What is acute coronary syndrome (ACS), including its definition, etiology, pathogenesis, pathophysiology changes, clinical features, heart sounds, electrocardiogram (ECG) readings, echocardiogram readings, treatment, and complications?

Acute Coronary Syndrome: Comprehensive Overview

Definition

Acute coronary syndrome (ACS) encompasses a spectrum of acute myocardial ischemic states including ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina (UA), all resulting from abrupt reduction in coronary blood flow. 1, 2

• STEMI represents complete coronary artery occlusion with persistent ST-segment elevation (>20 minutes), accounting for approximately 30% of ACS cases 1, 2
• NSTEMI involves myocardial necrosis with elevated cardiac biomarkers but without persistent ST-elevation, representing partial or intermittent arterial occlusion 1, 2
• Unstable angina presents with ischemic symptoms and ECG changes but without biomarker elevation indicating myocardial necrosis 1

Etiology

The primary cause is atherosclerotic plaque rupture, ulceration, fissure, or erosion with subsequent intraluminal thrombus formation in coronary arteries. 1, 3

• Vulnerable plaques are typically lipid-rich soft plaques with <50% stenosis severity prior to rupture 3
• Approximately 5-10% of cases occur without obstructive coronary disease, particularly in women 1
• Non-atherosclerotic causes include coronary vasospasm, spontaneous coronary artery dissection, and coronary embolism 1

Pathogenesis & Pathophysiology Flowchart

Pathogenesis Cascade:

1. Plaque Vulnerability Development 3

   • Lipid accumulation in arterial wall
   • Inflammatory cell infiltration
   • Thin fibrous cap formation
   • Increased mechanical stress

2. Acute Plaque Disruption 1, 3

   • Plaque rupture/erosion/ulceration
   • Exposure of thrombogenic material
   • Platelet adhesion and activation
   • Thrombin generation

3. Thrombus Formation 1

   • Complete occlusion → STEMI (transmural infarction)
   • Partial/intermittent occlusion → NSTEMI/UA (subendocardial ischemia)

4. Myocardial Consequences 1

   • Reduced coronary blood flow
   • Myocardial oxygen supply-demand mismatch
   • Cellular ischemia → necrosis (if prolonged)
   • Distal microembolization

Pathophysiological Changes:

Hemodynamic alterations:

• Decreased myocardial contractility in ischemic zones 1
• Elevated left ventricular end-diastolic pressure 1
• Reduced cardiac output in extensive infarction 1
• Potential cardiogenic shock in severe cases (10-15% mortality) 1

Structural changes:

• Regional wall motion abnormalities in affected myocardial segments 1
• Ventricular remodeling with chamber dilation (chronic phase) 1
• Potential mechanical complications: papillary muscle rupture, ventricular septal defect, free wall rupture 1

Clinical Features

Chest discomfort at rest is the cardinal symptom, affecting approximately 79% of men and 74% of women, described as pressure, tightness, pain, or burning. 2

Typical presentations:

• Retrosternal chest pain/pressure radiating to left arm, jaw, or back 2, 4
• Duration >20 minutes for STEMI; waxing/waning for NSTEMI/UA 1
• Associated diaphoresis, nausea, dyspnea 2

Atypical presentations (40% men, 48% women):

• Isolated dyspnea without chest pain 2
• Epigastric pain mimicking gastrointestinal pathology 1
• Syncope or presyncope 1
• More common in elderly, diabetics, and women 1

Physical examination findings:

• Often unremarkable in uncomplicated cases 1
• Diaphoresis and pallor 4
• Signs of heart failure: pulmonary rales, elevated jugular venous pressure 1
• Hypotension or hypertension 1
• Fourth heart sound (S4) from decreased ventricular compliance 4

Heart Sounds

S4 gallop is the most common auscultatory finding, reflecting atrial contraction against a stiffened ischemic ventricle. 4

• S3 gallop indicates ventricular dysfunction and heart failure complicating infarction 4
• New systolic murmur suggests:
  • Mitral regurgitation from papillary muscle dysfunction/rupture 1
  • Ventricular septal defect from septal rupture 1
• Pericardial friction rub may develop 24-72 hours post-infarction (pericarditis) 4

ECG Readings

A 12-lead ECG must be obtained within 10 minutes of presentation and compared with previous tracings. 1, 2

STEMI Pattern:

• Persistent ST-segment elevation ≥1 mm in two contiguous leads 1
• Hyperacute T waves (early finding) 2
• Development of pathological Q waves (>0.04 seconds duration) indicating transmural necrosis 1
• Reciprocal ST-depression in opposite leads 2

NSTEMI/UA Patterns:

• ST-segment depression ≥0.5 mm (31% of NSTE-ACS) 2
• T-wave inversions (12% of cases) 2
• Combined ST-depression and T-wave inversions (16%) 2
• Normal or non-specific changes (41% of NSTE-ACS) 2
• Transient ST-elevation (<20 minutes) 1
• Pseudo-normalization of previously inverted T waves 1

Critical pitfall: Bundle branch block or pacemaker rhythm (7% of cases) obscures ST-segment analysis and requires alternative diagnostic approaches 1

Echocardiogram Findings

Echocardiography should be performed to assess left ventricular function and identify mechanical complications. 1, 5

Structural Changes:

Ventricular wall motion:

• Regional wall motion abnormalities in the distribution of the culprit artery (hypokinesis, akinesis, or dyskinesis) 1
• Pattern consistent with ischemic territory helps localize affected coronary artery 1

Valvular complications:

• Mitral regurgitation from papillary muscle dysfunction or rupture 1
• Severity ranges from mild (ischemic dysfunction) to severe (complete rupture) 1

Chamber changes:

• Reduced left ventricular ejection fraction (LVEF) proportional to infarct size 5
• Left ventricular dilation in extensive infarction 1
• Right ventricular involvement in inferior STEMI 1

Hemodynamic Changes:

• Elevated left ventricular end-diastolic pressure from reduced compliance 1
• Decreased cardiac output in large infarctions 1
• Diastolic dysfunction with impaired relaxation 5
• Evidence of increased filling pressures: dilated inferior vena cava, reduced respiratory variation 5

Mechanical complications detected:

• Ventricular septal rupture (left-to-right shunt) 1
• Free wall rupture with pericardial effusion/tamponade 1
• Left ventricular thrombus formation 1

Treatment

Immediate Management (First 10 Minutes):

For STEMI, immediate reperfusion with primary PCI within 120 minutes reduces mortality from 9% to 7%. 2

STEMI reperfusion strategy:

• Primary PCI preferred if available within 120 minutes of first medical contact 1, 2
• Fibrinolytic therapy if PCI unavailable: alteplase, reteplase, or tenecteplase at full dose for patients <75 years; half dose for ≥75 years 2
• Transfer for PCI within 24 hours after fibrinolysis 1

Pharmacological Treatment (All ACS):

Antiplatelet therapy:

• Aspirin 75-150 mg daily indefinitely (Class I recommendation) 1, 5
• P2Y12 inhibitor for 12 months: clopidogrel, ticagrelor, or prasugrel 5
• Dual antiplatelet therapy is mandatory unless contraindications exist 5

Anticoagulation:

• Low-molecular-weight heparin (LMWH) or unfractionated heparin during acute phase 1
• Continue until revascularization or hospital discharge 1

Anti-ischemic therapy:

• Beta-blockers orally or IV unless contraindicated (heart failure, bradycardia, hypotension) 1, 5
• Nitrates oral or IV for persistent/recurrent chest pain 1, 5
• Calcium channel blockers if beta-blockers contraindicated 1

GPIIb/IIIa inhibitors:

• Indicated for high-risk NSTE-ACS undergoing early invasive strategy 1
• Abciximab or eptifibatide infusion for 12-24 hours 1

Risk Stratification for NSTE-ACS:

High-risk features requiring early invasive strategy (angiography within 24-48 hours): 1, 5

• Persistent or recurrent ischemia despite medical therapy
• ST-segment depression or transient ST-elevation
• Elevated troponin levels
• Hemodynamic instability or cardiogenic shock
• Life-threatening arrhythmias (ventricular tachycardia/fibrillation)
• Diabetes mellitus
• GRACE score >140

For high-risk NSTE-ACS, prompt invasive angiography and revascularization within 24-48 hours reduces mortality from 6.5% to 4.9%. 2

Low-risk patients:

• Negative troponin on repeat testing at 6-12 hours 1
• No recurrent chest pain 1
• Normal or minimal ECG changes 1
• Managed with ischemia-guided strategy: stress testing before discharge 1

Long-Term Secondary Prevention:

Lipid management:

• High-intensity statins initiated immediately and continued indefinitely 5
• Target LDL <70 mg/dL or 50% reduction from baseline 1

ACE inhibitors:

• Recommended for all patients with LVEF <40%, diabetes, hypertension, or chronic kidney disease 1
• Reduce cardiovascular death and recurrent MI 1

Beta-blockers:

• Continue for at least 6 weeks post-MI, indefinitely if LVEF reduced 5

Lifestyle modifications:

• Smoking cessation, dietary modification, exercise rehabilitation 1
• Control of hypertension, diabetes, and obesity 1

Complications

Early Complications (Hours to Days):

Arrhythmias:

• Ventricular fibrillation/tachycardia (most common cause of sudden death in first 48 hours) 1
• Bradyarrhythmias and heart block (especially inferior STEMI) 1
• Atrial fibrillation (10-20% of cases) 1

Mechanical complications:

• Papillary muscle rupture causing acute severe mitral regurgitation (days 2-7) 1
• Ventricular septal rupture (days 3-5, mortality >90% without surgery) 1
• Free wall rupture with cardiac tamponade (days 1-5, often fatal) 1

Hemodynamic complications:

• Cardiogenic shock (10% of STEMI, 50-80% mortality) 1
• Acute heart failure from extensive myocardial damage 1, 5
• Right ventricular infarction with hypotension (inferior STEMI) 1

Subacute/Late Complications (Days to Weeks):

Pericarditis:

• Early pericarditis (24-72 hours post-infarction) 4
• Dressler syndrome (weeks to months, autoimmune) 4

Ventricular remodeling:

• Progressive LV dilation and dysfunction 1
• Development of chronic heart failure 1

Thromboembolic events:

• Left ventricular thrombus formation with systemic embolization 1
• Deep vein thrombosis/pulmonary embolism from immobilization 1

Recurrent ischemia:

• Recurrent MI (5-10% within 30 days without optimal therapy) 1
• Post-infarction angina requiring revascularization 1

Monitoring During Hospitalization:

Continuous cardiac monitoring for at least 24 hours post-reperfusion to detect arrhythmias. 5

• Serial troponin measurements at 6-12 hour intervals 1, 5
• Daily ECGs to assess for evolution of infarction or recurrent ischemia 5
• Echocardiography to evaluate ventricular function and detect mechanical complications 5
• Close surveillance for recurrent chest pain, heart failure signs, or hemodynamic instability 5