Report of methamphetamine use and cardiomyopathy in three patients

Sadeghi, Roxana; Agin, Khosrow; Taherkhani, Maryam; Najm-Afshar, Leila; Nelson, Lewis S.; Abdollahi, Mohammad; Shadnia, Shahin

doi:10.1186/2008-2231-20-20

Cited by 23 publications

(16 citation statements)

References 21 publications

(19 reference statements)

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“…They are consistent with results of several recent meta-analyses (OR=1.87; 95% CI=1.5–2.33) (Nikfar et al 2012b) and (OR=1.45; 95% CI=1.22–1.72) (Ross et al 2013) that found a modest elevation in risk of spontaneous miscarriage with antidepressant treatment. However, confounding as a result of unmeasured or incompletely measured health factors such as prior pregnancy loss, obesity, substance abuse, etc, may confound the findings.…”

Section: Spontaneous Abortionsupporting

confidence: 92%

Antidepressant Use in Pregnant and Postpartum Women

Yonkers

Blackwell²,

Glover

et al. 2014

Annu. Rev. Clin. Psychol.

104

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Women in their reproductive years are at increased risk of experiencing depressive and anxiety disorders. As such, it is likely that pregnant women will undergo treatment with antidepressants. We review the risk of adverse pregnancy outcomes and perinatal and neonatal complications of the offspring related to in utero exposure to antidepressants. The literature shows that antidepressant exposure is associated with fetal growth changes and shorter gestations, although effects are small. There are a number of reports of transitory neonatal signs after exposure to antidepressants. No specific pattern of malformations has been consistently associated with antidepressants, with the possible exception of paroxetine and cardiac malformations. There is inconclusive evidence of a link between antidepressants in late pregnancy and persistent pulmonary hypertension in the newborn. While antidepressant use in pregnancy is well studied, confounding factors that can adversely affect pregnancy and birth outcomes may contribute to some of the findings.

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Section: Spontaneous Abortionsupporting

confidence: 92%

Antidepressant Use in Pregnant and Postpartum Women

Yonkers

Blackwell²,

Glover

et al. 2014

Annu. Rev. Clin. Psychol.

104

View full text Add to dashboard Cite

show abstract

“…3. Methamphetamine (crystal meth): as for cocaine and amphetamines above, there are reports of cardiomyopathy [73], hypertension, aortic dissection, acute coronary syndromes, pulmonary arterial hypertension and methamphetamine-associated cardiomyopathy [74] and in rat models cardiac pathology [75]. Recommendations as for Cocaine and Ecstasy above.…”

Section: Heartmentioning

confidence: 99%

Effects of drug abuse, smoking and alcohol on donor hearts and lungs

et al. 2019

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Potential heart and lung donors with a history of illicit drugs and/or smoking and alcohol are frequently offered, though there is no clear guidance on when it is safe to use these organs. A review of the literature on effects of drugs, alcohol and smoking on donor outcomes, and the effects of these on the intact heart and lung was undertaken. There has been a marked increase in deaths from opioid abuse in many developed countries, though recent evidence suggests that outcomes after cardiothoracic transplantation are equivalent to nonopioid donor causes of death. For donor smoking, there is an increased risk with lung transplantation; however, that risk is less when compared to further waiting on the transplant list for a nonsmoking alternative. Heavy alcohol consumption does not adversely affect heart transplantation, and there is no clear evidence of adverse outcomes after lung transplantation. There are no overall effects of cannabis or cocaine on survival after heart or lung transplantation. In all these cases, careful donor assessment can establish if a particular organ can be used. In most cases, use of drugs requires careful assessment, but is not in of itself a contraindication to cardiothoracic transplantation.

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“… 1 , 2 , 3 , 4 , 5 In particular, METH has been associated with a myriad of adverse effects on the circulatory system, including cardiomyopathy, hypertension, arrhythmia, myocardial ischemia, acute coronary syndrome, cardiac failure and sudden death. 6 , 7 , 8 In METH abusers with acute aortic dissection or coronary syndrome, vascular structural alterations have been found in the myocardium in a number of clinical cases, indicating that METH can cause toxic effects on the blood vessels. 9 , 10 The above studies suggest that vascular endothelial cells may be a key target in METH-caused cardiovascular pathophysiologic alterations.…”

mentioning

confidence: 99%

Nupr1/Chop signal axis is involved in mitochondrion-related endothelial cell apoptosis induced by methamphetamine

et al. 2016

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Methamphetamine (METH) abuse has been a serious global public health problem for decades. Previous studies have shown that METH causes detrimental effects on the nervous and cardiovascular systems. METH-induced cardiovascular toxicity has been, in part, attributed to its destructive effect on vascular endothelial cells. However, the underlying mechanism of METH-caused endothelium disruption has not been investigated systematically. In this study, we identified a novel pathway involved in endothelial cell apoptosis induced by METH. We demonstrated that exposure to METH caused mitochondrial apoptosis in human umbilical vein endothelial cells and rat cardiac microvascular endothelial cells in vitro as well as in rat cardiac endothelial cells in vivo. We found that METH mediated endothelial cell apoptosis through Nupr1–Chop/P53–PUMA/Beclin1 signaling pathway. Specifically, METH exposure increased the expression of Nupr1, Chop, P53 and PUMA. Elevated p53 expression raised up PUMA expression, which initiated mitochondrial apoptosis by downregulating antiapoptotic Bcl-2, followed by upregulation of proapoptotic Bax, resulting in translocation of cytochrome c (cyto c), an apoptogenic factor, from the mitochondria to cytoplasm and activation of caspase-dependent pathways. Interestingly, increased Beclin1, upregulated by Chop, formed a ternary complex with Bcl-2, thereby decreasing the dissociative Bcl-2. As a result, the ratio of dissociative Bcl-2 to Bax was also significantly decreased, which led to translocation of cyto c and initiated more drastic apoptosis. These findings were supported by data showing METH-induced apoptosis was significantly inhibited by silencing Nupr1, Chop or P53, or by PUMA or Beclin1 knockdown. Based on the present data, a novel mechanistic model of METH-induced endothelial cell toxicity is proposed. Collectively, these results highlight that the Nupr1–Chop/P53–PUMA/Beclin1 pathway is essential for mitochondrion-related METH-induced endothelial cell apoptosis and may be a potential therapeutic target for METH-caused cardiovascular toxicity. Future studies using knockout animal models are warranted to substantiate the present findings.

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Report of methamphetamine use and cardiomyopathy in three patients

Cited by 23 publications

References 21 publications

Antidepressant Use in Pregnant and Postpartum Women

Antidepressant Use in Pregnant and Postpartum Women

Effects of drug abuse, smoking and alcohol on donor hearts and lungs

Nupr1/Chop signal axis is involved in mitochondrion-related endothelial cell apoptosis induced by methamphetamine

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