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Biomedical subjects

Steven B Karch

Publications and source records attributed to Steven B Karch.

12 recordsLinked to original sources
PubMed2005

Sudden cardiac death during anabolic steroid abuse: morphologic and toxicologic findings in two fatal cases of bodybuilders.

We report two cases of sudden cardiac death (SCD) involving previously healthy bodybuilders who were chronic androgenic-anabolic steroids users. In both instances, autopsies, histology of the organs, and toxicologic screening were performed. Our findings support an emerging consensus that the effects of vigorous weight training, combined with anabolic steroid use and increased androgen sensitivity, may predispose these young men to myocardial injury and even SCD.

Adult↗
PubMed2005

Cardiac pathology in death from electrocution.

To better characterize the morphologic changes in electrocution, morphologic changes in the hearts of 21 subjects, who died instantaneously of electrocution, were compared to the hearts of decedents with different types of death. Sixteen myocardial samples per heart were processed for histological examination, and sections were prepared with a variety of specific stains. The frequency, location and extent of myocellular segmentation (stretching and/or rupture) of intercalated discs and associated changes of myocardial bundles and single myocells [myofibre break-up (MFB)] were recorded, quantitatively analysed and statistically evaluated. The frequency of MFB was maximal in cases of electrocution (90%). The findings show that MFB is an ante-mortem change and may be a distinct finding in electrocution.

Adult↗
PubMed2005

Cocaine cardiovascular toxicity.

Cocaine abuse kills thousands every year. Preexisting coronary artery disease appears to account for many of the deaths, but often the mechanism is much more complex. There exists a widely held but utterly mistaken notion that cocaine-related deaths are due to drug overdose. Except in the case of drug couriers ("body packers") with massive drug exposure, death is not dose related, and cocaine blood levels cannot be used to predict toxicity. Most deaths occur after prolonged drug use, which initiates a series of changes at the molecular, cellular, and tissue levels. All of these changes favor sudden death. Potentially lethal myocardial alterations include hypertrophy, fibrosis, and microangiopathy. Recently it has become clear that genetic causes, such as fully or partially expressed congenital long QT syndrome, may also play a role. The relative importance of each of these factors is reviewed.

Cardiomegaly↗
PubMed2004

Demographic, pathologic, and toxicological profiles of 127 decedents testing positive for ephedrine alkaloids.

The relative toxicity of ephedra-containing dietary supplements is disputed. In order to ascertain the magnitude of the problem, we reviewed all autopsies in our Medical Examiner's jurisdiction, from 1994 to 2001, where ephedrine or any its isomers (E+) were detected. Toxicology testing results were tabulated and anatomic findings in E+ cases were compared to those in a control group of drug-free trauma victims. Of 127 E+ cases identified, 33 were due to trauma. Decedents were mostly male (80.3%) and mostly Caucasian (59%). Blood ephedrine concentrations were <0.49 mg/l in 50% of the cases, range 0.07-11.73 mg/l in trauma victims, and 0.02-12.35 mg/l in non-trauma cases. Norephedrine (NE) was present in the blood of 22.8% (mean of 1.81 mg/l, S.D.=3.14 mg/l) and in the urine of 36.2% (mean of 15.6 mg/l, S.D.=21.50mg/l). Pseudoephedrine (PE) was present in the blood of 6.3% (8/127). More than 88% (113/127) of the decedents also tested positive for other drugs, the most common being cocaine (or its metabolites) and morphine. The most frequent pathologic diagnoses were hepatic steatosis (27/127) and nephrosclerosis (22/127). Left ventricular hypertrophy was common, and coronary artery disease (CAD) detected in nearly one third of the cases. The most common findings in E+ deaths are those generally associated with chronic stimulant abuse, and abuse of other drugs was common in those with CAD. There were no cases of heat stroke or rhabdomyolysis. In most cases, norephedrine was not detected, suggesting it plays no role in ephedrine toxicity.

Adolescent↗
PubMed2004

Channelling the Emperor: what really killed Napoleon?

Arsenic was present in Napoleon's hair before he arrived on Saint Helena and the findings at necropsy are consistent only with the diagnosis of ulcerating, regionally invasive, gastric carcinoma. The question of whether Napoleon died of, or merely with, arsenic poisoning is illuminated by developments in the treatment of promyelocytic leukaemia. Arsenic trioxide induces remission in many, but treatment can be complicated by QT prolongation, torsades de pointes and sudden death. At clinically relevant concentrations, arsenic blocks both I(Kr) and I(ks) channels and, at the same time, activates I(K-ATP) channels. The balance of these forces is easily disrupted, and QT prolongation is worsened by hypokalaemia. Napoleon was chronically treated with tartar emetic for gastrointestinal symptoms, and the day before he died he was given a huge dose of calomel (mercurous chloride) as a purgative. Both treatments would have caused potassium wastage. In addition, the Emperor was being treated with a decoction containing 'bark'-presumably 'Jesuit's bark'. The quinine in Jesuit's bark is another cause of QT prolongation. It is likely that the immediate cause of the Emperor's death was torsades de pointes, brought on by chronic exposure to arsenic and a medication error.

Arsenic Poisoning↗