Purpose: Acute myocardial infarction (AMI) is the most common cause of death in the world. Comprehensive risk assessment of patients presenting with chest pain and eliminating undesirable results should decrease morbidity and mortality rates, increase the quality of life of patients, and decrease health expenditure in many countries. In this study, the advantages and disadvantages of the enzymatic and nonenzymatic biomarkers used in the diagnosis of patients with AMI are given in historical sequence, and some candidate biomarkers – hFABP, GPBB, S100, PAPP-A, RP, TNF, IL6, IL18, CD40 ligand, MPO, MMP9, cell-adhesion molecules, oxidized LDL, glutathione, homocysteine, fibrinogen, and D-dimer procalcitonin – with a possible role in the diagnosis of AMI are discussed. Methods: The present study was carried out using meta-analyses, reviews of clinical trials, evidence-based medicine, and guidelines indexed in PubMed and Web of Science. Results: These numerous AMI biomarkers guide clinical applications (diagnostic methods, risk stratification, and treatment). Today, however, TnI remains the gold standard for the diagnosis of AMI. Details in the text will be given of many biomarkers for the diagnosis of AMI. Conclusion: We evaluated the advantages and disadvantages of routine enzymatic and nonenzymatic biomarkers and the literature evidence of other candidate biomarkers in the diagnosis of AMI, and discuss challenges and constraints that limit translational use from bench to bedside.

Blood is pumped into the cardiac muscle through arteries called the coronary arteries. Over time, the accumulation of cholesterol, coagulation factors, and cells on the walls of these arteries causes the walls to thicken and lose their elasticity, resulting in the development of atherosclerosis. When the blood supply of the heart is diminished by atherosclerosis, it can be restored by bypass surgery, in which atherosclerosis-free vein and/or artery grafts taken from another area of the body are used to replace the atherosclerotic vessels. These biological grafts used in surgery differ in biochemical composition and long-term patency. Although the great saphenous vein (GSV) has been the most popular graft material in revascularization for years, it has recently been superseded by the internal mammarian artery (IMA), which has a lower incidence of recurrence of atherosclerosis. The aim of the present review is briefly to address the structure of the cardiovascular system and blood vessels, and then, in the light recent data, to present the biochemical compositions and individual advantages of the graft materials used to restore an impaired blood supply to the heart.

Individual or combined administration of ILO and SIL reduced myocardial ischaemia and NO levels, and increased irisin levels. Elevated levels of irisin obtained by drug administration could possibly contribute to accelerated wound recovery by local heat production. Sildenafil was more effective than iloprost in eliminating ischaemia and may be the first choice in offsetting the effects of ischaemia in the future.

Enzyme-positive acute coronary syndrome (EPACS) can cause injury to or death of the heart muscle owing to prolonged ischaemia. Recent research has indicated that in addition to liver and brain cells, cardiomyocytes also produce adropin. We hypothesised that adropin is released into the bloodstream during myocardial injury caused by acute coronary syndrome (ACS), so serum and saliva levels rise as the myocytes die. Therefore, it could be useful to investigate how ACS affects the timing and significance of adropin release in human subjects Samples were taken over three days after admission, from 22 EPACS patients and 24 age- and gendermatched controls. The three major salivary glands (submandibular, sublingual and parotid) were immunohistochemically screened for adropin production, and serum and saliva adropin levels were measured by an enzyme-linked immunosorbent assay (ELISA). Salivary gland cells produce and secrete adropin locally. Serum adropin, troponin I, CK and CK-MB concentrations in the EPACS group became gradually higher than those in the control group up to six hours (p < 0.05), and troponin I continued to rise up to 12 hours after EPACS. The same relative increase in adropin level was observed in the saliva. Troponin I, CK and CK-MB levels started to decrease after 12 hours, while saliva and serum adropin levels started to decrease at six hours after EPACS. In samples taken four hours after EPACS, when the serum adropin value averaged 4.43 ng/ml, the receiver operating characteristic curve showed that the serum adropin concentration indicated EPACS with 91.7% sensitivity and 50% specificity, while when the cut-off adropin value in saliva was 4.12 ng/ml, the saliva adropin concentration indicated EPACS with 91.7% sensitivity and 57% specificity. In addition to cardiac troponin and CK-MB assays, measurement of adropin level in saliva and serum samples is a potential marker for diagnosing EPACS.