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  • Author: Ashvarya Mangla, MBBS, MD; Chief Editor: Eric B Staros, MD  more...
Updated: Jan 14, 2015

Reference Range

Troponins are protein molecules that are part of cardiac and skeletal muscle. Smooth muscle cells do not contain troponins.

Three types of troponins exist—troponin I, troponin T, and troponin C. Each subunit has a unique function: Troponin T binds the troponin components to tropomyosin, troponin I inhibits the interaction of myosin with actin, and troponin C contains the binding sites for Ca2+ that helps initiate contraction.[1]

This review discusses troponin as a marker of cardiac injury, its testing, utility, appropriateness use criteria, and interpretation of abnormal values.

Abnormal values

Troponins are generally undetectable in healthy patients, although this may eventually change as more sensitive assays become available. The absolute abnormal value varies depending on the clinical setting in which the patient is evaluated and the assay used. In a patient who presents with chest pain and possible myocardial infarction (MI), an abnormal value is that above the 99th percentile of the healthy population as a cutoff using an assay with acceptable precision.

The 99th percentile cutoff point for cardiac troponin T (cTnT) is well-known at 0.01 ng/mL (with 10% coefficient of variance value at the 99th percentile of 0.03 ng/mL), as only one cTnT assay exists.[2]

In contrast, several different assays are commercially available for cardiac troponin I (cTnI), so the 99th percentile cut point varies based on the assay being used.[3, 4, 5]

The 99th percentile of a reference decision limit (medical decision cutoff) for cardiac troponin (cTn) assays should be determined in each local laboratory with internal studies using the specific assay that is used in clinical practice or validating a reference interval that is based on findings in the literature.[2] Clinicians need to be aware of the reference range for the assay in use at their institution. Table 1 shows the calculated 99th upper reference limit values for some of the available troponin assays.

The cutoff values are different for MI in the setting of percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). Currently, CABG-related MI is defined as (1) biomarker level elevations more than 5 times the upper reference limit plus either new pathological Q waves or new left bundle branch block (LBBB), (2) angiographically documented new graft or native coronary artery occlusion, or (3) imaging evidence of new loss of viable myocardium.

For PCI in patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile upper reference limit indicate periprocedural myocardial necrosis. By convention, increases of biomarkers above 3 x 99th percentile upper reference limit have been designated as defining PCI-related MI.

In patients undergoing CABG or PCI in whom baseline cardiac enzyme values are abnormal, it is difficult to confirm periprocedural MI.

The following are 99th percentile cutoff values for acute MI (as suggested by the ESC/ACC) for some of the commonly used troponin I assays:[6]

  • DPC Immulite: 0.40
  • Abbott AxSYM: 0.30
  • Bayer ACS:Centaur: 0.15
  • Ortho Vitros: 0.10
  • Bayer ACS:180: 0.07
  • Dade Dimension RxL, second generation: 0.07
  • Beckman Access, second generation: 0.04
  • Byk-Sangtec Liaison: 0.036
  • Dade Status CS: 0.03
  • Roche Elecsys, third generation: 0.01


Troponins are released in response to myocardial injury regardless of cause. Ischemia is the most common cause of cardiac muscle damage, and the initial assays were developed as a marker to detect the presence of myocardial ischemia; however, elevation of troponin levels can occur in myriad conditions other than ischemic damage.

Troponin release in cardiac injury

It is proposed that there is a small cytosolic pool and a larger muscular pool of troponins. During cardiac injury, depending on the severity, troponins are released from both pools. An initial small elevation occurs when troponins are released from the cytosolic pool, when troponin molecules in the cytosol of cardiac muscle diffuse across the sarcolemma into the surrounding lymphatics and blood vessels, becoming detectable in blood. If the injury persists and necrosis progresses, further troponins are released from the muscular pool.[7, 8]

Pattern of rise and fall

When measured with older generation assays, elevated troponin levels can be detected 6-12 hours after onset of myocardial injury, peaking at about 24 hours, followed by a gradual decline over several days (up to 2 weeks).

Modern assays can detect troponins as early as 3-4 hours after onset of myocardial damage. This has increased the sensitivity of point-of-care troponin testing in patients who present initially to the emergency department with symptoms suggestive of ischemia and myocardial damage. Most current guidelines recommend rechecking troponins 6-12 hours after the initial assessment and up to 24 hours after symptom onset.[3, 9] In patients in whom subendocardial non–ST-segment elevation myocardial infarction (NSTEMI) is highly suspected, the troponin levels may be re-evaluated earlier, at 3-4 hours, as the markers may be detectable sooner.[10, 11, 12]

Troponin T and troponin I

Troponin T and troponin I are different molecules with different roles. While an elevation of either specifies myocardial damage, their absolute values differ. One standardized assay exists for troponin T, while multiple assays are available for troponin I; each has a different cutoff value, as these assays target distinct epitopes..

Clinicians need to be aware of the abnormal reference range for the assays used in their practice and that absolute values from different assays do not correlate.

Causes of troponin elevation other than myocardial infarction

Causes of troponin elevation other than MI include the following:

Elevated troponin levels should always be evaluated in a clinical context. While the incidence of elevated troponin levels in the general population is low and is generally associated with an underlying cardiac structural abnormality, any level of troponin elevation is associated with a worse prognosis in age- and disease-matched cohorts. This is especially true in critically ill patients with a diagnosis other than acute coronary syndrome, in whom elevated troponin levels have been shown to be associated with increased mortality.[13, 14, 15, 16]

There are various causes of troponin level elevation in the absence of coronary artery disease, discussed below.

Damage due to relative myocardial ischemia (type 2 myocardial infarction) from a supply-demand mismatch

The troponin level may be elevated in the setting of a demand for an increased cardiac output and relatively inadequate myocardial blood flow. This can occur in sepsis,[14] septic shock, systemic inflammatory response system (SIRS), hypotensive shock, hypovolemic shock,[17] cardiac arrhythmias (eg, supraventricular tachycardia, atrial fibrillation with rapid ventricular rate, tachyarrhythmias).[18, 19] In patients with acute exacerbation of congestive heart failure due to etiologies even other than MI, troponin levels may be elevated because of the inability of the weak heart to maintain appropriate coronary perfusion.

Tachycardia from any etiology increases the cardiac oxygen demand and, owing to reduced diastolic filling time, reduces coronary perfusion. This relative supply demand mismatch can cause myocardial damage to some extent, increasing the level of troponins.

In the setting of sepsis, septic shock, and acidosis, in addition to the increased myocardial oxygen demand, a relative myocardial depression contributes to demand ischemia.

Elevation of cardiac troponin levels has been noted in the setting of aortic valve disease. Individuals with aortic stenosis often have increased left ventricular thickness, and this increased muscle mass may contribute to demand-based subendocardial ischemia.[20] This also holds true for individuals with left ventricular hypertrophy.[21]

Hypertensive emergency, coronary vasculitis, and aortic dissection may also cause an elevated troponin level due to type 2 MI.

Elevated troponin levels caused by direct cardiac damage from agents other than ischemia

Cardiac contusion due to blunt chest wall trauma can raise the level of troponins stemming from direct injury to the ventricular muscle fibers. The combination of ECG and troponins had a high negative predictive value in diagnosing significant blunt cardiac injury, and, in the absence of other compelling reasons for hospitalization, these patients can be safely discharged.[22]

Myocarditis from any etiology (eg, viral, fungal, mycobacterial, bacterial) may elevate troponin levels owing to direct injury to the ventricular myocyte.[23] This causes membranous damage, myocyte necrosis, and release of troponin from the injured or necrosed myocytes.[24] Similarly, troponin levels may be elevated in the absence of ischemia in acute pericarditis due to ventricular myocyte injury.[25]

Patients who receive CPR or external defibrillation[26] or shocks from an implantable cardioverter defibrillator may also have elevated troponin levels due to ventricular muscle damage.

Medications and chemicals that are directly cardiotoxic may also elevate troponins. Such agents include chemotherapeutic drugs such as cyclophosphamide, anthracyclines, and bevacizumab and chemicals such as carbon monoxide. Studies in patients receiving chemotherapeutic agents with known cardiotoxicity have shown that those who develop elevated troponin levels in the absence of ischemia are at an increased future risk of developing left ventricular failure and cardiomyopathy.[27]

Infiltrative disorders such as amyloidosis may also cause elevate troponin levels.

Individuals who develop rhabdomyolysis with cardiac involvement may also have elevated troponin levels.

Multiple factors

Troponin elevation in stroke

Both ischemic and hemorrhagic stroke have been associated with elevated troponin levels and ECG changes, although the degree of elevation is typically much less than that seen with acute MI. The exact etiology of this remains unclear, but autonomic dysfunction following stroke with an imbalance in the sympathetic and parasympathetic outflow to the heart may be a possible explanation.

In the setting of stroke, the sympathetic input to the heart increases and catecholamines surge, which can affect the cardiac myocyte and increase troponin levels. levels of other cardiac markers are often normal in this setting. In patients with stroke or subarachnoid hemorrhage, elevated troponin levels have been associated with poor cardiac and neurological prognosis.[28]

Peripartum cardiomyopathy and Takotsubo cardiomyopathy have also been associated with elevated troponin levels.

Troponin elevation with pulmonary disease

The presence of significant pulmonary disease strains the right ventricle by increasing the right ventricular afterload. This can result from acute pulmonary embolism and chronic obstructive pulmonary disease (COPD) in the setting of pulmonary hypertension.

Increased troponin levels may be seen with a large pulmonary embolism, presumably owing to increased right heart strain.[29] Elevated troponin levels in the setting of acute pulmonary embolism portends a worse prognosis than in patients without elevated troponin levels.[30]

Similarly, troponin levels may be elevated in the setting of acute exacerbation of COPD and associated with increased in-hospital mortality.[31]

Troponin elevation with renal disease

The evaluation of elevated troponin levels in patients with chronic kidney disease presents many challenges. In many asymptomatic patients with kidney disease, especially those on hemodialysis, troponin levels may be elevated.[32]

In the absence of other clinical features of ischemia, elevated troponins alone may not be reliable and may be falsely positive, leading to unnecessary investigations. This is further confounded by the fact that patients with renal insufficiency are at an increased risk for silent ischemia and that cardiovascular diseases continue to be the leading cause of mortality in patients with kidney diseases.

Nonetheless, even asymptomatically elevated troponin levels are associated with a worse long-term prognosis in patients with chronic kidney disease.[33]

In many cases, troponin T is more elevated than troponin I in patients with chronic kidney disease, even at baseline.[32, 33] Although the exact reason for this is unknown, it has been postulated to result from a higher unbound cytosolic pool of troponin T, leading to early release and a higher molecular weight of troponin T (resulting in a delayed clearance from the kidneys).[34]


Collection and Panels

The troponin sample assay relies on serum levels of troponin. The sample collected is whole blood through venipuncture. No special patient preparation is needed, and fasting is not required. Blood for the test can be drawn at any time of the day.

The tubes in which the sample is collected are different for troponin T and troponin I, and the clinician should refer to the package insert for requirements. Generally, troponin T requires sample collection in heparinized test tubes (green top), while EDTA (purple top) or heparinized tubes are used for troponin I.[6, 35] Most specimens require centrifugation prior to running the test in order to separate the serum from the cellular components.

Sample storage

The clinician should refer to the assay’s package insert for instructions. In general, for troponin T, the blood sample should not be frozen or refrigerated immediately, and it can be stored at room temperature for up to 8 hours for analyses.[6]

Laboratory turnaround time

Currently, the consensus is that the turnaround time for troponin measurement in the setting of chest pain should be 60 minutes, and individual laboratories should strive to achieve this time.[36]



Troponins are protein molecules that are part of cardiac and skeletal muscle. Smooth muscle cells do not contain troponins.

Three types of troponins exist—troponin I, troponin T, and troponin C. Each of the 3 troponin subunits has a unique function. Troponin T binds the troponin components to tropomyosin. Troponin I inhibits the interaction of myosin with actin. Troponin C contains the binding sites for the Ca2+ that helps to initiate contraction.[1]

The skeletal and cardiac muscle troponin T and troponin I are immunologically distinct entities.[7] Separate sets of genes code for these proteins. Thus, the cardiac troponin assays, which rely on antigen antibody interaction, are specific for cardiac troponins and can be used to differentiate between the skeletal and cardiac troponins.

Cardiac troponin levels do not rise in the presence of skeletal damage without cardiac myocyte damage. However, this is not the case for creatine kinase MB, which, being present to some extent in skeletal muscle and several other tissues such as the intestines, tongue, diaphragm, uterus, and prostate, may be elevated upon injury to these tissues, potentially resulting in false-positive results.[37] . Because of this, troponin testing is superior to creatine kinase MB testing.

Ischemic heart disease

Ischemic heart disease is a leading cause of death worldwide. Much advancement in early diagnosis and management of patients presenting with varying manifestations of ischemic heart disease has been made.

Electrocardiography (ECG) was one of the earliest diagnostic modalities introduced to evaluate ischemic injury to the heart. Despite its usefulness, ECG continues to be nonsensitive in diagnosing ischemic cardiac events, as ECG findings are normal in many patients with ischemic injury.

The introduction of various markers of cardiac injury, such as creatinine kinase MB, troponins, and myoglobins, has revolutionized the diagnosis of myocardial injury. The cardiac troponins, by virtue of being the most sensitive and specific, have become the preferred biomarker for evaluation of patients with suspected MI.[2, 38, 9]


Troponin values should be evaluated upon clinical suspicion of MI.

Detection of myocardial infarction

Per the 2007 guidelines of the ACC/AHA, the term acute MI should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia. One of the criteria is detection of rising and falling cardiac biomarker levels, with at least one value above the 99th percentile of the upper reference limit. The preferred marker for diagnosis of MI in this setting is troponin.[38] This is the single most important use of troponin in clinical medicine. The troponins are specific to cardiac muscle, rise fairly early in cardiac injury, and stay elevated longer than some of the other cardiac biomarkers such as CK-MB and myoglobin. Normal serial troponin values effectively rule out acute myocardial ischemia.

Determining infarct size

Peak troponin values can provide an estimate of the infarct size and the severity of myocardial damage. These values are more sensitive in the setting of transmural infarction (ST-segment–elevation MI [STEMI]) than in subendocardial infarctions (NSTEMI).[39, 40] This correlation holds true for both troponin T[41, 39] and troponin I[42] (peak or values at 72-96 hours). Higher values generally correlate with a larger infarct

Significance of degree of troponin elevation

The degree of troponin elevation correlates well with both the 30-day mortality and long-term mortality. Various clinical trials have evaluated the degree of elevation of both troponin I and troponin T and found that higher elevations at presentation and peak are associated with worse long-term outcomes. The absolute values have been used to guide treatment decisions and to identify patients who are at an increased risk of death.[43, 44, 45, 46]

Prognostic value of the timing of elevation

Patients who present with elevated troponin levels at baseline tend to have worse outcomes than those in whom troponin levels are elevated at 8 hours. Outcomes are best in patients in whom troponin levels never elevate.[47]

In both STEMI and NSTEMI, elevated levels of troponin T and troponin I at presentation are associated with a worse prognosis in terms of both short-term and long-term mortality.

How often to perform troponin testing and the need for serial testing

In patients with MI, there is a lag before troponin elevations can be detected.Thus, the markers should be serially monitored upon suspicion for acute coronary syndrome (ACS). The initial recommendations were to check the markers every 6 hours until the expected peak was reached. However, with the more sensitive assays now available, very low concentrations of elevated cardiac markers can be detected, and evidence has demonstrated that checking troponins 3-4 hours after the initial draw can help in early diagnosis of ACS.[47]


Some of the analytical interfering factors that may lead to falsely elevated troponin results include the following:[9, 48, 49, 50]

  • Incompletely clotted specimen (eg, in patients with coagulopathy or on anticoagulant therapy) [51]
  • Heterophile antibodies, human anti-animal antibodies [52]
  • Rheumatoid factor [53, 54] and autoantibodies
  • Elevated bilirubin levels [55]
  • Immunocomplex formation [56]
  • Markedly elevated alkaline phosphatase levels [57]
  • Analyzer malfunction [58]
Contributor Information and Disclosures

Ashvarya Mangla, MBBS, MD Adult Hospitalist Services, OSF Saint Francis Medical Center; Clinical Assistant Professor of Medicine, University of Illinois College of Medicine at Peoria

Ashvarya Mangla, MBBS, MD is a member of the following medical societies: American College of Physicians, American Heart Association

Disclosure: Nothing to disclose.


Saurabh Gupta, MD, FACC, FSCAI Director, Cardiac Catheterization Laboratories, Co-Director, Multidisciplinary HeartValve Clinic, Assistant Professor of Medicine (Cardiology), Division of Cardiovascular Diseases, Associate Program Director, Interventional Cardiology Fellowship Program, Oregon Health and Science University School of Medicine

Saurabh Gupta, MD, FACC, FSCAI is a member of the following medical societies: American College of Cardiology, Oregon Medical Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

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