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CLINICAL PRACTICE |
Address correspondence to Gary E. Ross, DO, Physician Director Quality Improvement, St John Oakland Hospital, 27351 Dequindre Rd, Madison Heights, MI 48071-3499. E-mail: gary.ross{at}stjohn.org
The authors present a practical approach for physicians in clinical practice to use cardiac troponins in the interpretation of heart disease and myocardial damage. Laboratory results that fall within the intermediate area of facility-specific cutoff reference values for elevated troponin levels confer lower risks to patients than do higher levels of cardiac troponin. Perhaps not surprisingly, the actual anatomy of the vessels at cardiac catheterization does not correlate well with the troponin level.
In the six cases presented here, the patients' low levels of troponin release are discussed using the new term minimal myocardial infarction, which is synonymous with conditions that would previously have been diagnosed as unstable angina. Elevated levels of cardiac troponin provide a very sensitive measure for clinicians diagnosing patients with myocardial necrosis, but such measures are also useful in defining a broad spectrum of disease. Whenever the troponin levels are elevated (barring laboratory error), the patient has a poorer prognosis. The greatest challenge for physicians is in determining which patients with cardiac troponin elevation will best benefit from heart catheterization and percutaneous intervention.
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Considering these significant changes, it has become necessary for physicians to familiarize themselves with the appropriate interpretation of cTnI patterns. From a retrospective review of 2388 medical records, we present the case histories of 6 patients who presented for presumptive cardiac complaints to the Emergency Department (ED) of St John Macomb Hospital in Warren, Mich, one of the 8 hospitals affiliated with St John Health.
These cases represent the range of educational scenarios required for understanding and interpreting cTnI and creatine kinase isoenzyme MB (CK-MB) patterns in clinical practice. The principles of interpretation are similar for both cTnI and cardiac troponin T (cTnT). Cardiac troponin I was selected for this review due to its more prevalent use at the St John Health hospitals.
The accompanying graphs are used as educational tools to display the pattern of cardiac markers for each case and appear with the appropriate interpretation of the results. Furthermore, several scenarios demonstrate where the results of cardiac markers may be misleading.
Guidelines to aid physicians in diagnosing AMI—in the absence of definitive electrocardiograms (ECGs)—and unstable angina are constantly refined for special clinical settings (eg, percutaneous coronary artery intervention, cardiac surgery) in view of the continued research involving cardiac markers and treatment modalities. Current guidelines can be accessed online (Figure 2) from the American College of Cardiology (ACC), the American Heart Association, and the National Academy of Clinical Biochemistry.
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Methods
All 2388 patients who presented to the ED of St John Macomb Hospital from
September 1998 to March 2001 for apparent cardiac complaints were potential
subjects for this study. No other predetermined selection criteria were used
for this general pool of patients. Results from cTnI and CK-MB were available
at presentation to the ED and subsequently if the patients were either kept
for observation in the ED or admitted from the ED.
For each patient, a review of the medical records was undertaken and included a thorough review of available laboratory findings, results of ECG and echocardiogram, the cardiologist's diagnostic impressions and prescribed course of treatment, and the discharge diagnosis. The most common diagnoses—and those diagnoses that best illustrate (as determined by the authors) the use of cardiac markers in complex clinical presentations—were considered for this review.
The laboratory methods for the measurements of cTnI and creatine kinase (CK) at the treating institution were as follows:
The manufacturer's diagnostic criteria for cTnI and CK-MB were optimized at St John Health after a separate and independent study of 903 patients during 1997 and 1998 (unpublished data, 1998) using a receiver operator characteristic (ROC) curve analysis computer program, ROCKIT 0.9B (Beta Version, University of Chicago, Chicago, Ill).16 (See http://www-radiology.uchicago.edu/krl/top-page11.htm for more information.) The ROC curve is a mathematical tool for obtaining the best relationship of sensitivity and specificity for diagnostic decisions and thereby to define the reference cutoff values.13
The diagnostic criteria for cTnI (ng/mL) were: <0.5, normal; 0.5 through
4.5, suggests myocardial injury; >4.5, suggests AMI. The diagnostic
criteria for myocardial infarction from the CK-MB and CK-MB Index were: CK-MB
10.5 and CK-MB Index 3.9%. The diagnostic criteria for cTnI and CK-MB
used in this review were indistinguishable from those derived from an
independent study of 303 patients (unpublished data, 1998) at an affiliate
hospital of St John Health.
The figures presented for each case presentation use multiples of the upper reference limit rather than absolute y-axis coordinates. The reason for this is that the methodology for determining cTnI has not been standardized between manufacturers. Therefore, because of manufacturer inconsistency, multiples of the upper reference limit have become the standard format for presentation.1
Case Presentations
Case 1: Minimal Myocardial Infarction Previously Defined as Unstable Angina
A 77-year-old man presented to the ED with chest pain. His vital signs were
within normal limits. There was no adventitious respiratory noise, the abdomen
was soft, and the chest wall was not tender. The heart rate and rhythm were
regular. The chest radiograph showed no acute disease. The results of the
patient's ECG on presentation showed a right bundle branch block. Multiple
ECGs throughout admission did not demonstrate acute or evolutionary changes
consistent with AMI or ischemia. The patient also underwent a
ventilation-perfusion scan. The results were negative for pulmonary
embolism.
A plot of cTnI over time and results of cardiac markers (Figure 3 and Table 1) clearly indicated a classic rise and fall of cTnI below the AMI decision limit (>4.5 ng/dL). However, this plot represents the typical pattern for cTnI expected in unstable angina.5 There was no increase in CK-MB.
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The new ACC definition of myocardial infarction defines this pattern of troponin release as minimal myocardial infarction (MMI).1-2 The sensitivity of troponin makes it possible for physicians to define infarcts of minimal size. There is a continuous relation between MMI defined by troponin elevation and infarcts when other cardiac markers are present, and even larger infarcts complicated by heart failure or shock. Therefore, with the new ACC definition of myocardial infarction, any necrosis caused by ischemia is labeled a myocardial infarction.2
Case 2: Classic Acute Myocardial Infarction With Late Presentation of Patient
A 76-year-old man with type 1 diabetes mellitus, diminished mental status,
and low blood sugar (25 mg/dL) presented to the ED with the chief complaint of
weakness. The patient was discharged from the ED with the diagnosis of insulin
reaction.
The following day, the patient returned to the ED with similar symptoms. The patient had a pulse of 100, respiratory rate of 12, and arterial blood pressure of 110 +/– 80 mm Hg. During the chest examination, the attending physician noted diminished lung sounds bilaterally and heart sounds that were normal and fairly regular.
The patient's ECG during the second visit to the ED showed atrial fibrillation at a well-controlled rate (90 beats/min) and evidence of an old septal myocardial infarction. Multiple ECGs performed throughout the patient's hospital stay did not demonstrate any new AMI. However, there were changes in the ventricular response rate from the atrial fibrillation. The patient was treated with intravenous diltiazem to control the rapid heart rate.
The CK-MB and CK-MB Index were not indicative of AMI. However, two successive cTnI results were above the AMI decision limit (Table 2). The shape of the cTnI vs time curve (Figure 4) and its computerized extrapolation based on a normative case of cTnI, as seen in Figure 1, suggested that this patient presented after the initial AMI. The longer biological half-life of cTnI, which stays elevated for approximately 7 days after an AMI, makes it especially useful in the diagnosis of AMI in a late presentation.
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Case 3: Previously Labeled Unstable Angina With Rapid Rise in Cardiac Troponin I—Acute Myocardial Infarction or Minimal Myocardial Infarction?
An 82-year-old woman presented to the ED with complaints of non-radiating
chest pain on the left side and shortness of breath. She was taking multiple
nitroglycerin tablets sublingually without relief of pain. This patient had a
medical history of chronic obstructive pulmonary disease, myocardial
infarction, and multiple angioplasties during the prior two years.
The patient's chest radiograph was consistent with pulmonary edema. An echocardiogram was performed. Although it was a suboptimal study, the echocardiogram showed left ventricular dysfunction involving the left anterior wall, consistent with prior myocardial infarction and reduced left ventricular ejection fraction. The ECG on presentation, as well as multiple ECGs during hospitalization, showed non-specific ST-T changes consistent with ischemia. There was no evidence of AMI.
A review of cardiac markers (Table 3) indicated a rapid rise in cTnI from 2.3 to 11.6 ng/mL within 15.5 hours without any concomitant increase in CK. Similarly, a plot of cTnI over time also indicated a gradual, though not steep, increase in cTnI during 26 hours—a pattern that is not characteristic of AMI. The attending physician assigned the diagnosis of AMI; however, we questioned this diagnosis during our review of cases for this study. We believe that this patient had an MMI, which was previously labeled "unstable angina." This conclusion was supported by the shape of the simulated curve of cTnI over time (Figure 5). All cTnI values fell below the AMI decision level.
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Obviously, specimens were not available to confirm our computer-simulated curve. However, the cTnI assay on the original specimen, which was previously reported to have a cTnI of 11.6 (Table 3), was repeated. The repeat result of this specimen was 3.1 instead of 11.6, and this value complements the MMI diagnosis. Thus, the sudden rise in cTnI in the specimen in question was not due to clinical reasons, but was due instead to artifact.17-19
It is advised that a minimum of two elevated values (above the AMI decision level) should be recorded on either the ascending or descending limb of the cTnI vs time curve to confirm a diagnosis of AMI (Figure 1). A general recommendation for using cTnI is to request the retesting of the original specimen when the result is in question. At the same time, it is of value to request a test on a new specimen.
Case 4: Skeletal Muscle Injury and Acute Myocardial Infarction
An 88-year-old woman presented to the ED after falling in her home. She was
admitted with an acute intertrochanteric fracture of the left femur.
She had a history of atrial fibrillation, but no other known cardiac disease. A 2-dimensional echocardiogram with Doppler was performed, demonstrating normal global left ventricular systolic function. An ECG obtained in the ED showed ST-T wave abnormalities consistent with possible anterolateral ischemia. Throughout the patient's hospital stay, multiple ECGs showed no evidence of an AMI. Nine days after hospital admission, the patient underwent an open reduction internal fixation of the intertrochanteric left femur fracture.
The cardiac marker results prior to femur surgery (Table 4) and their plot over time (Figure 6) indicated a biphasic distribution.
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A few hours after the fracture, there was a significant increase in CK and CK-MB levels. In fewer than 24 hours, however, these markers showed an inflection point, suggesting that this initial burst of both CK and CK-MB was of skeletal muscle origin.
In contrast to the rise and fall pattern of CK and CK-MB, cTnI followed a classic pattern of sudden rise without exhibiting any minima, consistent with the fact that the concentration of cTnI is independent of skeletal muscle damage and reflects myocardial damage. Approximately 40 hours after the femur fracture, both CK and CK-MB exhibited classic indications of AMI, suggesting that their origin was myocardial tissue.
Case 5: Inflammatory Skeletal Muscle Disease Without Malignancy
A 74-year-old woman was admitted to the inpatient rehabilitation unit
because of progressive weakness and difficulty in walking. In view of her
numerous other complications, she was transferred back and forth from the
rehabilitation unit to the general care unit and intensive care unit (ICU) of
the hospital.
During the patient's longest continuous stays in the general care unit and ICU, an electromyelogram (EMG) was performed. The results were consistent with inflammatory myopathy. Echocardiography indicated hypokinetic left ventricular wall motion at the apex with an estimated ejection fraction of 50% to 55%. Results from the patient's multiple ECGs showed a complete left bundle branch block that remained essentially unchanged.
The persistent elevation of CK, CK-MB, and the CK-MB Index (Table 5)—in agreement with the EMG data—without a concomitant increase in cTnI above its AMI decision level-clearly indicated that the origin of CK-MB was skeletal muscle. Whenever there is a persistent and relatively constant increase in the CK-MB Index (eg, 9%–11.5%), as seen in this patient (Table 5), it is strongly suggestive that skeletal muscle, rather than cardiac tissue, is the origin of the high levels of CK-MB.
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This patient had markedly persistent elevation of serum ferritin (Table 6), and in the absence of any pathologic evidence of malignancy, it suggested acute inflammation rather than merely anemia. This patient also had an acute episode of herpes simplex virus 1 and 2 infection, and both IgG and IgM antibodies were markedly elevated, but subsequently resolved (Table 6). Furthermore, low levels of C3 and C4 complement activity and decreased serum immunoglobulin antibodies (Table 6) were compatible with infection.
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We postulate that the herpes simplex virus 1 and 2 infection affecting the cardiac muscle had caused a slight release of cTnI from the cardiac muscle (Table 5). It is also possible that, in view of the formation of immune complexes (due to infection) with the low levels of cTnI in this patient, the results (Table 5) demonstrated marker elevations that were false elevations for underlying coronary artery disease.
In summary, the cTnI results must be interpreted with caution in cases of infection and immune complex formation.20
Case 6: Skeletal Muscle Injury and Minimal Myocardial Infarction Followed by an Acute Myocardial Infarction
A 76-year-old man with type 1 diabetes mellitus fell on the ground,
resulting in an admission to the hospital for an intertrochanteric fracture of
the left hip.
This patient was in the hospital for 46 days. He initially underwent surgical repair of the hip. He also had bradycardic episodes diagnosed as sick sinus syndrome, necessitating pacemaker insertion. Subsequently, the patient developed acute deep venous thrombosis in the right upper extremity and aspiration pneumonia. The swelling of the upper extremity progressed and led to a compartment syndrome that necessitated a fasciotomy.
The initial ECG showed an old infarct with anterolateral ischemic changes, but multiple ECGs performed throughout the patient's hospitalization did not demonstrate changes consistent with a new AMI. Unexpectedly, an echocardiogram revealed normal left ventricular function and pulmonary hypertension.
The patient was discharged 46 days after his presentation to the ED. The final diagnoses and procedures completed included open reduction internal fixation of the hip fracture, myocardial infarction, aspiration pneumonia, sick sinus syndrome with secondary pacemaker insertion, deep venous thrombosis, and a fasciotomy to treat the right upper extremity compartment syndrome. The patient also had a shock liver and azotemia secondary to hypoperfusion.
An examination of the cardiac marker results (Table 7) during this patient's initial days of hospitalization demonstrated a cTnI level that did not increase above the AMI decision level. There was a significant increase in CK from its baseline value (63 U/L on November 10 and 245 U/L on November 14), primarily from skeletal muscle injury. The level of CK-MB and its index were not diagnostic of AMI. However, the shape of the cTnI plot over time (Figure 7) suggested an episode of MMI, which would have been labeled unstable angina prior to the availability of the troponin assay (eg, increased cTnI above the normal range, but below the AMI decision limit, and without a concomitant increase in CK-MB and its index above the threshold level for AMI).
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Soon afterward, this patient's laboratory test showed a sudden burst of cardiac markers (Figure 7 and Table 7), depicting skeletal muscle injury after hip fracture and followed by MMI and a large AMI.
Comment
These six case presentations were chosen to illustrate the most appropriate
interpretation of cTn I patterns in a variety of clinical scenarios. This
review article is intended to help convey in practical terms current thinking
regarding proper interpretation of cardiac troponin values.
Cardiac troponins are very sensitive for detecting even a minimal amount of myocardial damage.1,2,21 Elevations of cardiac troponin can occur without elevation of total CK and CK-MB.15 Unfortunately, there is currently no standardization among manufacturers of reagents for measuring cardiac troponin, of cutoff values for AMI, or of what the values define, such as minimal AMI and larger AMI.21
With the new ACC definitions, any elevation of cardiac troponin is indicative of an AMI as opposed to unstable angina. The new ACC guidelines suggest quantifying the size of AMI. In studies conducted prior to these revised guidelines, low levels of elevation were sometimes diagnosed as unstable angina.5,6,22 Cases in which cardiac troponin was actually released in small amounts and other cardiac markers were negative for increased values were likewise labeled as unstable angina prior to the availability of troponin assays. The cases presented demonstrate the analysis of troponin values using two decision limits: the first to define an abnormal and an intermediate zone, and the second, a cutoff value that is less sensitive and defines a myocardial infarction similar to that previously quantified by the WHO criteria.2,23
What was previously referred to as a level of troponin elevation in the range expected for "unstable angina," the new definition defines as minimal AMI. This level is often still too low to correlate with an AMI based on the WHO criteria. The WHO criteria require two of the following three conditions for the diagnosis of AMI: (1) ischemic symptoms, (2) ECG changes consistent with ischemia, and (3) elevated enzyme levels. Creatine kinase isoenzyme MB criteria were used until the new ACC guidelines were released in November 2002.2,3
The approach described in this review is controversial,2,22 yet it demonstrates the need to interpret cardiac troponin with an understanding that this test is very sensitive and can be used to make the diagnosis of minor myocardial damage.21
The actual cutoff values for myocardial infarction when a positive cardiac catheterization is likely, however, is based on the facility's ROC curves and conforms to the facility-defined decision limits. The elevations of cardiac troponin in the intermediate zone carry with them a significant risk to the patient for an adverse outcome in 30 days.22,24 Also, the greater the troponin level, the greater the likelihood of visualizing thrombus during heart catheterization, as well as the lower the odds of a thrombolysis in myocardial infarction grade 3 flow.1,25
If one wants to use the strictest definition of myocardial infarction, as presented in the new guidelines, the higher level cutoff decision value defines an AMI that is similar to the AMI population as defined by the WHO criteria. The area described as intermediate with low-level troponin release defines an acute MMI. Another reason for having two decision levels is that the confidence level for the value of cardiac troponin in the intermediate zone is large with older troponin assays. The newer equipment that is on the market is supposed to have narrow confidence levels for minimal releases of troponin.
Still another reason to have two decision levels is to better understand cardiac troponin release in patients in the ICU who either do not present with cardiac disease or those who present with hypoperfusion states and have troponin release. The reference cutoff value for such patients, marking true coronary disease, should be higher than that used for patients with probable coronary disease on presentation.15 Despite the higher cutoff value, release of cardiac troponin is still associated with a poorer prognosis.
With the new criteria, cTnI or cTnT is used for the diagnosis of AMI. When comparing the WHO criteria with the new ACC criteria, physicians should note that a significant number of patients who are now diagnosed with AMI under the ACC guidelines would have been missed by the WHO criteria.2,3
The many benefits of evaluating troponin, compared to other cardiac markers, are discussed elsewhere.1,15 Cardiac troponin I and cTnT have been recommended by the ACC as the preferred markers for physicians assessing myocardial damage.2 The biochemistry of the troponins has been nicely discussed previously1 and therefore is not discussed in this review.
From the hospitals of St John Health in Michigan: St John Oakland Hospital (Ross) in Madison Heights; St John Detroit Riverview Hospital (Bever, Uddin); St John Macomb Hospital (Devireddy) in Warren; and St John Hospital and Medical Center (Gardin, Ross) also in Detroit.
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This article has been cited by other articles:
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  D. M. Bunk and M. J. Welch Characterization of a New Certified Reference Material for Human Cardiac Troponin I Clin. Chem., February 1, 2006; 52(2): 212 - 219. [Abstract] [Full Text] [PDF]
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