Coronary Artery Disease

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Coronary Artery Disease

• Etiology:
  • reduced myocardial perfusion due to reduced O2 supply (more common) or increased O2 demand
• Causes:
  • Coronary atherosclerotic plaque rupture
  • occurs when the fibrous cap ruptures
  • Nearly 50% at sites with <50% luminal narrowing
  • Thrombus develops on top of the disrupted plaque
  • Statins, exercise and ACE inhibitors stabilize the fibrous cap of a coronary atheroma, reducing the likelihood of rupture
• Other Etiologies:
  • Spasm at site of atherosclerotic plaque
  • Normal coronary arteries with spasm
    • Prinzmetal’s angina (may have transient ST elevation)
    • Arterial inflammation (Kawasaki disease)
  • Cocaine-induced (treat with NTG and benzodiazepines; avoid beta-blockers)

Coronary Artery Disease Types

Asymptomatic CAD

• No Pain
  
• No Relief of Pain
  
• No Bio Markers
  
• No ST Changes
  
• <50% occlusive

Stable Angina

• + Pain with excursion
  
• + Relief with rest
  
• No Biomarkers
  
• No ST Changes
  
• 70% Occlusive `

Unstable Angina

• + Pain at rest
  
• No Relief
  
• No biomarkers
  
• No ST Changes
  
• 90% occlusive

NSTEMI

• Note: 
  • Unstable Angina and NSTEMI have similar clinical presentations but differ in severity:
  • NSTEMI and sometimes UA cause ST-segment depression or prominent T-wave inversion but not ST-segment elevation on
    EKG
  • NSTEMI = Ischemia severe enough to cause myocardial injury with release of biomarkers (troponin)
• Presentation:
  • + Pain at rest
    
  • No Relief
    
  • + Biomarkers
    
  • No ST Changes
    
  • 90% occlusive
• Management: 
  • Ischemia-guided strategy: (lower risk patients, preference for low intervention)
    • 1. Aspirin (non-enteric coated, chewable)
    • 2. P2Y12 inhibitor (clopidogrel, ticagrelor)
    • 3. Anticoagulation (heparin)
  • Early invasive strategy: (higher risk patients)
    • 1. Aspirin (non-enteric coated, chewable)
    • 2. P2Y12 inhibitor (clopidogrel, ticagrelor)
    • 3. Anticoagulation (heparin)
    • 4. Consider Glycoprotein IIb/IIIa receptor blockers [Tirofiban (Aggrastat), Eptifibatide (Integrilin), Abciximab (ReoPro)] before invasive treatment
  • Invasive strategy in higher risk patients
    • Symptoms or ischemia despite adequate medical therapy
    • Previous PCI or CABG, unless prior coronary angiography data indicate that no further revascularization is feasible
    • Evidence of significant cardiac disease (EF <40%, large anterior or multiple perfusion defects or wall motion abnormalities on echocardiography, high-risk TIMI or GRACE scores, Duke treadmill score ≤−11, Markedly elevated troponin levels, ventricular arrhythmias)
    • Fibrinolytic therapy has no role in NSTEMI

STEMI

• Note:
  • STEMI has ST-segment elevation on EKG (with Q wave later)
    
  • Warrants immediate reperfusion therapy
• Presentation:
  • + Pain at rest
    
  • No Relief
    
  • + Biomarkers
    
  • + ST changes
    
  • 100% occlusive
• EKG:
  • ST segments
    • Elevation occurs immediately post plaque-rupture and is consistent with myocardial injury.
    • Resolution of ST elevation suggests reperfusion.
    • Persistent ST elevation may be seen with aneurysm formation.
    • ST depression indicates myocardial ischemia.
  • Q waves
    • Develop ~12 hours post plaque-rupture, and are indicative of (electrically) dead myocardium (MI).
    • Typically permanent.
• Management:
  • Reperfusion as quickly as possible, within 12 hours (if no contraindications)
  • Percutaneous coronary intervention (PCI) is preferred
  • Fibrinolytic therapy is indicated
  • If onset of symptoms plus time to transport to a PCI-capable hospital is more than 12 hours
  • If time from first medical contact at the non-PCI capable hospital to device time at PCI-capable hospital is more than 2 hours

Troponin

• High sensitivity and specificity for myocardial necrosis
• Detected 3-6 hours after the onset of ischemia and remains elevated for 7-14 days post-MI
• Normal levels exclude myocardial infarction, but do not exclude unstable angina
• Non-ischemic causes that elevate troponin levels

Types of MI

• Anterior/anteroseptal
  • LAD (Left Anterior Descending)
  • Leads V1 – V4
• Lateral
  • Circumflex Artery
  • Leads V5 – V6
• Inferior
  • RCA (Right Coronary Artery)
  • Leads II, III, aVF

Percutaneous Coronary Intervention (PCI) With Stent

• Bare metal stent (BMS)
  • Bare metal acts as foreign body, increasing risk of in-stent thrombosis
  • Endothelialization may progress to in-stent stenosis
• Drug-eluting stent (DES)
  • Delay endothelialization, maintaining bare metal longer and reduce the rate of in-stent stenosis
  • Sirolimus (Cypher), tacrolimus (Mahoroba), paclitaxel (Taxus)

Dual Antiplatelet Therapy (DAPT)

• Aspirin 81 mg plus P2Y12 inhibitor: clopidogrel (Plavix), prasugrel (Effient), ticagrelor (Brilinta)
• In patients with ACS treated with BMS or DES implantation, DAPT should be given for at least 12 months (Class I).
• After one year, may stop P2Y12 inhibitor but continue aspirin indefinitely.
• If stents placed for stable coronary artery disease (scheduled catheterization rather than ACS)
  • After BMS implantation, DAPT for at least 1 month (Class I).
  • After DES implantation, DAPT for at least 6 months (Class I).
• Extending DAPT beyond one year following a myocardial infarction decreases the risk of a major cardiovascular event without increasing the likelihood of a major bleeding event, especially with clopidogrel

Clopidogrel (Plavix)

• Delayed onset of antiplatelet activity compared to aspirin
  • if used alone need to first treat with heparin or glycoprotein IIb/IIIa inhibitor
• Comparable to aspirin in reducing ischemic events
• Loading dose 600 mg before PCI then continued at 75 mg/day, along with aspirin (DAPT): better than aspirin alone 
• Metabolized to active form by cytochrome p450 enzyme CYP2C19; poor metabolizers risk therapeutic failure due to non-activation.
• Currently, prasugrel and ticagrelor have no genetic links to response and are “reasonable” alternatives.

Coronary Artery Bypass Graft)

• Improved survival for
  • Left main coronary artery stenosis
  • 3-vessel disease with abnormal left ventricular function (LVEF <50%)
  • 2- or 3-vessel disease with >75% stenosis of the proximal left anterior descending artery (LAD).
  • Patients with diabetes have better 8-year survival with CABG than with PTCA.
  • After CABG, DAPT for at least one year to reduce graft occlusion
• Acutely
  • Use only if coronary anatomy is not suitable for PCI