SECTION 5: CORONARY AND PERIPHERAL VASCULAR o Metabolic Regulation: Adjust flow to match demand
DISEASE (exercise, stress)
o Autoregulation: Maintains appropriate flow despite BP
changes
273: ISCHEMIC HEART DISEASE
Pathogenesis of Ischemia
Definition & Overview • Atherosclerosis:
• Ischemic Heart Disease (IHD): Condition characterized by inadequate o Reduces ability to increase perfusion when demand rises.
myocardial oxygen supply relative to demand. o Severe lesions reduce resting flow.
• Primary Cause: Atherosclerosis of epicardial coronary arteries • Other Causes:
leading to regional myocardial underperfusion. o Coronary spasm (Prinzmetal's angina)
• Focus of Chapter: Chronic IHD; acute presentations (e.g., ACS) o Thrombi, embolism, ostial narrowing (e.g., aortitis)
discussed separately. o Congenital anomalies (rare in adults)
• Increased Demand Ischemia:
Epidemiology & Global Trends o LVH (e.g., aortic stenosis) → subendocardial ischemia
• Leading Cause of Death & Disability in developed nations. • Reduced O₂ Capacity:
• U.S. Prevalence: ~20.1 million with IHD. o Severe anemia, CO poisoning lowers ischemia threshold.
• Myocardial Infarction (MI) History: 3–4% population prevalence. • Multiple Contributors:
• Risk Factors: o Often combined supply and demand imbalance (e.g., LVH +
o Genetic predisposition anemia + atherosclerosis)
o High-fat, energy-dense diet • Microvascular Angina:
o Smoking o Abnormal constriction/failure to dilate of resistance vessels.
o Sedentary lifestyle
• Socioeconomic Trends: Coronary Atherosclerosis
o Increasing prevalence among low-income groups in • Primary Site: Epicardial arteries
developed countries. • Major Risk Factors:
o Primary prevention efforts have delayed onset to later life. o ↑ LDL, smoking, HTN, DM
• Improvements in Mortality: • Endothelial Dysfunction:
o Decline in IHD mortality attributed ~50% to treatment and o Loss of vasomotor control, antithrombosis, anti-
~50% to prevention. inflammation.
• Emerging Global Trends: o Leads to constriction, thrombosis, leukocyte/platelet
o Obesity, insulin resistance, Type 2 DM are rising adhesion.
worldwide. • Plaque Development:
o Urbanization, Western diets in emerging economies. o Lipid, smooth muscle cells, fibroblasts, matrix
o Rapidly increasing IHD prevalence globally. accumulation.
• Global Burden: • “Vulnerable Vessel” + “Vulnerable Blood”:
o Estimated 197.2 million affected globally. o Hypercoagulability + endothelial dysfunction (esp. in DM).
o Significant contribution to DALYs (Disability-Adjusted Life • Site Preference:
Years). o Branch points (↑ flow turbulence).
• Populations at High Risk: • Degree of Stenosis:
o Men from South Asia (India, Middle East) particularly o >50% diameter reduction: limits demand flow increase.
vulnerable. o >80% reduction: limits resting flow.
• Plaque Rupture:
Pathophysiology of IHD o Exposure of contents triggers platelet aggregation and
Myocardial Oxygen Supply & Demand coagulation cascade → thrombus.
• Demand Factors (MVO₂): • Collateral Circulation:
o Heart rate o Develops with gradual stenosis; sustains rest perfusion but
o Myocardial contractility insufficient during stress.
o Myocardial wall tension (stress)
• Supply Factors: Effects of Ischemia
o Blood oxygen-carrying capacity (inspired O₂, pulmonary Mechanics:
function, hemoglobin) • ↓ O₂ tension leads to regional hypokinesia, akinesia, dyskinesia.
o Coronary blood flow (majority during diastole)
• Affects LV function → transient failure.
• Coronary Resistance Vessels:
o R1: Epicardial arteries • Papillary muscle involvement → mitral regurgitation.
o R2: Prearteriolar vessels Cellular Level:
o R3: Arteriolar/intramyocardial capillaries • Normal: Oxidizes fatty acids, glucose → CO₂ + H₂O.
• Key Regulatory Mechanisms: • Ischemia: Glucose → lactate, ↓ pH, ↓ ATP/creatine phosphate.
• Ion Disturbances: ↑ Na⁺, Ca²⁺ influx; K⁺ leakage.
, • Reversibility: o Substernal, can radiate to shoulders, arms (especially ulnar
o ≤20 mins: reversible (no collaterals) side), back, neck, jaw, teeth, epigastrium.
o >20 mins: irreversible → necrosis. o Rarely radiates above mandible or below umbilicus.
ECG Changes: o Excludes trapezius radiation (typical of pericarditis).
• T-wave inversion: nontransmural ischemia. • Duration:
• ST depression: patchy subendocardial ischemia. o Crescendo-decrescendo in nature.
o Typically lasts 2–5 minutes.
• ST elevation: severe transmural ischemia.
Electrical Instability: • Triggers:
o Physical exertion (exercise, sexual activity, hurrying).
• Can cause ventricular arrhythmias (VT, VF).
o Emotional stress (anger, fright, frustration).
• Sudden cardiac death: often due to ischemia-induced arrhythmias.
• Relief:
Asymptomatic vs. Symptomatic IHD
o Rest or sublingual nitroglycerin within 1–5 minutes.
Asymptomatic IHD: • Nighttime Occurrence:
• Begins <20 years old (autopsy studies). o Can occur at rest (angina decubitus) or during sleep.
o May reflect episodic tachycardia, oxygen desaturation, or
• Silent ischemia: ECG changes without symptoms. increased intrathoracic volume during recumbency.
• Coronary artery calcification (CAC): detected by CT, quantified by
CAC score. ANGINA PATTERNS
• Unrecognized infarcts: found at autopsy (scars, collateral vessels). • Stable Exertional Angina: Fixed threshold; predictable onset at defined
• Silent MI: ~25% not clinically recognized, similar prognosis to exertion level.
symptomatic MI. • Variable Threshold Angina: Varies within the day due to coronary
• Sudden death: often initial manifestation. vasomotor tone changes.
Symptomatic IHD: • Precipitating Factors: Cold exposure, heavy meals, unfamiliar exertion.
• Stable/unstable angina, MI.
• Can fluctuate: symptomatic ↔ asymptomatic ↔ sudden death. ANGINAL EQUIVALENTS (Especially in elderly/diabetics)
• Ischemic cardiomyopathy: • Dyspnea
o Heart failure from chronic ischemic damage, even without • Nausea
prior symptoms. • Fatigue
• Faintness
Key Clinical Takeaways
• IHD results from mismatch between oxygen supply and demand, RISK FACTOR ASSESSMENT IN HISTORY
primarily due to atherosclerosis. • Family history: IHD <55 years (men) or <65 years (women).
• Global burden rising with lifestyle changes in emerging economies. • Diabetes mellitus, hyperlipidemia, hypertension, smoking.
• Multifactorial pathogenesis: demand ↑, supply ↓, endothelial • Peripheral artery disease symptoms (claudication, stroke, TIA).
dysfunction, thrombosis.
• Presentation spectrum: asymptomatic → angina → MI → sudden CLINICAL RED FLAGS (Suggestive of unstable IHD)
death. • Angina with less exertion than before.
• Management strategies depend on understanding supply-demand • Occurs at rest.
dynamics, plaque stability, and myocardial vulnerability.
STABLE ANGINA PECTORIS (SAP)
• Awakens from sleep.
Definition
DIFFERENTIAL DIAGNOSIS (Non-IHD causes of chest pain)
• Episodic clinical syndrome caused by transient myocardial ischemia.
• Sharp, fleeting, localized submammary pain unlikely ischemic.
• Typically occurs when myocardial oxygen demand exceeds supply due
to fixed coronary artery obstruction.
• Chest tenderness, reproducibility suggest musculoskeletal source.
PHYSICAL EXAMINATION
EPIDEMIOLOGY
• ~70% of angina pectoris patients are male, higher proportion <50 years • Often normal when asymptomatic.
old. • Signs of Atherosclerosis:
• In women, presentations are often atypical and occur later (>60 years). o Carotid bruits.
o Peripheral pulses diminished.
CLINICAL HISTORY
o Abdominal aortic aneurysm.
Typical Features • Signs of Risk Factors:
• Occurs typically in men >50 years and women >60 years. o Xanthelasmas, xanthomas (hyperlipidemia).
o Hypertension evidence (AV nicking, light reflex in fundi).
• Described as: o Nicotine stains.
o Heaviness, pressure, squeezing, smothering, or choking.
o Rarely described as sharp pain. • Signs Suggesting Alternative Diagnosis:
o Aortic stenosis/regurgitation murmurs.
• Levine’s Sign: Clenched fist over sternum to describe discomfort. o HOCM murmur.
• Location: o Pulmonary hypertension signs.
, • During Attack: May reveal transient LV failure signs:
o S3/S4, mitral regurgitation murmur, pulmonary edema. Stress Echocardiography
• Rest vs. stress-induced wall motion abnormalities.
LABORATORY EXAMINATION • Dobutamine or exercise-induced ischemia.
• Urinalysis: Diabetes, renal disease. • More sensitive than ECG alone.
• Bloodwork: CMR (Cardiac MRI) Stress Testing
o Lipid profile (Total, LDL, HDL, TG). • Dobutamine-induced ischemia.
o Glucose, HbA1c. • Comprehensive ventricular assessment.
o Creatinine, hematocrit.
o Thyroid function (if indicated). Coronary Calcium Scoring (EBCT / MDCT)
• Other: • Agatston score quantifies calcified plaque.
o hs-CRP (1–3 mg/L): Independent risk factor for IHD. • Correlates with age and atherosclerosis burden.
• Chest X-ray: • Not primary diagnostic tool but adjunctive.
o Assess heart size, ventricular aneurysm, pulmonary
congestion.
FUNCTIONAL CLASSIFICATION (Canadian / NYHA)
ELECTROCARDIOGRAM (ECG) • Canadian Cardiovascular Society Angina Grading:
o I: Only strenuous exertion.
• Often normal at rest. o II: Slight limitation.
• Possible findings: o III: Marked limitation.
o Old MI (Q waves). o IV: Angina at any level, possible rest.
o LVH, repolarization abnormalities (ST/T changes). • NYHA Functional Class: For overall cardiac functional capacity.
o Conduction defects.
• Dynamic changes during angina (ST depression/elevation). CHALLENGES IN DIAGNOSIS
• LVH on ECG = poor prognosis indicator. • Women more often have angina without flow-limiting epicardial disease
(microvascular angina).
STRESS TESTING
• Diagnostic testing may require coronary reactivity testing (adenosine,
Exercise ECG (Treadmill/Bruce Protocol)
acetylcholine).
• Monitors: ECG, BP, symptoms. • Management includes endothelial function improvement:
• Endpoints: o Nitrates, beta-blockers, calcium channel blockers, statins,
o Chest pain, SOB, fatigue. ACE inhibitors.
o ST depression >2 mm. • Abnormal nociception: May respond to imipramine.
o BP drop >10 mmHg. CORONARY ARTERIOGRAPHY (CAG)
o Arrhythmia development. General Principles:
• Positive Test (Ischemia): • Visualizes lumen of coronary arteries; detects or excludes obstructive
o ST depression >1 mm, flat/downsloping, >0.08s duration. coronary artery disease (CAD).
o Upsloping ST changes are nonspecific.
• Does not assess arterial wall pathology; early atherosclerosis without
• Prognostic Indicators: luminal narrowing can go undetected.
o Early onset ST depression.
o Persistence >5 min post-exercise. • Atherosclerosis distribution:
o Failure of BP rise. o Scattered throughout coronary tree
o Common at branch points
• Contraindications: Rest angina <48h, unstable rhythm, severe AS, o Early growth in intima/media causes outward bulging
acute myocarditis, heart failure, PH, endocarditis.
(remodeling) without luminal narrowing.
o Later, growth leads to luminal narrowing and ischemia.
Sensitivity/Specificity
• Sensitivity ~75%. Indications for Coronary Arteriography:
• False positives: Informed by ISCHEMIA Trial (Stable IHD, EF >35%):
o Young asymptomatic men, premenopausal women, digitalis, • Early invasive strategy does not reduce MI or death, but improves
conduction defects, resting ECG abnormalities. angina relief.
• Circumflex disease may result in false negatives. Specific Indications:
1. Severe angina despite medical therapy being considered for PCI or
IMAGING IN STRESS TESTING CABG.
Nuclear Imaging (Thallium-201 / Technetium-99m) 2. Diagnostic uncertainty in symptomatic patients.
• Detect reversible ischemia (perfusion defect on stress, not rest). 3. Survivors of cardiac arrest with possible ischemic etiology.
• PET with N-13 ammonia, rubidium-82. 4. Angina or ischemia on noninvasive testing with LV dysfunction
Pharmacologic Stress (Non-exercise) evidence.
• Adenosine (coronary steal). Other Indications:
• Dobutamine (increases MVO₂). • Negative/nondiagnostic stress tests requiring definitive diagnosis.
• Combined with imaging. • Recurrent admissions with suspected ACS but no diagnosis.
, • Occupations involving public safety (e.g., pilots, firefighters, police) 3. Activity Adjustment: Educate on activity tolerance, pacing tasks.
with suspicious symptoms/tests. 4. Risk Factor Modification:
• Aortic stenosis or HCM with angina—exclude IHD. o Weight loss
• Men >45, women >55 prior to cardiac surgery (valve).
o BP, glucose, lipid control
o Smoking cessation
• Post-MI patients at high risk (recurrent angina, heart failure, o Diet: ↓ saturated/trans fats, calories
arrhythmias). o Physical activity tailored to ischemic threshold
• Suspected coronary spasm or nonatherosclerotic causes (e.g., 5. Drug Therapy
Kawasaki disease). 6. Consider Revascularization
Noninvasive Alternatives: RISK FACTOR TREATMENT DETAILS:
• CT Angiography: Higher radiation vs. conventional CAG. • Obesity: Associated with DM, HTN, dyslipidemia.
• CMR Angiography: Limited by cardiac motion, especially with • Smoking cessation: Essential.
tachycardia. • HTN Management: Lowers LVH, ischemia.
PROGNOSIS IN IHD
• DM Control: LDL <70 mg/dL, BP <130/80.
Key Prognostic Factors: • Dyslipidemia:
• Age o Statins: Mainstay; lower LDL 25–50%.
o PCSK9 inhibitors: Potent LDL-lowering.
• LV function (most critical prognostic indicator) o Other agents: Fibrates, niacin, icosapent ethyl.
• Location/severity of coronary lesions
• Severity/activity of ischemia PHARMACOTHERAPY FOR ANGINA:
High-Risk Indicators: Nitrates:
• New-onset angina, unstable angina, early post-MI angina. • Mechanism: Venodilation → ↓ preload; coronary dilation; NO-mediated
• Angina unresponsive to medical therapy. smooth muscle relaxation.
• Signs/symptoms of heart failure (pulmonary edema, S3, MR). • Uses: Sublingual for acute relief/prophylaxis; long-acting for prevention.
• Echocardiographic, radionuclide, or x-ray evidence of cardiomegaly / • Tolerance management: Drug-free interval daily.
reduced EF (<0.40).
High-Risk Findings on Noninvasive Testing: Beta Blockers:
• Exercise limitations: <6 min, stage II Bruce protocol. • ↓ HR, BP, myocardial O2 demand.
• Strongly positive exercise test: • Post-MI survival benefit.
o ≥0.1 mV ST depression before stage II complete. • Avoid in: asthma, bradycardia, AV block.
o ≥0.2 mV at any stage. • Preferred agents: β1-selective (metoprolol, atenolol).
o ST depression >5 min post-exercise.
o Systolic BP fall >10 mmHg during exercise. Calcium Channel Blockers:
o Exercise-induced VT. • Coronary vasodilation; ↓ contractility.
• Imaging findings: large/multiple perfusion defects, increased lung • Verapamil/diltiazem: Risk of conduction block, bradycardia.
uptake, ↓ EF during stress.
• Dihydropyridines (amlodipine, felodipine): Useful with BBs, especially
• Ambulatory ECG: frequent silent ST deviation. with HTN.
Cardiac Catheterization Prognostic Findings:
• Avoid short-acting dihydropyridines.
• Elevated LVEDP, LV volumes, reduced EF.
• Left main >50% stenosis or proximal LAD stenosis = higher risk. Antiplatelet Agents:
• Plaques with fissures / filling defects = vulnerable lesions. • Aspirin (75–162 mg/d): Reduces events.
• LV dysfunction + CAD = highest mortality. • Clopidogrel: For aspirin intolerance; used with aspirin post-ACS or
• Prognosis worsens with: stenting.
o Established MI • Ticagrelor / Prasugrel: More potent than clopidogrel but ↑ bleeding risk.
o Extent of ischemia
o LV dysfunction Other Therapies:
• Greater number of risk factors (age >75, HTN, dyslipidemia, DM, • ACE inhibitors: For HTN, DM, LV dysfunction.
obesity, PVD, cerebrovascular disease, prior MI) worsens prognosis. • Ranolazine: Inhibits late Na current; for refractory angina.
Novel Prognostic Markers:
• SGLT2 inhibitors: CV protective; BP, weight, glucose control.
• High CRP, extensive coronary calcification, carotid IMT on
ultrasound.
• Avoid NSAIDs; if unavoidable, minimize dose/duration.
• Nicorandil (outside US): K+ channel opener.
TREATMENT OF STABLE ANGINA PECTORIS • Ivabradine: ↓ HR in patients with high resting HR and LV dysfunction.
Management Plan:
1. Education/Reassurance: Disease understanding; encourage activity, Special Considerations:
rehab. • Women with IHD: Underdiagnosed, under-treated; equal benefit from
2. Identify/Treat Aggravating Conditions: HTN, obesity, anemia, statins, BBs, CABG.
hyperthyroidism, hypoxia. • Heart Failure + Angina:
DISEASE (exercise, stress)
o Autoregulation: Maintains appropriate flow despite BP
changes
273: ISCHEMIC HEART DISEASE
Pathogenesis of Ischemia
Definition & Overview • Atherosclerosis:
• Ischemic Heart Disease (IHD): Condition characterized by inadequate o Reduces ability to increase perfusion when demand rises.
myocardial oxygen supply relative to demand. o Severe lesions reduce resting flow.
• Primary Cause: Atherosclerosis of epicardial coronary arteries • Other Causes:
leading to regional myocardial underperfusion. o Coronary spasm (Prinzmetal's angina)
• Focus of Chapter: Chronic IHD; acute presentations (e.g., ACS) o Thrombi, embolism, ostial narrowing (e.g., aortitis)
discussed separately. o Congenital anomalies (rare in adults)
• Increased Demand Ischemia:
Epidemiology & Global Trends o LVH (e.g., aortic stenosis) → subendocardial ischemia
• Leading Cause of Death & Disability in developed nations. • Reduced O₂ Capacity:
• U.S. Prevalence: ~20.1 million with IHD. o Severe anemia, CO poisoning lowers ischemia threshold.
• Myocardial Infarction (MI) History: 3–4% population prevalence. • Multiple Contributors:
• Risk Factors: o Often combined supply and demand imbalance (e.g., LVH +
o Genetic predisposition anemia + atherosclerosis)
o High-fat, energy-dense diet • Microvascular Angina:
o Smoking o Abnormal constriction/failure to dilate of resistance vessels.
o Sedentary lifestyle
• Socioeconomic Trends: Coronary Atherosclerosis
o Increasing prevalence among low-income groups in • Primary Site: Epicardial arteries
developed countries. • Major Risk Factors:
o Primary prevention efforts have delayed onset to later life. o ↑ LDL, smoking, HTN, DM
• Improvements in Mortality: • Endothelial Dysfunction:
o Decline in IHD mortality attributed ~50% to treatment and o Loss of vasomotor control, antithrombosis, anti-
~50% to prevention. inflammation.
• Emerging Global Trends: o Leads to constriction, thrombosis, leukocyte/platelet
o Obesity, insulin resistance, Type 2 DM are rising adhesion.
worldwide. • Plaque Development:
o Urbanization, Western diets in emerging economies. o Lipid, smooth muscle cells, fibroblasts, matrix
o Rapidly increasing IHD prevalence globally. accumulation.
• Global Burden: • “Vulnerable Vessel” + “Vulnerable Blood”:
o Estimated 197.2 million affected globally. o Hypercoagulability + endothelial dysfunction (esp. in DM).
o Significant contribution to DALYs (Disability-Adjusted Life • Site Preference:
Years). o Branch points (↑ flow turbulence).
• Populations at High Risk: • Degree of Stenosis:
o Men from South Asia (India, Middle East) particularly o >50% diameter reduction: limits demand flow increase.
vulnerable. o >80% reduction: limits resting flow.
• Plaque Rupture:
Pathophysiology of IHD o Exposure of contents triggers platelet aggregation and
Myocardial Oxygen Supply & Demand coagulation cascade → thrombus.
• Demand Factors (MVO₂): • Collateral Circulation:
o Heart rate o Develops with gradual stenosis; sustains rest perfusion but
o Myocardial contractility insufficient during stress.
o Myocardial wall tension (stress)
• Supply Factors: Effects of Ischemia
o Blood oxygen-carrying capacity (inspired O₂, pulmonary Mechanics:
function, hemoglobin) • ↓ O₂ tension leads to regional hypokinesia, akinesia, dyskinesia.
o Coronary blood flow (majority during diastole)
• Affects LV function → transient failure.
• Coronary Resistance Vessels:
o R1: Epicardial arteries • Papillary muscle involvement → mitral regurgitation.
o R2: Prearteriolar vessels Cellular Level:
o R3: Arteriolar/intramyocardial capillaries • Normal: Oxidizes fatty acids, glucose → CO₂ + H₂O.
• Key Regulatory Mechanisms: • Ischemia: Glucose → lactate, ↓ pH, ↓ ATP/creatine phosphate.
• Ion Disturbances: ↑ Na⁺, Ca²⁺ influx; K⁺ leakage.
, • Reversibility: o Substernal, can radiate to shoulders, arms (especially ulnar
o ≤20 mins: reversible (no collaterals) side), back, neck, jaw, teeth, epigastrium.
o >20 mins: irreversible → necrosis. o Rarely radiates above mandible or below umbilicus.
ECG Changes: o Excludes trapezius radiation (typical of pericarditis).
• T-wave inversion: nontransmural ischemia. • Duration:
• ST depression: patchy subendocardial ischemia. o Crescendo-decrescendo in nature.
o Typically lasts 2–5 minutes.
• ST elevation: severe transmural ischemia.
Electrical Instability: • Triggers:
o Physical exertion (exercise, sexual activity, hurrying).
• Can cause ventricular arrhythmias (VT, VF).
o Emotional stress (anger, fright, frustration).
• Sudden cardiac death: often due to ischemia-induced arrhythmias.
• Relief:
Asymptomatic vs. Symptomatic IHD
o Rest or sublingual nitroglycerin within 1–5 minutes.
Asymptomatic IHD: • Nighttime Occurrence:
• Begins <20 years old (autopsy studies). o Can occur at rest (angina decubitus) or during sleep.
o May reflect episodic tachycardia, oxygen desaturation, or
• Silent ischemia: ECG changes without symptoms. increased intrathoracic volume during recumbency.
• Coronary artery calcification (CAC): detected by CT, quantified by
CAC score. ANGINA PATTERNS
• Unrecognized infarcts: found at autopsy (scars, collateral vessels). • Stable Exertional Angina: Fixed threshold; predictable onset at defined
• Silent MI: ~25% not clinically recognized, similar prognosis to exertion level.
symptomatic MI. • Variable Threshold Angina: Varies within the day due to coronary
• Sudden death: often initial manifestation. vasomotor tone changes.
Symptomatic IHD: • Precipitating Factors: Cold exposure, heavy meals, unfamiliar exertion.
• Stable/unstable angina, MI.
• Can fluctuate: symptomatic ↔ asymptomatic ↔ sudden death. ANGINAL EQUIVALENTS (Especially in elderly/diabetics)
• Ischemic cardiomyopathy: • Dyspnea
o Heart failure from chronic ischemic damage, even without • Nausea
prior symptoms. • Fatigue
• Faintness
Key Clinical Takeaways
• IHD results from mismatch between oxygen supply and demand, RISK FACTOR ASSESSMENT IN HISTORY
primarily due to atherosclerosis. • Family history: IHD <55 years (men) or <65 years (women).
• Global burden rising with lifestyle changes in emerging economies. • Diabetes mellitus, hyperlipidemia, hypertension, smoking.
• Multifactorial pathogenesis: demand ↑, supply ↓, endothelial • Peripheral artery disease symptoms (claudication, stroke, TIA).
dysfunction, thrombosis.
• Presentation spectrum: asymptomatic → angina → MI → sudden CLINICAL RED FLAGS (Suggestive of unstable IHD)
death. • Angina with less exertion than before.
• Management strategies depend on understanding supply-demand • Occurs at rest.
dynamics, plaque stability, and myocardial vulnerability.
STABLE ANGINA PECTORIS (SAP)
• Awakens from sleep.
Definition
DIFFERENTIAL DIAGNOSIS (Non-IHD causes of chest pain)
• Episodic clinical syndrome caused by transient myocardial ischemia.
• Sharp, fleeting, localized submammary pain unlikely ischemic.
• Typically occurs when myocardial oxygen demand exceeds supply due
to fixed coronary artery obstruction.
• Chest tenderness, reproducibility suggest musculoskeletal source.
PHYSICAL EXAMINATION
EPIDEMIOLOGY
• ~70% of angina pectoris patients are male, higher proportion <50 years • Often normal when asymptomatic.
old. • Signs of Atherosclerosis:
• In women, presentations are often atypical and occur later (>60 years). o Carotid bruits.
o Peripheral pulses diminished.
CLINICAL HISTORY
o Abdominal aortic aneurysm.
Typical Features • Signs of Risk Factors:
• Occurs typically in men >50 years and women >60 years. o Xanthelasmas, xanthomas (hyperlipidemia).
o Hypertension evidence (AV nicking, light reflex in fundi).
• Described as: o Nicotine stains.
o Heaviness, pressure, squeezing, smothering, or choking.
o Rarely described as sharp pain. • Signs Suggesting Alternative Diagnosis:
o Aortic stenosis/regurgitation murmurs.
• Levine’s Sign: Clenched fist over sternum to describe discomfort. o HOCM murmur.
• Location: o Pulmonary hypertension signs.
, • During Attack: May reveal transient LV failure signs:
o S3/S4, mitral regurgitation murmur, pulmonary edema. Stress Echocardiography
• Rest vs. stress-induced wall motion abnormalities.
LABORATORY EXAMINATION • Dobutamine or exercise-induced ischemia.
• Urinalysis: Diabetes, renal disease. • More sensitive than ECG alone.
• Bloodwork: CMR (Cardiac MRI) Stress Testing
o Lipid profile (Total, LDL, HDL, TG). • Dobutamine-induced ischemia.
o Glucose, HbA1c. • Comprehensive ventricular assessment.
o Creatinine, hematocrit.
o Thyroid function (if indicated). Coronary Calcium Scoring (EBCT / MDCT)
• Other: • Agatston score quantifies calcified plaque.
o hs-CRP (1–3 mg/L): Independent risk factor for IHD. • Correlates with age and atherosclerosis burden.
• Chest X-ray: • Not primary diagnostic tool but adjunctive.
o Assess heart size, ventricular aneurysm, pulmonary
congestion.
FUNCTIONAL CLASSIFICATION (Canadian / NYHA)
ELECTROCARDIOGRAM (ECG) • Canadian Cardiovascular Society Angina Grading:
o I: Only strenuous exertion.
• Often normal at rest. o II: Slight limitation.
• Possible findings: o III: Marked limitation.
o Old MI (Q waves). o IV: Angina at any level, possible rest.
o LVH, repolarization abnormalities (ST/T changes). • NYHA Functional Class: For overall cardiac functional capacity.
o Conduction defects.
• Dynamic changes during angina (ST depression/elevation). CHALLENGES IN DIAGNOSIS
• LVH on ECG = poor prognosis indicator. • Women more often have angina without flow-limiting epicardial disease
(microvascular angina).
STRESS TESTING
• Diagnostic testing may require coronary reactivity testing (adenosine,
Exercise ECG (Treadmill/Bruce Protocol)
acetylcholine).
• Monitors: ECG, BP, symptoms. • Management includes endothelial function improvement:
• Endpoints: o Nitrates, beta-blockers, calcium channel blockers, statins,
o Chest pain, SOB, fatigue. ACE inhibitors.
o ST depression >2 mm. • Abnormal nociception: May respond to imipramine.
o BP drop >10 mmHg. CORONARY ARTERIOGRAPHY (CAG)
o Arrhythmia development. General Principles:
• Positive Test (Ischemia): • Visualizes lumen of coronary arteries; detects or excludes obstructive
o ST depression >1 mm, flat/downsloping, >0.08s duration. coronary artery disease (CAD).
o Upsloping ST changes are nonspecific.
• Does not assess arterial wall pathology; early atherosclerosis without
• Prognostic Indicators: luminal narrowing can go undetected.
o Early onset ST depression.
o Persistence >5 min post-exercise. • Atherosclerosis distribution:
o Failure of BP rise. o Scattered throughout coronary tree
o Common at branch points
• Contraindications: Rest angina <48h, unstable rhythm, severe AS, o Early growth in intima/media causes outward bulging
acute myocarditis, heart failure, PH, endocarditis.
(remodeling) without luminal narrowing.
o Later, growth leads to luminal narrowing and ischemia.
Sensitivity/Specificity
• Sensitivity ~75%. Indications for Coronary Arteriography:
• False positives: Informed by ISCHEMIA Trial (Stable IHD, EF >35%):
o Young asymptomatic men, premenopausal women, digitalis, • Early invasive strategy does not reduce MI or death, but improves
conduction defects, resting ECG abnormalities. angina relief.
• Circumflex disease may result in false negatives. Specific Indications:
1. Severe angina despite medical therapy being considered for PCI or
IMAGING IN STRESS TESTING CABG.
Nuclear Imaging (Thallium-201 / Technetium-99m) 2. Diagnostic uncertainty in symptomatic patients.
• Detect reversible ischemia (perfusion defect on stress, not rest). 3. Survivors of cardiac arrest with possible ischemic etiology.
• PET with N-13 ammonia, rubidium-82. 4. Angina or ischemia on noninvasive testing with LV dysfunction
Pharmacologic Stress (Non-exercise) evidence.
• Adenosine (coronary steal). Other Indications:
• Dobutamine (increases MVO₂). • Negative/nondiagnostic stress tests requiring definitive diagnosis.
• Combined with imaging. • Recurrent admissions with suspected ACS but no diagnosis.
, • Occupations involving public safety (e.g., pilots, firefighters, police) 3. Activity Adjustment: Educate on activity tolerance, pacing tasks.
with suspicious symptoms/tests. 4. Risk Factor Modification:
• Aortic stenosis or HCM with angina—exclude IHD. o Weight loss
• Men >45, women >55 prior to cardiac surgery (valve).
o BP, glucose, lipid control
o Smoking cessation
• Post-MI patients at high risk (recurrent angina, heart failure, o Diet: ↓ saturated/trans fats, calories
arrhythmias). o Physical activity tailored to ischemic threshold
• Suspected coronary spasm or nonatherosclerotic causes (e.g., 5. Drug Therapy
Kawasaki disease). 6. Consider Revascularization
Noninvasive Alternatives: RISK FACTOR TREATMENT DETAILS:
• CT Angiography: Higher radiation vs. conventional CAG. • Obesity: Associated with DM, HTN, dyslipidemia.
• CMR Angiography: Limited by cardiac motion, especially with • Smoking cessation: Essential.
tachycardia. • HTN Management: Lowers LVH, ischemia.
PROGNOSIS IN IHD
• DM Control: LDL <70 mg/dL, BP <130/80.
Key Prognostic Factors: • Dyslipidemia:
• Age o Statins: Mainstay; lower LDL 25–50%.
o PCSK9 inhibitors: Potent LDL-lowering.
• LV function (most critical prognostic indicator) o Other agents: Fibrates, niacin, icosapent ethyl.
• Location/severity of coronary lesions
• Severity/activity of ischemia PHARMACOTHERAPY FOR ANGINA:
High-Risk Indicators: Nitrates:
• New-onset angina, unstable angina, early post-MI angina. • Mechanism: Venodilation → ↓ preload; coronary dilation; NO-mediated
• Angina unresponsive to medical therapy. smooth muscle relaxation.
• Signs/symptoms of heart failure (pulmonary edema, S3, MR). • Uses: Sublingual for acute relief/prophylaxis; long-acting for prevention.
• Echocardiographic, radionuclide, or x-ray evidence of cardiomegaly / • Tolerance management: Drug-free interval daily.
reduced EF (<0.40).
High-Risk Findings on Noninvasive Testing: Beta Blockers:
• Exercise limitations: <6 min, stage II Bruce protocol. • ↓ HR, BP, myocardial O2 demand.
• Strongly positive exercise test: • Post-MI survival benefit.
o ≥0.1 mV ST depression before stage II complete. • Avoid in: asthma, bradycardia, AV block.
o ≥0.2 mV at any stage. • Preferred agents: β1-selective (metoprolol, atenolol).
o ST depression >5 min post-exercise.
o Systolic BP fall >10 mmHg during exercise. Calcium Channel Blockers:
o Exercise-induced VT. • Coronary vasodilation; ↓ contractility.
• Imaging findings: large/multiple perfusion defects, increased lung • Verapamil/diltiazem: Risk of conduction block, bradycardia.
uptake, ↓ EF during stress.
• Dihydropyridines (amlodipine, felodipine): Useful with BBs, especially
• Ambulatory ECG: frequent silent ST deviation. with HTN.
Cardiac Catheterization Prognostic Findings:
• Avoid short-acting dihydropyridines.
• Elevated LVEDP, LV volumes, reduced EF.
• Left main >50% stenosis or proximal LAD stenosis = higher risk. Antiplatelet Agents:
• Plaques with fissures / filling defects = vulnerable lesions. • Aspirin (75–162 mg/d): Reduces events.
• LV dysfunction + CAD = highest mortality. • Clopidogrel: For aspirin intolerance; used with aspirin post-ACS or
• Prognosis worsens with: stenting.
o Established MI • Ticagrelor / Prasugrel: More potent than clopidogrel but ↑ bleeding risk.
o Extent of ischemia
o LV dysfunction Other Therapies:
• Greater number of risk factors (age >75, HTN, dyslipidemia, DM, • ACE inhibitors: For HTN, DM, LV dysfunction.
obesity, PVD, cerebrovascular disease, prior MI) worsens prognosis. • Ranolazine: Inhibits late Na current; for refractory angina.
Novel Prognostic Markers:
• SGLT2 inhibitors: CV protective; BP, weight, glucose control.
• High CRP, extensive coronary calcification, carotid IMT on
ultrasound.
• Avoid NSAIDs; if unavoidable, minimize dose/duration.
• Nicorandil (outside US): K+ channel opener.
TREATMENT OF STABLE ANGINA PECTORIS • Ivabradine: ↓ HR in patients with high resting HR and LV dysfunction.
Management Plan:
1. Education/Reassurance: Disease understanding; encourage activity, Special Considerations:
rehab. • Women with IHD: Underdiagnosed, under-treated; equal benefit from
2. Identify/Treat Aggravating Conditions: HTN, obesity, anemia, statins, BBs, CABG.
hyperthyroidism, hypoxia. • Heart Failure + Angina:
