|Year : 2016 | Volume
| Issue : 4 | Page : 505-506
Elevated troponin levels and typical chest pain: Is always acute coronary syndrome?
Department of Medicine and Cardiology, Air Force Hospital, Jorhat, Assam, India
|Date of Web Publication||12-Jul-2016|
Department of Medicine and Cardiology, 5 Air Force Hospital, Jorhat, Assam
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kumar A. Elevated troponin levels and typical chest pain: Is always acute coronary syndrome?. Med J DY Patil Univ 2016;9:505-6
Cardiac troponin T (cTnT) and troponin I (cTnI) are the most specific and sensitive laboratory markers of myocardial cell injury and therefore have replaced creatine kinase MB (CK-MB) as the gold standard. Unexplained elevations of troponins are rare, but may sometimes cause confusion. A rise of troponins reflects irreversible myocardial cell necrosis. Accordingly, abnormal values have been described in various conditions not related to acute coronary disease, such as myocarditis, pulmonary embolism, acute heart failure, septic shock, and as a result of cardiotoxic drugs as well as after electrical cardioversions.
The troponin complex consists of three subunits — troponin C, troponin I, and troponin T — and is located on the myofibrillar thin (actin) filament of striated (skeletal and cardiac) muscle. The cardiac isoforms cTnT and cTnI are only expressed in cardiac muscle. Hence, cTnT and cTnI are more specific than CK values for myocardial injury and, because of their high sensitivity, they may even be elevated when CK-MB concentrations are not.
There are some noncardiac conditions leading to rise in troponin levels discussed in the following paragraphs.
One of these is chronic renal failure. Acute coronary syndromes are frequently observed in renal failure; however, the use of troponin for diagnosis is inconvenient since cTn levels may be elevated in the absence of an acute ischemic event. Heart failure is also a common comorbidity in renal failure, in which troponins increase without any evidence of ischemia or infarct. Decreased clearance is another proposed explanation for troponin elevation in renal failure. In renal failure, cTnT elevation is seen more frequently than cTnI. Patients with acute heart failure/acute pulmonary edema constitute an important proportion of emergency department admissions. Troponin levels may rise without overt ischemia in heart failure. In subarachnoid hemorrhage, electrocardiographic manifestations were first mentioned by Byer in 1947. Today, the most widely accepted theory is the catecholamine hypothesis. It is possible that acute brain injury results in a massive release of norepinephrine from the myocardial sympathetic nerve terminals to the myocardial interstitium, which may subsequently lead to myocyte necrosis and contractile dysfunction in addition to sympathetic nerve terminal damage.
Ischemic cerebrovascular accident can also lead to rise in troponin levels. The proposed mechanisms regarding troponin release in the early phase of ischemic cerebrovascular disease include secondary cardioembolic cerebral ischemia related to primary myocardial damage, secondary central nervous system activation to primary cerebral ischemia, and cerebral disease-related heart failure. Acute massive or submassive pulmonary embolism is associated with elevated serum cTn levels. Troponin has been proposed as a risk determinant that may help in the decision of performing thrombolysis or embolectomy. Massive pulmonary embolism may cause cardiogenic shock and acute right ventricular dilatation, and release of endothelial mediators such as thromboxane, serotonin, and endothelin contributes to right ventricular ischemia and damage. Troponin elevation was found to be an independent predictor of the need for noninvasive mechanical ventilation and mortality in patients who were admitted with acute exacerbation of chronic obstructive pulmonary disease. Worsened pulmonary hypertension, hypoxia, and hypercapnia contribute to myocardial damage during the acute exacerbation period. The myocardial depressing factors released in sepsis and other inflammatory conditions cause troponin to be fragmented into low molecular weight particles in situ. These fragments are secreted into the circulation in the presence of increased membrane permeability. Since there is no necrosis, the myocyte damage is not permanent. Myocardial depression is completely reversible in patients who recover from sepsis. Competitive endurance sports have been suggested to be associated with elevations in cardiac biomarkers, especially cTns. Middleton et al. suggested that the increased myocardial demand related to endurance exercise could physiologically increase the turnover of cTns. Another proposal was that stress induces free radical overload, which causes a transient increase in membrane permeability and leads to troponin leakage from the cytosol. Exercise-induced dehydration, hemoconcentration, and altered acid-base balance were also reported to be associated with this increased membrane permeability. Troponin elevation was not found to be associated with any functional impairment using either echocardiography or cardiac magnetic resonance imaging. In light of the current knowledge, there seems to be no prognostic implication of troponin elevation. Direct cardiac trauma may cause troponin elevation due to the impairment of cardiac myocyte integrity. Although troponins are not found in the pericardium, they may be elevated because of the involvement of the epicardium in the inflammatory process in acute pericarditis. In addition, some myocardial damage may take place, and the pattern of troponin release in acute pericarditis mimics that of acute coronary syndromes. In contrast to acute coronary syndromes, troponin positivity was not associated with poor prognosis. Acute myocarditis may mimic myocardial infarction since chest pain, segmental wall motion abnormalities, and myocardial necrosis proven by troponin elevation exist in both conditions. It has also been found that troponin is more sensitive than CK-MB and correlates well with the symptoms of heart failure at 1 month after acute myocarditis. How long the troponins remain elevated depends on the inflammation severity. Supraventricular or ventricular tachycardia, atrial fibrillation with high ventricular response, or any other tachycardia may cause troponin elevation by increasing the myocardial oxygen demand without epicardial coronary stenosis. Temporal myocyte damage due to hemodynamic compromise is the mechanism responsible for this phenomenon.
| Conclusion|| |
Although cTns have been accepted as the gold standard in the diagnosis and risk stratification of acute coronary syndromes, misinterpretation of detectable troponin levels in the emergency department or other in-hospital settings may lead to confusion in terms of diagnosis and choice of suitable therapy options. Physicians should be aware of the nonischemic causes of troponin positivity as well as their pathophysiology and clinical impact in an effort to prevent unnecessary invasive and noninvasive treatments and coronary care unit admissions.
| References|| |
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