CORE Metadata, citation and similar papers at core.ac.uk Provided by Cognitive Sciences ePrint Archive Int J Cur Bio Med Sci. 2011; 1(2): 30 – 34. Contents lists available at CurrentSciDirect Publications International Journal of Current Biological and Medical Science CurrentSciDirect Journal homepage: www.currentscidirect.com Publication Original article The combinational effect of cardiac and biochemical markers in diabetic patients with cardiovascular disease Palanisamy Pasupathi*a, YY Raoa, Farook Ja, Boopathi subramaniyamb, Sathiyamoorthy Subramaniyamb, Babu Shankar Ponnushaa, Athimoolam Ambikaa *a Department of clinical Biochemistry , KG Hospital and Post Graduate Medical Institute, Coimbatore, Tamil Nadu, India. b Korean Ginseng Center and Ginseng Genetic Resource Bank, Kyung Hee University, 1 Seocheon, Giheung- gu, Yongin-si, Gyeonggi-do, 449-701, South Korea. c Tutor in Department of Anatomy ,Annapoorana medical college,Salem,tamilnadu. A R T I C L E I N F O A B S T R A C T Keywords: Background: Clinicopathological correlations, as well as several angiographic studies, suggest Atherosclerosis Glycated haemoglobin that diabetic patients have more extensive atherosclerotic disease, affecting the coronary cardiovascular subjects diabetes arteries in particular. We sought to examine the combinational effect of cardiac and biochemical markers in diabetic patients with cardiovascular disease. Method: The study population constituted 50 healthy subjects, 50 cardiovascular subjects with diabetes and 50 cardiovascular subjects without diabetes. The population was subjected to biochemical and cardiac marker analysis and the results were verified. Results and discussion: Studies suggest that glycated hemoglobin values in the abnormal range can identify persons at increased risk for coronary heart disease, stroke, and death before the diagnosis of diabetes, indicating that glycated hemoglobin is a useful marker of cardiovascular risk and death from any cause. c Copyright 2011. CurrentSciDirect Publications. IJCBMS - All rights reserved. 1. Introduction Type 2 diabetes is associated with multiple abnormalities, all of abnormalities of the autonomic nerve fibers were demonstrated which can contribute to vascular disease. The most notable of histologically in diabetic patients who died after painless these abnormalities include obesity, insulin resistance, myocardial infarction. Furthermore, diabetic patients with silent hyperglycemia, dyslipidemia, hypertension, and renal disease. myocardial ischemia show evidence of diffuse abnormalities in m- Although a number of these disorders are often grouped together iodobenzylguanidine imaging, suggesting that abnormalities of in an entity termed "metabolic syndrome,” the increased risk for pain perception may be linked to sympathetic denervation [1]. atherosclerotic disease in insulin-resistant patients correlates Cardiac markers are biomarkers measured to evaluate heart best with these abnormalities when each is considered function. They are often discussed in the context of myocardial individually. These abnormalities promote heart disease by infarction, but other conditions can lead to an elevation in cardiac inducing atherosclerosis, endothelial cell dysfunction, oxidative marker level. Cardiac marker tests identify blood chemicals s t r e s s , i n f l a m m a t i o n , a n d va s c u l a r r e m o d e l i n g . associated with myocardial infarction (MI), commonly known as a heart attack. The myocardium is the middle layer of the heart wall There could be several explanations for the different patterns of composed of heart muscle. Infarction is tissue death caused by an symptoms in patients with diabetes mellitus, including different interruption in the blood supply to an area. thresholds of pain sensitivity, psychological denial, or the presence of autonomic neuropathy leading to sensory denervation. The Cardiac troponin T (cTnT) and troponin I (cTnI) are cardiac latter seems to be more likely in diabetic patients, because regulatory proteins that control the calcium mediatedinteraction autonomic neuropathy is a common feature of diabetes, and between actin and myosin. The cardiac forms of these regulatory proteins are coded by specific genes and theoretically have the * Corresponding Author : Dr.Palanisamy Pasupathi Ph.D., FLS (UK)., potential of being unique to the myocardium. Indeed, cTnI has not Department of clinical Biochemistry, Institute of Laboratory Medicine been identified outside the myocardium.Cardiac troponin T is KG Hospital and Post Graduate Medical Institute, expressed to a small extent in skeletal muscle; however, the Coimbatore, Tamil Nadu, India. Mobile: 9787572244 current cTnT assay does not identify skeletal troponins [2]. Email: [email protected] c Copyright 2011. CurrentSciDirect Publications. IJCBMS - All rights reserved. Palanisamy Pasupathi et al. / Int J Cur Bio Med Sci. 2011; 1(2): 30 – 34. 31 The measurement of serum cTnI and cTnT is superior in terms markers, including total creatine kinase (total CK), creatine of sensitivity and specificity to cardiac muscle enzyme kinase-MB (CK-MB), the MB isoforms, and myoglobin, as well as measurements in the identification of cardiac muscle the troponins - cardiac troponin T (cTnT) and cardiac troponin I damage.Raised cardiac troponin concentrations are now accepted (cTnI) - are all used for assessment of the suspected acute as the standard biochemical marker for the diagnosis of myocardial infarction (AMI) patient. Myoglobin is released rapidly myocardial infarction. Cardiac troponins are detected in the serum after tissue injury and may be elevated as early as 1 hour after by the use of monoclonal antibodies to epitopes of cTnI and cTnT. myocardial injury. Myoglobin is also cleared rapidly by renal These antibodies are highly specific for cardiac troponin and have excretion, so abnormal levels may return to baseline values in six negligible crossreactivity with skeletal muscle troponins. Cardiac to twelve hours[4]. troponins may not be detected in the serum for up to four hours According to the American Heart Association, studies have after the onset of an acute coronary event and should be repeated shown that too much homocysteine in the blood is related to a after 12 hours if the troponin concentration on admission is not higher risk of coronary heart disease, stroke, and peripheral raised in an individual presenting with chest pain. vascular disease; and that it may also have an effect on Creatine kinase is an enzyme responsible for transferring a atherosclerosis. High levels of homocysteine are the result of a lack phosphate group from ATP to creatine. It is composed of M and/or of certain B vitamins, inheritance, or dietary excess and have been B subunits that form CK-MM, CKMB, and CK-BB isoenzymes. Total implicated in vascular-wall injury. Many risk factors, including CK (the activity of the MM, MB, and BB isoenzymes) is not family history of heart disease, smoking, obesity, lack of exercise, myocardial-specific. However, the MB isoenzyme (also called CK- diabetes, high levels of low-density lipoprotein cholesterol (LDL or 2) comprises about 40% of the CK activity in cardiac muscle and "bad" cholesterol), low levels of high-density lipoprotein 2% or less of the activity in most muscle groups and other tissues. cholesterol (HDL or "good" cholesterol), and high blood pressure In the proper clinical setting, MB is both a sensitive and specific have been documented to increase the risk of stroke and heart marker for myocardial infarction. MB usually becomes abnormal disease. With so many other risk factors, it has been difficult to three to four hours after an MI, peaks in 10–24 hours, and returns determine whether high levels of homocysteine are an to normal within 72 hours. However, an elevated serum MB may independent risk factor for the development these diseases. occur in people with severe skeletal muscle damage (such as in However, a substantial number of controlled, well-designed, and muscular dystrophy or a crush injury) and renal failure. In such well-documented studies have shown that individuals who have cases, the CK index (MB divided by total CK) is very helpful. If the high levels of homocysteine in the blood are at increased risk of index is under 4%, a nonmyocardial cause of a high MB should be developing blocked blood vessels, a condition known as occlusive suspected. CK-MB is considered the benchmark for cardiac arterial disease or at risk to worsen atherosclerosis ("hardening of markers of myocardial injury. Measurement of CK-MB may be the arteries"). performed via electrophoresis or immunoassays; the latter Either BNP or NT-proBNP may be used to help diagnose heart demonstrates better analytical sensitivity and better precision[3] failure and to grade the severity of that heart failure. Both BNP and CK-MB forms can be used to determine whether thrombolytic NT-proBNP levels in the blood are used for screening, diagnosis of therapy (such as treatment with tissue plasminogen activator to acute congestive heart failure (CHF) and may be useful to establish dissolve a blood clot in the coronary artery) has succeeded. MB prognosis in heart failure, as both markers are typically higher in forms are different molecular forms of MB found in the circulation. patients with worse outcome. The plasma concentrations of both When MB is released into the blood, part of the M subunit is BNP and NT-proBNP are also typically increased in patients with removed by an enzyme in the plasma. This results