Clinical Pearl Series Edited from Yale-G First Aid: Crush USMLE Step 2CK & Step 3 by Yale Gong, MD, Sr. Medical Advisor at www.medicine.net (Copyrighted)

Coronary artery disease (CAD) is a narrowing or blockage of coronary arteries causing reduced blood supply to the heart and ischemic heart disease. The most common presenting forms of CAD are angina pectoris, myocardial infarction (MI), and acute coronary syndrome.

Etiology and risk factors of CAD

The basic mechanisms of CAD are that coronary O2 demand surpasses supply due to decreased blood flow secondary to atherosclerotic narrowing of the coronary artery (Cor-A), leading to cardiac dysfunctioning. It's fatal if there is narrowing of 1-2 major coronary arteries that causes > 75% decrease in cross-sectional area (or 50% decrease in diameter).

Factors that increase oxygen demand: Physical exertion or stress, emotional or mental stress (including anxiety), large meals, etc.

Factors that lower the oxygen-carrying capacity of the blood: Anemia, carbon monoxide (CO) poisoning, platelet microthrombi at the site of coronary stenosis (focal damage), etc.

Major risk factors

Age (male > 45, female > 55 y/a), male gender, smoking, hypertension, diabetes, heredity, atherosclerosis, dyslipidemia (LDL>200mg/dL, HDL<40mg/dL), physical inactivity, obesity and overweight, stress, excess alcohol use, and postmenopausal women.

Prognostic indicators

(1) Left ventricular function—Ejection fraction (EF): Normal > 50%; if < 50%, associated with increased mortality.

(2) Severity—Vessels involved: Left main coronary artery or > 2 arteries indicating worse prognosis.

Preventive therapies of CAD

(1) Lifestyle modification for risk reduction (highly important!): Smoking cessation; reduction of stress, weight, LDL, and triglyceride; regular exercise; treatment of diabetes, hypertension, anemia, and COPD. Omega-3 fatty acids (DHA and EPA) and nuts intake can lower risk of CVDs.

(2) Antiplatelet therapy: Low-dose aspirin daily is very effective in prevention of angina. New antiplatelet drug (P2Y₁₂ inhibitor)—ticlopidine or clopidogrel is an alternative to aspirin in patient who cannot tolerate aspirin. Note that ticlopidine can cause neutropenia.

(3) Lipid management: Keeping LDL levels lower than 100mg/dL and HDL higher than 40 mg/dL by excercise, diet control, and medication.

Angina Pectoris

Angina pectoris mostly refers to“stable angina”, a paroxysmal chest pain resulting from cardiac ischemia—an imbalance between oxygen supply and demand, and is most commonly caused by the inability of atherosclerotic coronary arteries to perfuse the heart under conditions of increased myocardial oxygen consumption. Stable angina is the type when the pressure chest pain is precipitated by predictable factors (exercise, exertion, etc.), and alleviated by rest or nitrates within 15 min.

Unstable angina is angina that occurs at any time and in need of beta-blockers, or calcium blockers and longer time to be alleviated. It is considered a pre-MI condition, carrying high risk for myocardial infarction.

Prinzmetal (variant) angina: Chest pain occurs at rest or stress without the usual precipitating factor of exertion, due to coronary artery spasm, and alleviated immediately by a Ca-blocker.

Microvascular angina (cardiac syndrome X): It refers to angina pectoris (ischemia) with signs associated with decreased blood flow to heart tissue but with normal coronary arteriogram.

Myocardial Infarction (MI)

MI is ischemic myocardial necrosis as a result of an abrupt reduction in the coronary blood flow to a segment of myocardium, usually due to a thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis. MI is associated with a 30% mortality rate and 50% pre-hospital deaths. Early diagnosis and treatment during the first 30-60 min of onset is crucial to save life!

Acute Coronary Syndrome (ACS)

ACS refers to any group of symptoms attributed to obstruction of the coronary arteries. ACS usually occurs as a result of one of three conditions: EKG/ECG ST-elevation myocardial infarction (30%), non-ST-elevation myocardial infarction (25%), or unstable angina (38%).

It is difficult to determine the precise etiology from its history and physical examination alone. The risk factors for ACS are the same as for CAD.

Diagnostic guidelines for ACS

1. The most common symptom prompting diagnosis of ACS is pressure-like chest pain (> 30 min with infarction), often radiating to the left arm, and associated with anxiety, nausea, and diaphoresis.

2. Lab diagnosis: (1) EKG/ECG is abnormal immediately at onset of typical chest pain. ST-T elevation progresses to Q-waves or left branch block over up to 7 days. (2) Abnormal myoglobin starts 1-4 hours after chest pain and lasts 1-2 days; CK-MB starts 4-6 hours and lasts 3 days; troponin starts 2-4 hours and lasts 7-10 days. Troponin cannot distinguish a reinfarction occurring several days after the first onset. Renal inefficiency can result in a false increase in troponin.

3. Reinfarction: If a patient presents with a new chest pain within a few days of the first infarction or attack, perform an ECG to detect new ST segment abnormalities. Elevated CK-MB levels after several days indicate new infarction.

Therapeutic guidelines for ACS

1. All patients with an ACS should receive a P2Y₁₂ inhibitor. For patients undergoing an invasive approach, either prasugrel or ticagrelor has been preferred to clopidogrel.

2. ST-elevation MI: Oxygen, aspirin and beta1 blockers should be started ASAP for best benefits. Primary percutaneous cornorary intervention (PCI) within 90 min of first medical contact is the goal. Thrombolysis within 30 min in hospital and 6-12 hours of onset of symptoms reduces mortality.

3. Post-MI take-home medications: Aspirin (or clopidogrel if aspirin-intolerant), beta1 blockers (metoprolol), ACE-inhibitors (or ARB—angiotensin-R blockers if cough-persistent), and statins.

4. Glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban, eptifibatide): Useful in ACS with ST depression (non-ST elevation MI) and patients to undergo angioplasty and stenting. tPA is beneficial only with ST elevation MI. Heparin is best for non-ST elevation MI.

5. In non-ST elevation ACS, if patient is not better (persistent pain, S3 gallop, worse ECG changes, and rising troponin levels) after using all given medications, urgent angiography and possibly angioplasty (PCI) should be performed.

6. The most common cause of death is ventricular arrhythmia—tachycardia and fibrillation. Always get ready to perform immediate electrical cardioversion or defibrillation.

Contraindications: Do not use any“prophylactic antiarrhythmic medications for ventricular tachycardia or fibrillation” because it increases the risk of ventricular arrhythmia and mortality.

Do not use nitrates and sildenafil together, to avoid severe vascular complications (e.g.,hypotension).

Post-MI impotence: Erection problem is mostly due to anxiety. Sexual activity can be recovered when the patient is asymptomatic.

Plus: What is metabolic syndrome (Insulin resistance syndrome)?

It refers to any combination of hyperglycemia, hyperlipidemia, hyperuricemia, or/and hypertension ("a 4-High Cluster"). This syndrome associated genetic predisposition, lack of exercise, and body fat distribution increase the risk of developing diabetes and cardiovascular diseases.