Acute Coronary Syndromes - USMLE Step 2

SECTION 1

Historical Context & Motivation

The concept of acute coronary syndromes (ACS) has evolved dramatically over the past century, transforming from a largely fatal condition to one amenable to aggressive intervention. In the early 1900s, physicians recognized myocardial infarction as a distinct clinical entity, yet treatment options were limited to bed rest and morphine. The subsequent decades brought electrocardiography, coronary angiography, and ultimately percutaneous coronary intervention — each milestone reshaping how we diagnose and treat acute ischemic events. Today, ACS remains the leading cause of morbidity and mortality worldwide, but timely recognition and evidence-based management can profoundly improve patient outcomes.

1912 • Clinical Recognition of MI

James Herrick published his landmark paper describing coronary thrombosis as the cause of sudden cardiac death, establishing myocardial infarction as a survivable clinical entity rather than an immediate death sentence.

1958 • Coronary Angiography

Mason Sones accidentally injected contrast dye into a coronary artery during catheterization, inadvertently inventing selective coronary angiography and enabling direct visualization of coronary anatomy in living patients.

1977 • Balloon Angioplasty

Andreas Grüntzig performed the first percutaneous transluminal coronary angioplasty (PTCA), inaugurating the era of catheter-based coronary revascularization.

2000s • Troponin & Drug-Eluting Stents

Introduction of highly sensitive cardiac troponin assays refined the diagnosis of NSTEMI, while drug-eluting stents dramatically reduced in-stent restenosis rates after PCI.

2020s • Precision Medicine & Systems of Care

Current guidelines emphasize regionalized STEMI systems of care, door-to-balloon time goals under 90 minutes, and risk-stratified approaches to NSTE-ACS using validated scoring systems such as TIMI and GRACE.

The central question that drives the study of ACS is deceptively simple: when a patient presents with chest pain, how do you rapidly distinguish between stable angina, unstable angina, NSTEMI, and STEMI — and how does that classification dictate the urgency and nature of your intervention? This lesson addresses the pathophysiology underlying plaque rupture, the diagnostic criteria that differentiate ACS subtypes, and the evidence-based treatment algorithms you will encounter on Step 2 and in clinical rotations.

SECTION 2

Core Principles & Definitions

Acute coronary syndromes represent a spectrum of clinical presentations caused by acute myocardial ischemia, almost always resulting from atherosclerotic plaque disruption with superimposed thrombus formation. The unifying pathophysiological mechanism is a sudden reduction in coronary blood flow sufficient to cause myocardial injury. ACS is categorized based on ECG findings and biomarker evidence of myocardial necrosis into three entities: unstable angina (UA), non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Distinguishing among these entities is the critical first step in management.

Plaque Rupture & Thrombosis

A vulnerable plaque with a thin fibrous cap and large lipid core ruptures, exposing thrombogenic subendothelial collagen and tissue factor to circulating platelets and coagulation factors, leading to acute thrombus formation.

Spectrum of Occlusion

UA and NSTEMI typically result from partial (subtotal) occlusion or transient total occlusion with distal embolization, while STEMI arises from complete thrombotic occlusion of a coronary artery.

Biomarker Differentiation

Cardiac troponin I or T elevation distinguishes NSTEMI from UA. High-sensitivity troponin assays detect smaller quantities of myocardial necrosis, increasing diagnostic sensitivity but also necessitating clinical correlation to exclude non-ACS causes of troponin elevation.

ECG as the Gateway Decision

ST-segment elevation ≥ 1 mm in two contiguous leads (or new LBBB) prompts emergent reperfusion. Absence of ST-elevation directs patients down the NSTE-ACS pathway, where risk stratification guides timing of angiography.

Time = Myocardium

Myocardial necrosis begins within 20–40 minutes of total occlusion, progressing transmurally over 6–12 hours. Early reperfusion — whether pharmacological or mechanical — limits infarct size and preserves ventricular function, making rapid triage paramount.

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KEY TAKEAWAY

Think of ACS like a pipe that is clogging. In unstable angina, the blockage is partial and transient — flow is compromised but the downstream tissue survives intact. In NSTEMI, the partial blockage or distal embolization is severe enough that some downstream cells die, releasing troponin into the circulation like a chemical distress signal. In STEMI, the pipe is completely blocked — without urgent intervention, the entire territory of myocardium supplied by that artery will necrose. The ECG is your first tool to separate the 'complete blockage' (STEMI) from the 'partial blockage' (NSTE-ACS), and troponin is your second tool to separate NSTEMI from UA within the partial-blockage group.

SECTION 3

Visual Explanation — The ACS Spectrum

The ACS spectrum begins with a vulnerable plaque that ruptures, forming a thrombus. The degree of occlusion and the resulting ECG changes and troponin levels differentiate unstable angina (negative troponin), NSTEMI (positive troponin, no ST elevation), and STEMI (positive troponin, ST elevation in contiguous leads).

As the diagram illustrates, the pathophysiological continuum begins with a vulnerable atherosclerotic plaque characterized by a thin fibrous cap and a large, lipid-rich necrotic core. When this cap ruptures or erodes, the exposure of subendothelial collagen and tissue factor triggers platelet adhesion, activation, and aggregation, followed by the coagulation cascade and thrombus formation. The clinical presentation depends on whether the thrombus is partially or completely occlusive and whether sufficient ischemia occurs to produce cardiomyocyte death detectable by troponin. The 12-lead ECG serves as the initial branching point: ST-segment elevation in a territorial distribution immediately classifies the patient as STEMI and triggers emergent reperfusion therapy, while its absence directs the patient into the NSTE-ACS pathway where serial troponin measurements become the key differentiator.

SECTION 4

Pathophysiological Mechanisms & Diagnostic Markers

The Ischemic Cascade

When coronary blood flow is abruptly compromised, the myocardium undergoes a predictable sequence of events known as the ischemic cascade. This concept is clinically important because different diagnostic modalities detect abnormalities at different stages of the cascade. The earliest changes are biochemical — depletion of ATP and accumulation of lactate — followed by diastolic dysfunction (detectable by echocardiography), then systolic wall motion abnormalities, and subsequently ECG changes (ST-segment deviation). Chest pain is actually a relatively late manifestation. This explains why some patients develop silent ischemia with ECG or biomarker evidence of injury before symptom onset, a phenomenon particularly common in diabetic patients with autonomic neuropathy.

Troponin Kinetics

Cardiac troponin I (cTnI) and troponin T (cTnT) are structural proteins in the contractile apparatus of cardiomyocytes. When myocardial necrosis occurs, these proteins are released into the circulation. With conventional assays, troponin becomes detectable 3–6 hours after the onset of ischemia, peaks at 12–24 hours, and remains elevated for 7–14 days. High-sensitivity troponin (hs-cTn) assays detect much lower concentrations and may become positive within 1–3 hours, enabling rapid rule-in or rule-out protocols. The 2020 ESC guidelines endorse a 0/1-hour or 0/2-hour algorithm: if the initial hs-cTnT or hs-cTnI is below the limit of detection and the delta at 1–2 hours is minimal, MI can be ruled out with a negative predictive value exceeding 99%.

ECG Localization of Ischemia

ECG Territory	Leads with ST Elevation	Culprit Artery	Reciprocal Changes
Anterior	V₁–V₄ (may extend to V₅–V₆)	Left anterior descending (LAD)	ST depression in II, III, aVF
Inferior	II, III, aVF	Right coronary artery (RCA) ~85%; Left circumflex (LCx) ~15%	ST depression in I, aVL
Lateral	I, aVL, V₅, V₆	Left circumflex (LCx) or diagonal of LAD	ST depression in III, aVF
Posterior	V₇–V₉ (posterior leads); ST depression V₁–V₃ = reciprocal	LCx or posterior descending (PDA)	Tall R waves, ST depression V₁–V₃
Right Ventricular	V₃R–V₄R (right-sided leads); inferior ST elevation	Proximal RCA	Associated with inferior STEMI

ECG localization of STEMI by lead territory and culprit artery

⚠

Clinical Pearl

Always obtain right-sided leads (V₄R) in any patient with an inferior STEMI to evaluate for right ventricular infarction. RV infarction is preload-dependent — these patients may become profoundly hypotensive with nitroglycerin or diuretics, both of which reduce preload.

SECTION 5

Classification & Risk Stratification

Once a patient is categorized into the NSTE-ACS pathway (no persistent ST elevation), clinicians must stratify the risk of adverse outcomes to guide the urgency of invasive management. Two validated scoring systems dominate clinical practice and board examinations: the TIMI risk score and the GRACE score. The TIMI score for NSTE-ACS assigns one point each for seven variables and is straightforward to calculate at the bedside. The GRACE score is more complex but provides a more precise estimate of in-hospital and 6-month mortality. Both inform decisions regarding early invasive strategy versus initial conservative management.

The NSTE-ACS management algorithm illustrates how initial medical therapy is identical regardless of risk category. The risk stratification step determines the timing and urgency of invasive angiography: conservative strategy with selective catheterization for low-risk patients, early invasive approach within 24–72 hours for intermediate-risk patients, and urgent catheterization within 2 hours for high-risk patients with hemodynamic instability or refractory angina.

TIMI Risk Score for NSTE-ACS

✓ Age ≥ 65 years (1 point)
✓ ≥ 3 CAD risk factors — hypertension, diabetes, dyslipidemia, smoking, family history (1 point)
✓ Known coronary stenosis ≥ 50% (1 point)
✓ ASA use within the past 7 days (1 point)
✓ ≥ 2 anginal episodes within 24 hours (1 point)
✓ ST deviation ≥ 0.5 mm on presenting ECG (1 point)
✓ Elevated cardiac biomarkers (1 point)

Each variable contributes one point, yielding a total score of 0–7. Patients with a TIMI score of 0–2 are considered low risk (< 8% risk of death, MI, or urgent revascularization at 14 days), while a score of 5–7 identifies high risk patients (> 26% event rate). The simplicity of TIMI makes it ideal for rapid bedside use, though the GRACE score is considered more accurate for mortality prediction.

SECTION 6

Worked Clinical Example

Clinical Vignette: 62-Year-Old Male with Chest Pain

1
Step 1 — Presentation & Initial Assessment

A 62-year-old male with a history of hypertension, type 2 diabetes mellitus, and hyperlipidemia presents to the ED with 45 minutes of substernal chest pressure radiating to the left arm, associated with diaphoresis and nausea. He takes aspirin 81 mg daily. Vital signs: BP 148/92, HR 88, RR 18, SpO₂ 97%. An ECG is obtained within 10 minutes of arrival.

First priority: Obtain and interpret the 12-lead ECG within 10 minutes to identify or exclude STEMI.
2
Step 2 — ECG Interpretation

The ECG shows 2 mm ST-segment depression in leads V₃–V₅ and T-wave inversions in leads I and aVL. There is no ST-segment elevation in any territory. The rhythm is normal sinus. This ECG pattern is consistent with NSTE-ACS — the absence of ST elevation rules out STEMI and directs us down the NSTE-ACS pathway.

ECG diagnosis: NSTE-ACS (ST depression and T-wave inversions without ST elevation).
3
Step 3 — Initial Medical Therapy (MONA-B plus anticoagulation)

Initiate the following: Aspirin 325 mg chewed (loading dose), heparin (unfractionated heparin or enoxaparin), nitroglycerin sublingual or IV for ongoing pain, a beta-blocker (metoprolol) if no contraindications, a high-intensity statin (atorvastatin 80 mg), and supplemental oxygen only if SpO₂ < 90%. Morphine may be considered for refractory pain but is used cautiously given data suggesting possible harm. A P2Y₁₂ inhibitor (ticagrelor or clopidogrel) is initiated pending the invasive strategy decision.

Medications administered: ASA 325 mg, enoxaparin 1 mg/kg SQ, NTG SL, metoprolol 25 mg PO, atorvastatin 80 mg.
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Step 4 — Risk Stratification with TIMI Score

Calculate the TIMI score: Age ≥ 65? No (62) = 0. ≥ 3 CAD risk factors? Yes (HTN, DM, HLD) = 1. Known coronary stenosis ≥ 50%? Unknown/No = 0. ASA use within 7 days? Yes = 1. ≥ 2 anginal episodes in 24 hours? Only 1 described = 0. ST deviation ≥ 0.5 mm? Yes (2 mm depression) = 1. Elevated biomarkers? Pending — initial troponin drawn at presentation.

TIMI score: 3 (minimum) — will be 4 if troponin returns positive, placing the patient in the intermediate-to-high risk category favoring an early invasive strategy.
5
Step 5 — Troponin Result & Management Decision

The initial hs-cTnI returns at 1,240 ng/L (reference < 26 ng/L), confirming myocardial necrosis. The TIMI score is now 4, and the patient is classified as having an NSTEMI. Given his intermediate-to-high risk profile, an early invasive strategy is indicated: coronary angiography within 24 hours. Ticagrelor 180 mg loading dose is administered. Angiography reveals a 95% stenosis of the proximal LAD with TIMI 2 flow. PCI with drug-eluting stent is performed, restoring TIMI 3 flow.

Final diagnosis: NSTEMI due to 95% LAD stenosis, treated with PCI and DES. Discharge on DAPT (ASA + ticagrelor × 12 months), high-intensity statin, β-blocker, ACE inhibitor.

SECTION 7

Comparing ACS Subtypes & Treatment Strategies

Feature	Unstable Angina	NSTEMI	STEMI
Pathology	Partial occlusion, no necrosis	Partial occlusion ± embolization, subendocardial necrosis	Complete occlusion, transmural necrosis
ECG	ST depression, T-wave inversions, or normal	ST depression, T-wave inversions, or normal	ST elevation ≥ 1 mm in ≥ 2 contiguous leads (or new LBBB)
Troponin	Negative	Positive	Positive
Acute Treatment	Antiplatelet, anticoagulation, anti-ischemic Rx; risk-stratified invasive approach	Antiplatelet, anticoagulation, anti-ischemic Rx; early invasive strategy (24–72 h)	Emergent reperfusion: primary PCI (preferred) or fibrinolysis within 12 h
Time Target	Risk-dependent; stress test or cath within days	Cath within 24–72 h; < 2 h if very high risk	Door-to-balloon < 90 min (PCI); door-to-needle < 30 min (fibrinolysis)
Fibrinolysis	Contraindicated	Contraindicated	Indicated if PCI not available within 120 min

Comparison of ACS subtypes: pathology, diagnosis, and management

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KEY TAKEAWAY

A critical board-tested concept is that fibrinolysis is only indicated for STEMI — administering thrombolytics to an NSTE-ACS patient increases bleeding risk without benefit and can be harmful. Think of it this way: fibrinolysis is a blunt tool that dissolves clot indiscriminately. In STEMI, the entire vessel is blocked, so the benefit of restoring any flow outweighs the bleeding risk. In NSTE-ACS, there is still some residual flow through the partially occlusive thrombus, and fibrinolysis may paradoxically destabilize the thrombus without improving outcomes.

Reperfusion Strategy Selection in STEMI

The choice between primary PCI and fibrinolysis in STEMI depends primarily on the availability of a PCI-capable facility within a timely window. Current ACC/AHA guidelines recommend primary PCI as the preferred reperfusion strategy when it can be performed within 90 minutes of first medical contact at a PCI-capable hospital, or within 120 minutes if transfer from a non–PCI-capable hospital is required. If these time targets cannot be met, fibrinolysis should be administered within 30 minutes of hospital arrival (door-to-needle time), provided the patient presents within 12 hours of symptom onset and has no absolute contraindications. After fibrinolysis, patients should be transferred for routine angiography within 3–24 hours (pharmacoinvasive strategy).

SECTION 8

Complications & Advanced Considerations

Understanding the complications of acute myocardial infarction is essential for Step 2 and clinical practice. Complications are broadly categorized by their temporal relationship to the index event and by mechanism — mechanical, arrhythmic, inflammatory, or thromboembolic. Recognizing these entities early is critical because many are rapidly fatal without intervention.

Complication	Typical Timing	Mechanism & Key Features	Management
Ventricular fibrillation / VT	First 24–48 hours	Electrical instability due to ischemia; most common cause of early death in MI	Defibrillation, amiodarone, β-blockers; correct electrolytes
Cardiogenic shock	Hours to days	Extensive LV necrosis (usually > 40% of LV mass); hypotension, pulmonary edema, end-organ hypoperfusion	Emergent revascularization, inotropes, vasopressors, mechanical circulatory support (IABP, Impella)
Free wall rupture	3–5 days (up to 2 weeks)	Transmural necrosis weakens myocardium → hemopericardium, cardiac tamponade; often fatal	Emergent pericardiocentesis + surgical repair
Ventricular septal rupture	3–5 days	New harsh holosystolic murmur with thrill; left-to-right shunt → acute heart failure	Surgical repair; stabilize with vasodilators, IABP
Papillary muscle rupture	2–7 days	Acute severe mitral regurgitation; new systolic murmur, pulmonary edema; more common with inferior MI (posteromedial papillary muscle)	Emergent mitral valve repair/replacement
Dressler syndrome	2–10 weeks post-MI	Autoimmune pericarditis; pleuritic chest pain, friction rub, diffuse ST elevation, fever	NSAIDs, colchicine; avoid anticoagulation (risk of hemorrhagic pericarditis)
LV thrombus / embolism	Days to weeks	Mural thrombus forms on akinetic/dyskinetic segments (especially anterior/apical MI); risk of systemic embolization (stroke)	Anticoagulation (warfarin or DOAC); echocardiographic surveillance

Major post-MI complications by timing, mechanism, and management

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High-Yield Board Tip

Differentiating ventricular septal rupture from papillary muscle rupture on Step 2: both present with a new murmur and acute hemodynamic deterioration 3–7 days post-MI. The key differentiator is the step-up in oxygen saturation from RA to RV on right heart catheterization — present in VSD (left-to-right shunt), absent in MR. Echocardiography will also demonstrate the specific lesion.

Looking forward, ongoing research into personalized antiplatelet therapy guided by platelet function testing and pharmacogenomics (e.g., CYP2C19 polymorphisms affecting clopidogrel metabolism) may refine DAPT strategies. Additionally, advances in intracoronary imaging with optical coherence tomography (OCT) and intravascular ultrasound (IVUS) are improving our understanding of plaque morphology and stent optimization. These technologies represent the frontier of ACS management, bridging the gap between population-level guidelines and truly individualized care.

SECTION 9

Practice Problems

Question 1: CONCEPTUAL

A 55-year-old woman presents with 2 hours of substernal chest pressure radiating to her left arm. Her ECG shows ST depression in leads V₄–V₆, and her initial high-sensitivity troponin I is within normal limits. A repeat troponin drawn 3 hours later remains normal. What is the most likely diagnosis, and why does this differ from NSTEMI?

Show answer

The most likely diagnosis is unstable angina. Both UA and NSTEMI present with ischemic symptoms and ECG changes (ST depression, T-wave inversions) without ST elevation, placing them in the NSTE-ACS category. The critical differentiator is the troponin level: in unstable angina, myocardial ischemia is severe enough to cause symptoms and ECG changes but does not produce sufficient cardiomyocyte necrosis to release detectable troponin. In NSTEMI, the ischemia crosses the threshold into actual myocardial cell death, releasing troponin into the circulation. Serial negative troponins over a clinically appropriate observation period (typically at least 3–6 hours with high-sensitivity assays) effectively rules out myocardial necrosis and establishes UA as the diagnosis. Step-by-step reasoning: 1. The patient presents with classic ischemic chest pain (substernal pressure, 2 hours duration). 2. ECG shows ST depression in V₄–V₆ — this rules out STEMI (which requires ST elevation) and places her in the NSTE-ACS category. 3. Initial high-sensitivity troponin I is within normal limits. 4. Repeat troponin at 3 hours remains normal — serial negative troponins rule out myocardial necrosis (NSTEMI requires detectable troponin rise and/or fall). 5. Conclusion: Ischemia without necrosis = Unstable Angina. If troponin had risen, the diagnosis would be NSTEMI.

Question 2: BASIC CALCULATION

A 68-year-old man with hypertension, diabetes, and hyperlipidemia presents with new-onset chest pain at rest. He has been taking aspirin for secondary prevention. His ECG shows 1.5 mm ST depression in leads V₂–V₅, and his troponin T is elevated at 0.85 ng/mL. He has had one anginal episode in the past 24 hours. Calculate his TIMI risk score for NSTE-ACS and interpret the result.

Show answer

The TIMI score is calculated by assigning one point for each criterion met. Age ≥ 65: Yes (68) = 1 point. ≥ 3 CAD risk factors (HTN, DM, HLD): Yes = 1 point. Known coronary stenosis ≥ 50%: Not stated, likely unknown = 0 points. Aspirin use within 7 days: Yes = 1 point. ≥ 2 anginal episodes in 24 hours: Only 1 episode described = 0 points. ST deviation ≥ 0.5 mm: Yes (1.5 mm depression) = 1 point. Elevated cardiac biomarkers: Yes (troponin 0.85) = 1 point. Total TIMI score = 5/7, placing him in the high-risk category with an estimated 14-day event rate (death, MI, or urgent revascularization) exceeding 26%. This score strongly supports an early invasive strategy with coronary angiography within 24 hours.

Question 3: INTERMEDIATE

A 72-year-old woman arrives at a non–PCI-capable hospital with 90 minutes of crushing chest pain. Her ECG shows 3 mm ST elevation in leads II, III, and aVF with reciprocal ST depression in leads I and aVL. The nearest PCI center is 2 hours away by transport. What is the appropriate reperfusion strategy, and what additional ECG evaluation should you perform before initiating treatment?

Show answer

This patient presents with an inferior STEMI (ST elevation in II, III, aVF with reciprocal changes). Since the estimated time to PCI exceeds 120 minutes from first medical contact, the patient does not meet the time window for primary PCI transfer. Therefore, fibrinolytic therapy should be administered within 30 minutes of arrival (door-to-needle < 30 min), followed by transfer for routine angiography within 3–24 hours (pharmacoinvasive strategy). Before initiating treatment, you must obtain right-sided ECG leads (V₃R–V₄R) to evaluate for concurrent right ventricular infarction, which occurs in approximately 30–50% of inferior STEMIs due to proximal RCA occlusion. If RV involvement is present, avoid nitroglycerin and diuretics (which reduce preload), and administer IV fluids to maintain adequate RV filling pressure.

Question 4: APPLIED

A 58-year-old man undergoes successful primary PCI with drug-eluting stent placement to the LAD for an anterior STEMI. On post-MI day 4, he develops sudden hemodynamic collapse with a new harsh holosystolic murmur at the left sternal border and a palpable thrill. Swan-Ganz catheterization reveals a step-up in oxygen saturation from the right atrium to the right ventricle. What is the diagnosis, what is the mechanism, and what is the definitive management?

Show answer

The diagnosis is ventricular septal rupture (VSR), a mechanical complication of transmural MI that typically occurs 3–5 days post-infarction when necrotic myocardium undergoes maximal softening before scar formation. The step-up in oxygen saturation from RA to RV on Swan-Ganz catheterization is pathognomonic — it confirms a left-to-right shunt through the ventricular septal defect. The new holosystolic murmur with a thrill is the classic auscultatory finding. This must be distinguished from acute mitral regurgitation due to papillary muscle rupture, which also presents with a new murmur but does not produce an oxygen step-up. Definitive management is emergent surgical repair. Temporizing measures include an intra-aortic balloon pump (IABP) to reduce afterload and augment coronary perfusion, and vasodilators such as nitroprusside. Mortality without surgery exceeds 90%.

Question 5: CRITICAL THINKING

A 50-year-old woman presents with acute chest pain and an ECG showing ST elevation in leads V₁–V₃ with new-onset heart failure. Initial troponin is markedly elevated. Coronary angiography reveals normal coronary arteries without evidence of atherosclerotic disease. Ventriculography shows apical ballooning with hyperkinesis of the basal segments. Discuss the differential diagnosis, the most likely condition, and how the pathophysiology differs from typical ACS. How should this patient be managed differently from a standard STEMI?

Show answer

The most likely diagnosis is Takotsubo cardiomyopathy (stress cardiomyopathy / apical ballooning syndrome), which mimics STEMI with ST elevation, troponin elevation, and wall motion abnormalities but occurs in the absence of obstructive coronary artery disease. The pathophysiology involves catecholamine-mediated myocardial stunning, often precipitated by intense emotional or physical stress — it differs fundamentally from typical ACS because there is no atherosclerotic plaque rupture or thrombosis. The classic pattern is apical and mid-ventricular akinesis with compensatory basal hyperkinesis, giving the ventricle a 'takotsubo' (octopus trap) shape on ventriculography. Management differs from standard STEMI in several important ways: since there is no culprit lesion, PCI is not indicated; supportive care with beta-blockers and ACE inhibitors is the mainstay; patients with severe LV dysfunction may require temporary hemodynamic support; and anticoagulation may be considered if LV thrombus develops in the akinetic apex. The prognosis is generally favorable, with most patients recovering LV function within weeks to months, though in-hospital mortality is approximately 4–5% due to complications such as cardiogenic shock, LV outflow tract obstruction, or arrhythmias. This case underscores the importance of coronary angiography in confirming the etiology of apparent STEMI and maintaining a broad differential that includes non-atherosclerotic causes of acute myocardial injury.

SUMMARY

Acute Coronary Syndromes — Summary

Summary

Acute coronary syndromes comprise a clinical spectrum — unstable angina, NSTEMI, and STEMI — unified by the pathophysiology of atherosclerotic plaque disruption with superimposed thrombosis. The initial 12-lead ECG is the gateway decision point: ST elevation triggers emergent reperfusion therapy (primary PCI preferred, door-to-balloon < 90 minutes; fibrinolysis if PCI unavailable within 120 minutes). Absence of ST elevation directs patients into the NSTE-ACS pathway, where serial troponin measurements differentiate NSTEMI (positive troponin = myocardial necrosis) from unstable angina (negative troponin = ischemia without necrosis).

For NSTE-ACS, risk stratification using TIMI or GRACE scores determines the urgency of invasive angiography: conservative management for low-risk patients, early invasive strategy within 24–72 hours for intermediate risk, and urgent catheterization within 2 hours for high-risk patients. All ACS patients receive dual antiplatelet therapy (ASA + P2Y₁₂ inhibitor), anticoagulation, high-intensity statin therapy, beta-blockers, and ACE inhibitors as part of secondary prevention. Awareness of post-MI complications — from ventricular arrhythmias and mechanical ruptures to Dressler syndrome — is essential for both clinical care and Step 2 success.