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 CADStable AnginaUnstable AnginaNSTEMISTEMI
Vessel Occlusion < 50% 70% 90% 90% 100%
Chest PainExerciseAt Rest At Rest At Rest
Troponins Increased Increased
ReliefRest and Nitrates
TreatmentsMonitorStress TestStress TestMedicationCath lab

PresentationAssociated sxs Risk Factors Physical Exam Treatment Medication
1. Substernal chest pain
2. Worse with exertion
3. Relieved with NTG

1 or 0/3 = non anginal
2/3 = atypical
3/3 = typical
family history
age >45 in males
age >55 in females
chest pain
Chest pain EKG
If EKG shows ST elevation 
– go emergently to cath
If EKG shows no ST elevations
– get troponins
If troponins elevated
– go urgently to cath
If troponins not elevated
– get stress test
If stress test is positive
– electively go to cath
If Cath shows 1 or 2 vessels issue
– 1-2 vessels = stent placement
If cath shows 3 vessel issue
– 3+ vessels (or big proximal vessels) = CABG
*Beta Blocker

* = will definitely go home with
** = maybe go home with

No nitrates for pts with: right sided MI (leads 2,3, AVF)
(right ventricle is preload dependent)

Asymptomatic CAD

Stable Angina

Unstable Angina


  • 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
    • NSTEMI = Ischemia severe enough to cause myocardial injury with release of biomarkers (troponin)
  • Presentation:
  • 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


  • Note:
  • Presentation:
  • 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


  • 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

EKG LeadsArteries
Anterior MISTEMI in V1-V4LAD and diagonal branches
Lateral MISTEMI in I, aVL and V5-V6LCA
Posterior MIST depression in V1 and V2 (Reciprocal change)PDA

  • 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