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Predicting Heart Attacks is Now Possible

Research shows that levels of MPO are elevated long before a patient actually develops a heart attack due to plaque instability. This new finding is going to help many patients prevent heart attacks.

Until very recently family history, life style (smoking), occupation, weight and BMI were used to predict the statistical probability of a patient suffering a heart attack. These observations were not accurate and could not be used until after the patient had suffered a heart attack. The risk factors were identified after the event therefore useless for prevention. Knowing these risk factors was useful for educating the patient after he had a heart attack.

Scientists have now identified and enzyme known as myeloperoxide (MPO) which is present in the body in measurable quantities. The research I am quoting is about to be published in the July 10, 2007, The Journal of the American College of Cardiology. The evidence will state that elevated levels of myeloperoxidase (MPO) in healthy males and females will increase the likelihood of a heart attack by 50% over 8 years when similar data is compared with patients who had the lower levels of myeloperoxide (MPO). This study suggests that elevated levels of MPO can predict the patient's probability of getting heart attack years before it happens with significantly more accuracy. Pro inflammatory enzyme and myeloperoxidase (MPO) might help identify healthy individuals who are at risk for a heart attack.

The myeloperoxide prediction is independent and a better predictor of coronary artery disease after considering the traditional risk factors. Elevated levels also predicted disease risk in patients who had lower-risk features at baseline presentation of risk factors.

MPO was previously thought to be a bactericidal enzyme. It has now gained prominence because it has a role in plaque formation which is responsible for coronary artery occlusion. It is reasonable to conclude that elevated levels of MPO can therefore be used to predict the probability of a future likelihood of a myocardial infarction (heart attack).

3,375 adult males and females who were free of Coronary Artery Disease were entered for this study. The nested case study was done in nine European Countries. It involved community-based populations who were being studies for cancer and nutrition. Serum was collected and frozen from patients at the start of the study as way back as 1995. At the end of the study serum MPO was measures using commercially available assay. Follow up studies showed that 1,138 patients developed coronary artery diseases of varying significance. The 2,237 patients who did not develop CAD served as the controls. Analysis showed that patients who developed CAD had significantly higher MPO levels when compared with controls.

Detailed comparisons of MPO levels and traditional CAD risk factors revealed a strong relationship. Further, analysis of CRP, white blood cell count was also positive. As expected a negative association with baseline HDL, and with smoking status was present.

When MPO data was stratified into quartiles the risk for CAD increased with higher MPO levels. Patients in the top quartile had higher CAD odds ratios when compared with patients in the bottom quartile. When the other risk factors were taken into consideration, the differences between the upper and lower quartiles remained very significant. Baseline MPO formed a more accurate association in male patients of both sexes who had died. The exact figures and more research details are available in the Cardiology Journal.

In this study MPO's association with future risk of coronary artery disease is weaker than had been documented in research involving patients with acute coronary syndrome (ACS). The difference suggests that MPO might be a more potent marker of plaque instability than of coronary artery disease risk or atheroma burden. It is known that MPO is derived predominantly from activated neutrophils and monocytes. Therefore elevated levels of MPO as seen in acute coronary syndrome could indicate the influx and migration of the cells toward unstable plaque.

There are some limitations of this study. One is the fact that deaths were as documented on the death certificate. So patients who had CAD but died of other causes were excluded from this study.

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