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

• Nonischemic cardiovascular
  • Aortic dissection
  • Myocarditis/pericarditis
  • Hypertrophic cardiomyopathy
  • Cardiac injury/rhabdomyolysis
  • Cardiac arrhythmias
  • Infiltrative cardiac disease
  • Congestive heart failure
• Chest wall/musculoskeletal
  • Cervical disk disease
  • Costochondritis
  • Herpes zoster
  • Neuropathic pain
  • Rib fracture
• Pulmonary
  • Pulmonary embolism
  • Pneumonia
  • Tension pneumothorax
  • Pleurisy
• Gastrointestinal
  • Esophageal reflux
  • Cholecystitis
  • Peptic ulcer disease
  • Esophageal spasm
  • Pancreatitis
  • Esophageal rupture
• Other
  • Sepsis/shock
  • Burns (>30% of body)
• Psychiatric
  • Depression
  • Panic attack
  • Somatization with psychogenic pain disorder

Screening

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

• Hypertension
• Hyperlipidemia
• Diabetes mellitus
• Tobacco use
• Family history
• Obesity (including metabolic syndrome)
• Physical inactivity
• Increasing age

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

Click the plus sign to expand the table of additional tests.

Test Name and Number	Comments
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 by MAFD 0051537 Method: Quantitative Multiplex Bead Assay