Ischemic Heart Disease (IHD), also known as coronary artery disease (CAD), is one of the leading causes of morbidity and mortality globally. IHD encompasses a spectrum of clinical conditions that arise from reduced coronary blood flow, resulting in myocardial ischemia. The clinical manifestations range from stable angina, reflecting chronic ischemia, to acute coronary syndromes (ACS) such as unstable angina, NSTEMI, and STEMI, which carry higher risk for myocardial injury and death. Understanding the types, pathophysiology, and clinical features of IHD is essential for diagnosis, management, and prevention.
1. Introduction
IHD is characterized by an imbalance between myocardial oxygen supply and demand, usually due to atherosclerotic obstruction of coronary arteries. The severity and duration of ischemia determine the type of clinical presentation.
Key Points:
- IHD can be chronic or acute, depending on plaque stability and degree of coronary obstruction.
- Clinical types include:
- Stable Angina – Predictable, exertional chest pain
- Unstable Angina – New-onset or worsening chest pain
- NSTEMI – Partial-thickness myocardial necrosis without ST elevation
- STEMI – Full-thickness myocardial infarction with ST elevation
- ECG, cardiac biomarkers, and imaging are critical for differentiating types.
2. Stable Angina
2.1 Definition
Stable angina, also called effort angina, is chest discomfort precipitated by physical exertion or emotional stress and relieved by rest or nitrates. It represents chronic, reversible myocardial ischemia caused by fixed atherosclerotic plaques.
2.2 Pathophysiology
- Caused by fixed coronary artery stenosis (≥50% luminal narrowing) that limits blood flow during increased oxygen demand.
- Myocardium remains viable at rest due to adequate perfusion.
- Plaques are generally stable with thick fibrous caps, resistant to rupture.
Mechanisms:
- Exertion increases heart rate and contractility → increased oxygen demand.
- Fixed stenosis prevents increased blood flow → ischemia.
- Subendocardial myocardium is most vulnerable due to higher wall stress.
2.3 Clinical Features
- Chest pain: Retro-sternal, pressure-like, radiating to left arm/jaw
- Duration: 1–15 minutes, relieved by rest or nitrates
- Precipitating factors: Exercise, emotional stress, cold exposure
- Associated symptoms: Shortness of breath, diaphoresis, fatigue
2.4 Diagnosis
- ECG at rest: Usually normal
- Stress ECG: ST-segment depression during exertion
- Coronary angiography: Identifies stenotic lesions
- Non-invasive imaging: Myocardial perfusion scan, echocardiography
2.5 Management
- Lifestyle modifications: Exercise, smoking cessation, diet
- Medications:
- Nitrates: Relieve angina
- Beta-blockers: Reduce heart rate and oxygen demand
- Calcium channel blockers: Reduce afterload and vasospasm
- Antiplatelets: Prevent thrombus formation
- Statins: Plaque stabilization
- Revascularization:
- Percutaneous coronary intervention (PCI)
- Coronary artery bypass grafting (CABG) in multi-vessel disease
3. Unstable Angina (UA)
3.1 Definition
Unstable angina is chest pain at rest, of new onset, or worsening frequency, indicating acute coronary syndrome without myocardial necrosis. It is more dangerous than stable angina and may precede NSTEMI or STEMI.
3.2 Pathophysiology
- Caused by plaque disruption or erosion, leading to partial thrombosis or transient occlusion.
- Myocardial perfusion is intermittently reduced.
- Plaques are vulnerable, with thin fibrous caps and lipid-rich cores.
- Inflammatory mediators (e.g., cytokines, CRP) contribute to instability.
3.3 Clinical Features
- Chest pain at rest or with minimal exertion
- Pain duration: >20 minutes, unpredictable
- Increasing severity in previously stable angina
- Associated symptoms: Dyspnea, nausea, diaphoresis
3.4 Diagnosis
- ECG: May show ST-segment depression or T-wave inversion; often normal at rest
- Cardiac biomarkers: Normal troponin (distinguishes UA from NSTEMI)
- Risk stratification: TIMI or GRACE scores
- Coronary angiography: Identifies culprit lesions
3.5 Management
- Hospitalization for monitoring and early intervention
- Medications:
- Antiplatelets: Aspirin + P2Y12 inhibitor
- Anticoagulants: Heparin
- Anti-ischemic therapy: Nitrates, beta-blockers
- Statins: Plaque stabilization
- Revascularization: PCI or CABG depending on angiographic findings and risk profile
4. Non-ST Elevation Myocardial Infarction (NSTEMI)
4.1 Definition
NSTEMI is myocardial necrosis without ST-segment elevation. Partial-thickness (subendocardial) infarction occurs due to partial or transient coronary artery occlusion.
4.2 Pathophysiology
- Plaque rupture or erosion → thrombosis
- Incomplete coronary occlusion → subendocardial ischemia
- Oxygen supply-demand mismatch contributes to injury
- Inflammatory processes and microvascular obstruction exacerbate ischemia
4.3 Clinical Features
- Similar to unstable angina:
- Chest pain at rest or minimal exertion
- Radiating discomfort, nausea, diaphoresis
- More severe or prolonged than unstable angina
- Can progress to STEMI if thrombus propagates
4.4 Diagnosis
- ECG: ST-segment depression, T-wave inversion, no ST elevation
- Cardiac biomarkers: Elevated troponin I/T confirms myocardial necrosis
- Risk stratification: Guides timing of invasive procedures
- Imaging: Echocardiography can show regional wall motion abnormalities
4.5 Management
- Anti-ischemic therapy: Nitrates, beta-blockers, calcium channel blockers
- Antiplatelets and anticoagulants: Aspirin, P2Y12 inhibitors, heparin
- High-risk patients: Early PCI within 24–72 hours
- Statins: Plaque stabilization
- Monitoring: Telemetry for arrhythmias, hemodynamic instability
5. ST Elevation Myocardial Infarction (STEMI)
5.1 Definition
STEMI is full-thickness myocardial infarction with ST-segment elevation on ECG, resulting from complete coronary artery occlusion.
5.2 Pathophysiology
- Plaque rupture with complete thrombosis → cessation of blood flow
- Transmural myocardial necrosis occurs rapidly (minutes to hours)
- Infarcted myocardium cannot contract → decreased cardiac output
- Electrical instability → arrhythmias, conduction blocks
- Inflammatory response leads to healing and scar formation
5.3 Clinical Features
- Sudden, severe chest pain at rest
- Pain lasts >20–30 minutes, unrelieved by rest or nitrates
- Radiation to left arm, jaw, or neck
- Associated symptoms: Sweating, nausea, vomiting, dyspnea, syncope
- Signs: Hypotension, tachycardia, pulmonary congestion if extensive
5.4 Diagnosis
- ECG:
- ST-segment elevation in leads corresponding to infarct territory
- Reciprocal ST depression in opposite leads
- Development of pathological Q waves in hours to days
- Cardiac biomarkers: Troponin and CK-MB elevated
- Coronary angiography: Identifies culprit artery for PCI
5.5 Management
- Immediate reperfusion:
- Percutaneous coronary intervention (PCI) is preferred
- Thrombolytic therapy if PCI unavailable within guideline timelines
- Adjunctive therapy:
- Antiplatelets: Aspirin + P2Y12 inhibitor
- Anticoagulants: Heparin
- Beta-blockers, ACE inhibitors, statins
- Monitoring and supportive care:
- Telemetry for arrhythmias
- Management of heart failure or cardiogenic shock
- Long-term care:
- Cardiac rehabilitation
- Lifestyle modification
- Secondary prevention with medications
6. Comparison of IHD Types
| Feature | Stable Angina | Unstable Angina | NSTEMI | STEMI |
|---|---|---|---|---|
| Cause | Fixed plaque | Plaque disruption | Partial occlusion | Complete occlusion |
| Pain | Exertional | At rest or minimal exertion | Severe, prolonged | Severe, persistent |
| ECG | Normal at rest | ST depression/T inversion or normal | ST depression/T inversion | ST elevation |
| Cardiac biomarkers | Normal | Normal | Elevated troponin | Elevated troponin |
| Infarction | None | None | Subendocardial | Transmural |
| Risk | Low-moderate | High | High | Very high |
| Management | Lifestyle, meds, possible revascularization | Hospitalization, meds, early PCI | Medications + early PCI | Emergent reperfusion therapy |
7. Pathophysiological Continuum
- IHD represents a spectrum from stable plaque to acute rupture:
- Stable plaque → Stable angina
- Plaque instability → Unstable angina
- Partial thrombosis → NSTEMI
- Complete thrombosis → STEMI
- Understanding this continuum guides risk assessment, monitoring, and therapy.
8. Clinical Implications
- Early recognition of ACS (UA/NSTEMI/STEMI) reduces mortality and infarct size.
- Differentiation of stable vs unstable forms guides timing of interventions.
- Risk stratification (TIMI, GRACE) identifies patients for early invasive therapy.
- Chronic management (statins, antiplatelets, beta-blockers) prevents progression from stable angina to ACS.
9. Diagnostic Strategies
- History and physical exam: Characterize chest pain, risk factors
- ECG: Detect ischemia or infarction
- Cardiac biomarkers: Troponin I/T, CK-MB
- Stress testing: Evaluate stable angina
- Coronary angiography: Visualize anatomy, guide PCI
- Imaging: Echocardiography for wall motion abnormalities, viability
10. Treatment Overview
10.1 Lifestyle Measures
- Smoking cessation, exercise, diet, weight management
10.2 Pharmacologic Therapy
- Antianginals: Nitrates, beta-blockers, calcium channel blockers
- Antiplatelets: Aspirin, P2Y12 inhibitors
- Anticoagulants: Heparin, low-molecular-weight heparin
- Statins: LDL reduction, plaque stabilization
- ACE inhibitors/ARBs: Reduce remodeling and blood pressure
10.3 Revascularization
- PCI for occlusive lesions or ACS
- CABG for multi-vessel or left main disease
10.4 Monitoring
- Telemetry for arrhythmias
- Serial ECGs
- Biomarkers to assess infarct progression
11. Prognosis
- Stable angina: Low risk of immediate infarction if well-controlled
- Unstable angina/NSTEMI: High risk; early intervention improves outcomes
- STEMI: High mortality if untreated; early reperfusion critical
- Prognosis improves with risk factor modification, medical therapy, and timely revascularization.
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