Serum troponin

I are regulatory proteins involved in myocardial contractility. They are released into the plasma in response to cardiac damage. Elevated serum troponins are more predictive of adverse outcomes in unstable angina or myocardial infarction than the conventional assay of CK2. 

Hamm CW, Heeschen C, Goldmann B, et al. Benefit of abciximab in patients with refractory unstable angina in relation to serum troponin T levels. N Eng J Med 1999 340 1623-1629. 

PTCA and 1 hour afterward. Reduction in primary outcome variables was 30% in favor of abciximab and was again maintained over 6 months (52). Patients with elevated serum troponin T levels showed a particular benefit (53). Finally, patients with acute MI benefited from abciximab given as an adjunct to primary PTCA in the RAPPORT trial (54). 

A 16-year-old girl developed pericarditis associated with clozapine. There were electrocardiographic changes and serial rises in serum troponin I, a highly sensitive and specific marker of myocardial injury. 

An 83-year-old white man became distressed and had nausea and facial flushing after 10 minutes of a slow infusion of vancomycin (1 g scheduled over 2 hours). Despite interruption, he developed suffocating respiratory distress requiring intubation and mechanical ventilation. Uncharacteristic of anaphylactoid reactions, he became severely hypertensive. Subsequently, his condition rapidly normalized. During the acute event, there was an increase in serum troponin concentration. 

Wallace KB, Hausner E, Herman E, et al. Serum troponins as biomarkers of drug-induced cardiac toxicity. Tox Path. 2004 32 106-121. 

Figure 44-27 Rates of cardiac events after randomization (with or without therapy, abciximab) and during 6 months of followup among patients with serum cardiac troponin T concentrations above and below the diagnostic cutoff. (Data from Hamm CW, Heeschen C, Goldmann B, Vahanian A, Adgey j, Miguel CM, et a. Benefit of ABCIXIMAB in patients with refroctory unstab/e angina in relation to serum troponin T levels. N Engl j Aled 1999 340 1623-9.)...

Typically, no laboratory tests are abnormal however, if the patient has intermediate- to high-risk features for unstable angina, electrocardiographic changes are seen, and serum troponin or creatine kinase concentrations may become abnormal (Table 15-3). 

Cardiac troponin complex consists of three parts. Troponin T facilitates contraction, troponin 1 (cTnl) inhibits actin-myosin interactions, and troponin C binds to calcium ions. Troponin I and T are specific to the heart, but cTnT is also expressed by injured skeletal muscle. In the course of cell damage, cardiac troponin is released from myocytes, facilitated by increased membrane permeability that allows smaller troponin fragments to traverse the membrane. Complicating the use of troponin levels is the fact that in cases where there is cardiac injury without cardiac cell membrane disruption, serum troponin level can increase. Also, altered ion homeostasis may not be reflected in troponin levels. 

The patient, a 63-year-old Caucasian female, was hospitalized on 4 April 2002 though 10 April 2002 for a non-ST segment elevation myocardial infarction (non-Q-wave MI per chart documentation). She had a negative adenosine stress test after the initial event. Her serum cardiac-specific troponin I (cTnl) concentration 24 hours after her onset of chest pain was 1.4 pg/L (upper limit of normal is 0.3 ng/mL), and her creatine kinase (CK) MB level was 12.5 pg/L (upper limit of normal 6.0 ng/mL). Three days post-event her cTnl level was 0.5 pg/L and her CK-MB level was 4.5 pg/L (Fig. 5-1). MB refers to one of the isoenzyme forms of CK found in serum. The form of the enzyme that occurs in brain (BB) does not usually get past the blood-brain barrier and therefore is not normally present in the serum. The MM and MB forms account for almost all of the CK in serum. Skeletal muscle contains mainly MM, with less than 2% of its CK in the MB form. MM is also the predominant myocardial creatine kinase and MB accounts for 10%-20% of creatine kinase in heart muscle. 

Figure 5-1. Time-course of changes in serum cardiac troponin I and creatine kinase MB (CK-MB) following myocardial infarction and subsequent reinfarction during hospitalization. Cardiac-specific troponin I (cTNI), open squares CK-MB, filled circles. Reprinted fromApple and Murakami (2005).

Apple FS, Falahati A, Paulsen PR, et al. Improved detection of minor ischemic myocardial injury with measurement of serum cardiac troponin I. Clin Chem 43 2047-2051,1997. 

Herman EH, Zhang J, Lipshultz SE, et al. Correlation between serum levels of cardiac troponin-T and the severity of the chronic cardiomyopathy induced by doxorubicin. / Clin Oncol 1999 17(7) 2237 13. 

Apak, I., Iltumur, K., Tamam, Y., Kaya, N. (2005). Serum cardiac troponin T levels as an indicator of myocardial injury in ischemic and hemorrhagic stroke patients. Tohoku J. Exp. Med. 205 93-101. 

Cirrhotic cardiomyopathy This term is defined as a left ventricular functional disorder due to stress (e. g. hyperdynamic circulation) or as pharmacological stimulation. But also the possibility of (toxically induced ) subclin-ical myocardial damage is discussed, especially because elevated troponin 1 serum values are detectable in every third patient. (81, 142, 187) (Troponin is connected with propomyosin in the actin filaments at regular intervals and, as a relaxing protein , has an important function in muscle metabolism, also in the heart). 

Antmann EM, Grudzien C, Sachs DB. Evaluation of a rapid bedside assay for detection of serum cardiac troponin T. JAMA 1995 273 1279-82. 

The changes of serum CK and its MB isoenzyme following a myocardial infarction are discussed in Chapter 44. Other cardiac conditions have been reported to increase serum CK and CK-MB in serum. These conditions include cardioversion, cardiopulmonary bypass and coronary artery bypass surgery, cardiac transplantation, myocarditis, pericarditis, and pulmonary embolism. Despite improvements, in the diagnostic performance and practicality of CK and CK-MB assays, there is no controlled cUnicai impact trial showing that these tests are effective for decisions to send a patient home or to the appropriate level of care of admission for patients with suspected acute cardiac ischemia, either as one-time or serial tests.For diagnosis of acute myocardial infarction, it is now advantageous to use more cardiac-specific nonenzymatic tests, such as cardiac troponin I orT. 

Figure 44-10 Cardiac troponin i imprecision profiles for human serum pools using different cTnl assays, with 0% CV concentration indicated by the dashed line. (From Panteghini M, Pagani F, Yeo KT, Apple FS, Christenson RH, Dati F, et al. Evaluation of the impredsion at low range concentrations of the assays for cardiac troponin determination. Clin Chem 2004 50 327-32.)...

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