heroin and Death--Sudden--Cardiac

The recreational use of illicit drugs remains an enormous and growing problem throughout the United States of America and around the world. Cocaine is most frequently thought of when considering the cardiovascular toxicity of illicit drugs. The association of cocaine use with sudden death due to myocardial ischaemia and infarction is well recognised, and this risk appears to be amplified by concomitant cigarette smoking and alcohol consumption. Like cocaine, amphetamine and its derivatives lead to indirect stimulation of the autonomic nervous system through the release of norepinephrine, dopamine, and serotonin in nerve terminals of the central and autonomic nervous systems. However, amphetamine lacks the ion channel-blocking properties of cocaine. Also similar to cocaine, coronary artery spasm may be induced in individuals with or without atherosclerotic disease and may lead to myocardial infarction. With the movement across the United States of America to legalise marijuana, or cannabis, for medicinal and recreational purposes, it is important to consider its potential deleterious effects. Marijuana has long been thought to have very few adverse effects with the exception of long-term dependence. There are, however, scattered reports of acute adverse events up to and including sudden death. These appear to be due to myocardial infarction. In conclusion, the incidence of sudden death associated with the use of these drugs varies from rare in the case of marijuana use to not infrequent with some drugs such as cocaine. It is important for care providers to recognise the potential for drug abuse when caring for a sudden cardiac arrest survivor.

Topics: Adolescent; Alcohol Drinking; Amphetamines; Cannabis; Cocaine; Death, Sudden, Cardiac; Heroin; Humans; Illicit Drugs; Myocardial Infarction; Smoking; Substance-Related Disorders

Pulmonary edema complicating heroin overdosage is a well recognized entity and regarded as the major mechanism contributing to death in heroin addicts. It's pathogenesis is unknown, several mechanisms are discussed: hypoxia-induced increase of pulmonary capillary permeability, depressed myocardial contractility, centrally induced respiratory depression, primary toxic effects on the alveolar capillaries and acute anaphylactic shock. The present study included opiate-related deaths (n=23) and a control group of sudden cardiovascular deaths (n=12) to verify the hypothesis, that defects of the alveolar capillary membranes and/or an acute anaphylactic reaction leads to pulmonary congestion, edema and hemorrhages. Lung specimens were obtained from these 35 autopsies of persons autopsied in the Institute of Forensic Medicine, University of Bonn, in 1997 and 1998. All specimens were examined with hematoxylin-eosin, prussian blue and investigated with immunohistological methods using primary antibodies against collagen IV, laminin and IgE. Defects of the basal laminae of the alveoli were found, demonstrated by laminin and collagen IV, and the number of IgE-positive cells was counted in both groups. There was an increased but not significant number of IgE-positive cells in the heroin-group and defects of the epithelial and endothelial basal laminae were found in both groups without significant differences.

Topics: Anaphylaxis; Antibodies; Basement Membrane; Capillaries; Capillary Permeability; Cause of Death; Collagen; Coloring Agents; Death, Sudden, Cardiac; Drug Overdose; Endothelium, Vascular; Epithelial Cells; Female; Hemorrhage; Heroin; Heroin Dependence; Humans; Hypoxia; Immunoglobulin E; Immunohistochemistry; Laminin; Male; Myocardial Contraction; Narcotics; Pulmonary Alveoli; Pulmonary Edema; Respiration