Acute Myocardial Infarction (AMI) is the most common cause of mortality, and cardiac troponin I (cTnI) is the gold standard for AMI diagnosis. Cardiac troponins, as a regulator of skeletal and cardiac muscle contractions, consist of troponin C (TnC), troponin I (TnI), and troponin T (TnT). In comparison with creatine kinase-MB, lactate dehydrogenase, and myoglobin, cardiac troponin I (cTnI) is more specific to myocardial tissue injury, because it is made only in heart muscle. Upon acute myocardial infarction (AMI), cTnI fragments are released into the blood serum from dead cells. The cTnI concentration level in normal patients is very low, approximately 1 pg/mL, but in AMI patients’ blood, it increases up to100 ng/mL. Thus for AMI detection, cTnI is attracted more consideration. In the normal heart muscle cases, cTnI exists in blood at trace levels. Upon the myocardial damage, the levels of cTnI rise, so the limits of detection (LODs) of the given methods are important for early diagnosis of heart failure. Nowadays, almost all the current cTnI assay methods are based on immune assessment methodologies.
This thesis is including three electrochemical sensors for cardiac troponin I (cTnI) determination. In order to attain selectivity in the field of protein determination, three known components including antibody, aptamer, and molecular imprinting polymers (MIPs), each designed for the corresponding protein, are used as the diagnostic component in the sensor design. In spite of excellent performance of antibodies, some limitations are reported in usage them for the design of protein sensors and some of which are discussed in this thesis. Considering the limitations for the use of antibodies and in order to propose a new probe for cTnI sensing, we have applied aptamer and MIP as diagnostic species. Then, relying on the computational modeling data, a new molecule has been introduced as a diagnostic species in the cTnI determination sensor. so in the first study, a simple