Ischemic Heart Disease - IHD

  • Diagnosis
  • Screening
  • Background
  • Lab Tests
  • References
  • Related Content

Indications for Testing

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

Laboratory Testing

  • Newer markers (diagnostic significance not proven)
    • Oxidative stress – lipoprotein-associated phospholipase A2, myeloperoxidase
    • Tissue necrosis – C-reactive protein, 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 typically posterior MI, right ventricular infarction


  • 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 on EKG
      • >2 anginal events in preceding 24 hours
      • Acetylsalicylic acid (ASA) treatment in previous 7 days
      • Increased cardiac markers (troponins preferred)
      • Prior AMI, congestive heart failure (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

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

Patients with ischemic heart disease (IHD) fall into 2 groups: stable angina secondary to ischemic heart disease (coronary artery disease [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.


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

Risk Factors


  • 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

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

Troponin I 0090613
Method: Chemiluminescent Immunoassay


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


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


Troponins preferred

Additional Tests Available

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


Detects inflammatory processes

Interleukin 6 0051537
Method: Quantitative Multiplex Bead Assay


Diagnosis and treatment of chest pain and acute coronary syndrome (ACS). Institute for Clinical Systems Improvement - Nonprofit Organization. 2004 November (Revised 2012 November). NGC: 009521

General References

Anaya P, Moliterno D. The evolving role of cardiac troponin in the evaluation of cardiac disorders. Curr Cardiol Rep. 2013; 15(11): 420. PubMed

Baker J, Reinhold J, Redwood S, Marber M. Troponins: redefining their limits. Heart. 2011; 97(6): 447-52. PubMed

Christenson E, Christenson R. Characteristics of cardiac troponin measurements. Coron Artery Dis. 2013; 24(8): 698-704. PubMed

Christenson R, Phillips D. Sensitive and high sensitivity next generation cardiac troponin assays: more than just a name. Pathology. 2011; 43(3): 213-9. PubMed

Keller T, Zeller T, Peetz D, Tzikas S, Roth A, Czyz E, Bickel C, Baldus S, Warnholtz A, Fröhlich M, Sinning C, Eleftheriadis M, Wild P, Schnabel R, Lubos E, Jachmann N, Genth-Zotz S, Post F, Nicaud V, Tiret L, Lackner K, Münzel T, Blankenberg S. Sensitive troponin I assay in early diagnosis of acute myocardial infarction. N Engl J Med. 2009; 361(9): 868-77. PubMed

Kumar A, Cannon C. Acute coronary syndromes: diagnosis and management, part I. Mayo Clin Proc. 2009; 84(10): 917-38. PubMed

Lee-Lewandrowski E, Januzzi J, Grisson R, Mohammed A, Lewandrowski G, Lewandrowski K. Evaluation of first-draw whole blood, point-of-care cardiac markers in the context of the universal definition of myocardial infarction: a comparison of a multimarker panel to troponin alone and to testing in the central laboratory. Arch Pathol Lab Med. 2011; 135(4): 459-63. PubMed

Muthu V, Kozman H, Liu K, Smulyan H, Villarreal D. Cardiac troponins: bench to bedside interpretation in cardiac disease. Am J Med Sci. 2014; 347(4): 331-7. PubMed

Senter S, Francis G. A new, precise definition of acute myocardial infarction. Cleve Clin J Med. 2009; 76(3): 159-66. PubMed

Sherwood M, Newby K. High-sensitivity troponin assays: evidence, indications, and reasonable use. J Am Heart Assoc. 2014; 3(1): e000403. PubMed

Tanindi A, Cemri M. Troponin elevation in conditions other than acute coronary syndromes. Vasc Health Risk Manag. 2011; 7: 597-603. PubMed

Tiwari R, Jain A, Khan Z, Kohli V, Bharmal R, Kartikeyan S, Bisen P. Cardiac troponins I and T: molecular markers for early diagnosis, prognosis, and accurate triaging of patients with acute myocardial infarction. Mol Diagn Ther. 2012; 16(6): 371-81. PubMed

Twerenbold R, Jaffe A, Reichlin T, Reiter M, Mueller C. High-sensitive troponin T measurements: what do we gain and what are the challenges? Eur Heart J. 2012; 33(5): 579-86. PubMed

References from the ARUP Institute for Clinical and Experimental Pathology®

Knoblock R, Lehman C, Smith R, Apple F, Roberts W. False-positive AxSYM cardiac troponin I results in a 53-year-old woman. Arch Pathol Lab Med. 2002; 126(5): 606-9. PubMed

Medical Reviewers

Last Update: January 2016