Cardiovascular fatality

CS392 Bachs, L. and H. Morland. Acute cardiovascular fatalities following cannabis use. Forensic Sci Int 2001 124(2-3) 200-203. 

Systemic anaphylaxis is the most dramatic and potentially fatal manifestation of immediate hypersensitivity, accounting for more than 500 deaths annually [ 1 ]. Despite these alarming findings, there is surprisingly limited interest and little information on how the cardiovascular system is involved in fatal and near-fatal allergic diseases. 

Contraindications are the same as for immunotherapy for inhalant allergy, but are relative in nature because of the life-saving potential of venom immunotherapy. Elderly patients, especially with preexisting cardiovascular disease, are at a high risk to develop severe or even fatal anaphylaxis [26]. Therefore, venom immunotherapy is often recommended in patients over 50-60 years of age. Since (3-blocker treatment is associated with a significantly increased survival rate in patients with coronary heart... 

Muller UR Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol 2007 7 337-341. Pumphrey RSH Lessons for management of anaphylaxis from a study of fatal reactions. Clin Exp Allergy 2000 30 11444-11450. 

In some countries such as Japan, pretesting with intravenous injection of 0.5-1 ml of RCM as a means of predicting severe or fatal reactions had been performed. This approach had been abandoned after severe cardiovascular reactions to these minute amounts RCM were described [34]. The possibility to react to low amounts of allergen is regarded to be typical for IgE-mediated reactions. 

Disulfiram works by irreversibly blocking the enzyme aldehyde dehydrogenase, a step in the metabolism of alcohol, resulting in increased blood levels of the toxic metabolite acetaldehyde. As levels of acetaldehyde increase, the patient experiences decreased blood pressure, increased heart rate, chest pain, palpitations, dizziness, flushing, sweating, weakness, nausea and vomiting, headache, shortness of breath, blurred vision, and syncope. These effects are commonly referred to as the disulfiram-ethanol reaction. Their severity increases with the amount of alcohol that is consumed, and they may warrant emergency treatment. Disulfiram is contraindicated in patients who have cardiovascular or cerebrovascular disease, because the hypotensive effects of the disulfiram-alcohol reaction could be fatal in such patients or in combination with antihypertensive medications. Disulfiram is relatively contraindicated in patients with diabetes, hypothyroidism, epilepsy, liver disease, and kidney disease as well as impulsively suicidal patients. 

Poor sleep architecture and fragmented sleep secondary to OSA can cause excessive daytime sleepiness (EDS) and neu-rocognitive deficits. These sequelae can affect quality of life and work performance and may be linked to occupational and motor vehicle accidents. OSA is also associated with systemic disease such as hypertension, heart failure, and stroke.21-23 OSA is likely an independent risk factor for the development of hypertension.24 Further, when hypertension is present, it is often resistant to antihypertensive therapy. Fatal and non-fatal cardiovascular events are two- to threefold higher in male patients with severe OSA.25 OSA is associated with or aggravates biomarkers for cardiovascular disease, including C-reactive protein and leptin.26,27 Patients with sleep apnea often are obese and maybe predisposed to weight gain. Hence, obesity may further contribute to cardiovascular disease in this patient population. 

Sertindole (Serdolect) Schizophrenia Cardiovascular (QT-interval prolongation, potentially fatal arrhythmias) 2000 [57]... 

Terfenadine (Seldane) Allergy Cardiovascular (potentially fatal heart condition) 1998 [58]... 

Neuroleptic malignant syndrome is an acute iatrogenic condition caused by neuroleptics, characterized by tremor, catatonia, fluctuating consciousness, hyperthermia, and cardiovascular instability. It is relatively uncommon, occuring in 1-1.5% of patients but is fatal in 11-38%, most often due to cardiovascular collapse (Jahan et al. 1992). The pathogenesis of neuroleptic malignant syndrome is poorly understood, but it is believed to result from altered dopamine and serotonin transmission in the hypothalamus, spinal cord, and striatum. Treatment includes discontinuation of neuroleptics and administration of drugs that increase dopamine transmission bromocriptine or L-dopa (Jahan etal. 1992 Baldessarini 1996). 

Cardiovascular (CV) risk NSAIDs may cause an increased risk of serious CV thrombotic events, myocardial infarction (Ml), and stroke, which can be fatal. This risk may increase with duration of use. Patients with CV disease or risk factors for CV disease may be at higher risk. 

Cardiovascular events There have been rare reports following administration of botulinum toxin type A for other indications of adverse events involving the cardiovascular system, including arrhythmia and Ml, some with fatal outcomes. Some of these patients had risk factors including pre-existing cardiovascular disease. 

Myocardial toxicity, manifested in its most severe form by potentially fatal CHF, may occur either during therapy with mitoxantrone or months to years after termination of therapy. Mitoxantrone use has been associated with cardiotoxicity this risk increases with cumulative dose. In cancer patients, the risk of symptomatic CHF was estimated to be 2.6% for patients receiving up to a cumulative dose of 140 mg/m. For this reason, monitor patients for evidence of cardiac toxicity and question them about symptoms of heart failure prior to initiation of treatment. Monitor patients with multiple sclerosis (MS) who reach a cumulative dose of 100 mg/m for evidence of cardiac toxicity prior to each subsequent dose. Ordinarily, patients with MS should not receive a cumulative dose greater than 140 mg/m. Active or dormant cardiovascular disease, prior or concomitant radiotherapy to the mediastinal/pericardial area, previous therapy with other anthracyclines or anthracenediones, or concomitant use of other cardiotoxic drugs may increase the risk of cardiac toxicity. Cardiac toxicity with mitoxantrone may occur at lower cumulative doses whether or not cardiac risk factors are present (see Warnings and Administration.and.Dosage). 

Ingestion of concentrated solutions of carbon tetrachloride can cause death in humans within hours to days. The principal clinical signs observed in fatal cases include gastrointestinal irritation, central nervous system depression and cardiovascular disturbances, with death usually resulting from severe injury to kidney and/or liver (Guild et al. 1958 reviewed in von Oettingen 1964). 

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