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Diagnostic Efficiency of Creatine Kinase (CK), CKMB and Troponin I in Patients with Suspected Acute Myocardial Infarction

Date : 21 Dec, 2018

Cardiovascular Disease (CVD) is a major cause of death globally with Coronary Heart Disease (CHD) being the single most important cause of death in middle-aged men. Because of the frequency and severity of CVD, diagnosis must be rapid and accurate. Diagnosis on an Electrocardiogram is not the absolute criterion, particularly in the case of small infarctions. Assays of plasma markers are thus of importance to confirm the clinical hypothesis.

Coronary Heart Disease

They measure intracellular cardiac tissue molecules released into the circulation after the onset of CVD. Cytoplasmic Creatine Kinase (CK) is a dimer composed of M and B subunits that associate to form CK-MM, CK-MB and CK-BB isoenzymes. In patients having significant myocardial disease, the CK-MB isoenzyme comprises approximately 20% of the total CK in this tissue. CK-MB is diagnostically sensitive for myocardial injury.

The diagnosis of Acute Myocardial Infraction (AMI) is usually predicated on the WHO criteria of chest pain, ECG changes, and increases in biochemical markers of myocardial injury. Unfortunately, about half of the patients with ‘typical’ symptoms do not have AMI. The diagnosis of AMI is particularly difficult in the elderly, where relatively minor symptoms may reflect acute ischemia. The ECG is specific for AMI, but lacks sensitivity. It also provides additional information regarding localization and the extent of the injury. Sometimes, it is not easy to distinguish remote injury from a more recent one. In contrast, biochemical markers have excellent sensitivity for diagnosing AMI. By combining the most sensitive and the most specific tests, diagnostic accuracy can be enhanced.

Cardiac Troponin I (cTnI) is a very reliable marker of cardiac tissue injury. It is considered to be a more sensitive marker compared to CK-MB & Lactate Dehydrogenase (LDH).  It is released into blood in 4-6 hours from the onset of an acute myocardial infarction, reaching its peak level in 16-30 hours. This makes it a very valuable marker for the late diagnosis of Acute Myocardial Infarction (AMI).

ErbaQik Troponin I

Qualitative determination of Troponin I is based on Chromatographic Immunoassay Tech. It is

  • Highly sensitive and specific
  • Easy to perform
  • Qualitative results of cTnI cassettes are read visually without any instrument
  • No other reagent is needed 
  • It takes less than 15 minutes to be sure
  • Detection Limit: > 0.5 ng/m
  • Relative Sensitivity: 95%
  • Relative Specificity: 97%
  • Pack Size: 20 Tests 

Case study:

I. Patient’s history:

The patient was a 76-year-old white male with chronic renal failure and long-standing hypertension who was admitted for L2-L5 posterior lumbar fusion. He experienced a period of intraoperative hypotension that extended to the postoperative period and required temporary treatment with pressor agents. Several hours postoperatively routine ECG showed T-wave changes in lateral leads, and subsequently a new Left Bundle Branch Block (LBBB). There was no previous ECG for comparison. At that time the patient did not have any chest pain, shortness of breath or any other symptoms. His physical exam was unremarkable, except for a new third heart sound. There was no history of prior cardiac events. The results of the first set of cardiac enzymes (CK, CK-MB, Troponin I was consistent with a new Myocardial Infarction (MI).

Past medical history was also significant for hyperlipidemia, gout, right leg Deep Venous Thrombosis (DVT), multiple back surgeries, bilateral knee replacements and cataract removals. Medications included allopurinol, trazodone, pravachol, aspirin, verapamil and lisinopril. The patient did not consume alcohol and did not smoke. His father died at the age of 60 of MI. The patient remained asymptomatic, and his later ECGs showed normal sinus rhythm, with persistent LBBB. Repeated sets of cardiac enzymes confirmed the presence of MI. Transthoracic echocardiogram showed left ventricular hypertrophy and global hypokinesis. The medical regimen was readjusted and patient was transferred for cardiac rehabilitation.

II. ECG findings:

Day Time Results

Day 1 – 2.55 PM: ST-T wave abnormality compatible with lateral ischemia
Day 1 – 9.00 PM: LBBB and sinus tachycardia
Day 2 – 5.39 AM: Nonspecific intra ventricular conduction delay and T wave abnormality
compatible with lateral ischemia
Day 2 – 4.00 PM: Septal infarct pattern, age undetermined. ST abnormality compatible
with lateral subendocardial injury or infarction. ST abnormality is more marked than T wave abnormality previously, and ST is new.
Day 3 – 7.00 AM: Normal sinus rhythm. Left ventricular conduction defect. As compared
to day 2 supraventricular tachycardia is no longer present and QRS duration has decreased.
Day 7 – 7.00 AM: Normal sinus rhythm with premature ectopic complexes. LBBB with
associated repolarization abnormality. As compared to day 3, no significant change.

III. Laboratory data:

Cardiac enzyme levels
DAY TIME Total CPK (normal 0-200 IU/L)
CPK- MB (normal <7 IU/L)
TROPONIN I (normal < 1.5 ng/mL)

IV. Case discussion:

The patient presented in the first case developed ECG changes that were initially interpreted as nonspecific, until elevated cardiac enzymes were found. At that time, he was asymptomatic, and remained that way during his hospital course. He experienced only intraoperative and brief postoperative hypotension. Nevertheless, his laboratory results indicated the presence of ‘silent’ Myocardial Infarction.

ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart disease. When it fails to show conclusive evidence of infarction, the crucial step in ruling in/out the diagnosis of AMI is the measurement of myocardial enzymes in the serum. The rate of release of specific proteins differs depending on their intracellular location, molecular weight, and the local blood and lymphatic flow. The temporal pattern of marker protein release is of diagnostic importance.

Ruling out AMI requires a test with high diagnostic sensitivity, whereas ruling in AMI requires a test with high diagnostic specificity. These diagnostic strategies often require different decision thresholds for different biochemical markers. The ideal marker of myocardial injury would provide early diagnosis, assessment of the success of reperfusion after thrombolytic therapy, detection of re-occlusion and reinfarctions, determination of infarct size, and detection of perioperative MI during cardiac or non-cardiac surgery. Acceptable biochemical markers of ischemic heart disease are now considered to include myoglobin, CK-MB, total CK, and cardiac Troponins T and I. Enzyme CK has three isoforms composed of two chains (M and B chains), MM, MB and BB. The MB fraction is found predominantly in cardiac muscle. It is important to show both; a rise in the serum concentration of CK-MB, and a rise in the ratio of CK-MB to total CK to diagnose MI.

Furthermore, it is important to obtain serial samples for CK-MB and total CK from a patient with suspected MI to demonstrate a rise or fall in isoenzyme concentration. Typically, CKMB begins to rise 4-8 hours after the MI, peaks within the first 24 hours, and can be used to establish the diagnosis of the MI. The CK-MB returns to normal range after 48-72 hours.

TROPONIN use in current practice:

In practice, the ordering criteria for troponin in emergency departments are often less stringent than in the controlled conditions of a clinical research study. In a busy Emergency Department (ED), the need for rapid ED turnover times drives the practice of initial bundling of laboratory tests to eliminate time-consuming sequential processes (clinical evaluation followed by testing). Thus, Troponin tests often are drawn before the ordering physician examines the patient and takes a detailed history. This practice is reinforced by the need to rapidly establish a diagnosis for patients with Acute Coronary Syndromes (ACS) and is also motivated by defensive medicine to minimize medico-legal liability. Similar ordering practices also often occur in other areas of hospitals, such as Intensive Care Units. As a result, Troponin testing is used as a screening test in a broad spectrum of non-ACS patients including patients with endstage renal disease, sepsis, and congestive heart failure, all of which are known to have elevated Troponin levels.


  1. Henry JB. Clinical diagnosis and management by laboratory methods. 19th edition, 1996;88-89.
  2. Moqensen J, Kruse TA, Borglum AD. Assignment of the human cTnI gene (TNNI3) to chromosome 19q13.4 by radiation hybrid mapping. Cytogenet Cell Genet 1997;79:272.
  3. Adams JE, Schectman KB, Landt Y, Ladenson JH, Jaffe AS. Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I. Clin Chem 1994;40:1291.
  4. Jaffe AS, Landt Y, Parvin CA, Abendschein D, Geltman EM, Ladenson JH. Comparative sensitivity of cardiac troponin I and lactate dehydrogenase isoenzymes for diagnosing acute myocardial infarction. Clin Chem 1996;42:1770.
  5. Fiocchi R, Vernocchi A, Gariboldi F, Senni M, Mamprin F, Gamba A. Troponin I as a specific marker for heart damage after hearttransplantation in a patient with Becker type muscular dystrophy. J Heart Lung Transplant 1997;16:969.
  6. Stanton E, Jackowski G, Worron I, Lawrence M, Tanser P, Luxton G, Bonnell R, Gawas Y. Biochemical differentiation between the different classes of unstable angina. J Heart Failure 1995;2:A387.
  7. Luscher Ms, Thygesen K, Ravkilde J, Heickendorff L. Applicability of cardiac troponin T and I for eary risk stratification in unstable coronary artery disease. TRIM study group. Thrombin inhibition in myocardial ischemia. Circulation 1997;96:2578.
  8. Green GB, Li DJ, Bessman ES, Cox JL, Kelen GD, Chan DW. The prognostic significance of troponin I and troponin T. Acad Emerg Med 1998;5:758.
  9. Hamm CW, Goldmann BU, Heeschen C, Kreymann G, Berger J, Meinertz T. Emergency room triage of patients with acute chest pain by means of rapid testing for cardiac troponin T or troponin I. N Engl J Med 1997;337:1648.
  10. McLaurin M, Apple FS, Henry TD, Sharkey SW. Cardiac troponin I and T concentrations in patients with cocaine associated chest pain. Ann Clin Biochem 1996;33:1.
  11. Vuori J, Huttunen K, Vuotikka P, Vaananen HK. The use of myoglobin/carbonic anhydrase III ratio as a marker for myocardialdamage in patients with renal failure. Clin Chim Acta 1997;265:33-40 contributed by Sanja Dacic,MD, PhD and Mohamed A Virji, MD, PhD
  12. Indian Journal of Clinical Biochemistry, 2004, 19 (1) 113-117
  13. Landesberg G: The pathophysiology of perioperative myocardial infarction: Facts and perspectives. J Cardiothorac Vasc Anesth 2003; 17:90–100Landesberg, G