Cocaine-related deaths present significant diagnostic challenges due to the nonspecific nature of cardiac histopathology and the limited reliability of postmortem toxicology, often affected by redistribution phenomena. This study investigated the postmortem heart expression and distribution of an anti-cocaine monoclonal antibody, aiming to evaluate immunohistochemistry (IHC) as a potential complementary tool for diagnosing cocaine-related fatalities. Fifteen cases of acute cocaine-related death, with toxicological data exclusively positive for cocaine, were examined and compared to ten cases negative for drug abuse. Cardiac samples from the lateral left ventricular wall and interventricular septum underwent IHC using an experimentally optimized protocol. All cocaine-related cases demonstrated clear and widespread immunopositivity, with varying staining intensities across a semi-quantitative scale. Immunostaining localized consistently to nuclear and myofibrillar compartments and showed no association with postmortem interval (mean PMI 72.33 h; range 30–144). Control samples exhibited no staining. Positive immunostaining also highlighted cardiomyocyte alterations related to cocaine toxicity, particularly hypercontracted fibers with myofibrillar rhexis and contraction band necrosis. While these findings align with the established cocaine-induced myocardial injury, the intense nuclear staining observed may further reflect oxidative DNA damage associated with cocaine exposure. This study provides novel evidence supporting the applicability of anti-cocaine IHC in postmortem investigations. The technique may serve as a valuable adjunct in detecting cocaine distribution within cardiac tissue, particularly when toxicological data are inconclusive or unavailable.

Anabolic-androgenic steroids (AAS) comprise testosterone and synthetic androgenic compounds that differ substantially in pharmacokinetics, receptor activity, route of administration, hepatic metabolism, and clinical risk. From a forensic perspective, the central problem is not simply to catalogue adverse effects but to determine how verified exposure, chronology, co-use of other substances, clinical and electrocardiographic findings, pathological alterations, and toxicological results should be integrated when evaluating an individual death. This critical narrative review therefore distinguishes therapeutic testosterone replacement from non-medical and supraphysiological AAS exposure and examines the evidence connecting exposure to endocrine, cardiovascular, hepatic, renal, musculoskeletal, neuropsychiatric, and immunological findings. Human prospective and observational data support associations between androgen abuse and endocrine suppression, erythrocytosis, adverse lipid changes, increased blood pressure, and left-ventricular structural or functional alterations, with recovery of selected measured parameters reported in the studied cohorts. Electrocardiographic studies also report prolonged repolarization indices and impaired heart-rate recovery in AAS-using bodybuilders; however, these intermediate markers do not by themselves establish an individual risk of fatal ventricular arrhythmia. Forensic autopsy series describe myocardial hypertrophy, fibrosis, coronary disease, and other lesions in AAS-associated deaths, but these findings are not specific and require correlation with toxicology, clinical history, circumstances, and alternative causes. The detailed immunological literature is predominantly mechanistic, in vitro, or experimental and currently provides limited direct forensic evidence in human AAS users. Similarly, Raman spectroscopy is best regarded as a developing adjunct for forensic trace or analytical applications rather than a validated method for confirming AAS accumulation or cause of death in post-mortem tissue. We propose a structured forensic framework in which exposure is first verified, the temporal and pharmacological context is reconstructed, findings are assessed for specificity and plausibility, co-exposures and competing causes are examined, and the final opinion explicitly communicates the degree of certainty and the limitations of the evidence.