Troponin elevated

Selvanayagam JB, Porto I, Channon K, et al, Troponin elevation after percutaneous coronary intervention directly represents the extent of irreversible myocardial injury insights from cardiovascular magnetic resonance imaging, Circulation 2005 ... 

Although troponin elevation suggests necrosis, biomarkers of myocardial ischemia are equally important. Ischemia-modified albumin was reported to be highly sensitive for a diagnosis of ischemia in patients with chest pain presenting to the emergency room (12). Further study needs to be done on this sensitive biomarker for myocardial ischemia. 

Creatine kinase is a protein necessary for ATP generation. One of its forms, CK-MB, is found mainly in the myocardium and upon tissue damage, such as myocardial infarction (Ml), becomes elevated. It takes up to 24 h for the elevated level to reach its peak. A difficulty resides in the fact that unlike troponin, an assay does not allow us to distinguish between cardiac and skeletal muscle damage. Also, in about a third of Ml cases while CK-MB levels stay neutral, troponin elevation is noted. The normal level of troponin in the blood is less than 0.3 pg/1 while for CK-MB it is less than 3.0 ng/ml. For humans, the CK is in the range of 55-170 lU/1 (international units per liter) and is less specific than CK-MB for cardiac tissue damage. 

Jensen, J.K., Atar, D., Mickley, H. (2007). Mechanism of troponin elevations in patients with acute ischemic stroke. Am. J. Cardiol. 99 867-70. 

It is important to remember other reasons for troponin elevation without Ml - heart or kidney failure, hypertensive crises, etc.)... 

A patient with transient electrolyte shift or a presumed cause for cardiac arrest, may or may not benefit from an ICD. Survivors of cardiac arrest due to ventricular arrhythmia should not be assumed as due to reversible cause unless this can be proven with high level of certainty. Consider the fact that it is often not clear what is the cause or the effect of a cardiac arrest Hypokalemia and slight troponin elevation are two common findings after an arrest even if they are not the cause. Be careful not to jump to conclusions as to what caused a cardiac arrest. If the cause is not completely clear it is better to err on the side of an ICD implant rather than to rely on unfounded and potentially dangerous clinical assumptions. 

The precise definition of a myocardial infarction is a subject of detailed discussion in the literature. Different definitions can be used in clinical practice, clinical trials, and registries (White et al. 2014). In an attempt to standardize definitions, the Third Universal Definition of myocardial infarction is based on troponin elevation together with ischemic symptoms, ischemic ECG changes, and imaging evidence myocardial infarctions are classified into several types according to whether they are spontaneous, secondary to imbalance between coronary artery blood supply and demand, related to sudden death, or related to revascularization procedures (White et al. 2014). 

Biochemical markers (creatine kinase [CK], CK-MB fraction, troponin I and troponin T) are elevated in Ml (ST-segment elevation Ml and non-ST-segment elevation Ml), but normal in chronic stable angina and unstable angina. 

Describe the onset, peak, and duration of elevation of troponin and creatine kinase myocardial band in acute myocardial infarction. 

Risk-stratification of the patient with NSTE ACS is more complex, as in-hospital outcomes for this group of patients varies with reported rates of death of 0% to 12%, reinfarction rates of 0% to 3%, and recurrent severe ischemia rates of 5% to 20%.12 Not all patients presenting with suspected NSTE ACS will even have CAD. Some will eventually be diagnosed with non-ischemic chest discomfort. In general, among NSTE patients, those with ST-segment depression (Fig. 5-1) and/or elevated troponin and/or CK-MB are at higher risk of death or recurrent infarction. 

Troponins T or I Proteins found predominantly in cardiac muscle that regulate calcium-mediated interaction of actin and myosin troponins I and T are released into the blood from myocytes at the time of myocardial cell necrosis after infarction. These biochemical markers become elevated and are used in the diagnosis of myocardial infarction. 

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. 

ACS can be classified into UA, myocardial infarction (Ml) without ST-segment elevation [non-ST-elevation Ml (NSTEMI)], or STEMI. The presence of cardiac troponin in ACS indicates worse prognosis than the absence of troponin (9). 

Cardiac enzyme elevation (creatine kinase-MB, cardiac troponin) may occur on average in 20% to 30% of patients after PCI and is associated with adverse clinical outcomes in the short- and long-term (64), Magnetic resonance imaging... 

Biomarkers help establish the presence of myocardial necrosis. There are nearly two dozen biomarkers currently under study Most experience is with creatinine kinase, creatinine kinase MB, troponin I or 7) and myoglobin, Others are under study (Fig. I) (3). Two other biomarkers currently available are C-reactive protein (CRP) and brain natriuretic peptide (BNP), Even minor elevations of troponin I orT have had prognostic importance, In the tactics TIMI 18 study, troponin levels between 0,1 ng/mL and more than 1,5 ng/mL were found in 60% of the 1821 patients (9), In this study, troponin... 

Troponin levels are an important addition to stratify risk in the ACS patient with history and electrocardiographic changes. However, abnormal troponins are found in other conditions as well, notably pulmonary embolus and sepsis, when ACS patients are excluded. These authors suggest that elevated troponin levels are not specific for ACS (II). This requires clinical evaluation (Table 2). 

Table 2 Nonthrombotic causes for elevated cardiac troponin level diagnosis...

Multiple biomarkers are under study. Well-studied and commercially available biomarkers include CK-MB, troponin I or T CRR and BNR and recently, myeloperoxidase, Each of these biomarkers is an independent predictor of death, myocardial infarction, or congestive heart failure. Utilizing the opus TIMI 16 patients, Sabatine et al. studied CRP BNP and troponin in 450 patients. These authors found a 30-day risk of death increased in proportion to the number of these biomarkers that were elevated at baseline (25). They validated the concept in the tactics TIMI 18 patients (26). These two trials of over 2000 patients with NSTEMI, troponin, CRR and BNP provided independent prognostic information. 

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