7.1 Coronary Artery Disease & Acute Coronary Syndromes
Key Takeaways
- Primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy for ST-elevation myocardial infarction (STEMI) when it can be performed within 90 minutes of first medical contact at a PCI-capable facility, or within 120 minutes if transfer is required.
- Fibrinolytic therapy (e.g., alteplase, tenecteplase) is indicated for STEMI within 30 minutes of hospital arrival (door-to-needle time) when transfer to a PCI center cannot achieve reperfusion within 120 minutes and there are no absolute contraindications.
- Right ventricular infarction occurs in 30% to 40% of inferior STEMIs (right coronary artery occlusion) and presents with hypotension, jugular venous distension, and clear lung fields; management requires IV normal saline boluses while avoiding preload-reducing agents such as nitrates, opioids, and diuretics.
- TIMI risk score >=3 in patients with non-ST-elevation acute coronary syndrome (NSTEMI/Unstable Angina) indicates high risk and warrants an early invasive management strategy (coronary angiography within 24 hours).
- Mechanical complications post-myocardial infarction typically present 3 to 14 days after the index event: papillary muscle rupture causes acute severe mitral regurgitation with giant v waves, interventricular septum rupture causes a harsh holosystolic murmur with oxygen saturation step-up in the right ventricle, and free wall rupture causes cardiac tamponade and PEA.
Coronary Artery Disease & Acute Coronary Syndromes
Coronary artery disease (CAD) remains the leading cause of mortality worldwide. On USMLE Step 2 CK, candidates are evaluated on their ability to differentiate stable ischemic heart disease from acute coronary syndromes (ACS), interpret electrocardiograms (EKGs), select appropriate non-invasive diagnostic testing, and execute time-sensitive pharmacologic and invasive reperfusion strategies.
Stable Ischemic Heart Disease & Diagnostic Workup
Stable angina pectoris presents as predictable, exertional substernal chest pressure that is relieved by rest or sublingual nitroglycerin within 5 minutes. The underlying pathophysiology is stable atherosclerotic plaque producing fixed luminal narrowing (typically $\ge 70%$ obstruction).
When evaluating chest pain, clinicians first establish the pre-test probability of CAD based on age, sex, and symptom character (typical vs. atypical vs. non-cardiac).
Diagnostic Testing Algorithm
| Patient Profile & Baseline EKG | Recommended Initial Test | Clinical Rationale & Pearls |
|---|---|---|
| Low-to-Intermediate Risk, normal resting EKG, able to exercise | Exercise ECG Stress Test | Positive test: $\ge 1\text{ mm}$ horizontal or downsloping ST depression. |
| Intermediate-to-High Risk, uninterpretable EKG (LBBB, ST changes, digoxin, LVH) | Pharmacologic Stress Imaging (Nuclear MPI or Echo) | Adenosine/Regadenoson (coronary vasodilators) or Dobutamine (inotropic/chronotropic). Avoid adenosine in severe asthma. |
| Prior CABG / Stent or uninterpretable exercise capacity | Stress Echocardiography or Myocardial Perfusion Imaging (MPI) | Detects inducible wall motion abnormalities or reversible perfusion defects. |
| Low-to-Intermediate Risk, acute chest pain, low troponin | Coronary Computed Tomography Angiography (CCTA) | High negative predictive value to rule out CAD. |
| High Pre-test Probability or severe refractory angina | Invasive Coronary Angiography | Diagnostic and therapeutic gold standard allowing percutaneous intervention. |
Important Test-Taking Pearl: If a patient has a Left Bundle Branch Block (LBBB) or a ventricular paced rhythm, exercise stress testing and dobutamine stress testing are unreliable due to septal motion artifacts. Regadenoson or adenosine myocardial perfusion imaging is the diagnostic procedure of choice.
Acute Coronary Syndromes: Pathophysiology & Risk Stratification
Acute coronary syndromes represent a spectrum of acute myocardial ischemia resulting from atheromatous plaque rupture or erosion with superimposed thrombosis. ACS is divided into three distinct entities based on cardiac biomarkers and EKG findings:
- Unstable Angina (UA): Ischemic symptoms at rest, new-onset severe angina, or crescendo angina. Cardiac troponins are negative, and EKG may show ST depression or T-wave inversion.
- Non-ST-Elevation Myocardial Infarction (NSTEMI): Symptoms similar to UA, but with elevated cardiac troponins indicating myocardial necrosis. EKG displays ST depressions, T-wave inversions, or non-specific changes.
- ST-Elevation Myocardial Infarction (STEMI): Transmural myocardial ischemia causing ST-elevation in $\ge 2$ contiguous leads or a new LBBB, accompanied by troponin elevation.
Cardiac Biomarker Kinetics
- Cardiac Troponin I and T: Most sensitive and specific. Rise at 3–6 hours, peak at 18–24 hours, and remain elevated for 7–10 days.
- CK-MB (Creatine Kinase-MB): Rises at 4–6 hours, peaks at 18–24 hours, and returns to baseline within 48–72 hours. Useful for detecting early re-infarction if chest pain recurs 3–4 days post-MI.
Risk Stratification in UA/NSTEMI
The TIMI (Thrombolysis in Myocardial Infarction) Risk Score stratifies 14-day mortality and ischemic risk in UA/NSTEMI. One point is assigned for each criterion (Age $\ge 65$, $\ge 3$ CAD risk factors, known CAD stenosis $\ge 50%$, ASA use in past 7 days, severe angina $\le 24\text{ hours}$, elevated cardiac markers, ST deviation $\ge 0.5\text{ mm}$).
- TIMI Score 0–2 (Low Risk): Ischemia-guided medical management.
- TIMI Score $\ge 3$ (High Risk): Early invasive strategy with coronary angiography within 24 hours.
Acute Emergency Management & Reperfusion Protocols
Initial Medical Management (NSTEMI / UA / STEMI)
- Aspirin: Chewable non-enteric coated 162–325 mg immediately, followed by 81 mg daily indefinitely.
- P2Y12 Inhibitor: Loading dose of ticagrelor (180 mg) or prasugrel (60 mg) or clopidogrel (600 mg). Combined with aspirin for Dual Antiplatelet Therapy (DAPT) for at least 12 months post-PCI.
- Anticoagulation: Unfractionated heparin (UFH) drip or low-molecular-weight heparin (enoxaparin 1 mg/kg SC q12h) or fondaparinux.
- Nitrates: Sublingual or IV nitroglycerin for pain and preload reduction. Absolute Contraindications: Right ventricular infarction, severe aortic stenosis, or phosphodiesterase-5 inhibitor use (sildenafil within 24 hours, tadalafil within 48 hours).
- Beta-Blockers: Oral metoprolol or carvedilol within 24 hours. Avoid in acute heart failure, cardiogenic shock, or severe bradycardia.
- High-Intensity Statin: Atorvastatin 80 mg or rosuvastatin 40 mg initiated immediately regardless of baseline LDL level.
- ACE Inhibitors / ARBs: Initiated within 24 hours, especially in anterior MI, LVEF $<40%$, or hypertension.
STEMI EKG Localization & Reperfusion Timing
| EKG Leads | Affected Wall | Occluded Coronary Artery | Clinical Notes & Complications |
|---|---|---|---|
| V1–V4 | Anterior / Septal | Left Anterior Descending (LAD) | Highest risk of acute LV failure, cardiogenic shock, and free wall rupture. |
| I, aVL, V5–V6 | Lateral | Left Circumflex (LCX) | May present with isolated lateral ST elevations. |
| II, III, aVF | Inferior | Right Coronary Artery (RCA) | High risk of AV block and associated Right Ventricular (RV) Infarction. |
| V1–V3 ST depression with tall R waves | Posterior | Posterior Descending Artery (PDA) | Confirm with ST elevation in posterior leads V7–V9. |
Right Ventricular Infarction Management: Occurs in up to 40% of inferior MIs. Presenting features include hypotension, elevated JVD, and clear lungs. Diagnostic confirmation requires ST elevation in right-sided leads V3R–V4R. Treatment: Aggressive IV isotonic saline volume expansion to maintain RV preload. Avoid nitrates, opioids, and diuretics.
STEMI Reperfusion Guidelines
- Primary PCI (Preferred): First medical contact-to-balloon time $\le 90\text{ minutes}$ at a PCI-capable facility, or $\le 120\text{ minutes}$ if transfer to a PCI center is required.
- Fibrinolytic Therapy: Indicated if transfer to PCI cannot be achieved within 120 minutes. Door-to-needle time must be $\le 30\text{ minutes}$. Absolute contraindications include prior intracranial hemorrhage, active internal bleeding, ischemic stroke within 3 months, or suspected aortic dissection.
Post-Myocardial Infarction Complications Timeline
| Timeframe | Complication | Clinical Presentation | Management Strategy |
|---|---|---|---|
| First 24 Hours | Ventricular Arrhythmias (VF/VT) | Most common cause of pre-hospital death. Sudden cardiac arrest. | Defibrillation, amiodarone, ACLS protocol. |
| 1 to 3 Days | Peri-infarction Pericarditis | Pleuritic chest pain, pericardial friction rub, diffuse ST elevation. | High-dose Aspirin (650 mg tid). Avoid NSAIDs and steroids. |
| 3 to 14 Days | Papillary Muscle Rupture | Acute severe Mitral Regurgitation, sudden pulmonary edema, holosystolic murmur at apex radiating to axilla, giant v waves on PCWP. | Emergency surgical valve repair/replacement, intra-aortic balloon pump (IABP). |
| 3 to 14 Days | Interventricular Septum Rupture | Biventricular failure, harsh holosystolic murmur at left lower sternal border with thrill, oxygen saturation step-up from RA to RV. | Emergency surgical closure, IABP. |
| 3 to 14 Days | Free Wall Rupture | Sudden electromechanical dissociation (PEA), pericardial tamponade (Beck triad), death. | Pericardiocentesis, emergency surgery. |
| >2 Weeks to Months | Left Ventricular Aneurysm | Persistent ST-segment elevation weeks post-MI, heart failure, mural thrombus causing ischemic stroke. | Anticoagulation, surgical resection if symptomatic. |
| 2 to 10 Weeks | Dressler Syndrome | Autoimmune pericarditis, fever, leukocytosis, elevated ESR/CRP. | NSAIDs plus Colchicine. |
A 62-year-old man presents to the emergency department with 2 hours of crushing substernal chest pain. His blood pressure is 88/54 mmHg, pulse is 58/min, and oxygen saturation is 96% on room air. EKG demonstrates 2-mm ST-segment elevation in leads II, III, and aVF. Physical examination reveals jugular venous distension 5 cm above the sternal angle and clear lung fields bilaterally. Which of the following is the most appropriate next step in management?
A 68-year-old woman is admitted to the cardiac intensive care unit following an anterior wall STEMI treated with primary PCI 5 days ago. She suddenly develops severe shortness of breath and hypotension. Physical examination shows a blood pressure of 82/50 mmHg, pulse of 110/min, and bilateral pulmonary crackles halfway up the lung fields. A new harsh 4/6 holosystolic murmur is heard best at the apex, radiating to the axilla. Pulmonary artery catheterization shows giant v waves on the pulmonary capillary wedge pressure tracing. What is the underlying cause of this patient's acute clinical deterioration?
A 55-year-old man presents to a rural emergency department without on-site percutaneous coronary intervention (PCI) capabilities. He reports 90 minutes of severe substernal chest pain. EKG shows 3-mm ST elevations in leads V1 through V4. The nearest PCI-capable hospital is located 2.5 hours away, and estimated transport time will result in a first medical contact-to-balloon time of 160 minutes. The patient has no history of stroke, surgery, or bleeding disorders. Which reperfusion strategy should be initiated immediately?