Troponin tests measure the level of cardiac-specific troponin in the blood to help detect heart injury. An elevated troponin level in the blood may indicate a heart. Consequent to their findings, one of the most successful diagnostic investigations to date has been developed: the cardiac troponin (cTn). High-sensitivity assays can quantify cardiac troponins I and T (hs-cTnI, hs-cTnT) . were available, the most up-to-date or comprehensive information was used.
It is important to be aware cTn is highly specific for myocardial injury, which could be attributable to a myriad of underlying causes, emphasizing the notion that cTn is an organ-specific, not disease-specific biomarker. Furthermore, the ability to detect increased cTn using high-sensitivity assays following extreme exercise is disconcerting. It has been suggested troponin release can occur without cardiomyocyte necrosis, contradicting conventional dogma, emphasizing a need to understand the mechanisms of such release.
This review discusses basic troponin biology, the physiology behind its detection in serum, its use in the diagnosis of AMI, and some key concepts and experimental evidence as to why cTn can be elevated in chronic diseases. Cardiac troponinChronic diseaseRelease mechanismBiomarkerPrognosis 1.
Introduction Intensive investigation into the mechanisms of striated muscle contraction during the late 50 s and early 60 s led to evidence of a protein that resembled tropomyosin and regulated the calcium sensitivity of the actomyosin contractile apparatus.
This finding subsequently led to the discovery of troponin by Ebashi and Kodama in Elucidation of the physiologically distinct subunits of troponin by Greaser and Gergely 1 in has facilitated a quantum-leap in our understanding of the molecular physiology underpinning cardiac contraction. Consequent to their findings, one of the most successful diagnostic investigations to date has been developed: Whilst troponin is found in all forms of striated muscle, troponin in the heart is distinguished by regions of different amino acid sequences.
Another result of this study suggests that cardiac troponins might be useful parameter for detection of right ventricular dysfunction, prediction of mortality and massive disease in PE patients.
Cardiac Troponin T; cTnI: Left Ventricle; Thorax CT: Considering the mortality rates, PE should be diagnosed immediately and for the cases that necessitate, the decision of thrombolytic treatment should be made as early as possible [ 23 ]. Right ventricular function is an important prognostic factor in PE. Results of previous studies showed that right ventricular dysfunction is associated with poor prognosis and high mortality rates [ 4 ].
As a result of pulmonary arterial obstruction and increase in pulmonary vascular resistance, right ventricular after load increases and acute right ventricular dilatation develops with increase of right ventricular pressure up to pathological levels.
In addition, myocardial damage and ischemia might occur in some cases [ 256 ]. Cardiac troponins are biochemical markers that are highly sensitive to myocardial cell damage. They have been very helpful in diagnosis and prognosis of acute coronary syndrome. Since myocardial ischemia and damage were reported in acute PE without prominent coronary artery disease, recently several studies showed that cardiac troponins might increase in PE [ 5 - 13 ]. The primary outcomes of this study are to investigate the diagnostic importance of cardiac troponins in PE and to determine the role of cardiac troponins in differential diagnosis of PE from other pulmonary diseases e.
As secondary outcomes, this study also aims to evaluate 1 the relationship between levels of cardiac troponins and disease severity, and 2 the relationship between levels of cardiac troponins and right ventricular dysfunction.
PE was confirmed by highprobability ventilation-perfusion lung scanning according to PIOPED criteria or spiral computed thorax tomography [ 14 - 17 ].
An acute infection of the pulmonary parenchyma that was associated with some symptoms of acute pulmonary infection, accompanied by the presence of an acute infiltration on a chest radiograph or auscultatory findings consistent with CAP was defined as CAP [ 18 ]. Study design Fifty-nine patients diagnosed with acute PE were study group Group l and 58 patients diagnosed with pneumonia and asthma attack were evaluated as control group Group II.
Patients with pathology that may cause high levels of cardiac troponins acute myocardial infection, congestive heart failure, sepsisrenal failure, drug toxicity, cerebrovascular events, ultra-exercise, hypothyroidismCOPD, primary pulmonary hypertension were not included in the study [ 2021 ].
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Additionally, five cases 3 pulmonary embolism and 2 pneumonia admitted to our clinic were excluded due to unavailable cardiac troponin values. For all patients, symptoms, symptom durations, physical examination findings, predisposing factors for PE and risk factors smoking, hypercholesterolemiasystemic hypertensiondiabetes mellitusand atherosclerosis story in family for coronary artery disease were recorded at admission.
Severity of clinical presentation in patients with PE was divided into 3 groups according to Goldhaber: Laboratory analyses On admission; all the patients had physical examination, complete blood count, routine biochemical analysis, chest x-ray, Arterial Blood Gas Analysis ABGD-dimer level and ECG pathologies were recorded sinusoidal tachycardia, incomplete and complete right branch block, right axis deviation, non-specific ST variations, atrial fibrillation and atrial flutter.
Right ventricular dysfunction was evaluated as positive in the presence of at least one of the following signs [ 224 ]: Paradoxical septal movement 3. Right ventricular hypokinesis 4.