Coronary artery disease: Clinical sciences

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Coronary artery disease: Clinical sciences

OLD Internal Medicine - Clinical Sciences (Required)

OLD Internal Medicine - Clinical Sciences (Required)

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Decision-Making Tree

Transcript

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Coronary artery disease, or CAD, is caused by atherosclerosis of the coronary arteries, which occurs when plaque builds up in the vessels, eventually narrowing the lumen, and causing a mismatch between oxygen supply and demand of the heart. Over time, reduced oxygen supply can lead to myocardial ischemia or even infarction.

The diagnosis of CAD is based on atherosclerotic risk factors that categorize patients into low, intermediate, or high risk groups based on their probability for obstructive disease.

Now, if you suspect CAD, first perform an ABCDE assessment. This is to determine if the patient is unstable or stable.

If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, provide supplemental oxygen, and put them on continuous vital sign monitoring including blood pressure, heart rate, and pulse oximetry.

At this point, you should suspect CAD with acute coronary syndrome, which includes unstable angina, non-ST elevated myocardial infarction, or NSTEMI, or ST-elevated myocardial infarction, or STEMI.

Once you stabilize the patient, obtain a focused history and physical examination, and order serial troponin levels and an ECG.

Okay, let’s focus on unstable angina, your patient may report sudden chest discomfort that doesn’t improve with rest, and feelings of uneasiness or “impending doom”.

Other common symptoms include dizziness, shortness of breath, sweating, as well as nausea.

Physical exam typically reveals a distressed, anxious, and diaphoretic individual.

Ok, next take a look at the serial troponins. If there’s no myocardial infarction, troponins will typically be normal.

While ECG may or may not show signs of ischemia like ST segment depression or new T wave inversion.

This combination of history, physical exam, labs, and ECG findings are characteristic of unstable angina, where chest pain is caused by an insufficient supply of oxygen to the cardiac tissue.

In these individuals, treatment consists of Morphine, Oxygen, Nitrates, and Aspirin, also known as MONA, as well as a statin and a beta blocker. Additionally, your patient will likely need an invasive coronary angiography with or without revascularization.

Here’s a clinical pearl! A non-ST elevated myocardial infarction, or NSTEMI, can present with similar history, physical exam, and ECG findings as unstable angina, but troponin levels are typically elevated in NSTEMI by definition. However, troponins may initially not be detectable, and may even take hours to rise after presentation, so be sure to keep NSTEMI on your differential even if troponin is normal.

Okay, let’s return to the ABCDE assessment and take a look at stable patients. If your patient is stable, obtain a focused history and physical exam. Your patient will typically describe their chest discomfort or pain as a heavy pressure that is worse with exertion, cold weather, or highly stressful situations, and improves when these conditions subside. Your patient might also report shortness of breath with exertion.

They may also have ASCVD risk factors, such as increasing age, male sex, hypertension, diabetes mellitus, hyperlipidemia, tobacco use, and a family history of premature CAD.

Okay, moving on to the physical exam, you may find elevated blood pressure, decreased peripheral pulses, and bruits, which are all evidence of atherosclerotic disease.

You may also see xanthelasmas, or yellow cholesterol deposits on the eyelids, which indicate underlying hyperlipidemia. Finally, you might detect nicotine-stained fingertips in patients that use tobacco. These findings should make you suspect CAD, particularly stable angina.

Now, here’s a high-yield fact! The key thing that distinguishes stable from unstable angina is that pain improves with rest in stable angina, while pain remains present even at rest with unstable angina. You should also keep in mind that if your patient is a biologically female individual, has a positive history of diabetes mellitus, and reports back or epigastric burning or stabbing pain, you should think of atypical angina!

Now that you suspect CAD, your next step is to order labs.

These include a high-sensitivity troponin, fasting lipid panel, and hemoglobin A1C. Also, you should obtain a 12-lead ECG.

Labs typically reveal troponin levels as normal, lipid panel will reveal an elevated LDL, and hemoglobin A1C elevated too, which is common in patients with poorly controlled diabetes. On the flip side,

ECG could be normal, or show inverted T waves, which is a repolarization abnormality; pathological Q waves, indicating an old myocardial infarction; or a left bundle branch block.

All these findings are highly suggestive of CAD causing stable angina, so your next step is to assess the pretest probability of obstructive CAD. You can do this by using the patient’s age, sex, chest pain symptoms, and risk factors. This allows you to stratify the patient into a low, intermediate, or high risk group and determine the appropriate type of management.

Okay, lets first look at individuals who are at low risk. Patients who are low risk likely have non-obstructive CAD and do not require additional testing. Instead, you should encourage lifestyle modifications, such as a diet rich in fruits, vegetables, whole grains, and fish, as well as 150 minutes of moderate exercise each week, often divided up as 30 minutes 5 times a week, and sleep hygiene. Counsel your patient on tobacco cessation and weight loss, annual influenza vaccines, and mental health.

Sources

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  8. "Coronary Artery Disease" CDIM Core Medicine Clerkship Curriculum Guide, 4th ed. essay (2020)
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