CAD

Acute Coronary Syndrome

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Acute Coronary Syndrome, Myocardial Infarction

  • Risk Factors
  • Epidemiology
  1. Prevalence of CAD in U.S.: 27.6 million (11.5%) in U.S. (2014)
  2. Mortality: 370,000 per year in U.S. (2014)
  3. Incidence of Acute MI: 735,000/year in U.S. (2014)
    1. STEMI accounts for 30% of cases (typically younger patients)
    2. NSTEMI accounts for 70% of cases (typically older patients)
    3. Steg (2002) Am J Cardiol 90(4): 358-63 [PubMed]
  4. No prior coronary symptoms in >50% with fatal acute MI
  5. Coronary deaths account for up to 20% of all deaths in U.S.
  6. Average age of first Myocardial Infarction in U.S.
    1. Men: 65 years old
    2. Women: 72 years old
  7. References
    1. https://www.cdc.gov/nchs/fastats/heart-disease.htm
    2. https://www.cdc.gov/heartdisease/facts.htm
  • Pathophysiology
  • Atherosclerotic Plaque
  1. Form over 10-15 years in response to vascular injury
    1. Significant Plaque present in 75% of age >25 years
  2. Lipid core (atheroma)
    1. Injured endothelium attracts Macrophages
    2. Macrophages resorb LDL Cholesterol fatty streaks
    3. Lipids transform Macrophages into foam cells
  3. Surrounding wall (fibroatheroma)
    1. Surrounds lipid core
    2. Composed of fibroblasts and smooth muscle cells
  4. Acute MI or Acute Coronary Syndrome
    1. Occurs on Plaque rupture; results in vessel Occlusion
  • Pathophysiology
  • Postinfarction remodeling
  1. Early Phase (<72 hours)
    1. Infarct zone expansion
    2. Myocardial wall thinning and ventricular dilation
    3. Increased elevated myocardial wall stress throughout cardiac cycle
    4. Renin-Angiotensin System activated (increased BNP)
  2. Late Phase (>72 hours)
    1. Left ventricle generalized effects and ventricular dilation over time resulting in distorted ventricular shape
    2. Mural hypertrophy occurs in response to ventricular load (decreases rate of dilation, preserves contractility)
    3. Fibrous tissue replaces necrotic myocytes in the first 4 weeks after Myocardial Infarction
    4. Ventricular effects do not improve with revascularization
  3. References
    1. Sutton (2000) Circulation 101(25):2981-8 [PubMed]
  • History
  1. Coronary Artery Disease (prior PTCA or CABG?)
  2. Peripheral Arterial Disease
  3. Prior abnormal stress test
  4. Diabetes Mellitus
  5. Other risk factors
    1. See Coronary Artery Disease Risk Factors
    2. Hypertension
    3. Hyperlipidemia
    4. Tobacco Abuse
    5. Premature heart disease Family History (age <55 in father or brother, age <65 in mother or sister)
  • Symptoms
  1. See TIMI Risk Score
  2. See HEART Score
  3. See Angina Diagnosis
    1. Reviews the likelihood that Chest Pain is due to cardiovascular cause
    2. ACS is asymptomatic in 25% of Myocardial Infarctions
  4. Findings that most increase the likelihood of Acute Coronary Syndrome
    1. See Chest Pain
    2. Chest Pain radiation to the right chest or bilateral arms (or Shoulders)
    3. Exertional Chest Pain
    4. Chest Pain with diaphoresis
    5. Chest Pain associated with Vomiting (not only Nausea)
  5. Chest Pain due to Myocardial Infarction is similar to Angina
    1. Deep, poorly localized chest ache
      1. Worse with activity
      2. Better with rest and Nitroglycerin
    2. Radiation
      1. Arm, Shoulder, hand or upper back
      2. Radiation to right arm or bilateral arms is more suggestive of coronary syndrome
      3. May also radiate to neck, jaw or throat (less specific)
  6. Distinguishing features of Chest Pain due to Myocardial Infarction
    1. More intense than Angina
    2. More persistent than Angina (>30 minutes)
    3. Not fully relieved by palliative measures
      1. Rest
      2. Nitroglycerin (3 consecutive doses)
    4. Accompanied by systemic symptoms
      1. Vomiting
      2. Diaphoresis
      3. Apprehension
  • Signs
  1. Pallor
  2. Diaphoresis
  3. Tachycardia
  4. Signs of Congestive Heart Failure may also be present (higher risk findings)
    1. Rales on Lung Examination
    2. S3 Gallup Rhythm
    3. Jugular Venous Distention (esp. Right Ventricular Infarction)
  • Diagnosis
  1. Serum Cardiac Markers
    1. Serial Troponin
  2. Electrocardiogram
    1. See Electrocardiogram in Myocardial Infarction
    2. See Immediate Myocardial Infarction Management
    3. Evaluate Electrocardiogram carefully
      1. Ischemic changes (e.g. ST segment depression or T Wave inversion) are commonly missed
      2. Hyperacute T Waves (Peaked T Waves) precede ST Elevation
  3. Echocardiogram
    1. See Echocardiogram in Myocardial Infarction
  • Types
  1. Type 1
    1. Myocardial Infarction with Plaque rupture or erosion with thrombus formation (classic)
  2. Type 2
    1. Myocardial Infarction with imbalance between oxygen supply and oxygen demand WITHOUT Plaque rupture
    2. Examples: Serious arrhythmia, severe Anemia
  3. Type 3
    1. Sudden Cardiac Death before Troponins have time to rise
  4. Type 4 and 5
    1. Cardiac procedure (e.g. PCI, ) related Troponin elevation
  5. References
    1. Thygesen (2018) Circulation 138(2):e618-51 +PMID:30571511 [PubMed]
  • Complications
  1. Arrhythmia
    1. Ventricular Fibrillation
    2. Accelerated Idioventricular Rhythm
    3. Bradyarrhythmia
    4. Atrioventricular Block
  2. Congestive Heart Failure
  3. Cardiogenic Shock
  4. Acute Mechanical Complications
    1. Ventricular Septal Rupture
    2. Acute Mitral Regurgitation
  5. Pericarditis
  6. Ventricular aneurysm
  7. Recurrent Angina
  8. Dressler's Syndrome