Scenario 1: Myocardial Infarction
CC: “I woke up this morning at 6 a.m. with numbness in my left arm and pain in my chest. It feels tight right here (mid-sternal).” “My dad had a heart attack when he was 56-years-old and I am scared because I am 56-years-old.”
HPI: Patient is a 56-year-old Caucasian male who presents to Express Hospital Emergency Department with a chief complaint of chest pain that radiates down his left arm. He states this started this morning and has been getting worse, pointing to the mid-sternal area, “it feels like an elephant is sitting on my chest and having a hard time breathing”. He rates the pain as 9/10. Nothing has made the pain better or worse. He denies any previous episode of chest pain. Denies nausea, or lightheadedness. Nitroglycerin 0.4 mg tablet sublingual x 1 which decreased pain to 7/10.
Lipid panel reveals Total Cholesterol 424 mg/dl, high density lipoprotein (HDL) 26 mg/dl, Low Density Lipoprotein (LDL) 166 mg/dl, Triglycerides 702 mg/dl, Very Low-Density Lipoprotein (VLDL) 64 mg/dl
His diagnosis is an acute inferior wall myocardial infarction.
Question:
1. How does inflammation contribute to the development of atherosclerosis?
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Inflammation plays a key role in the development of atherosclerosis, a condition characterized by the buildup of plaque in the arteries. It begins with injury or damage to the artery walls. In response to the injury, the body's immune system activates an inflammatory response.
The initial step is the recruitment of inflammatory cells, particularly monocytes, to the site of injury. These monocytes then migrate into the inner layer of the arterial wall and transform into macrophages, which engulf and digest lipids, including oxidized low-density lipoproteins (LDL).
The accumulation of oxidized LDL within the arterial wall triggers an inflammatory cascade. The macrophages release various cytokines and chemokines, which attract more immune cells to the site of inflammation. These immune cells produce enzymes, such as matrix metalloproteinases (MMPs), which degrade the extracellular matrix of the arterial wall, leading to a weakening and thinning of the wall.
In addition, the activated immune cells release reactive oxygen species (ROS), which can further damage the arterial wall and promote inflammation. The inflammatory response also promotes the recruitment and proliferation of smooth muscle cells, which migrate into the inner layer of the artery and contribute to the formation of a fibrous cap over the plaque.
Over time, the accumulated lipids, immune cells, and fibrous tissue form a plaque, which narrows the artery and disrupts blood flow. If the plaque ruptures, it can cause the formation of a blood clot, leading to complete blockage of the artery and causing a myocardial infarction (heart attack).
Overall, inflammation contributes to the development of atherosclerosis by promoting the recruitment of immune cells, the release of cytokines and chemokines, the production of enzymes that degrade the arterial wall, and the formation of a plaque that can eventually lead to a heart attack.
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