Ischemic Heart Disease - IHD

Diagnosis

Indications for Testing

  • Patient presenting with chest pain who also has risk factors suggesting CAD
  • Clinical history and risk factor assessment

Laboratory Testing

  • Cardiac markers testing

    Cardiac Markers Testing

    Troponins

    • Useful to distinguish AMI from UA
    • Cardiac-specific troponins have amino acid sequences different from skeletal muscle forms and therefore are highly specific for cardiac injury
    • Preferred markers for the diagnosis of AMI – use in conjunction with EKG and clinical picture
      • Negative predictive value is 97-99%; low sensitivity in myocardial infarction (MI) <6 hours old
      • Should always be used in conjunction with clinical assessment
    • Elevated troponins indicate cardiac injury
    • Obtain blood sample at presentation and again after 6-9 hours – rising troponins confirm cardiac injury
      • Guideline* recommendation for diagnosis – maximal concentration >99th percentile of a reference control group in the first 24 hours
      • Guidelines* also recommend troponins be 5 times the 99th percentile during the first 72 hours following coronary artery bypass graft (CABG) to confirm CAD or related MI
    • Troponins can remain elevated 10-14 days after an event

    CK-MB (creatine kinase-MB isoenzyme)

    • Acceptable marker when troponins not available
    • Guideline* recommendation for diagnosis – maximal concentration >99th percentile of a reference control group in two successive samples or a maximal value >twice the upper limit of normal during the first 24 hours
      • Loss of specificity after 24 hours
    • Impaired use in organ injury (acute or chronic muscle, intestine, diaphragm, uterus and prostate damage)
      • Due to nonspecific elevations
    • Low sensitivity in early MI (<6 hours); late MI (>36 hours); minor damage MI

    Myoglobin

    • Not recommended as a standalone test
    • Very low specificity; high sensitivity in early detection of MI

    Natriuretic peptides (NP)

    • Atrial (ANP), brain or b-type (BNP) and N-terminal (Nt) metabolic peptides are released by cardiocytes
      • Release stimulated by ventricular wall stress
    • Function as powerful diuretics/natriuretics and as vascular smooth muscle relaxers
    • Elevated in conditions characterized by wall stretch, ventricular dilation or increased pressure
    • Most frequently used to diagnose heart failure

    Most guidelines* recommend serial sampling of cardiac markers and repeated EKG tracings over 24 hours to rule out AMI

    *Guidelines include European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, National Academy of Clinical Biochemistry, ESC/American College of Cardiology

  • BNP measures may give additional prognostic information about mortality during first cardiovascular events
  • Newer markers (diagnostic significance not proven)
    • Oxidative stress – lipoprotein-associated phospholipase A2, myeloperoxidase
    • Tissue necrosis – CRP, interleukin 6, other interleukins, fatty acid binding proteins, free fatty acid unbound to albumin

Imaging Studies

  • Stress testing
  • Echocardiography – wall motion abnormalities suggest AMI

Other Testing

  • Electrocardiogram (EKG) – may have false negatives
    • Typically demonstrates ST elevation, but not always (posterior MI, right ventricular infarction)

Prognosis

  • Use of TIMI (thrombolysis in myocardial infarction) risk score prognosticates 2-week, all-cause mortality in new or recurrent AMI
    • One point for each of the following
      • Age >65 years
      • History of diabetes mellitus, hypertension, angina
      • Documented coronary stenosis >50%
      • ST elevation
      • >2 anginal events in preceding 24 hours
      • ASA (acetylsalicylic acid) treatment in previous 7 days
      • Increased cardiac markers (troponins preferred)
      • Prior AMI, CHF, bypass surgery or percutaneous angioplasty
    • 1 point = 5%; 2 points = 8%; 3 points = 13%; 4 points = 20%; 5 points = 26%; ≥6 points = 41%

Differential Diagnosis

Screening

  • EKG, exercise treadmill, and electron beam computerized tomography may provide prognostic information about future events, but screening of asymptomatic patients is not recommended (U.S. Preventative Services Task Force)

Clinical Background

Patients with ischemic heart disease (IHD) fall into 2 groups: stable angina secondary to ischemic heart disease (coronary artery disease or CAD) and acute coronary syndromes (ACS). ACS is further grouped into acute myocardial infarction (AMI) and unstable angina (UA). CAD is the leading cause of death in the U.S.

Epidemiology

  • Incidence – >1,500,000 cases of ACS annually in U.S.
  • Age – peak onset is >50 years
  • Sex – M>F

Risk Factors

Pathophysiology

  • Atherosclerosis – disease of large and medium-sized arteries
  • Clot formation in the coronary arteries – ACS caused by rupture or erosion of plaques
    • Rupture of plaques leads to inadequate circulation with ischemia, resulting in myocardial cell death

Clinical Presentation

  • ACS
    • Substernal chest pain, dyspnea, gastric discomfort, diaphoresis, tachycardia or hypotension
      • Atypical pain site presentations are not uncommon – arm, back, jaw, neck
    • May auscultate S3 or S4, new murmur, pericardial friction rub or bibasilar rales
    • May be difficult to distinguish the chest pain of AMI or UA from other conditions such as gastroesophageal reflux disease (GERD)
  • CAD
    • May be asymptomatic
    • May present with symptoms similar to ACS or AMI
  • Sudden death event
    • Caused by ventricular fibrillation, ventricular tachycardia, electromechanical dissociation, and bradycardias
    • Most patients have underlying CAD or structural heart disease
    • High fatality rate associated with this event

Treatment

  • Early recognition of ACS is important to prevent complications
  • Use established guidelines for specific treatment strategies from the American Heart Association

Prevention

  • Aggressive management of risk factors

Indications for Laboratory Testing

  • Tests generally appear in the order most useful for common clinical situations
  • Click on number for test-specific information in the ARUP Laboratory Test Directory
Test Name and Number Recommended Use Limitations Follow Up
Troponin I 0090613
Method: Chemiluminescent Immunoassay

Determine if injury has occurred to heart muscle

First-line laboratory test for myocardial injury

False-positive results may occur in acute pulmonary embolism, acute and chronic heart failure, sepsis, stroke, renal failure

 
Troponin T 0098803
Method: Quantitative Electrochemiluminescent Immunoassay

Determine if injury has occurred to heart muscle

First-line laboratory test for myocardial injury

False-positive results may occur in acute pulmonary embolism, acute and chronic heart failure, sepsis, stroke, renal failure

Lower early sensitivity than troponin I for myocardial necrosis

 
Creatine Kinase, MB 0080480
Method: Chemiluminescent Immunoassay

Cardiac injury marker when troponins are not available

Troponins preferred

 
Additional Tests Available
 
Click the plus sign to expand the table of additional tests.
Test Name and NumberComments
Creatine Kinase, Total, Serum or Plasma 0020010
Method: Quantitative Enzymatic
Myoglobin, Serum 0020224
Method: Quantitative Electrochemiluminescent Immunoassay

May be used selectively by clinicians to evaluate causes of non-cardiac muscle injury

B-Type Natriuretic Peptide 0030191
Method: Quantitative Chemiluminescent Immunoassay
proBrain Natriuretic Peptide, NT 0050083
Method: Quantitative Electrochemiluminescent Immunoassay
Lipoprotein-Associated Phospholipase A2 (PLAC) 0081055
Method: Quantitative Enzyme-Linked Immunosorbent Assay
C-Reactive Protein 0050180
Method: Quantitative Immunoturbidimetry
Interleukin 6 0051537
Method: Quantitative Multiplex Bead Assay