الفهرس | Only 14 pages are availabe for public view |
Abstract Acute coronary syndrome (ACS) refers to a group of conditions that include ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina. It is a type of coronary heart disease (CHD), which is responsible for one-third of total deaths in people older than 35. Some forms of CHD can be asymptomatic, but ACS is always symptomatic. It is thought that most acute coronary syndromes (ACS) are the result of luminal thrombosis, although not all are associated with occlusive diseases. There are three main causes of coronary thrombosis such as plaque rupture, erosion, and calcified nodule. Based on the autopsy studies, the majority of thrombosis occurs from plaque rupture (55–65%), followed by erosion (30–35%) and, least frequent, calcified nodule (2–7%). Early diagnosis of ACS is essential because of improvement in prognosis following timely interventions. Currently, the diagnosis of ACS is based on elevation of (high-sensitive) cardiac troponin I or T (cTnI or cTnT), in the context of clinical and ECG findings. Unfortunately, these biomarkers are not consistently elevated within the first hours after symptom onset, requiring repetitive measurements and hindering early diagnosis. cTns cannot be detected until 6 to 12 h after coronary occlusion, even high-sensitive Tn can only be detected until 3 h after MI. H-FABP is 20 times more specific to cardiac muscle than myoglobin it is found at 10-fold lower levels in skeletal muscle than heart muscle and the amounts in the kidney, liver and small intestine are even lower again. |