Risk Stratification of Patients with Acute Coronary Syndrome and Congestive Heart Failure

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Citation
Asia Pacific Cardiology - Volume 1 Issue 1;2007:1(1):20-21

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Acute coronary syndrome (ACS) and congestive heart failure (CHF) are significant health risks affecting a large part of the population. In both diseases, early detection and initiation of treatment significantly reduce the risk of serious adverse events and death. B-type natriuretic peptide (BNP) and myeloperoxidase (MPO) have both shown considerable utility in the early diagnosis of patients with these conditions, as well as the ability to risk-stratify these patients. BNP, while initially identified as a marker of severity of heart failure, has recently demonstrated its ability to aid in the risk stratification of ACS patients. MPO has been identified as an early indicator of myocyte necrosis and a marker of risk for developing and worsening heart failure.

B-type Natriuretic Peptide as a Prognostic Tool in Acute Coronary Syndrome

While BNP is primarily used for the diagnosis of heart failure, many studies have been performed recently showing the prognostic value of BNP after hospitalisation for ACS. In the ACS setting, BNP levels most likely rise due to acute left ventricular stiffening as a result of myocardial ischaemia. In patients admitted to hospital with non-ST-elevation or ST-elevation myocardial infarctions (MIs), BNP levels above 80pg/ml were associated with a two-fold increased risk of death within two years. Additionally, these patients were at higher risk of new-onset or worsening CHF.1 Measurement of BNP levels in the months following presentation with ACS also appears to be important in risk stratification of these patients. Patients who had normal BNP levels at presentation but who demonstrated elevated BNP levels four months later were shown to be at a significantly higher risk of death or new-onset CHF than patients with high initial and low follow-up BNP levels.1

Myeloperoxidase – An Early Diagnostic Marker of Acute Coronary Syndrome

MPO is a haemoprotein that is involved in inflammatory processes. In acute coronary syndrome, MPO has emerged as an early marker of myocyte necrosis. The activation of leukocytes that occurs in patients with ACS is responsible for initiating the secretion of MPO.2 MPO degrades the protective collagen coating of plaques, causing them to become vulnerable to erosion and rupture.3 Additionally, MPO alters the characteristics of high-density lipoprotein (HDL) and low-density lipoprotein (LDL) by binding to apolipoprotein A1, causing oxidation and subsequently resulting in the destabilisation of plaques.3 The oxidative effects of MPO on HDL cause HDL molecules to become pro-inflammatory and pro-atherogenic. This contributes to the formation of atherosclerotic lesions.4 MPO has been implicated as a mechanistic link between inflammation and plaque instability, and therefore is believed to be a useful marker for predicting cardiovascular event risk.2

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References
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