Cardiomyopathy Cocaine Publications (208)

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Cardiomyopathy Cocaine Publications

2016Jul
J Forensic Leg Med
J Forensic Leg Med 2016 Jul 9;41:36-41. Epub 2016 Apr 9.
Consultant Pathologist/Toxicologist, P.O. Box 5139, Berkeley, CA, 94705, USA. Electronic address:

The term "positional asphyxia" was originally used to describe the situation in which the upper airways becomes compromised by sharp angulation of the head or neck, or where the chest wall is splinted and the diaphragm is prevented from moving because of an unusual position of the body. The term was redefined in the early 1980s to describe sudden death during physical restraint of an individual who is in a prone position. A large percent of reported victims were overweight males. Read More

Most were in early middle age and manifesting psychotic behavior at the time of death. Most were reported to have unremarkable autopsies, save for the finding, in many cases, of cocaine or methamphetamine (more recently synthetic cannabinoids and cathinones as well). As no cause of death was apparent (other than non-specific signs such as pulmonary edema), it became common practice to attribute death to force exerted on the decedent's back. When experimental studies with human volunteers disproved this notion, the term "restraint asphyxia" was substituted for positional asphyxia, but with nearly the exact same meaning. No experimental study has ever determined the actual amount of force necessary to cause asphyxia by force applied to the back (although the range of required static force is known), nor the duration for which it must be applied. This review discusses the epidemiology and the evidence for and against the theory of "restraint/positional" asphyxia. It also considers alternative theories of causation, including the findings of studies suggesting that cardiac channelopathies/cardiomyopathies may explain many cases of ARD.

2016Sep
Addict Biol
Addict Biol 2016 Sep 22;21(5):1030-42. Epub 2016 Mar 22.
National Laboratory of Gender Medicine of the National Institute of Biostructures and Biosystems, Osilo, Sassari, Italy.

Although sex differences in several aspects of substance use disorders (SUDs) have been identified, less is known about the importance of possible sex differences in side effects induced by substances of abuse or by medications used to treat SUDs. In the SUD field, the perception of certain subjective effects are actively sought, while all other manifestations might operationally be considered side effects. This article was aimed at reviewing sex differences in side effects induced by alcohol, nicotine, heroin, marijuana and cocaine and by medications approved for alcohol, nicotine and heroin use disorders. Read More

A large body of evidence suggests that women are at higher risk of alcohol-induced injury, liver disease, cardiomyopathy, myopathy, brain damages and mortality. The risk of tobacco-induced coronary heart disease, lung disease and health problems is higher for women than for men. Women also experience greater exposure to side effects induced by heroin, marijuana and cocaine. In addition, women appear to be more vulnerable to the side effects induced by medications used to treat SUDs. Patients with SUDs should be advised that the risk of developing health problems may be higher for women than for men after consumption of the same amount of substances of abuse. Doses of medications for SUD women should be adjusted at least according to body weight. The sex differences observed also indicate an urgent need to recruit adequate numbers of female subjects in pre-clinical and clinical studies to improve our knowledge about SUDs in women.

2016Feb
Am. J. Physiol. Heart Circ. Physiol.
Am J Physiol Heart Circ Physiol 2016 Feb 18;310(4):H516-23. Epub 2015 Dec 18.
Raabe College of Pharmacy, Ohio Northern University, Ada, Ohio.

Methamphetamine is one of the most common illicit drugs abused during pregnancy. The neurological effects of prenatal methamphetamine are well known. However, few studies have investigated the potential effects of prenatal methamphetamine on adult cardiovascular function. Read More

Previous work demonstrated that prenatal cocaine exposure increases sensitivity of the adult heart to ischemic injury. Methamphetamine and cocaine have different mechanisms of action, but both drugs exert their effects by increasing dopaminergic and adrenergic receptor stimulation. Thus the goal of this study was to determine whether prenatal methamphetamine also worsens ischemic injury in the adult heart. Pregnant rats were injected with methamphetamine (5 mg·kg(-1)·day(-1)) or saline throughout pregnancy. When pups reached 8 wk of age, their hearts were subjected to ischemia and reperfusion by means of a Langendorff isolated heart system. Prenatal methamphetamine had no significant effect on infarct size, preischemic contractile function, or postischemic recovery of contractile function in male hearts. However, methamphetamine-treated female hearts exhibited significantly larger infarcts and significantly elevated end-diastolic pressure during recovery from ischemia. Methamphetamine significantly reduced protein kinase Cε expression and Akt phosphorylation in female hearts but had no effect on these cardioprotective proteins in male hearts. These data indicate that prenatal methamphetamine differentially affects male and female sensitivity to myocardial ischemic injury and alters cardioprotective signaling proteins in the adult heart.

2016Oct
Cardiovasc. Toxicol.
Cardiovasc Toxicol 2016 Oct;16(4):381-9
Department of Graduate Medical Education, Scripps Mercy Hospital, 4077 Fifth Avenue, MER-35, San Diego, CA, 92103, USA.
2015Dec
Crit Care Nurs Clin North Am
Crit Care Nurs Clin North Am 2015 Dec 19;27(4):469-81. Epub 2015 Aug 19.
School of Nursing and Knight Cardiovascular Institute, Oregon Health and Science University, Mail Code: SN-2N, 3455 SW, US Veterans Hospital Road, Portland, OR 97239-2941, USA. Electronic address:

Cardiotoxicity is a broad term that refers to the negative effects of toxic substances on the heart. Cancer drugs can cause cardiotoxicity by effects on heart cells, thromboembolic events, and/or hypertension that can lead to heart failure. Rheumatoid arthritis biologics may interfere with ischemic preconditioning and cause/worsen heart failure. Read More

Long-term and heavy alcohol use can result in oxidative stress, apoptosis, and decreased contractile protein function. Cocaine use results in sympathetic nervous system stimulation of heart and smooth muscle cells and leads to cardiotoxicity and evolution of heart failure. The definition of cardiotoxicity is likely to evolve along with knowledge about detecting subclinical myocardial injury.

2015Nov
Am. J. Physiol. Heart Circ. Physiol.
Am J Physiol Heart Circ Physiol 2015 Nov 18;309(9):H1453-67. Epub 2015 Sep 18.
Laboratory of Cardiovascular Physiology and Tissue Injury, National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland;

Mitochondria has an essential role in myocardial tissue homeostasis; thus deterioration in mitochondrial function eventually leads to cardiomyocyte and endothelial cell death and consequent cardiovascular dysfunction. Several chemical compounds and drugs have been known to directly or indirectly modulate cardiac mitochondrial function, which can account both for the toxicological and pharmacological properties of these substances. In many cases, toxicity problems appear only in the presence of additional cardiovascular disease conditions or develop months/years following the exposure, making the diagnosis difficult. Read More

Cardiotoxic agents affecting mitochondria include several widely used anticancer drugs [anthracyclines (Doxorubicin/Adriamycin), cisplatin, trastuzumab (Herceptin), arsenic trioxide (Trisenox), mitoxantrone (Novantrone), imatinib (Gleevec), bevacizumab (Avastin), sunitinib (Sutent), and sorafenib (Nevaxar)], antiviral compound azidothymidine (AZT, Zidovudine) and several oral antidiabetics [e.g., rosiglitazone (Avandia)]. Illicit drugs such as alcohol, cocaine, methamphetamine, ecstasy, and synthetic cannabinoids (spice, K2) may also induce mitochondria-related cardiotoxicity. Mitochondrial toxicity develops due to various mechanisms involving interference with the mitochondrial respiratory chain (e.g., uncoupling) or inhibition of the important mitochondrial enzymes (oxidative phosphorylation, Szent-Györgyi-Krebs cycle, mitochondrial DNA replication, ADP/ATP translocator). The final phase of mitochondrial dysfunction induces loss of mitochondrial membrane potential and an increase in mitochondrial oxidative/nitrative stress, eventually culminating into cell death. This review aims to discuss the mechanisms of mitochondrion-mediated cardiotoxicity of commonly used drugs and some potential cardioprotective strategies to prevent these toxicities.

Acute myocardial infarction (AMI) during pregnancy and the puerperium is a rare but devastating event. The objective of this study was to describe the clinical and epidemiological features of pregnancy-related AMI.
A retrospective study was conducted using Texas hospital inpatient data (years 2004-2007). Read More

Diagnoses and procedures had been coded using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). Adjusted odds ratios (OR) for hospital mortality and length of stay >4 days (prolonged length of stay [PLOS]) were calculated using logistic regression with Firth's bias correction and multiple imputation.
103 women with pregnancy-related AMI were identified in the statewide hospital database (6.5 cases per 100,000 births). The prevalence of cardiomyopathy was 16.5%. Approximately 14% of the pregnancies were complicated by preeclampsia/eclampsia. A history of cocaine use was noted in 3 patients. Congestive heart failure was present in 18 patients (17.5%). Two patients had attempted suicide and 1 died in the hospital. The overall hospital mortality rate was 9.7%. Placement of coronary artery stents was the most common coronary revascularization procedure (11 patients or 10.7%). The adjusted hospital mortality OR for women 35-39 years old (versus 30-34 years old) was 6.29 (P = .07). Patients with preeclampsia were more likely to have PLOS than patients whose deliveries were not complicated by preeclampsia (OR, 3.84; P = .06).
While AMI in pregnancy remains a rare occurrence, it is associated with significant morbidity and a high case-fatality rate.

2015Mar
Oman Med J
Oman Med J 2015 Mar;30(2):77-82
Department of Cardiology, Sana'a University, Sana'a, Yemen.

Recent reports suggest that 20 million people worldwide are regularly using khat as a stimulant, even though the habit of chewing khat is known to cause serious health issues. Historical evidence suggests khat use has existed since the 13th century in Ethiopia and the southwestern Arabian regions even before the cultivation and use of coffee. In the past three decades, its availability and use spread all over the world including the United States and Europe. Read More

Most of the consumers in the Western world are immigrant groups from Eastern Africa or the Middle East. The global transport and availability of khat has been enhanced by the development of synthetic forms of its active component. The World Health Organization considers khat a drug of abuse since it causes a range of health problems. However, it remains lawful in some countries. Khat use has long been a part of Yemeni culture and is used in virtually every social occasion. The main component of khat is cathinone, which is structurally and functionally similar to amphetamine and cocaine. Several studies have demonstrated that khat chewing has unfavorable cardiovascular effects. The effect on the myocardium could be explained by its effect on the heart rate, blood pressure, its vasomotor effect on the coronary vessels, and its amphetamine-like effects. However, its direct effect on the myocardium needs further elaboration. To date, there are few articles that contribute death among khat chewers to khat-induced heart failure. Further studies are needed to address the risk factors in khat chewers that may explain khat-induced cardiotoxicity, cardiomyopathy, and heart failure.

2015Nov
Intensive Care Med
Intensive Care Med 2015 Nov 8;41(11):1965-6. Epub 2015 Apr 8.
Department of Cardiothoracic Surgery, University Hospital of Liege, Liege, Belgium.