Cardiomyopathy Cocaine Publications (208)
Cardiomyopathy Cocaine Publications
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.
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.
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.
For patients with two or more admissions during the entire time period, the trajectories of NYHA functional class and EF over time were determined (n = 58). MAC has significantly increased from 1.8 to 5.6 % of total CHF patients admitted (n = 3705). Among patients who stopped using methamphetamine, NYHA functional class significantly improved, while among patients who continued methamphetamine use, NYHA was significantly worsened (p < 0.001). Significantly more patients with improved EF stopped using methamphetamine than continued (p = 0.05). There was a significant increase in the prevalence of MAC during the study period for all CHF patients admitted in our hospital system. Continued methamphetamine use is associated with worsening functional status, while cessation of methamphetamine is associated with improvement in functional status.
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.
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.
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.
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.