Biomarkers of Cardiovascular Damage

Abstract

Acute coronary syndromes (ACS) are due to the rupture or erosion of atheromatous plaques. This produces, depending on plaque size, vascular anatomy and degree of collateral circulation, progressive tissue ischaemia which may progress to cardiomyocyte necrosis. This may then result in cardiac remodelling. Serum biomarkers are available which can be used for diagnosis of all of these stages. Markers to detect myocardial ischaemia at the pre-infarction stage are potentially the most interesting but also the most challenging. An ischaemia marker offers the opportunity to intervene to prevent progression to infarction. The problems with potential ischaemia markers are specificity and the reference diagnostic standard against which they can be judged. To date, only one, ischaemia-modified albumin®, has reached the point where clinical studies can be performed. The measurement of the cardiac troponins, cardiac troponin T and cardiac troponin I, have become recognised as the diagnostic reference standard for myocardial necrosis. The sensitive nature of these tests has also revealed that myocardial necrosis is also found in a range of other clinical situations, highlighting the need to use all clinical information for diagnosis of acute myocardial infarction. The measurement of B-type natriuretic peptides can be shown to be diagnostic and prognostic in both ACS and detecting the sequelae of post-infarction myocardial insufficiency. The role of the B-type natriuretic peptides in detection of cardiac failure, both acute and chronic, is well defined but remains the subject of further studies, in ACS.

Heat-Killed Trypanosoma cruzi Induces Acute Cardiac Damage and Polyantigenic Autoimmunity

“…It has been previously validated in a murine model of experimental autoimmune myocarditis, and demonstrates greater utility than creatine kinase or anti-cardiac myosin antibodies [45], [46], [47], [48], [49]. Increased serum cTnI levels positively correlate with increased levels of histopathological changes in the myocardium, and serum markers are a facile means of tracking cardiac injury [47].…”

Protective effects of caspase-9 and poly(ADP-ribose) polymerase inhibitors on ischemia-reperfusion-induced myocardial injury

“…Electrical pacing has not been used in the study because it is reported to release norepinephrine (Nayler et al, 1985). Infarct size in the present study is assessed macroscopically because a good correlation has been noted between infarct size measured macroscopically and microscopically (Banka et al, 1981;Collinson and Gaze, 2007). The duration of 30 min ischemia and 120 min reperfusion employed in this study has been reported to produce apoptosis (Maulik et al, 1999).…”

Mid-regional-pro-adrenomedullin plasma levels are increased in obese adolescents

“…It might be that, in obese adolescents, the excess in fat mass causes MRproADM overproduction, drowning out its age-related changes. The higher MR-proADM plasma levels found in obese adolescents are unlikely to be attributable to cardiovascular alterations, since both BNP and NTproBNP, considered sensitive biomarkers of cardiac dysfunction used in the diagnostic and prognostic staging of chronic and acute cardiac conditions across all ages [33], resulted in normal range and comparable between obese and normalweight adolescents. The pathophysiological role of ADM secreted by adipose tissue in obese subjects is still speculative.…”