Polymorphisms in CYP2D6 may predict methamphetamine related heart failure

Sutter, Mark E.; Gaedigk, Andrea; Albertson, Timothy E; Southard, Jeffrey; Owen, Kelly P.; Mills, Lisa D.; Diercks, Deborah B.

doi:10.3109/15563650.2013.818684

Cited by 24 publications

(17 citation statements)

References 20 publications

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“…Vulnerability to the development of methamphetamineassociated cardiomyopathy appears to be genetically influenced. Cytochrome P450 polymorphism profiling may identify methamphetamine abusers at elevated risk of cardiomyopathy; CYP2D6 'extensive metabolisers' appear to be significantly more prone to both methamphetamineinduced cardiomyopathy and psychosis [33].…”

Section: Methamphetamine-associated Cardiomyopathymentioning

confidence: 99%

The Cardiac Complications of Methamphetamines

Paratz

Cunningham

MacIsaac

2016

Heart, Lung and Circulation

121

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Methamphetamines are increasingly popular drugs of abuse in Australia, and are rising in purity. The rising popularity and purity of methamphetamines has notably increased demands upon Australian medical services. Methamphetamines are sympathomimetic amines with a range of adverse effects upon multiple organ systems. Cardiovascular complications are the second leading cause of death in methamphetamine abusers, and there appears to be a high prevalence of cardiac pathology. Cardiovascular pathology frequently seen in methamphetamine abusers includes hypertension, aortic dissection, acute coronary syndromes, pulmonary arterial hypertension and methamphetamine-associated cardiomyopathy. The rising prevalence of methamphetamine abuse is likely to increase the burden of cardiovascular pathology in Australians. A National Parliamentary Enquiry was opened in March 2015 to address concerns regarding the medical and social impacts of methamphetamine abuse. From April 2015, a National 'Ice Taskforce' was also created in parallel. Reversal of cardiac pathology appears to be achievable with abstinence from methamphetamines and initiation of appropriate treatment. It is key to appreciate that the pathogenesis of methamphetamine-induced cardiac complications arises as a result of the specific toxic effects of methamphetamines. Clinical management is hence individualised; suggested management approaches for methamphetamine-induced cardiac complications are detailed within this article.

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Section: Methamphetamine-associated Cardiomyopathymentioning

confidence: 99%

The Cardiac Complications of Methamphetamines

Paratz

Cunningham

MacIsaac

2016

Heart, Lung and Circulation

121

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show abstract

“…CYP2D6 is responsible for the first step of MA metabolism. Correlating to this, a small prospective case‐control study showed a, albeit statistically insignificant, trend that individuals with an increased CYP2D6 metabolism were more likely to develop DCM . A clinical case of a patient with MA abuse is depicted in Figure .…”

Section: Cardiac Complicationsmentioning

confidence: 72%

Methamphetamine‐related cardiovascular diseases

2020

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Aims Abuse of crystal methamphetamine (MA) poses a growing problem for health services worldwide. This review summarizes the current literature on the effects of MA on the cardiovascular system. Methods and results This article is a presentation of a case report and review of the current literature. In Europe, especially the eastern countries and the eastern states of Germany are affected. MA increases the concentration of catecholamines in the synaptic gap leading to euphoria, alertness, and hunger suppression as well as psychiatric and gastrointestinal complications. MA consumption is associated with hypertension, acute and chronic myocardial toxicity, stroke, coronary artery disease, and sudden cardiac death. Although many aspects of the underlying pathophysiology remain unknown, catecholaminemediated pathologies appear to play an important role. The duration of MA consumption is the most important determinant for the prognosis. Conclusions Awareness is needed as cardiac complications are important causes of morbidity and mortality in patients with MA consumption. Drug abstinence is the mainstay of therapy, cardiac and other complications should be treated according to the respective guidelines. Incompliance to therapy and frequent relapses are the main challenges for successful treatment. Further research is required to improve the understanding of this rapidly increasing cardiomyopathy.

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“…Indeed, (Berezin, 2016d;Fazakas et al, 2016;Friedrich et al, 2013;Hofman et al, 2010;Kolder et al, 2012;McNamara et al, 2014;Sutter et al, 2013). As biomarkers particularly used to scrutiny single nucleotide polymorphisms (SNPs) of genes encoding enzymes related to oxidative stress (Berezin, 2016e), genotype of guanine nucleotide-binding proteins (G-proteins) beta-3 subunit (GNB3) (Fazakas et al, 2016), transcription factor Islet-1 gene (McNamara et al, 2014), troponin T (Friedrich et al, 2013), CYP2D6 polymorphism (Hofman et al, 2010), cardiac myosin binding protein-C mutations (Friedrich et al, 2013), renin-angiotensin-aldosterone system polymorphism (Sutter et al, 2013) etc. Indeed, it is well known that angiotensin-converting enzyme (ACE) I/D gene D allele was associated with higher overall mortality as compared with the I allele in HF patients and that the effect could be modified by ACE inhibitors' given (Kolder et al, 2012).…”

Section: Genetic Biomarkersmentioning

confidence: 99%

Up-to-date clinical approaches of biomarkers’ use in heart failure

Berezin¹

2017

Biomed. Res. Ther.

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Heart failure (HF) is considered a leading cause of death in patients with established cardiovascular (CV) and metabolic diseases. Although current treatment strategy has improved survival rate and clinical outcomes of HF, the HF prevalence exhibits growth especially in older patients' population and survivors after coronary atherothrombotic events. Current clinical guidelines regarding treatment and prevention of HF claim the role of biological markers as pretty easy and powerful tool for diagnosis, risk stratification, and prognostication of HF. However, there is not clear whether all these biological markers are able to equally predict CV death and HF-related outcomes in patients with acute and chronic HF as well as in various phenotypes of HF. The aim of the review is to discuss a role of in risk stratification and individual treatment in patients with different phenotypes of HF.

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Polymorphisms in CYP2D6 may predict methamphetamine related heart failure

Abstract: Our study demonstrates a trend that individuals with decreased metabolic activity were less likely to develop heart failure. While not statistically significant, a signal is present that extensive metabolizers may be at increased risk for the development of a cardiomyopathy.

Cited by 24 publications

References 20 publications

The Cardiac Complications of Methamphetamines

The Cardiac Complications of Methamphetamines

Methamphetamine‐related cardiovascular diseases

Up-to-date clinical approaches of biomarkers’ use in heart failure

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