Modifiable Risk Factors for Coronary Artery Disease

Cardiovascular 
Mr. W.G. is a 53-year-old white man who began to experience chest discomfort while playing tennis with a friend. At first, he attributed his discomfort to the heat and having had a large breakfast. Gradually, however, discomfort intensified to a crushing sensation in the sternal area and the pain seemed to spread upward into his neck and lower jaw. The nature of the pain did not seem to change with deep breathing. When Mr. G. complained of feeling nauseated and began rubbing his chest, his tennis partner was concerned that his friend was having a heart attack and called 911 on his cell phone. The patient was transported to the ED of the nearest hospital and arrived within 30 minutes of the onset of chest pain. In route to the hospital, the patient was placed on nasal cannula and an IV D5W was started. Mr. G. received aspirin (325 mg po) and 2 mg/IV morphine. He is allergic to meperidine (rash). His pain has eased slightly in the last 15 minutes but is still significant; was 9/10 in severity; now7/10. In the ED, chest pain was not relieved by 3 SL NTG tablets. He denies chills. 

Case Study Questions

1. For patients at risk of developing coronary artery disease and patients diagnosed with acute myocardial infarct, describe the modifiable and non-modifiable risk factors.
2. What would you expect to see on Mr. W.G. EKG and which findings described on the case are compatible with the acute coronary event?
3. Having only the opportunity to choose one laboratory test to confirm the acute myocardial infarct, which would be the most specific laboratory test you would choose and why?
4. How do you explain that Mr. W.G temperature has increased after his Myocardial Infarct, when that can be observed and for how long? Base your answer on the pathophysiology of the event.
5. Explain to Mr. W.G. why he was experiencing pain during his Myocardial Infarct. Elaborate and support your answer.

1. Modifiable and Non-Modifiable Risk Factors for Coronary Artery Disease (CAD):
   • Modifiable Risk Factors:
     • Smoking: Smoking increases the risk of CAD by damaging the blood vessels and promoting atherosclerosis.
     • Diet: A diet high in saturated and trans fats, cholesterol, and salt can contribute to CAD.
     • Physical inactivity: Lack of regular physical activity can lead to obesity and increase CAD risk.
     • Hypertension: High blood pressure is a major risk factor for CAD.
     • Diabetes: Poorly controlled diabetes can damage blood vessels and accelerate atherosclerosis.
     • Obesity: Excess body weight, especially around the waist, is a risk factor for CAD.
     • High cholesterol levels: Elevated LDL cholesterol levels can lead to plaque buildup in the arteries.
   • Non-Modifiable Risk Factors:
     • Age: The risk of CAD increases with age, especially after 45 for men and 55 for women.
     • Gender: Men are generally at higher risk than women, but the risk for women increases after menopause.
     • Family history: A family history of CAD increases the likelihood of developing the condition.
     • Genetics: Some genetic factors can predispose individuals to CAD.
2. EKG Findings for Mr. W.G.:
   • In the case of an acute coronary event like a myocardial infarction (MI), the EKG (Electrocardiogram) can show specific changes:
     • ST-segment elevation (STEMI): ST-segment elevation in multiple contiguous leads indicates an ongoing myocardial infarction. It signifies complete occlusion of a coronary artery and requires immediate intervention.
     • T-wave inversion: T-wave changes may be seen in some leads, indicating myocardial ischemia.
     • Pathological Q-waves: These may develop in the days to weeks following an MI, indicating previous myocardial damage.
   • In Mr. W.G.’s case, the description of crushing chest pain that radiates to the neck and lower jaw, along with EKG findings of chest pain not relieved by nitroglycerin, is compatible with an acute coronary event.
3. Most Specific Laboratory Test to Confirm MI:
   • The most specific laboratory test to confirm an acute myocardial infarction (MI) is the measurement of cardiac troponin levels (troponin I or troponin T). Cardiac troponins are highly sensitive and specific markers for myocardial injury.
   • Troponins are released into the bloodstream when there is damage to the heart muscle, such as during an MI. Elevated troponin levels indicate myocardial damage, making it a crucial diagnostic tool for confirming MI.
4. Increased Temperature after MI:
   • After a myocardial infarction, it is possible for a patient’s temperature to increase, and this can be observed within the first 24 hours following the event.
   • This increase in temperature is often due to the body’s inflammatory response to the cardiac tissue damage. When the heart muscle is injured, inflammation occurs as the body’s immune system responds to the injury. This can lead to a mild fever or elevated body temperature as part of the healing process.
5. Explanation of Pain during MI:
   • Mr. W.G. experienced pain during his myocardial infarction due to the insufficient oxygen supply to his heart muscle. Myocardial infarction occurs when one or more coronary arteries become blocked, usually by a blood clot, leading to reduced or interrupted blood flow to a portion of the heart muscle.
   • The pain, often described as crushing or pressure-like, occurs because the heart muscle is deprived of oxygen (ischemia) and begins to die (infarction). This lack of oxygen causes nerve endings in the heart to become irritated, sending pain signals to the brain.
   • The pain can radiate to the neck, jaw, and other areas because of the complex network of nerves that transmit signals from the heart. Additionally, the pain may not change with deep breathing because it is not related to lung issues but rather the heart’s inadequate blood supply.