

Cardiovascular Responses Elicited by the “Binge” Administration of Methamphetamine

Chloroephedrine: contaminant of methamphetamine synthesis with cardiovascular activity

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