1.1 Ischemic Heart Disease & Acute Coronary Syndromes
Key Takeaways
- Ischemic heart disease is a blueprint subsection of Cardiovascular Disease, the largest category on the exam at 14%.
- Type 1 myocardial infarction reflects plaque rupture with thrombus; type 2 reflects supply-demand mismatch and is managed by correcting the precipitant.
- NSTE-ACS risk scores such as TIMI and GRACE determine whether an early invasive or an ischemia-guided strategy is appropriate.
- Primary PCI is preferred when it can be delivered within the guideline door-to-balloon window; fibrinolysis is the fallback when timely PCI is unavailable.
- Non-cardiac chest pain and coronary spasm are explicitly named blueprint topics and appear as distractors in ACS vignettes.
Acute coronary syndromes (ACS) represent a spectrum of acute myocardial ischemia ranging from unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI) to ST-segment elevation myocardial infarction (STEMI). Mastery of ACS diagnosis, emergency triage, invasive versus conservative pathways, antithrombotic pharmacology, and post-infarction complications is a cornerstone of the ABIM Internal Medicine certification exam.
1. Pathophysiology and Spectrum of Ischemic Heart Disease
Coronary atherosclerosis begins with endothelial injury, subendothelial accumulation of low-density lipoprotein (LDL) particles, leukocyte recruitment, and foam cell formation. Over decades, this process generates fibroatheromatous plaques characterized by a lipid-rich necrotic core covered by a fibrous cap composed of vascular smooth muscle cells and extracellular collagen matrix.
Mechanisms of Acute Coronary Occlusion
- Plaque Rupture (~70% of ACS): Thin-cap fibroatheromas (cap thickness <65 µm) infiltrated by activated macrophages that secrete matrix metalloproteinases (MMPs). Rupture exposes highly thrombogenic subendothelial core components (tissue factor, collagen) to circulating blood, initiating platelet adhesion, activation, and thrombin generation resulting in an occlusive red (erythrocyte-fibrin rich) or non-occlusive white (platelet-rich) thrombus.
- Plaque Erosion (~25-30% of ACS): Endothelial denudation without cap rupture, more frequent in premenopausal women, smokers, and non-calcified plaques. Platelet-rich thrombus forms directly on a proteoglycan- and hyaluronan-rich matrix.
- MINOCA (Myocardial Infarction with Non-Obstructive Coronary Arteries): Defined as acute MI criteria met with <50% stenosis on invasive angiography. Etiologies include epicardial coronary vasospasm (Prinzmetal/variant angina), coronary microvascular dysfunction, spontaneous coronary artery dissection (SCAD), coronary embolism/thrombus with spontaneous lysis, and myocarditis or Takotsubo cardiomyopathy mimicking ACS.
Clinical & Diagnostic Differentiation of Chest Pain Syndromes
| Feature | Stable Angina | Unstable Angina (UA) | NSTEMI | STEMI |
|---|---|---|---|---|
| Pathophysiology | Fixed flow-limiting stenosis (>70%) | Subtotal thrombus / transient occlusion | Subtotal thrombus causing myocardial necrosis | Total transmural coronary artery occlusion |
| Symptom Pattern | Predictable on exertion, relieved by rest/sublingual nitroglycerin <5 min | Occurs at rest (>20 min), new onset (CCS Class III), or crescendo pattern | Prolonged rest pain (>20 min), chest pressure radiating to left arm/jaw | Severe, persistent substernal crushing pain >30 min, diaphoresis, dyspnea |
| High-Sensitivity Troponin | Normal (<99th percentile URL) | Normal (<99th percentile URL) | Elevated with dynamic rise/fall above 99th percentile | Elevated with dynamic rise/fall above 99th percentile |
| 12-Lead ECG Findings | Normal or non-specific ST-T changes at rest | Transient ST depression (>=0.5 mm), T-wave inversions, or non-diagnostic | ST-segment depression (>=0.5 mm), deep T-wave inversions, or transient ST elevation | Persistent ST elevation (>=1 mm in >=2 contiguous limb leads; >=2.0 mm in men >=40y / >=2.5 mm in men <40y / >=1.5 mm in women in V2-V3) or new LBBB with Sgarbossa criteria |
ECG Pearl — Posterior MI & Sgarbossa Criteria:
- Posterior STEMI: ST depressions in leads V1–V3 with tall, wide R waves (R/S ratio >1) and upright T waves represent reciprocal changes of the posterior wall (LCx or PDA occlusion). Always obtain posterior leads (V7–V9); ST elevation >=0.5 mm in V7–V9 confirms posterior STEMI and warrants immediate primary PCI.
- Sgarbossa Criteria in LBBB / Paced Rhythm: (1) Concordant ST elevation >=1 mm in any lead (5 points); (2) Concordant ST depression >=1 mm in V1–V3 (3 points); (3) Modified Smith-Sgarbossa: Excessively discordant ST elevation >=1 mm with ST/S ratio <= -0.25 (2 points). A score >=3 has >90% specificity for acute STEMI.
2. Risk Stratification in NSTE-ACS
Risk stratification determines whether an invasive (coronary angiography +/- revascularization) or conservative (ischemia-guided) strategy is indicated, as well as the optimal timing of catheterization.
Clinical Risk Scores
-
TIMI Risk Score for UA/NSTEMI (7 variables, 1 point each):
- Age >= 65 years
- >=3 CAD risk factors (HTN, DM, hyperlipidemia, smoking, family history)
- Known CAD (coronary stenosis >= 50%)
- Aspirin use in the past 7 days
- Severe angina (>=2 episodes in past 24 hours)
- ST-segment deviation >= 0.5 mm
- Positive cardiac biomarkers (elevated troponin)
- Score interpretation: 0-2 = Low risk (4.7-8.3% 14-day death/MI/urgent revascularization); 3-4 = Intermediate risk (13.2-19.9%); 5-7 = High risk (26.2-40.9%).
-
GRACE Risk Score: Calculates in-hospital and 6-month mortality using 8 variables: age, heart rate, systolic BP, serum creatinine, Killip class, cardiac arrest at admission, ST-segment deviation, and elevated biomarkers. A GRACE score >140 indicates high risk.
-
HEART Score for Emergency Department Chest Pain:
- History (highly suspicious = 2, moderately = 1, slightly = 0)
- ECG (significant ST depression = 2, non-specific repolarization = 1, normal = 0)
- Age (>=65y = 2, 45-64y = 1, <45y = 0)
- Risk factors (>=3 risk factors or known CAD = 2, 1-2 risk factors = 1, none = 0)
- Troponin (>=3x normal = 2, 1-3x normal = 1, <=normal = 0)
- Score 0-3: Low risk (0.9-1.7% 6-week MACE); candidates for early discharge without inpatient admission.
- Score 4-6: Moderate risk (12-16.6% MACE); requires observation and provocative testing.
- Score 7-10: High risk (50-65% MACE); mandates admission and early invasive angiography.
3. Acute STEMI Management & Reperfusion Timing
Every minute of coronary occlusion correlates with progressive transmural myocardial necrosis. Time is myocardium.
Primary Percutaneous Coronary Intervention (PCI)
- First-line reperfusion therapy: Primary PCI is superior to fibrinolysis in reducing mortality, recurrent MI, and intracranial hemorrhage when performed expeditiously.
- Time benchmarks:
- Door-to-Balloon (D2B) time <= 90 minutes for patients presenting directly to a PCI-capable facility.
- Door-to-Balloon time <= 120 minutes (First Medical Contact to Device) for patients presenting to a non-PCI center requiring inter-hospital transfer.
Intravenous Fibrinolysis
- Indication: Indicated for patients with symptom onset <=12 hours when the anticipated transfer time to primary PCI exceeds 120 minutes.
- Time benchmark: Door-to-Needle (D2N) time <= 30 minutes.
- Agent of choice: Single weight-based IV bolus Tenecteplase (TNK-tPA) (30 mg for <60 kg up to 50 mg for >=90 kg) due to lower non-cerebral bleeding rates and ease of administration compared to Alteplase.
- Absolute Contraindications to Fibrinolysis:
- Any prior intracranial hemorrhage (ICH)
- Known structural cerebral vascular lesion (e.g., arteriovenous malformation)
- Known malignant intracranial neoplasm (primary or metastatic)
- Ischemic stroke within the preceding 3 months (excluding acute ischemic stroke <4.5 hours)
- Suspected aortic dissection
- Active internal bleeding or bleeding diathesis (excluding menses)
- Significant closed-head or facial trauma within the preceding 3 months
- Pharmacoinvasive Strategy: Following fibrinolysis, all patients should be transferred to a PCI-capable facility for routine angiography and PCI within 2 to 24 hours, or emergent rescue PCI if fibrinolysis fails (<50% ST resolution at 60-90 minutes, ongoing chest pain, hemodynamic instability).
A 62-year-old man presents to the emergency department of a rural community hospital with 2 hours of crushing substernal chest pressure. His ECG reveals 4-mm ST-segment elevation in leads II, III, and aVF with reciprocal ST depression in leads I and aVL. The nearest PCI-capable hospital is a 2.5-hour transport away. He has no history of stroke, head trauma, or active bleeding, and his blood pressure is 138/84 mmHg. What is the most appropriate next step in management?