N334: Coronary Artery Disease and Acute Coronary Syndrome

Coronary Artery Disease (CAD)

Narrowing or blockage of the coronary arteries due to atherosclerosis

• Pathophysiology: Plaque buildup reduces oxygenated blood flow to the myocardium

• Risks Factors:

  • Modifiable: Smoking, obesity, hypertension, dyslipidemia

  • Non-modifiable: Age, family, history, genetics

• Contributing Factors:

  • DM, Metabolic Syndrome, Homocysteine Level

  • Psychological States, Mood Disorders

Myocardial Ischemia

Oxygen demand > oxygen supply

• Myocardial oxygen demand exceeds the available supply from coronary blood flow, leading to insufficient oxygen delivery to the heart muscle

• S/S: Chest pain or discomfort, radiating pain (shoulder, neck, arms, back, teeth, or jaw), SOB, N/V, sweating, fatigue, dizziness, symptoms during exertion (improves with rest)

  • Angina: Chest pain resulting from lack of oxygen

Collateral Circulation Response

Forms as a response to ensure adequate blood supply when primary coronary arteries are compromised

• Helps maintain heart function and reduce the severity of angina

ACS Testing

• EKG: First-line; differentiates UA, NSTEMI, STEMI; shows ischemia/injury (decreased T and ST; increased ST and Q)

• Serial Cardiac Biomarkers:

  • hs-Troponin I/T (most specific): Check at 0, 3, 6 hours; high or rising/falling levels suggest heart injury (MI)

    • Troponin is released when heart muscle is damaged

  • CK-MB: Check at 0, 6, 12 hours; > 5 ng/mL or >5% of total CK suggest heart injury

• Imaging:

  • Echocardiogram: Heart function and wall motion

  • Coronary Angiography: Diagnostic test that uses a catheter and dye to view coronary arteries and plan revascularization

Approaches to Angina

• Rapid 12-Lead ECG: In 10 minutes after arrival to check for ACS

• High-Sensitivity Troponin: Detect myocardial infarction (MI)

• Immediate Medications:

  • Aspirin: First medication given; 162-325 mg orally to inhibit platelet aggregation

  • Nitroglycerin (NTG): Sublingual administration for chest pain (angina); avoid in hypotensive patients (<90 mmHg) or those using PDE5 inhibitors (e.g., sildenafil)

  • Morphine: Use if chest pain persists despite NTG treatment

• Oxygen: Administer if hypoxic (SaO2 < 90%) or in respiratory distress

• Risk and Imaging: Assess risk and cause of chest pain

• Early Re-perfusion Therapy: Consider PCI within 90 min if STEMI diagnosis

Acute Coronary Syndrome (ACS)

A spectrum of conditions associated with reduced blood flow to the heart

• Three Main Types:

  • Stable Angina

  • Unstable Angina (UA)

  • Myocardial Infarction (MI): STEMI and NSTEMI

• Etiology: Most caused by plaque rupture and thrombosis leading to reduced coronary perfusion

Stable Angina

Predictable chest pain triggered by exertion or stress, relieved by rest or nitroglycerin

• Diagnosis:

  • Electrocardiogram (ECG): Typically normal, unless during an episode

    • Typically will have an angiography as well

  • Stress Test: Used to assess blood flow and cardiac function

• Treatment:

  • Medications: Nitrates, beta-blockers, calcium channel blockers

  • Lifestyle Changes: Diet, exercise, smoking cessation

Unstable Angina

Unpredictable chest pain, occurs at rest, and is more severe

• Diagnosis:

  • EKG: May show ischemic changes, but no ST-elevation

  • Cardiac Biomarkers: Normal

• Treatment:

  • Antiplatelet Therapy: Aspirin, P2Y12 inhibitors (e.g., Clopidogrel)

  • Anticoagulants: Heparin or low molecular weight heparin

  • Beta-blockers and statins for long-term management

Myocardial Infarction (MI)

Acute necrotic event of the myocardium resulting from the sudden loss of blood supply to the tissue due to prolonged lack of blood supply, primarily caused by the blockage of coronary arteries

• Pathogenesis:

  • Atherosclerosis → plaque → thrombus → increased platelets → increased fibrin → embolus

  • Embolus/spasm → NO blood flow → infarction (MI) → necrosis

• Can be STEMI or NSTEMI

• S/S:

  • “Elephant sitting on my chest”

  • Heaviness, pressure

  • “Indigestion” feeling, N/V

  • Unrelieved by NTG or rest

  • Radiation

  • Severity is vague

  • Timing: Continuous, lasts longer than 15-30 minutes

  • May have no pain — especially with DM

  • EKG changes

  • POSITIVE cardiac markers

MI on EKG

• T-Wave Inversion (decreased T): Indicates temporary myocardial ischemia

• ST depression (decreased ST): Sign of subendocardial ischemia (partial-thickness wall affected, decreased O2)

• ST elevation (increased ST): Sign of transmural myocardial injury (full-thickness wall affected, prolonged O2 reduction → some permanent damage)

• Q waves (Q): Indicates myocardial infarction (necrosis, dead cells → no conduction or contraction)

ST-Elevation Myocardial infarction (STEMI)

• Characterized by complete occlusion of a coronary artery

• ECG: ST-segment elevation in 2 or more contiguous leads

• Cardiac Biomarkers: Elevated troponins and CK-MB

• Treatment: Immediate PCI (within 90 minutes) or thrombolytics (if PCI unavailable)

Non-ST-Elevation Myocardial Infarction (NSTEMI)

• Involves partial blockage and typically results in less severe damage

• ECG: ST depression, T-wave inversions, or normal

• Cardiac Biomarkers: Elevated indicating myocardial damage

• Treatment: Early invasive PCI or medical management (antiplatelets, anticoagulants, beta-blockers, and statins)

Effects of MI on the Heart

• Loss of muscle function

• Decreased cardiac output

• Electrical instability

• Ventricular remodeling

• Valve dysfunction

• Pericarditis

• Heart rupture

• Reduced exercise tolerance

Initial Medications for Chest Pain/ACS

• Oxygen: Maintain SpO2 > 94% → support myocardial oxygenation

• Aspirin (160-325 mg orally or chewed): Decreased platelet aggregation → early antithrombotic effect

• P2Y12 Inhibitor (Clopiodogrel 600 mg loading, Prasugrel, Ticagrelor): Decreased platelet aggregation → part of DAPT in confirmed ACS

• Nitroglycerin (0.4 mg SL every 5 min, max 3 doses/15 min): Decreased preload and afterload → relieve ishcemic chest pain

• Morphine (2-4 mg IV slowly, repeat PRN): Decreased pain and sympathetic drive → decrease myocardial oxygen demand

STEMI-Specific Medications

• Anticoagulants (Heparin, Enoxaparin): Prevent clot formation, stabilize patient

• Beta-blockers (Metoprolol): Decrease HR and myocardial O2 demand, decrease arrhythmia risk and cardiac death

• ACEIs/ARBs (Lisinopril, Losartan): Decrease mortality and prevent HR, protect myocardium if given within 24 hours

• Statins (Atorvastatin): Decrease cholesterol and stabilize plaques, decrease recurrent events

• Glycoprotein IIb/IIIa Inhibitors (Abciximab, Eptifibatide, Tirofiban): Decrease platelet aggregation, prevent thrombotic complications during PCI

Percutaenous Coronary Intervention (PCI)

Preferred reperfusion strategy for STEMI → < 90 minutes from first medical contact to balloon inflation (“door-to-balloon” time)

• Balloon angioplasty with stenting (bare-metal or drug-eluting) → restores coronary blood flow, limits infarct size

• Often combined with antiplatelets, anticoagulants, and GP IIb/IIIa inhibitors

• Decrease mortality, recurrent MI, and complications

Thrombolytics

Reperfusion if PCI is unavailable within 120 minutes

• Alteplase, Tenecteplase, Reteplase

• Increase clot breakdown, restore coronary blood flow

• < 30 minutes from hospital arrival (“door-to-needle” time)

Percutaneous Coronary intervention (PCI)

Preferred for STEMI and high-risk NSTEMI patients

• Balloon angioplasty and stenting to restore coronary blood flow

Coronary Artery Bypass Grafting (CABG)

Indicated for patients with multivessel disease or left main coronary artery disease

• Improves long-term survival in certain high-risk patients

Post ACS Management and Prevention

• Lifestyle Modifications:

  • Smoking cessation, weight management, regular physical activity

  • Dietary changes to manage cholesterol and hypertension

• Medications:

  • DAPT: Continue for 12 months post-PCI

  • Beta-blockers, ACE inhibitors, and statins for long-term risk reduction

• Cardiac Rehabilitation: Structured exercise and education programs for recovery