Top Bio Markers for Heart Disease

Top Bio-Markers For Heart Disease
 Homocystine,  Theoretically, an elevated level of homocysteine in the blood (hyperhomocysteinemia) is believed to cause narrowing and hardening of the arteries (atherosclerosis). This narrowing and hardening of the vessels is thought to occur through a variety of ways involving elevated homocysteine. The blood vessel narrowing in turn leads to diminished blood flow through the affected arteries. Elevated levels of homocysteine in the blood may also increase the tendency to excessive blood clotting. Blood clots inside the arteries can further diminish the flow of blood. The resultant lack of blood supply to the heart muscles may cause heart attacks, and the lack of blood supply to the brain causes strokes. Elevated homocysteine levels also have been shown to be associated with formation of blood clots in veins (deep vein thrombosis and pulmonary embolism).


 

 Blood Sugar; Lowering blood sugar levels could reduce the risk of coronary heart disease in both diabetics and non-diabetics, according to researchers at the Johns Hopkins Bloomberg School of Public Health and other institutions. The researchers found that Hemoglobin A1c (HbA1c)-a measure of long-term blood glucose level-predicts heart disease risk in both diabetics and non-diabetics. An elevated blood glucose level is the defining feature of diabetes, but until now it was unclear whether elevated glucose levels contributed independently to increasing heart-disease risk. The study is published in the September 12, 2005, issue of Archives of Internal Medicine.

 C-Reactive Protein; The elevation of CRP has also been recently linked to atherosclerosis and heart disease. Atherosclerosis, or cholesterol plaquing of the arteries, is known to have an inflammatory component that is thought to cause the rise in CRP levels in the blood. Atherosclerosis is also felt to be affected by age and other cardiovascular risk factors including diabetes mellitus, high cholesterol, high blood pressure, and cigarette smoking. In atherosclerosis, the blood vessel wall becomes injured. This injury acts as focus of inflammation and leads to the formation of plaques in the blood vessel walls. The plaques typically contain blood cells of inflammation, cholesterol deposits, and debris from the injured cells in the blood vessel lining. The accumulation of these elements leads to narrowing of the wall of the blood vessel.

Fibrinogen has been identified as a major independent risk factor for cardiovascular disease. Fibrinogen has also been associated with traditional cardiovascular risk factors, suggesting that elevation of fibrinogen may be a pathway by which these risk factors exert their effect. There are several mechanisms by which fibrinogen may increase cardiovascular risk. First, it binds specifically to activated platelets via glycoprotein IIb/IIIa, contributing to platelet aggregation. Second, increased fibrinogen levels promote fibrin formation. Third, it is a major contributor to plasma viscosity. Finally, it is an acute-phase reactant that is increased in inflammatory states.

 Lipoprotein(a) [Lp(a)] has been considered a cardiovascular risk factor for many year Owing to incomplete scientific evidence, screening for and treatment of high Lp(a) levels have to date been performed principally by lipid specialists. However, during the last few years, major advances have been achieved in understanding the causal role of elevated Lp(a) in premature cardiovascular disease These new findings have prompted the present critical appraisal of the evidence base in the form of a Consensus Paper.
Lipoprotein(a) is a plasma lipoprotein consisting of a cholesterol-rich LDL particle with one molecule of apolipoprotein B100 and an additional protein, apolipoprotein(a), attached via a disulfide bond (Figure 1 Elevated Lp(a) levels can potentially increase the risk of CVD (i) via prothrombotic/anti-fibrinolytic effects as apolipoprotein(a) possesses structural homology with plasminogen and plasmin but has no fibrinolytic activity and (ii) via accelerated atherogenesis as a result of intimal deposition of Lp(a) cholesterol, or both.

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