BACKGROUND: Although myeloperoxidase (MPO) monitoring is predictive for cardiovascular outcomes in suspected acute coronary syndromes, the value of serial testing is unknown.
METHODS: We investigated the relationship between serial MPO concentrations in 490 individuals with acute chest pain and incident major adverse cardiac events (MACE) during 6 months of follow-up. We measured MPO with the CardioMPO assay, and cardiac troponin I (cTnI), with the Abbott Architect assay.
RESULTS: Plasma MPO concentrations during the first 16 h were higher in individuals who experienced MACE. Higher MPO quartiles predicted a greater likelihood of 6-month MACE at baseline [OR (95%CI), 2.4 (1.4–4.1), P = 0.001 for highest vs lowest quartile] and all subsequent time points, with strongest predictive ability found in 16-h postbaseline samples [9.9 (4.7–20.9), P < 0.001 for highest vs lowest quartile]. MPO was predictive for MACE among individuals whose cTnI remained normal (<0.028 µg/L). The lowest rate of missed cases was found when MPO was <640 pmol/L at baseline and all other time points. Serial MPO monitoring predicted MACE risk better than baseline MPO measurements alone (c statistic 0.813 vs 0.602; P = 0.002), including in individuals whose cTnI remained normal (c statistic 0.903; P = 0.009). Combined serial cTnI and MPO testing improved accuracy for predicting 6-month MACE, reduced the number of missed MACE events from cTnI testing alone, and improved risk classification in 26.1% of patients.
CONCLUSIONS: MPO concentrations are predictive of outcome up to 16 h after presentation with chest pain and predict events missed by cTnI testing, supporting a potential role in rapid patient triage.
Stephen J. Nicholls1,2,3,*, W.H. Wilson Tang1,2,3, Danielle Brennan1, Marie-Luise Brennan1,2,3, Shirley Mann2,3, Steven E. Nissen1 and Stanley L. Hazen1,2,3
1 Department of Cardiovascular Medicine, and
2 Department of Cell Biology, and
3 Center for Cardiovascular Diagnostics and Prevention, Cleveland Clinic, Cleveland, OH
Sunday
Monday
Proteinase 3 and prognosis of patients with acute myocardial infarction.
Abstract
A multimarker approach may be useful for risk stratification in AMI (acute myocardial infarction) patients, particularly utilizing pathways that are pathophysiologically distinct. Our aim was to assess the prognostic value of PR3 (proteinase 3) in patients post-AMI.
We compared the prognostic value of PR3, an inflammatory marker, with an established marker NT-proBNP (N-terminal pro-B-type natriuretic peptide) post-AMI. We recruited 900 consecutive post-AMI patients (700 men; age, 64.6±12.4 years) in a prospective study with follow-up over 347 (0-764) days. Plasma PR3 was significantly higher in patients who died [666.2 (226.8-4035.5) ng/ml; P<0.001] or were readmitted with heart failure [598 (231.6-1803.9) ng/ml, P<0.004] compared with event-free survivors [486.9 (29.3-3118.2) ng/ml]. Using Cox modelling, log10 PR3 [HR (hazard ratio), 3.80] and log10 NT-proBNP (HR, 2.51) were significant independent predictors of death or heart failure.
When patients were stratified by plasma NT-proBNP (median, 1023 pmol/l), PR3 gave additional predictive value for death or heart failure, in both the patients in whom NT-proBNP level was above the median (log rank for trend, 12.54; P<0.0004) and those with NT-proBNP level below the median (log rank for trend, 3.83; P<0.05). Neither marker predicted recurrent AMI.
In conclusion, this is the first report showing a potential role for the serine protease PR3 in determining mortality and incidence of heart failure following AMI, independent of established conventional risk factors. PR3 may represent a clinically useful marker of prognosis after an AMI as part of a multimarker strategy.
A multimarker approach may be useful for risk stratification in AMI (acute myocardial infarction) patients, particularly utilizing pathways that are pathophysiologically distinct. Our aim was to assess the prognostic value of PR3 (proteinase 3) in patients post-AMI.
We compared the prognostic value of PR3, an inflammatory marker, with an established marker NT-proBNP (N-terminal pro-B-type natriuretic peptide) post-AMI. We recruited 900 consecutive post-AMI patients (700 men; age, 64.6±12.4 years) in a prospective study with follow-up over 347 (0-764) days. Plasma PR3 was significantly higher in patients who died [666.2 (226.8-4035.5) ng/ml; P<0.001] or were readmitted with heart failure [598 (231.6-1803.9) ng/ml, P<0.004] compared with event-free survivors [486.9 (29.3-3118.2) ng/ml]. Using Cox modelling, log10 PR3 [HR (hazard ratio), 3.80] and log10 NT-proBNP (HR, 2.51) were significant independent predictors of death or heart failure.
When patients were stratified by plasma NT-proBNP (median, 1023 pmol/l), PR3 gave additional predictive value for death or heart failure, in both the patients in whom NT-proBNP level was above the median (log rank for trend, 12.54; P<0.0004) and those with NT-proBNP level below the median (log rank for trend, 3.83; P<0.05). Neither marker predicted recurrent AMI.
In conclusion, this is the first report showing a potential role for the serine protease PR3 in determining mortality and incidence of heart failure following AMI, independent of established conventional risk factors. PR3 may represent a clinically useful marker of prognosis after an AMI as part of a multimarker strategy.
Thursday
Projected Effect of Dietary Salt Reductions on Future Cardiovascular Disease
Background
The U.S. diet is high in salt, with the majority coming from processed foods. Reducing dietary salt is a potentially important target for the improvement of public health
Methods
We used the Coronary Heart Disease (CHD) Policy Model to quantify the benefits of potentially achievable, population-wide reductions in dietary salt of up to 3 g per day (1200 mg of sodium per day). We estimated the rates and costs of cardiovascular disease in subgroups defined by age, sex, and race; compared the effects of salt reduction with those of other interventions intended to reduce the risk of cardiovascular disease; and determined the cost-effectiveness of salt reduction as compared with the treatment of hypertension with medications.
Background
The U.S. diet is high in salt, with the majority coming from processed foods. Reducing dietary salt is a potentially important target for the improvement of public health.
Full Text of Background...
Methods
We used the Coronary Heart Disease (CHD) Policy Model to quantify the benefits of potentially achievable, population-wide reductions in dietary salt of up to 3 g per day (1200 mg of sodium per day). We estimated the rates and costs of cardiovascular disease in subgroups defined by age, sex, and race; compared the effects of salt reduction with those of other interventions intended to reduce the risk of cardiovascular disease; and determined the cost-effectiveness of salt reduction as compared with the treatment of hypertension with medications.
Full Text of Methods...
Results
Reducing dietary salt by 3 g per day is projected to reduce the annual number of new cases of CHD by 60,000 to 120,000, stroke by 32,000 to 66,000, and myocardial infarction by 54,000 to 99,000 and to reduce the annual number of deaths from any cause by 44,000 to 92,000. All segments of the population would benefit, with blacks benefiting proportionately more, women benefiting particularly from stroke reduction, older adults from reductions in CHD events, and younger adults from lower mortality rates. The cardiovascular benefits of reduced salt intake are on par with the benefits of population-wide reductions in tobacco use, obesity, and cholesterol levels. A regulatory intervention designed to achieve a reduction in salt intake of 3 g per day would save 194,000 to 392,000 quality-adjusted life-years and $10 billion to $24 billion in health care costs annually. Such an intervention would be cost-saving even if only a modest reduction of 1 g per day were achieved gradually between 2010 and 2019 and would be more cost-effective than using medications to lower blood pressure in all persons with hypertension.
Conclusions
Modest reductions in dietary salt could substantially reduce cardiovascular events and medical costs and should be a public health target
Kirsten Bibbins-Domingo, Ph.D., M.D., Glenn M. Chertow, M.D., M.P.H., Pamela G. Coxson, Ph.D., Andrew Moran, M.D., James M. Lightwood, Ph.D., Mark J. Pletcher, M.D., M.P.H., and Lee Goldman, M.D., M.P.H.
N Engl J Med 2010; 362:590-599
The U.S. diet is high in salt, with the majority coming from processed foods. Reducing dietary salt is a potentially important target for the improvement of public health
Methods
We used the Coronary Heart Disease (CHD) Policy Model to quantify the benefits of potentially achievable, population-wide reductions in dietary salt of up to 3 g per day (1200 mg of sodium per day). We estimated the rates and costs of cardiovascular disease in subgroups defined by age, sex, and race; compared the effects of salt reduction with those of other interventions intended to reduce the risk of cardiovascular disease; and determined the cost-effectiveness of salt reduction as compared with the treatment of hypertension with medications.
Background
The U.S. diet is high in salt, with the majority coming from processed foods. Reducing dietary salt is a potentially important target for the improvement of public health.
Full Text of Background...
Methods
We used the Coronary Heart Disease (CHD) Policy Model to quantify the benefits of potentially achievable, population-wide reductions in dietary salt of up to 3 g per day (1200 mg of sodium per day). We estimated the rates and costs of cardiovascular disease in subgroups defined by age, sex, and race; compared the effects of salt reduction with those of other interventions intended to reduce the risk of cardiovascular disease; and determined the cost-effectiveness of salt reduction as compared with the treatment of hypertension with medications.
Full Text of Methods...
Results
Reducing dietary salt by 3 g per day is projected to reduce the annual number of new cases of CHD by 60,000 to 120,000, stroke by 32,000 to 66,000, and myocardial infarction by 54,000 to 99,000 and to reduce the annual number of deaths from any cause by 44,000 to 92,000. All segments of the population would benefit, with blacks benefiting proportionately more, women benefiting particularly from stroke reduction, older adults from reductions in CHD events, and younger adults from lower mortality rates. The cardiovascular benefits of reduced salt intake are on par with the benefits of population-wide reductions in tobacco use, obesity, and cholesterol levels. A regulatory intervention designed to achieve a reduction in salt intake of 3 g per day would save 194,000 to 392,000 quality-adjusted life-years and $10 billion to $24 billion in health care costs annually. Such an intervention would be cost-saving even if only a modest reduction of 1 g per day were achieved gradually between 2010 and 2019 and would be more cost-effective than using medications to lower blood pressure in all persons with hypertension.
Conclusions
Modest reductions in dietary salt could substantially reduce cardiovascular events and medical costs and should be a public health target
Kirsten Bibbins-Domingo, Ph.D., M.D., Glenn M. Chertow, M.D., M.P.H., Pamela G. Coxson, Ph.D., Andrew Moran, M.D., James M. Lightwood, Ph.D., Mark J. Pletcher, M.D., M.P.H., and Lee Goldman, M.D., M.P.H.
N Engl J Med 2010; 362:590-599
Key predictor of cardiovascular death identified
ScienceDaily (Mar. 22, 2010) — Coronary Artery Disease (CAD) hospitalizes more than 160,000 Canadians every year, and almost one quarter of those patients die from this common form of heart disease. But now a team of Vancouver-based researchers has identified a key predictor of mortality in CAD patients, which means that specialists can better determine how to treat and improve outcomes for patients with CAD.
Coronary artery disease is the most frequent cause of heart disease and occurs when important blood vessels become narrow or blocked and can no longer give enough blood to meet the heart's demand.
In an article published in the Journal of the American College of Cardiology, researchers Claire Heslop, Dr. Jiri Frohlich, and Dr. John Hill from The Providence Heart + Lung Institute and the University of British Columbia detail their discovery, that high levels of an enzyme, myeloperoxidase , in the blood of CAD patients more than doubles the risk for death over a 13 year period. Myeloperoxidase is an enzyme associated with oxidative stress, which damages arterial tissue.
The research team, funded by the Heart and Stroke Foundation of BC & Yukon, looked at blood samples and records from a group of patients admitted to hospital in the early 1990s with symptoms of heart disease. Over a 13 year period, mortality was more than double for patients with high blood levels of myeloperoxidase than for those with lower levels.
Based on this work, the researchers were able to develop a new classification of risk for CAD patients based on their levels of myeloperoxidase. Measurement of the enzyme provides added predictive value for cardiovascular death when compared to traditional risk factors such as smoking and diabetes. "We hope that the discovery of new markers of cardiovascular risk will help identify specific patients who could benefit from more aggressive treatment strategies" said lead investigator, Dr. John Hill.
Patients whose records and samples were used in this study all consented to have their information used for research.
The Heart and Stroke Foundation of Canada has funded researchers across Canada for over 50 years. Every year, the Foundation presents grants, awards and scholarships to leading stroke and heart disease researchers who are committed to reducing and eliminating the effects of stroke and heart disease.
"We are proud to support Canadian researchers, such as Dr. Hill, Dr. Frohlich and Ms. Heslop , who are combining their efforts to develop new techniques to fight heart disease and identify factors in at-risk individuals," says Bobbe Wood, President and CEO of Heart and Stroke Foundation of BC & Yukon. "Since almost 40,000 deaths occur in Canada each year due to CAD, it's crucial to focus on better methods to treat such a devastating health problem."
Coronary artery disease is the most frequent cause of heart disease and occurs when important blood vessels become narrow or blocked and can no longer give enough blood to meet the heart's demand.
In an article published in the Journal of the American College of Cardiology, researchers Claire Heslop, Dr. Jiri Frohlich, and Dr. John Hill from The Providence Heart + Lung Institute and the University of British Columbia detail their discovery, that high levels of an enzyme, myeloperoxidase , in the blood of CAD patients more than doubles the risk for death over a 13 year period. Myeloperoxidase is an enzyme associated with oxidative stress, which damages arterial tissue.
The research team, funded by the Heart and Stroke Foundation of BC & Yukon, looked at blood samples and records from a group of patients admitted to hospital in the early 1990s with symptoms of heart disease. Over a 13 year period, mortality was more than double for patients with high blood levels of myeloperoxidase than for those with lower levels.
Based on this work, the researchers were able to develop a new classification of risk for CAD patients based on their levels of myeloperoxidase. Measurement of the enzyme provides added predictive value for cardiovascular death when compared to traditional risk factors such as smoking and diabetes. "We hope that the discovery of new markers of cardiovascular risk will help identify specific patients who could benefit from more aggressive treatment strategies" said lead investigator, Dr. John Hill.
Patients whose records and samples were used in this study all consented to have their information used for research.
The Heart and Stroke Foundation of Canada has funded researchers across Canada for over 50 years. Every year, the Foundation presents grants, awards and scholarships to leading stroke and heart disease researchers who are committed to reducing and eliminating the effects of stroke and heart disease.
"We are proud to support Canadian researchers, such as Dr. Hill, Dr. Frohlich and Ms. Heslop , who are combining their efforts to develop new techniques to fight heart disease and identify factors in at-risk individuals," says Bobbe Wood, President and CEO of Heart and Stroke Foundation of BC & Yukon. "Since almost 40,000 deaths occur in Canada each year due to CAD, it's crucial to focus on better methods to treat such a devastating health problem."
Sunday
Anti-apolipoprotein A-1 IgG as an independent cardiovascular prognostic marker affecting basal heart rate in myocardial infarction
AIMS :To assess the prognostic value of anti-apolipoprotein A-1 (anti-apoA-1) IgG after myocardial infarction (MI) and its association with major cardiovascular events (MACEs) at 12 months and to determine their association with resting heart rate (RHR), a well-established prognostic feature after MI. Anti-apoA-1 IgG have been reported in MI without autoimmune disease, but their clinical significance remains undetermined.
METHODS AND RESULTS: A total of 221 consecutive patients with MI were prospectively included, and all completed a 12-month follow-up. Major cardiovascular events consisted in death, MI, stroke, or hospitalization either for an acute coronary syndrome or heart failure. Resting heart rate was obtained on Holter the day before discharge under the same medical treatment. Neonate rat ventricular cardiomyocytes (NRVC) were used in vitro to assess the direct anti-apoA-1 IgG effect on RHR. During follow-up, 13% of patients presented a MACE. Anti-apoA-1 IgG positivity was 9% and was associated with a higher RHR (P = 0.0005) and higher MACE rate (adjusted OR, 4.3; 95% CI, 1.46–12.6; P = 0.007). Survival models confirmed the significant nature of this association. Patients with MACE had higher median anti-apoA-1 IgG values at admission than patients without (P = 0.007). On NRVC, plasma from MI patients and monoclonal anti-apoA-1 IgG induced an aldosterone and dose-dependent positive chronotropic effect, abrogated by apoA-1 and therapeutic immunoglobulin (IVIG) pre-incubation.
CONCLUSIONS: In MI patients, anti-apoA-1 IgG is independently associated with MACE at 1-year, interfering with a currently unknown aldosterone-dependent RHR determinant. Knowing whether anti-apoA-1 IgG assessment could be of interest to identify an MI patient subset susceptible to benefit from apoA-1/IVIG therapy remains to be demonstrated.
Nicolas Vuilleumier1,*, Michel F. Rossier1,2, Sabrina Pagano1, Magaly Python2, Emmanuel Charbonney3, René Nkoulou4, Richard James2, Guido Reber5, François Mach4 and Pascale Roux-Lombard6
METHODS AND RESULTS: A total of 221 consecutive patients with MI were prospectively included, and all completed a 12-month follow-up. Major cardiovascular events consisted in death, MI, stroke, or hospitalization either for an acute coronary syndrome or heart failure. Resting heart rate was obtained on Holter the day before discharge under the same medical treatment. Neonate rat ventricular cardiomyocytes (NRVC) were used in vitro to assess the direct anti-apoA-1 IgG effect on RHR. During follow-up, 13% of patients presented a MACE. Anti-apoA-1 IgG positivity was 9% and was associated with a higher RHR (P = 0.0005) and higher MACE rate (adjusted OR, 4.3; 95% CI, 1.46–12.6; P = 0.007). Survival models confirmed the significant nature of this association. Patients with MACE had higher median anti-apoA-1 IgG values at admission than patients without (P = 0.007). On NRVC, plasma from MI patients and monoclonal anti-apoA-1 IgG induced an aldosterone and dose-dependent positive chronotropic effect, abrogated by apoA-1 and therapeutic immunoglobulin (IVIG) pre-incubation.
CONCLUSIONS: In MI patients, anti-apoA-1 IgG is independently associated with MACE at 1-year, interfering with a currently unknown aldosterone-dependent RHR determinant. Knowing whether anti-apoA-1 IgG assessment could be of interest to identify an MI patient subset susceptible to benefit from apoA-1/IVIG therapy remains to be demonstrated.
Nicolas Vuilleumier1,*, Michel F. Rossier1,2, Sabrina Pagano1, Magaly Python2, Emmanuel Charbonney3, René Nkoulou4, Richard James2, Guido Reber5, François Mach4 and Pascale Roux-Lombard6
Thursday
Evaluation of erectile dysfunction and associated cardiovascular risk using structured questionnaires in Chinese type 2 diabetic men
ABSTRACT
Erectile dysfunction (ED) is not uncommon, but frequently underdiagnosed in type 2 diabetic men. In this study, we aimed to explore the frequency and severity of ED in Chinese type 2 diabetic men using a structured questionnaire. We furthermore sought to investigate the associations of ED with diabetes-related complications and metabolic indices.
A consecutive cohort of 313 Chinese type 2 diabetic men aged between 25 and 76 years attending a diabetic centre were recruited between October 2006 and June 2007. Of the study population, the frequency of ED was 39.3% according to the National Institutes of Health (NIH) Consensus Conference criteria, compared with 84.3% (41.7% of them having moderate to severe ED) as diagnosed by International Index of Erectile Function (IIEF-5) questionnaire.
After adjusting for potential confounding factors by multivariable logistic regression, ED defined by NIH criterion was associated with advanced age [OR = 1.05 (95% CI 1.01–1.09), p = 0.012], the presence of diabetic retinopathy [OR = 2.43 (95% CI 1.27–4.66), p = 0.008] and coronary heart disease [OR = 2.63 (95% CI 1.21–5.70), p = 0.015]. ED defined by IIEF-5 was associated with advanced age [OR = 1.12 (95% CI 1.06–1.17), p < 0.0001], use of insulin therapy [OR = 2.94 (95% CI 1.12–7.73), p = 0.029] and urinary albumin-creatinine ratio [OR = 2.29 (95% CI 1.05–5.01), p = 0.037].
In conclusion, ED was highly prevalent in Chinese type 2 diabetic men and was associated with multiple cardiovascular risk factors and complications. Advanced age, use of insulin therapy, the existence of microvascular complications such as retinopathy, albuminuria and coronary heart disease were associated with ED. NIH criteria diagnosed a much lower rate of ED compared with IIEF-5. Overall, structured questionnaires are useful and objective tools to detect ED, which should prompt a comprehensive risk assessment in these subjects
L. W. Yu*, A. P. Kong*†, P. C. Tong*, C. Tam*, G. T. Ko*, C.-S. Ho‡, W.-Y. So*, R. C. Ma*, C.-C. Chow* and J. C. Chan*
*Department of Medicine and Therapeutics , †Li Ka Shing Institute of Health Science , and ‡Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China
Erectile dysfunction (ED) is not uncommon, but frequently underdiagnosed in type 2 diabetic men. In this study, we aimed to explore the frequency and severity of ED in Chinese type 2 diabetic men using a structured questionnaire. We furthermore sought to investigate the associations of ED with diabetes-related complications and metabolic indices.
A consecutive cohort of 313 Chinese type 2 diabetic men aged between 25 and 76 years attending a diabetic centre were recruited between October 2006 and June 2007. Of the study population, the frequency of ED was 39.3% according to the National Institutes of Health (NIH) Consensus Conference criteria, compared with 84.3% (41.7% of them having moderate to severe ED) as diagnosed by International Index of Erectile Function (IIEF-5) questionnaire.
After adjusting for potential confounding factors by multivariable logistic regression, ED defined by NIH criterion was associated with advanced age [OR = 1.05 (95% CI 1.01–1.09), p = 0.012], the presence of diabetic retinopathy [OR = 2.43 (95% CI 1.27–4.66), p = 0.008] and coronary heart disease [OR = 2.63 (95% CI 1.21–5.70), p = 0.015]. ED defined by IIEF-5 was associated with advanced age [OR = 1.12 (95% CI 1.06–1.17), p < 0.0001], use of insulin therapy [OR = 2.94 (95% CI 1.12–7.73), p = 0.029] and urinary albumin-creatinine ratio [OR = 2.29 (95% CI 1.05–5.01), p = 0.037].
In conclusion, ED was highly prevalent in Chinese type 2 diabetic men and was associated with multiple cardiovascular risk factors and complications. Advanced age, use of insulin therapy, the existence of microvascular complications such as retinopathy, albuminuria and coronary heart disease were associated with ED. NIH criteria diagnosed a much lower rate of ED compared with IIEF-5. Overall, structured questionnaires are useful and objective tools to detect ED, which should prompt a comprehensive risk assessment in these subjects
L. W. Yu*, A. P. Kong*†, P. C. Tong*, C. Tam*, G. T. Ko*, C.-S. Ho‡, W.-Y. So*, R. C. Ma*, C.-C. Chow* and J. C. Chan*
*Department of Medicine and Therapeutics , †Li Ka Shing Institute of Health Science , and ‡Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China
Tuesday
Myeloperoxidase: A Useful Biomarker for Cardiovascular Disease Risk Stratification?
Clinical Chemistry. 2009;55:1462-1470
Abstract
Background: Inflammation and oxidative stress are associated with atherosclerosis. Myeloperoxidase (MPO) is linked to both inflammation and oxidative stress by its location in leukocytes and its role in catalyzing the formation of oxidizing agents. Recent evidence suggests that MPO activity precipitates atherogenesis. Measurement of MPO in plasma may therefore contribute to cardiovascular disease (CVD) risk stratification.
Content: Cross-sectional studies, case-control studies, and prospective-cohort studies investigating the relation between MPO and CVD have been evaluated. Differences in study populations, sample materials, sample handling, and assays were ascertained. Potential causal mechanisms linking MPO to accelerated atherosclerosis are discussed here. A majority of studies indicate that measurement of MPO in plasma was associated with improved CVD risk stratification above and beyond risk stratification results obtained with markers used in routine clinical practice. However, comparison of these epidemiological studies with regard to MPO and outcome is hampered because the reported MPO concentration depends on the assay method, sampling material, and preanalytical and analytical procedures. The link between MPO and CVD can, at least partly, be explained by MPO-dependent oxidation of LDL and HDL, subsequently leading to cholesterol accumulation in the arterial wall. Furthermore, MPO may reduce the bioavailability of nitric oxide, resulting in endothelial dysfunction. Finally, MPO destabilizes atherosclerotic plaques.
Summary: Increasing evidence suggests that MPO is causally linked to atherosclerosis and its measurement may improve CVD risk estimation. Before MPO can be used in routine clinical practice, however, standardization of sampling and laboratory procedures is needed
Abstract
Background: Inflammation and oxidative stress are associated with atherosclerosis. Myeloperoxidase (MPO) is linked to both inflammation and oxidative stress by its location in leukocytes and its role in catalyzing the formation of oxidizing agents. Recent evidence suggests that MPO activity precipitates atherogenesis. Measurement of MPO in plasma may therefore contribute to cardiovascular disease (CVD) risk stratification.
Content: Cross-sectional studies, case-control studies, and prospective-cohort studies investigating the relation between MPO and CVD have been evaluated. Differences in study populations, sample materials, sample handling, and assays were ascertained. Potential causal mechanisms linking MPO to accelerated atherosclerosis are discussed here. A majority of studies indicate that measurement of MPO in plasma was associated with improved CVD risk stratification above and beyond risk stratification results obtained with markers used in routine clinical practice. However, comparison of these epidemiological studies with regard to MPO and outcome is hampered because the reported MPO concentration depends on the assay method, sampling material, and preanalytical and analytical procedures. The link between MPO and CVD can, at least partly, be explained by MPO-dependent oxidation of LDL and HDL, subsequently leading to cholesterol accumulation in the arterial wall. Furthermore, MPO may reduce the bioavailability of nitric oxide, resulting in endothelial dysfunction. Finally, MPO destabilizes atherosclerotic plaques.
Summary: Increasing evidence suggests that MPO is causally linked to atherosclerosis and its measurement may improve CVD risk estimation. Before MPO can be used in routine clinical practice, however, standardization of sampling and laboratory procedures is needed
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