Autopsy Observation

The subject of the autopsy experience was a 43-year-old Caucasian female living in southeast Michigan who presented with no obvious cause of death. Other demographic data relating to the subject was limited. The family had requested an autopsy be conducted to determine the cause of death. Known comorbidities included hypertension and obesity. The subject went to bed on November 3rd, 2018 at approximately 2000, husband did not note any symptoms that the client exhibited the previous night. Husband woke at 0600 on November 4th, 2018, and was not able to rouse the subject.

At 0900 subject’s children found her unresponsive and called for emergency assistance. Emergency room staff were unable to revive the subject with a time of death being pronounced at 1000. It was noted that the subject was dead on arrival and did not receive any medications in the hospital therefore toxicology was believed to not be affected. Health history received from hospital report stated a subject had a history of smoking tobacco and possible prescription drug abuse.

The autopsy began with medical investigators taking photographs of the body while autopsy technicians examined the body for anything remarkable; nothing remarkable was found. The autopsy was conducted by a resident under the observation of a medical examiner who viewed from the observation deck. Autopsy technicians removed internal organs weighing each one to determine whether any organs were not within nominal range. Organs were then given to ta the resident for examination and dissection. The resident examined each organ to determine if any anomalies such as tumors, emboli, or other potential causes were present.

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Examination of the heart revealed some atherosclerotic plaque with 10%-20% occlusion. The medical examiner explained that typically this would not be enough plaque build-up to cause death, however, he would not rule this out as a possible cause until histology and toxicology were examined. Organ, brain tissue, and femoral blood was prepared and sent to a laboratory for testing. Until histology and toxicology results were returned cause of death was not immediately known. Approximately one week after autopsy observation, an email from the Oakland County Medical Examiner’s office was received ruling the cause of death to be acute myocardial infarct due to hypertensive and arteriosclerotic cardiovascular disease.

Pathophysiology of Arteriosclerosis Leading to Myocardial Infraction

Atherosclerosis is the most common type of arteriosclerosis and is caused by the hardening and loss of elasticity in arterial vessel walls due to the buildup of lipid lesions called plaques (Kelly, 2015). A chronic inflammatory condition, atherosclerosis results from a continued insult to the epithelial cells of vessel walls. Traditional factors contributing to damaged cells include hypertension, smoking, diabetes, hyperlipidemia, and autoimmunity (McCance & Huether, 2019). Typically damage to vessel walls does not occur because of one event but of a multitude of pathophysiologic conditions occurring over time.

Once epithelial cells become inflamed they begin to express adhesion molecules (McCance & Huether, 2019). The expression of adhesion molecules allows macrophages to adhere to the vessel walls which release inflammatory cytokines, further damaging the intima of the vessel. Injury to epithelial cells also affects the permeability of the endothelium allowing the accumulation of lipids (Kelly, 2015). The macrophages digest the lipids that have accumulated in the endothelium forming lesions called fatty streaks (McCance & Huether, 2019).

Fatty streaks release oxygen radicals which further damage the intima and promote aggregation of T cells leading to autoimmunity (McCance & Huether, 2019). Smooth muscle cells begin to proliferate in the injured vessels due to the secretion of growth factors from macrophages. Collagen produced from the smooth muscle cells covers the fatty streaks forming fibrous plaque which can calcify, protruding into the lumen of the vessel obstructing blood flow (McCance & Huether, 2019). If a plaque ruptures the clotting cascade is initiated and a thrombus is quickly formed. The sudden formation of a thrombus can abruptly occlude the vessel resulting in an acute myocardial infarction (McCance & Huether, 2019).

As noted above, acute myocardial infarction due to hypertension and arteriosclerotic cardiovascular disease was determined to be the cause of death for the subject of the autopsy observation. The subject displayed several known contributing factors to atherosclerosis including smoking tobacco, a higher body mass index (BMI), and hypertension. Obesity and higher blood pressures in the arterial vessels cause damage and weaken the vessel walls while toxic chemicals from cigarettes damage the epithelial cells of the intima. These factors promote plaque formation and can hasten atherogenesis leading to myocardial infarction.

Prevalence of Cardiovascular Disease in Women

Michigan ranks 8th in the nation for the number of deaths related to cardiovascular disease (CVD), with 200 per 1,000 deaths being attributed to CVD compared to the national average of 168 per 1,000 deaths (Centers for Disease Control and Prevention, 2018). Over the last decade deaths related to CVD have decreased in the United States, however, the number of women younger than 50 years dying from CVD has remained stagnant (Merz, Ramineni, Leong, Bairey Merz, 2018). Traditional risk factors such as hypertension, obesity, and smoking that increase the risk of CVD in men may pose a higher risk for women along with other sex-based links such as early menopause. Early transition to menopause has been shown to reduce vascular compliance and increase hyperlipidemia in women (Merz, Ramieni, Leong, Bairey Merz, 2018). Reduced vascular compliance and increased hyperlipidemia in the accumulation with other known factors like cigarette smoking and hypertension contribute to the increased risk of women under 50 years who die from CVD-related causes.

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Autopsy. (2022, Jun 29). Retrieved from

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