Ischemic Heart Disease¶
Chapter 284 | Part 6: Cardiovascular Disorders
KEY CLINICAL POINTS¶
- Ischemic heart disease (IHD) is the leading cause of mortality globally, driven by atherosclerosis, which disrupts myocardial oxygen supply-demand balance.
- Key diagnostic tools include 12-lead ECG, stress testing (exercise, pharmacologic, or imaging), and coronary angiography to assess coronary anatomy.
- Management involves risk factor modification, medical therapy (nitrates, beta-blockers, statins), and revascularization (PCI/CABG) for severe cases.
1. DEFINITION & OVERVIEW¶
Ischemic heart disease (IHD) refers to myocardial ischemia due to inadequate oxygen supply, typically from coronary artery atherosclerosis. It encompasses stable angina, unstable angina, myocardial infarction, and chronic ischemic heart failure.
Macrocirculation vs. Microcirculation¶
| Segment | Size | Function | Resistance Contribution |
|---|---|---|---|
| Epicardial arteries | >400 µm | Supply large myocardial regions | R1 |
| Small arteries | <400 µm | Regulate regional perfusion | R2 |
| Arterioles | <100 µm | Control microvascular flow | R3 |
| Capillaries | <10 µm | Exchange oxygen/nutrients | N/A |
1.1 Pathophysiology¶
IHD arises from a mismatch between myocardial oxygen supply and demand. Atherosclerosis narrows coronary arteries, reducing blood flow. Key determinants of myocardial oxygen demand include heart rate, contractility, and wall tension. Coronary flow is regulated by autoregulation and metabolic factors.
1.2 Clinical Spectrum¶
IHD ranges from asymptomatic coronary artery disease to acute coronary syndromes. Silent ischemia and microvascular angina are distinct entities with atypical presentations.
2. EPIDEMIOLOGY¶
IHD is the leading cause of death globally, with 18 million annual deaths. Prevalence is rising due to aging populations, urbanization, and lifestyle factors. In the US, ~20.5 million have IHD, with 3-4% experiencing myocardial infarction annually.
Functional Classification of Angina (Canadian Cardiac Society)¶
| Class | Description |
|---|---|
| I | No limitation of physical activity |
| II | Mild limitation, angina with exertion |
| III | Marked limitation, angina with minimal exertion |
| IV | Inability to perform any physical activity without angina |
2.1 Risk Factors¶
Modifiable: hypertension, hyperlipidemia, diabetes, obesity, smoking. Non-modifiable: age, family history, male sex, and ethnic predisposition.
2.2 Global Trends¶
Emerging economies show rising IHD rates due to Westernized diets. Women's risk increases post-menopause, with diabetes exacerbating atherogenesis.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Atherosclerosis is the primary cause, with plaque rupture and thrombosis leading to acute coronary syndromes. Microvascular dysfunction and coronary vasospasm contribute to variant angina.
Mechanisms of Myocardial Ischemia¶
| Mechanism | Effect |
|---|---|
| Oxygen supply < demand | Angina, ST-segment depression |
| Plaque rupture | Acute coronary syndrome |
| Microvascular dysfunction | Angina without obstructive CAD |
| Reperfusion injury | Myocardial necrosis, arrhythmias |
3.1 Atherosclerosis Mechanisms¶
LDL accumulation, endothelial dysfunction, inflammation, and foam cell formation drive plaque progression. Vulnerable plaques with high lipid content and low fibrous cap are prone to rupture.
3.2 Ischemia Effects¶
Transient ischemia causes ST-segment changes, while prolonged ischemia leads to necrosis. Myocardial stunning and hibernation occur with reperfusion.
4. CLINICAL FEATURES¶
Symptoms include chest discomfort (pressure, squeezing), dyspnea, fatigue. Atypical presentations are common in women and diabetics. Complications include heart failure, arrhythmias, and sudden cardiac death.
ECG Findings in Ischemia¶
| Finding | Clinical Correlation |
|---|---|
| ST-segment depression | Subendocardial ischemia |
| Finding | Clinical Correlation |
|---|---|
| ST-segment elevation | Transmural infarction |
| T-wave inversion | Myocardial injury or ischemia |
| Arrhythmias | Electrical instability |
4.1 Stable vs. Unstable Angina¶
Stable: predictable triggers, no new ECG changes. Unstable: new or worsening symptoms, ST-segment elevation, or new left bundle branch block.
4.2 Silent Ischemia¶
Asymptomatic myocardial ischemia detected by ECG or stress testing, more common in diabetics and elderly. Linked to increased mortality.
5. DIFFERENTIAL DIAGNOSIS¶
Distinguish IHD from pericarditis, myocarditis, pulmonary embolism, and cardiac arrhythmias. Atypical presentations in women and diabetics require careful evaluation.
5.1 Non-Cardiac Causes¶
Gastroesophageal reflux, musculoskeletal pain, anemia, and panic disorder can mimic angina.
5.2 Atypical Syndromes¶
Microvascular angina, coronary artery spasm, and cardiac neurosis present with chest discomfort without obstructive CAD.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis combines clinical assessment, ECG, stress testing, and imaging. Non-invasive tests include stress echocardiography, nuclear perfusion imaging, and coronary CT angiography.
Metabolic Equivalent Tasks (METs) by Functional Class¶
| Functional Class | METs |
|---|---|
| I | 5–7 |
| II | 3–5 |
| III | 1–3 |
| IV | <1 |
6.1 Stress Testing¶
Exercise ECG (Bruce protocol) or pharmacologic stress (adenosine, dobutamine) detects ischemia. Sensitivity ~75% for CAD detection.
6.2 Imaging Modalities¶
Coronary CT angiography (CCTA) assesses plaque burden and stenosis. Cardiac MRI evaluates myocardial viability and infarction.
7. MANAGEMENT & TREATMENT¶
Multimodal approach includes risk factor modification, medical therapy, and revascularization. Lifestyle changes, statins, beta-blockers, and nitrates form the cornerstone of treatment.
Antiplatelet Agents¶
| Drug | Dose | Use |
|---|---|---|
| Aspirin | 75–162 mg/d | Baseline therapy |
| Clopidogrel | 75 mg/d | With aspirin for ACS or stent placement |
| Prasugrel | 10 mg/d | For ACS patients |
| Ticagrelor | 90 mg bid | For ACS patients |
7.1 Medical Therapy¶
Antiplatelets (aspirin, clopidogrel), statins (atorvastatin, rosuvastatin), beta-blockers (metoprolol, bisoprolol), nitrates, and calcium channel blockers (dihydropyridines).
7.2 Revascularization¶
PCI for single-vessel disease; CABG for multivessel or left main disease. Drug-eluting stents reduce restenosis risk.
8. PROGNOSIS & COMPLICATIONS¶
Mortality is highest in left main or multivessel disease. Complications include heart failure, arrhythmias, and sudden cardiac death. Long-term outcomes depend on revascularization and risk factor control.
8.1 Predictors of Outcome¶
Left ventricular dysfunction, diabetes, and incomplete revascularization worsen prognosis. Early revascularization improves survival in high-risk patients.
8.2 Long-Term Risks¶
Recurrence of angina, myocardial infarction, and cardiovascular mortality persist despite optimal medical therapy.
9. SPECIAL CONSIDERATIONS¶
Women and diabetics have atypical presentations. Elderly patients require cautious drug dosing. Pregnancy necessitates avoidance of certain medications (e.g., ACE inhibitors).
9.1 Women with IHD¶
Atypical symptoms (e.g., dyspnea, fatigue). Higher risk of microvascular disease and worse outcomes post-MI.
10. KEY POINTS & CLINICAL PEARLS¶
- IHD management requires aggressive risk factor modification and early revascularization in high-risk patients.
- Stress testing is essential for diagnosing ischemia and guiding treatment decisions.
- PCI is preferred for single-vessel disease; CABG is optimal for multivessel or left main disease.
- Asymptomatic ischemia is common in diabetics and correlates with increased mortality.
- Long-term dual antiplatelet therapy (DAPT) reduces stent thrombosis but increases bleeding risk.