Acute Coronary Syndromes (ACS) and Ischemic Heart Disease

Overview of Ischemic Heart Disease (IHD) and Acute Coronary Syndromes (ACS)

Ischemic Heart Disease (IHD), also known as Coronary Artery Disease (CAD) or Coronary Heart Disease (CHD), is characterized by an inadequate oxygen supply to the myocardium due to narrowed or blocked coronary arteries. Acute Coronary Syndromes (ACS) represent a spectrum of clinical conditions associated with acute myocardial ischemia and include unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI).

• Stable Angina: Predictable chest pain with exertion, relieved by rest or nitroglycerin.

• Unstable Angina (UA): Unpredictable chest pain, often at rest, not relieved by nitroglycerin, may progress to MI.

• Myocardial Infarction (MI): Necrosis of myocardial tissue due to prolonged ischemia; classified as STEMI or NSTEMI based on ECG findings.

Pathophysiology of Atherosclerosis and ACS

Atherosclerosis is the underlying cause of most cases of IHD and ACS. It involves the accumulation of fatty deposits (plaque) within the arterial wall, leading to narrowing (stenosis) and reduced blood flow. Plaque rupture can trigger clot formation, resulting in partial or complete occlusion of the coronary artery.

• Plaque Formation: Composed of cholesterol, fatty substances, fibrin, and blood cells.

• Consequences: Can lead to stable angina, ACS, stroke, and peripheral artery disease (PAD).

Types of Angina and ACS

• Chronic Stable Angina: Predictable, exertion-induced chest pain, no/minimal ECG changes, normal troponin.

• Unstable Angina: Occurs at rest, unpredictable, ST depression or T-wave inversion on ECG, normal troponin.

• NSTEMI: Similar to UA but with elevated troponin, indicating myocardial injury.

• STEMI: Complete coronary artery occlusion, ST elevation on ECG, elevated troponin, myocardial necrosis.

Clinical Presentation and Risk Factors

Symptoms of ACS and Angina

• ACS: Chest heaviness, pressure, pain radiating to jaw/shoulder/arms, shortness of breath, diaphoresis, nausea/vomiting, lasts >5 minutes, not relieved by nitroglycerin, unpredictable onset.

• Stable Angina: Chest discomfort with exertion, relieved by rest or nitroglycerin, lasts ≤5 minutes, predictable onset.

• Atypical Symptoms: More common in women, elderly, and diabetics—may include vomiting, sweating, weakness, dizziness, fainting, or dyspepsia.

Risk Factors and Aggravating Factors

• Major Risk Factors: Hypertension, dyslipidemia, diabetes mellitus, chronic kidney disease, age, male sex, family history of premature MI, prior ACS, obesity, physical inactivity, smoking.

• Aggravating Factors: Cold exposure, physical exertion, emotional stress, hypotension/hypertension, arrhythmias.

• Drug Causes: NSAIDs, stimulants (cocaine, amphetamines), oral contraceptives, alcohol.

Diagnosis of ACS and Stable Angina

Diagnostic Tools

• Electrocardiogram (ECG): 12-lead ECG is essential for differentiating STEMI from NSTEMI/UA.

• Cardiac Biomarkers: Troponin I/T (preferred for sensitivity and specificity), CK-MB, and other non-specific markers (ALT/AST, LDH, myoglobin).

• Exercise Tolerance/Stress Tests: Assess myocardial perfusion during exertion.

• Coronary Angiogram: Visualizes coronary artery blockages using contrast dye.

Key Diagnostic Criteria Table

Management of ACS and Stable Angina

Goals of Therapy

• Restore blood flow to the infarcted artery (especially in STEMI).

• Prevent total occlusion (NSTEMI/UA).

• Reduce infarct size, prevent death/complications, relieve ischemic symptoms, minimize medication side effects.

Non-Pharmacological Measures

• Continuous ECG monitoring for high-risk patients.

• Coronary Artery Bypass Graft (CABG) or Percutaneous Coronary Intervention (PCI) as indicated.

• Rehabilitation, weight management, exercise programs, stress management.

Pharmacological Management

• Dual Antiplatelet Therapy (DAPT): ASA (lifetime) + P2Y12 inhibitor (usually 12 months).

• High-Intensity Statin: Target LDL <1.8 mmol/L or ≥50% reduction.

• Beta Blockers (BB): Mortality benefit, especially post-MI or with reduced LVEF.

• ACE Inhibitors (ACEi): Mortality benefit, especially with HTN, diabetes, LVEF <40%, or CKD.

• Nitrates: SL for acute relief, long-acting for chronic management (with nitrate-free interval to prevent tolerance).

• Heparin (UFH/LMWH): Anticoagulation during acute management.

• Other: Oxygen (if O2 <90%), morphine for pain, CCBs if BBs contraindicated (not in STEMI).

STEMI Treatment Algorithm

• ASA 160-325 mg STAT, NTG IV if SL ineffective, BB (when stable), heparin, P2Y12 inhibitor, O2/morphine PRN.

• PCI preferred within 120 minutes (ideally 90 minutes); if not feasible, thrombolysis within 12 hours of symptom onset.

• Continue DAPT, high-intensity statin, BB, ACEi, DVT prophylaxis if not ambulatory.

NSTEMI/UA Treatment Algorithm

• ASA, NTG, BB (or CCB if contraindicated), heparin, P2Y12 inhibitor, O2/morphine PRN.

• High-risk patients: Consider PCI +/- glycoprotein IIb/IIIa inhibitor.

• Continue DAPT, optimize antianginals, start ACEi and statin.

Stable Angina Management

• Symptom relief: Nitroglycerin (SL or spray), BB, long-acting CCB (avoid short-acting nifedipine).

• Mortality benefit: Antiplatelet (ASA or clopidogrel), BB, high-intensity statin, ACEi/ARB.

• Consider GLP1 agonists or SGLT2 inhibitors in type 2 diabetes for CV benefit.

• Stop NSAIDs and HRT due to increased CV risk.

Clinical Considerations and Special Populations

• Hold clopidogrel/ticagrelor before CABG (2-7 days/2-3 days, respectively).

• LMWH preferred over UFH except in renal dysfunction (CrCl ≤30 mL/min).

• Fibrinolysis (alteplase/tenecteplase) for STEMI within 12 hours of symptom onset; contraindications include history of stroke, recent surgery, active bleeding, severe hypertension.

• Educate patients and families on recognizing symptoms and when to seek emergency care.

Case Studies: Application of Knowledge

Case 1: 65-year-old Female with ACS

• Major risk factor: Type 2 diabetes mellitus.

• Immediate medication to reduce myocardial O2 demand: Metoprolol (beta-blocker).

• ASA therapy duration post-ACS: Indefinitely.

• Drug class worsening CV outcomes: NSAIDs.

Case 2: 58-year-old Male with Stable Angina

• Most likely diagnosis: Stable angina.

• Most likely trigger: Physical exertion.

• Next management step: Initiate a beta-blocker.

• Drug without proven mortality benefit in stable angina: Nitrates.

Summary Table: Pharmacological Measures in ACS and Stable Angina

Key Equations and Definitions

• Oxygen Supply vs. Demand: ACS results from an imbalance between myocardial oxygen supply and demand.

• Troponin: Cardiac biomarker for myocardial injury; elevation indicates MI.

• ECG Changes: ST elevation (STEMI), ST depression/T-wave inversion (NSTEMI/UA), or normal (stable angina).

Additional info: For further reading, refer to the Canadian Cardiovascular Society Guidelines and UpToDate resources on ACS and stable ischemic heart disease.