Acute Cardiomyopathy Secondary to Intravenous Amphetamine Abuse

Call, Thomas

doi:10.7326/0003-4819-97-4-559

Cited by 77 publications

(20 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Addiction to amphetamine poses enormous social and economic burdens. Serious and sometimes fatal cardiovascular toxicity associated with the use of this drug has been reported [2][3][4]. The illicit use of amphetamines has been shown to lead to tachyarrhythmias and sudden death [5,6].…”

Section: Introductionmentioning

confidence: 99%

Amphetamine activates connexin43 gene expression in cultured neonatal rat cardiomyocytes through JNK and AP-1 pathway

Shyu¹,

Wang²,

Yu³

et al. 2004

Cardiovascular Research

View full text Add to dashboard Cite

Objective: Amphetamine has been known to induce cardiac dysrhythmia and sudden death. However, the molecular mechanism for the induction of dysrhythmia is not known. Connexin43 (Cx43) plays an important role for arrhythmogenesis. This study was undertaken to test the hypothesis that amphetamine could induce Cx43 expression in cardiac myocytes. Methods: Neonatal Wistar rat cardiac myocytes were cultured under the stimulation of amphetamine. Cx43 mRNA and protein expression were examined by Northern and Western blots, respectively. We used c-Jun N-terminal kinase (JNK) inhibitor, SP600125, and JNK1 dsRNAi to investigate the signal pathway of amphetamine-induced expression of Cx43. Results: The level of Cx43 protein significantly increased from 4 to 24 h after addition of amphetamine (10 AM). The Cx43 mRNA increased maximally to 4.2-fold at 6 h after addition of amphetamine and returned to the baseline level at 48 h. These increases of Cx43 protein at 24 h were completely attenuated ( P < 0.001) by SP600125 (20 AM) and JNK1 dsRNAi. Amphetamine increased and SP600125 decreased the immunohistochemical labeling of Cx43. Amphetamine increased and SP600125 decreased the phosphorylated JNK and c-Jun proteins. Gel-shifting assay showed that DNA-binding activity of AP-1 increased after addition of amphetamine and SP600125 and JNK1 dsRNAi abolished the binding activity induced by amphetamine. Conclusions: These findings indicate that amphetamine activates Cx43 gene expression in cultured rat neonatal cardiac myocytes. Amphetamine mediates the Cx43 gene expression, at least in part, through the JNK pathway. These findings from our study suggest that Cx43 plays a role for the molecular mechanism of amphetamine-induced cardiac dysrhythmias.

show abstract

Section: Introductionmentioning

confidence: 99%

Amphetamine activates connexin43 gene expression in cultured neonatal rat cardiomyocytes through JNK and AP-1 pathway

Shyu¹,

Wang²,

Yu³

et al. 2004

Cardiovascular Research

View full text Add to dashboard Cite

show abstract

“…Amphetamines have sympathetic activators with the stimulation of α -and β -adrenergic receptors and various effects on the cardiovascular system such as hypertension and tachyarrhythmia [10]. Acute cardiomyopathy associated with amphetamines or similar drug use was also reported [11,12]. In this case, the patient presented with acute car- and congestive heart failure varies from 10% to 30% [13].…”

Section: Discussionmentioning

confidence: 93%

Amphetamine-Like Weight Reduction Drug Induced Acute Cardiomyopathy with Left Ventricular Thrombosis

et al. 2014

View full text Add to dashboard Cite

“…On at least one occasion the degree of left ventricular failure was severe enough to lead to death despite therapy [1]. Several authors report acute reversible left ventricular function following intravenous administration which is a common route of abuse along with smoking or ingesting the drug [3,4]. Fortunately our patient was not taking amphetamines during either of her pregnancies, as prenatal exposure has also been associated with cardiomyopathy in the neonate [5].…”

Section: Discussionmentioning

confidence: 99%

“…Full blood count with MCV of 84, urea and electrolytes normal. Liver function tests were marginally abnormal with bilirubin 22 mmol l -1 [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20], alkaline phosphatase 83 (30-100 IU l -1 ), ALT 70 (5-31 IU l -1 ) and albumin 28 g l -1 [35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50]. A diagnosis of amphetamine-related cardiomyopathy was made and she was commenced on a diuretic, warfarin and an ACE inhibitor.…”

mentioning

confidence: 99%

‘Ally McBeal heart?’– Drug induced cardiomyopathy in a young woman

Crean¹,

Pohl²

2004

Brit J Clinical Pharma

View full text Add to dashboard Cite

Dilated cardiomyopathy is relatively uncommon in women of child bearing age. When it does occur, it is most commonly as a sequela of pregnancy, viral myocarditis or excessive alcohol intake. However, individuals in this age group are also amongst the most likely to consume other recreational drugs. We present the case of a young woman whose long-term amphetamine habit resulted in severe impairment of left ventricular function.Mrs X was a 30-year-old mother of two children who was referred from her general practitioner with a four month history of ankle swelling, together with increased abdominal distension and breathlessness over the previous 3 days. Past medical history included an episode of pneumonia 7 years earlier, mild asthma (never requiring hospitalization), and regular panic attacks.Symptomatic enquiry revealed that she had been experiencing a sensation of panic most nights in the last 2 months when she found she had been waking from sleep breathless. These symptoms were eased by sitting forward and she was adamant that they were quite distinct from the symptoms she would typically experience during a traditional panic attack.She had a 20-pack year smoking history but professed only very occasional alcohol consumption. She did, however, admit to having taken amphetamines on a daily basis for the last 4 years. Her motivation for this habit was a desire to stay thin -and indeed she had initially begun to abuse the drug at a time when she was trying to give up smoking and subsequently gained weight. She purchased the drug illegally, consuming approximately one tablespoon per day. She estimated that she would utilize 15 g of amphetamine per month at a price of roughly 10 pounds sterling per gram.On examination she was thin with a BMI of 19 kg m -2 . Respiratory rate was increased and saturations on air were low at 92%. A sinus tachycardia of 120 bpm was present. Blood pressure was 125/90. The apex beat was displaced and the jugular venous pressure was elevated 8 cm. Auscultation revealed a gallop rhythm and a left basal effusion. There was hepatomegaly, mild ascites and peripheral pitting oedema.ECG demonstrated biphasic P waves in keeping with left atrial enlargement, a left ventricular hypertrophy and strain pattern, and Q waves in the anteroseptal leads. CXR showed cardiomegaly, interstitial pulmonary oedema and a small left pleural effusion.

show abstract

Acute Cardiomyopathy Secondary to Intravenous Amphetamine Abuse

Cited by 77 publications

References 6 publications

Amphetamine activates connexin43 gene expression in cultured neonatal rat cardiomyocytes through JNK and AP-1 pathway

Amphetamine activates connexin43 gene expression in cultured neonatal rat cardiomyocytes through JNK and AP-1 pathway

Amphetamine-Like Weight Reduction Drug Induced Acute Cardiomyopathy with Left Ventricular Thrombosis

‘Ally McBeal heart?’– Drug induced cardiomyopathy in a young woman

Contact Info

Product

Resources

About