Coronary artery disease: Clinical practice

Coronary artery disease can lead to myocardial ischemia which is when the myocardium isn’t getting a sufficient blood supply; so there isn’t enough oxygen to meet the heart’s demands.

And coronary artery disease is characterized by a type of chest pain called angina pectoris, which can be due to either vasospastic disease and atherosclerotic disease.

Vasospastic disease, also called Prinzmetal angina, is when for unclear reasons there’s transient vasoconstriction of a coronary artery, leading to transient ischemia.

These attacks generally occur at rest, during the night or early morning, and occur in clusters.

Atherosclerotic disease is when a coronary artery narrows due to build up of atherosclerotic plaque, and it can be further divided into stable angina, unstable angina, and myocardial infarction.

Unstable angina and myocardial infarction are collectively called acute coronary syndrome.

Patients with stable angina don’t feel pain at rest, but they do feel chest pain during intense physical exercise, because that’s when the myocardium has increased oxygen demand, which leads to transient or demand ischemia.

The chest pain stops when the exercise stops, so these patients often just rest rather than going to the emergency department or ED.

Now, angina is considered unstable if it presents at rest, or if it becomes more frequent, lasts longer, or occurs with less exertion than previous episodes of angina.

In unstable angina there’s prolonged myocardial ischemia, but there’s no myocardial cell death yet, so it’s not a myocardial infarction.

But if it’s not taken care of promptly, the ischemia can get prolonged and can lead to myocardial infarction, which is life-threatening.

When a patient comes into the ED with acute chest pain, a number of things have to be done within 10 minutes to confirm or exclude a myocardial ischemia.

The differential diagnosis includes gastroesophageal reflux, pulmonary embolism, aortic dissection, a pneumonia, or a panic attack.

The first step is to check the airway, breathing, and circulation, perform a quick physical exam, and attach cardiac and oxygen saturation monitors. And supplemental oxygen should be given if the oxygen level dips below 90%, and supplemental assisted ventilation should be given if the oxygen level dips below 80%.

Emergency resuscitation equipment should be nearby, including a defibrillator and airway equipment, just in case the patient goes into cardiac arrest.

All patients with suspected myocardial ischemia should be given 325 mg of aspirin, unless there’s a contraindication, like a history of an anaphylactic reaction or if they’ve already received it.

The aspirin can be given orally or as a rectal suppository.

In the meantime, IV access should be obtained, and blood should be drawn for initial laboratory work, including a CBC, electrolytes, creatinine and blood urea nitrogen, coagulation factors, lipids, and most importantly, cardiac biomarkers of acute myocardial damage, including a troponin T and I, which are essential for diagnosing a myocardial infarction.

Other cardiac biomarkers like creatine kinase or lactate dehydrogenase are less sensitive and specific than cardiac troponin, so the current guidelines recommend cardiac troponin as the only cardiac biomarker that should be measured in a patient with suspected myocardial infarction.

Troponins are generally found inside cardiomyocytes, so when they die, the biomarkers are released into the bloodstream, so their blood levels rise.

But it can take up to 6 hours for the elevation of cardiac biomarkers to be detectable, so troponin levels should be checked initially and then again at 6 hours.

If troponins are negative it may be that a patient is having unstable angina, a short attack of Prinzmetal angina, or a non cardiac cause of chest pain.

If troponins are positive, that means there’s cardiomyocyte death; which means that it’s a myocardial infarction.

Next, it’s important to get a clear history of the chest pain - and the acronym OPQRST can help.

O stands for onset, which is usually sudden and at rest, but may also occur while exercising.

P stands for provocation - so which activities provoke pain - and palliation, so which activities alleviate pain. Generally speaking, angina pectoris doesn’t improve or worsen with respiration or position.

Q stands for quality, which may be described as a pressure, heaviness, tightness, fullness, or squeezing.

R stands for radiation, which is most often to the neck, jaw, and left arm.

S stands for site, which typically is substernal or in the left chest, and the pain is usually diffuse and difficult to localize. If a person can point to the site of pain with a single finger it’s less likely due to cardiac ischemia.

Finally, T stands for time course, which typically lasts over 30 minutes.

Myocardial ischemia can also cause dyspnea, palpitations, nausea, and increased sweating.

And some important risk factors include being over 55 years old, being male, hypertension, hypercholesterolemia, diabetes mellitus, smoking, obesity, and family history of first degree relatives premature coronary artery disease, so males before the age of 55 years and females before the age of 65.

Also, women, older adults, and patients with diabetes often have atypical presentations like just dyspnea, epigastric pain or discomfort, syncope, or sudden death from cardiac arrest.

In individuals having myocardial ischemia - so those with unstable angina and myocardial infarction as well as Prinzmetal angina, nitrates should be used immediately to help widen the coronary arteries and help increase blood flow to the heart, which should relieve the pain and decrease the blood pressure.

Three sublingual doses of 0.4 mg of nitrates are generally given, one every five minutes.

If the patient has Prinzmetal angina, nitrates will lead to an immediate and full recovery, so nitrates help with both diagnosis and management.

And if the patient has unstable angina or a myocardial infarction, then pain and blood pressure should improve, so if there’s really no improvement at all, then intravenous nitrates may be needed.

Nitrates are contraindicated in case of hypotension, myocardial infarction of the right ventricle, and recent use of PDE-5 inhibitors like Sildenafil, because in these situations nitrates can cause really severe hypotension.

Additionally, some patients with ongoing chest pain or tachycardia should get beta blockers to lessen cardiac demand.

And if the patient is hypertensive, intravenous beta blockers can be used.

However, beta blockers are contraindicated in Prinzmetal angina, because they can worsen the coronary vasoconstriction.

They’re also contraindicated in bradycardia, cardiogenic shock, and acute decompensated heart failure - all of which can worsen with beta blockers.

Beta blockers are also contraindicated in cocaine-related acute coronary syndrome.

That’s because cocaine triggers a big release of sympathomimetic amines, and if the beta receptors are blocked by the beta blockers, then those sympathomimetic amines end up binding to alpha receptors, causing severe coronary vasoconstriction.

Now, patients with underlying heart failure must be given an intravenous loop diuretic like furosemide.

In addition, patients with severe and persistent chest pain can be given intravenous morphine sulfate at an initial dose of 2 to 4 mg, repeated every 5 to 15 minute intervals.

Basically, every patient suspected of having myocardial ischemia should get a standard 12-lead electrocardiogram or ECG within 10 minutes of arrival to an ED.

And the initial ECG is often not diagnostic, so it should be repeated at 5 to 10 minute intervals if there is high suspicion for myocardial ischemia.