Utility of myeloperoxidase in the differential diagnosis of acute coronary syndrome / Utilidad de la determinación de mieloperoxidasa en el diagnóstico diferencial del síndrome coronario agudo

Abstract Objectives: To determine the usefulness of myeloperoxidase in discriminating between patients with acute coronary syndrome and patients with chest pain by other causes. Methods: The study included all patients over 18 years of age who come consecutively to the emergency department from September 2015 to December 2015 with chest pain of non- traumatic origin. The initial patient evaluation was performed according to the study protocol for patients with suspected acute coronary syndrome (ACS) in our Emergency Department. This included the serial measurement of troponin, and in this case myeloperoxidase, with serialization on admission and at 6 h. For the determination of myeloperoxidase (MPO), a single step sandwich enzyme immunoassay by Siemens, automated on a Dimension analyser, was used. Results: Statistically significant differences were observed in the concentration of myeloperoxidase at time 0 among patients diagnosed with ACS: 505 (413) pmol/L, and non-ACS patients: 388 (195) pmol/L (p < .001), as well as at 6 h (p < .001). An area under the curve ROC of 0.824 was obtained at 6 h for ACS patients, with a confidence interval of 95% from 0.715 to 0.933 and a level of significance of p <.001. Statistically significant differences were also found in the concentration of myeloperoxidase at time 0 and at 6 h among patients with ACS and patients with heart disease other than coronary artery disease. Conclusions: The concentration of MPO helps to differentiate between ACS and non-ACS patients, as well as between ACS patients and patients with heart diseases other than coronary artery disease.

Resumen Objetivos: Conocer la utilidad de mieloperoxidasa (MPO) para discriminar entre pacientes con síndrome coronario agudo y dolor torácico de otras causas. Métodos: De septiembre a diciembre de 2015 se incluyeron todos los pacientes mayores de 18 años que acudieron de forma consecutiva al servicio de urgencias con dolor torácico de origen no traumático. La evaluación inicial del paciente se realizó de acuerdo con el protocolo de estudio para pacientes con sospecha de síndrome coronario agudo (SCA) en nuestro servicio de urgencias, que incluye la medición de troponina y en este caso MPO, con serialización al ingreso y a las 6 h. Para la determinación de MPO se utilizó un inmunoensayo enzimático de tipo sándwich, de una sola etapa de Siemens, automatizado en un equipo Dimension . Resultados: Se obtuvieron diferencias estadísticamente significativas en la concentración de MPO a tiempo 0 entre los pacientes con diagnóstico de SCA: 505 (413) pmol/l y los pacientes no SCA: 388 (195 pmol/l (p < 0.001), así como a las 6 h (p < 0.001). Se obtuvo a las 6 h un área bajo la curva ROC para pacientes con SCA de 0.824 con un intervalo de confianza del 95% de 0.715 a 0.933 y un grado de significación p < 0.001. También se obtuvieron diferencias estadísticamente significativas en la concentración de MPO tanto a tiempo 0 como a las 6 h entre pacientes con SCA y pacientes con enfermedad cardiaca diferente de enfermedad coronaria. Conclusiones: La concentración de MPO sirve para diferenciar entre pacientes SCA y pacientes que no son SCA, así como entre pacientes SCA y pacientes con otras enfermedades cardiacas diferentes a la enfermedad coronaria.

Paraoxonase 1 gene polymorphisms and enzyme activities in coronary artery disease and its relationship to serum lipids and glycemia / Polimorfismos en el gen de la paraoxonasa 1 y sus actividades enzimáticas en la enfermedad coronaria. Su relación con el perfil lipídico y la glucemia

Abstract Objectives Oxidative stress and inflammation are important processes in development of atherosclerosis. Paraoxonase 1 (PON1) is a bioscavenger enzyme associated with inflammation and oxidative stress. We evaluate the association of two single nucleotide polymorphisms in PON1 gene, and enzyme activities with lipid profile and glycemia. Methods This case-control study consisted of 126 patients with coronary artery disease (CAD) and 203 healthy controls. PON Q192R and L55M polymorphisms were detected by real-time PCR. Paraoxonase and arylesterase activities were determined spectrophotometrically. Blood glucose, cholesterol, triglycerides, HDL, and LDL were measured. Results PON1 QR192 polymorphism had a major effect on paraoxonase but no effect on arylesterase serum activities. Paraoxonase activity was higher in RR genotype and lowest in QQ genotype. Paraoxonase and arylesterase activities were higher in LL and lower in MM genotypes of PON1 LM55 polymorphism. RQ and LM variants showed intermediate activities between respective homozygous. Elevated concentrations of triglycerides in cases correlate with QQ variant or the presence of M allele. Glucose levels were elevated in cases with QQ variant or with the presence of M allele. Cholesterol and LDL did not show variations in control and cases with any variant of both polymorphisms. HDL is lower in cases with respect to controls independently of genotypes. All differences were significant with p < 0.05. Conclusions Our results confirm the relationship between variations in PON1 activities and lipid metabolism, and showed that genetically programmed low PON1 activities would have certain responsibility in the increase in glycemia and concomitantly the aggravation of atherosclerotic disease.

Resumen Objetivos La enzima paraoxonasa 1 (PON1), está asociada con el estrés oxidativo y la inflamación, procesos importantes en el desarrollo de la aterosclerosis. Evaluamos la asociación de 2 polimorfismos de un solo nucleótido en el gen PON1 y sus actividades enzimáticas con el perfil lipídico y la glucemia. Métodos Estudio caso-control en 126 pacientes con enfermedad coronaria y 203 controles sanos. Los polimorfismos PON Q192R y L55M fueron detectados por PCR en tiempo real y las actividades de paraoxonasa y arilesterasa por espectrofotometría. Se midieron glucemia, colesterol, triglicéridos, HDL y LDL. Resultados El polimorfismo PON1 QR192 afectó la actividad de paraoxonasa pero no la de arilesterasa. La actividad de paraoxonasa fue mayor en el genotipo RR y menor en QQ. Ambas actividades fueron mayores en el genotipo LL y menores en MM del polimorfismo PON1 LM55. Las variantes RQ y LM mostraron actividades intermedias entre los respectivos homocigotos. Concentraciones elevadas de triglicéridos en los casos correlacionaron con la variante QQ o la presencia del alelo M. Los niveles de glucosa fueron elevados en los casos QQ o con la presencia del alelo M. El colesterol y el LDL no variaron ni en los casos ni en los controles con ambos polimorfismos. El HDL fue menor en los casos respecto de los controles, independientemente del genotipo. Conclusiones Los resultados confirman la relación entre las variaciones en las actividades de PON1 y el metabolismo lipídico y mostraron que las bajas actividades de PON1 genéticamente programadas tendrían cierta responsabilidad en el aumento de la glucemia y, concomitantemente, en la agravación de la enfermedad aterosclerótica.

Serum Gamma-Glutamyltransferase Concentration Correlates with Framingham Risk Score in Koreans

Gamma-glutamyltransferase (GGT) is a novel coronary artery disease (CAD) risk factor, but its use as an independent factor for CAD risk prediction remains unclear in Asian population. This study examined the association between serum GGT concentration and Framingham risk score (FRS) in the Korean population. This cross-sectional study was performed on 30,710 Koreans. Besides FRS, body mass index, fasting blood glucose, liver enzymes, lipid profile, uric acid and high sensitive C-reactive protein data were used. The study subjects were grouped into quartiles according to the levels of GGT. Analyses relating GGT to FRS > or = 20% utilized multiple confounders adjusted logistic regression. Positive correlations were established between log-transformed GGT concentration and FRS (r = 0.38; P or = 20% were significantly increased from the lowest to highest GGT quartiles; these results remained significantly after adjustments for multiple confounders. Increased GGT concentration is associated with the increase in FRS. Serum GGT may be helpful to predict the future risk of CAD.

Presencia del alelo T para el polimorfismo rs2781666 G>T del gen arginasa 1 constituye un factor protector contra enfermedad arterial coronaria / The presence of T allele for rs2781666 G>T common variant of arginase 1 gene constitutes a protector factor against coronary artery disease in Southern Chilean subjects

Introducción: Variaciones moleculares en el gen de la arginasa I, ARGl, podrían provocar un aumento de la expresión de la enzima o de su actividad, lo que puede llevar a una disfunción endotelial al disminuir la producción de óxido nítrico por parte de la eNOS. Así, el objetivo del presente estudio fue investigar la posible asociación del polimorfismo rs2781666 G>T y la presencia de enfermedad coronaria (confirmada con angiografía) en individuos de la región de La Araucanía. Material y Métodos: En el presente estudio, de tipo casos y controles, fueron evaluados 247 sujetos, con edades entre 30 y 74 años; 124 individuos pacientes con enfermedad arterial coronaria (casos) y 123 controles. La genotipificación del polimorfismo rs2781666 del gen ARGl fue realizada mediante PCR- RFLR Resultados: La frecuencia del genotipo homocigoto TT para el polimorfismo rs2781666 del gen ARGl fue de 6.5 por ciento en el grupo casos y 8 por ciento en el grupo control, difiriendo significativamente (p=0.032). La frecuencia relativa del alelo T también presentó diferencias significativas entre casos y controles (0.230 vs. 0.325, p=0.031). La OR relacionada al alelo mutado T fue de 0.63 (I.C. 95 por ciento, 0.43 - 0.94), confirmando la presencia de la asociación observada. Conclusión: Los resultados obtenidos sugieren que el polimorfismo rs2781666 G>T del gen ARGl confiere protección contra enfermedad coronaria en la población analizada. Sin embargo, este resultado debe ser replicado en otros grupos poblacionales de nuestro país.

Background: Recent data support a role for arginase 1 (ARG1) in the initiation, development, and complications of coronary artery disease. Thus, in the present study we investigated the possible association between the rs2781666 G>T variant of ARG1 and the presence of CAD confirmed by angiography in Chilean subjects. Methods: A total of 124 unrelated patients with diagnosis of CAD confirmed by angiography (stenosis > 70 percent) and 123 healthy controls (30 - 74 years old) were included in this study. The rs2781666 G>T variant of the ARG1 gene was evaluated by PCR-RFLR Results: The frequency of TT homozygous genotype in CAD patients was lower when compared to control group (6.5 percent vs. 8.0 percent, p=0.032). Similarly, the T allele frequency was different between CAD and control groups (0.230 vs. 0.325, p=0.031). The OR for CAD related to T allele was 0.64 (95 percent CI. = 0.43-0.94), con-firming the association founded. Conclusion: These findings suggest that the T allele for rs2781666 polymorphism of the ARG1 gene constitutes an inherited protective factor against CAD in Southern Chilean subjects.

Paraoxonases : Structure, gene polymorphism & role in coronary artery disease.

Paraoxonases (PONs) i.e. PON1, PON2, PON3 are basically lactonases. Of these, PON1 in addition has an efficient esterase activity and can hydrolyze organophosphates. The PONs prevent low density lipoprotein cholesterol (LDL-C) from peroxidation, thereby preventing atherosclerosis. The PON1 is exclusively associated with high density lipoprotein cholesterol (HDL-C) and its antioxidant activity is largely attributed to PON1 located on it. At present, PON1 status i.e. its activity and concentration, is considered to be more important than polymorphism alone, in prevention of coronary artery disease (CAD). Its activity has been found to be affected by a number of pharmacological agents, diet and other factors, thereby becoming a promising target for pharmacological intervention. The PON2 prevents cell mediated lipid peroxidation. However, little is known about the role of PON3. This review describes the structure, gene polymorphism, and factors affecting the activity of PONs, and their role in prevention of CAD.

Actividades paraoxonasa y arilesterasa bajas en sujetos mexicanos con enfermedad arterial coronaria / Low paraoxonase and arylesterase plasma activities in mexican patients with coronary artery disease

PURPOSE: To determine the Paraoxonase-1 (PON1) activity as well as its pheno- and genotypes at position 192 in Mexican subjects with diagnosis of coronary heart disease (CHD). METHODS: We determined the PON1-192 polymorphism by PCR-RFLP, and serum PON1 activity, using either paraoxon (PONase activity) or phenylacetate (ARE activity) as substrates, in 155 clinically healthy individuals (control group), and 155 patients with at least one myocardial infarction (CHD group). The biochemical A/B phenotype was determined by the ratio of the NaCI 1 M-stimulated PONase activity divided by the ARE activity. RESULTS: We found significantly lower PONase and ARE activities in CHD patients as compared to controls (233.1 +/- 102.1 vs. 295.8 +/- 159.1 nmol/min/mL, and 103.1 +/- 33.7 vs 220.2 +/- 120.7 micromol/min/mL, respectively, p<0.05 for both). Allele and genotype frequencies for PON1-192 were similar in CHD patients and healthy controls. Moreover, in the control group, the PON1-192 Q/R genotype did not matched with the A/B phenotype as has been proposed by other studies. CONCLUSIONS: There were important differences in the ARE and PONase activities between Mexican CHD patients and controls, suggesting that PON1 activity could be a good marker of CHD risk, whereas PON1-192 lacks of value to assess such risk.

Mieloperoxidase e doença arterial coronariana: da pesquisa à prática clínica / Myeloperoxidase and coronary arterial disease: from research to clinical practice

A mieloperoxidase (MPO) é uma enzima derivada de leucócitos que catalisa a formação de numerosas espécies reativas oxidantes. Além de integrantes da resposta imune inata, evidências têm comprovado a contribuição desses oxidantes para o dano tecidual durante inflamação. A MPO participa de atividades biológicas pró-aterogênicas relacionadas à evolução da doença cardiovascular, incluindo iniciação, propagação e as fases de complicação aguda do processo aterosclerótico. Dessa forma, a MPO e sua cascata inflamatória representam um alvo atrativo para investigação prognóstica e terapêutica na doença aterosclerótica cardiovascular. Nesta revisão, apresentamos o estado da arte no entendimento das ações biológicas às evidências clínicas da relação entre MPO e doença arterial coronariana. Vários estudos apontam para o efeito independente dos níveis de MPO na evolução da doença e ocorrência de eventos em pacientes com síndrome coronariana aguda. Entretanto, ainda não é consistente o valor preditivo adicional dos níveis de MPO na estratificação de risco cardiovascular para incorporá-la à prática clínica como sinalizadora de vulnerabilidade de placa. Estudos adicionais são necessários para confirmar seu papel nas diferentes formas de apresentação da cardiopatia isquêmica, além da padronização do ensaio, ponto fundamental para a transição desse marcador do ambiente de pesquisa para uso na rotina clínica.

Myeloperoxidase (MPO) is an enzyme derived of leukocytes that catalyze formation of numerous reactive oxidant species. Besides members of the innate host defense, evidences have been proving the contribution of these oxidants to tissue injury during inflammation. MPO participates in proatherogenic biological activities related to the evolution of cardiovascular disease, including initiation, propagation and acute complications of atherosclerotic process. Thereby, MPO and its inflammatory cascade represents an attractive target for prognostical investigation and therapeutics in atherosclerotic cardiovascular disease. In this review, we present the state of the art in the understanding of biological actions to clinical evidences of the relationship between MPO and coronary arterial disease. Several studies point to the independent effect of MPO levels in the evolution of disease and incidence of events in patients with acute coronary syndrome. However, the additional predictive value of MPO levels in the cardiovascular risk assessment, to incorporate it to the clinical practice as marker of plaque vulnerability, is still not consistent. Additional studies are necessary to confirm its role in the different forms of presentation of ischemic disease, besides the standardization of the assay, fundamental point for transition of this marker from research atmosphere to use in clinical routine: : from laboratory to clinical practice.

Homocistéina e metilenotetrahidrofolato redutase em indivíduos submetidos à angiografia coronariana / Homocysteine and methylenetetrahydrofolate reductase in subjects undergoing coronary angiography

OBJETIVO: Determinar os níveis plasmáticos de homocisteína e a incidência do polimorfismo C677T no gene da enzima metilenotetrahidrofolato redutase (MTHFR) em um grupo de indivíduos submetidos a angiografia coronariana, buscando estabelecer a possível correlação entre esses parâmetros e a gravidade da doença arterial coronariana (DAC), bem como investigar a correlação entre hiper-homocisteinemia e a presença do polimorfismo. MÉTODOS: Vinte indivíduos com ausência de ateromatose nas coronárias (controles), quatorze indivíduos apresentando ateromatose leve/moderada e vinte e nove indivíduos apresentando ateromatose grave foram avaliados. RESULTADOS: Para o parâmetro homocisteína foram observadas diferenças significativas entre as médias dos grupos controle e ateromatose grave (p < 0,001). Entre os demais grupos não foram observadas diferenças significativas. O grupo ateromatose grave apresentou uma freqüência de 62,0 por cento e 6,9 por cento para o polimorfismo C677T no gene da enzima MTHFR, em heterozigose e homozigose, respectivamente. Entretanto, não foi observada correlação entre a presença da mutação e hiper-homocisteinemia. Foi observada uma correlação positiva da ordem de 41,91 por cento (p < 0,001) entre hiper-homocisteinemia e a presença de DAC. CONCLUSÃO: O achado mais importante deste estudo foi a associação entre hiper-homocisteinemia e a presença de estenose coronariana superior a 70 por cento; entretanto, permanece a dúvida se o aumento da concentração plasmática de homocisteína constitui um fator determinante para o agravamento da lesão aterosclerótica nas coronárias ou se o mesmo é uma conseqüência desta lesão.

OBJECTIVE: To determine plasma homocysteine levels and the incidence of methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism in a group of subjects who underwent coronary angiography, in an attempt to establish a correlation between these parameters and the severity of coronary artery disease (CAD), as well as investigate the correlation between hyperhomocysteinemia and the presence of polymorphism. METHODS: Twenty subjects with no coronary atheromatosis (controls), fourteen subjects with mild/moderate atheromatosis, and twenty-nine subjects with severe atheromatosis were evaluated. RESULTS: Significant differences were observed in mean homocysteine levels between the control and the severe atheromatosis groups (p < 0.001). No significant differences were observed among the other groups. The severe atheromatosis group showed rates of 62.0 percent and 6.9 percent for the C677T MTHFR gene polymorphism, in heterozygous and homozygous subjects, respectively. However, there was no correlation between the presence of mutation and hyperhomocysteinemia. A positive correlation of 41.91 percent (p < 0.001) was found between hyperhomocysteinemia and CAD. CONCLUSION: The most important finding of this study was the association between hyperhomocysteinemia and coronary stenosis > 70 percent; yet, whether elevated plasma homocysteine worsens atherosclerosis or is a consequence remains to be established.

Hyperhomocystinemia in patients with coronary artery disease

Hyperhomocystinemia has been related to an increased risk of cardiovascular disease in several studies. The C677T polymorphism for the gene that encodes the methylenetetrahydrofolate reductase enzyme (MTHFR) and low plasma folate levels are common causes of hyperhomocystinemia. Due to differences in nutritional patterns and genetic background among different countries, we evaluated the role of hyperhomocystinemia as a coronary artery disease (CAD) risk factor in a Brazilian population. The relation between homocysteine (Hcy) and the extent of CAD, measured by an angiographic score, was determined. A total of 236 patients referred for coronary angiography for clinical reasons were included. CAD was found in 148 (62.7 percent) patients and 88 subjects had normal or near normal arteries. Patients with CAD had higher Hcy levels [mean (SD)] than those without disease (14 (6.8) vs 12.5 (4.0) æM; P = 0.04). Hyperhomocystinemia (Hcy >17.8 æM) prevalence was higher in the CAD group: 31.1 vs 12.2 percent (P = 0.01). After adjustment for major risk factors, we found an independent association between hyperhomocystinemia and CAD (OR = 2.48; 95 percent CI = 1.02-6.14). Patients with a more advanced coronary score had a higher frequency of hyperhomocystinemia and tended to have higher mean Hcy levels. An inverse relation between plasma folate and Hcy levels was found (r = -0.14; P = 0.04). Individuals with the MTHFR C677T polymorphism had a higher prevalence of hyperhomocystinemia than those without the mutated allele. We conclude that hyperhomocystinemia is independently associated with CAD, with a positive association between Hcy level and disease severity.

Polymorphism of Matrix Metalloproteinase-3 Promoter Gene as a Risk Factor for Coronary Artery Lesions in Kawasaki Disease

Kawasaki disease (KD) is a major cause of acquired coronary artery diseases in childhood. The serum levels of matrix metalloproteinase (MMP)-3 and MMP-9 in KD have been reported to be significantly higher than other diseases. Several studies have demonstrated that MMP-3 5A/6A polymorphism and MMP-9 C-1562T polymorphism modify each transcriptional activity in allele specific manner. We hypothesized that these polymorphisms may play a role as a risk factor for development of coronary artery lesions (CAL) in KD. Eighty-three patients, diagnosed with KD in Cheju National University Hospital from January 2000 to February 2004, were divided into two groups according to the presence of CAL. Genotyping of MMP-3 and MMP-9 gene polymorphisms were determined by restriction fragment length polymorphism. With regard to MMP-3 gene polymorphism, the KD with CAL group had a higher frequency of 6A/6A genotype than control group (p=0.0127) and the KD without CAL group (p=0.0036). However, no significant differences in the allele and genotype distributions of the MMP-9 polymorphism were observed. These findings suggest that MMP-3 6A/6A genotype may be an independent risk factor for CAL formation in KD.

T1 and M1 polymorphism in glutathione S-transferase gene and coronary artery disease in North Indian population.

BACKGROUND: DNA damage has been found to play an important role in atherosclerosis and coronary artery disease. Genetic polymorphisms of the genes coding for enzymes involved in the metabolism of genotoxins result in different phenotypes with respect to their ability to detoxify these agents. In the present study the contribution of the polymorphism in the glutathione S-transferase gene to the development of coronary artery disease has been investigated. METHODS: One hundred and ninety seven angiographically proven patients with coronary artery disease and one hundred and ninety eight age-matched controls were genotyped for glutathione S- transferase polymorphism by polymerase chain reaction. Genotype frequencies were compared in patients and controls by Chi-square test. Binary logistic regression was used to examine the relationship between genotype and disease, incorporating other variables into the model. RESULTS: GSTT1 null genotype was significantly decreased in patients with coronary artery disease. No significant association was found with GSTM1 genotypes. No such association was seen with smokers. CONCLUSION: Null genotype of GSTT1 is protective against coronary artery disease in our population.

Angiotensin-converting enzyme gene polymorphism in coronary artery disease in north India.

BACKGROUND: The aim of this study was to investigate the role of angiotensin-converting enzyme gene polymorphism in patients with coronary artery disease in north India. METHODS AND RESULTS: One hundred forty-six patients with angiographically proven atherosclerotic coronary artery disease, and 146 age- and sex-matched control subjects (treadmill-negative) were included in the study. Genomic DNA was extracted and analyzed for angiotensin-converting enzyme insertion/deletion polymorphism. Two independent investigators scored the genotypes. CONCLUSIONS: When we compared the genotypes of patients with coronary artery disease with those of normal controls, it was seen that all three genotypes, i.e. DD, ID and II, were not statistically different among patients and controls. Further, we categorized the patient and control groups into 2 subgroups, i.e. below and above 50 years of age. Interestingly, it was observed that the DD genotype was significantly higher in patients in the higher age group (i.e. above 50 years of age). However, this needs further validation by studying patients with coronary artery disease from other parts of India.

Lipid peroxidation and antioxidant enzymes in coronary and peripheral artery disease.

There is a strong co-relation in between the levels of blood lipids in patients of different subgroups of CAD, however this is not present in the case of subgroups of patients in PAD. Moreover levels of MDA and antioxidant enzymes are also significantly altered in the subgroups of CAD but the correlation is weak in that of PAD. Thus these values may serve as a clinical support for experimental data and supplementary information regarding atheromatous disease.

Role of oxygen free radicals in causing endothelial damage in acute myocardial infarction.

OBJECTIVES: This work was done in order to study the oxidant and anti-oxidant status in a disease resulting from endothelial injury. The disease selected for study was acute myocardial infarction. METHODS: Sixty patients of acute myocardial infarction were selected after being diagnosed in accordance to the guidelines laid down by the WHO. Thirty subjects were included as controls. Plasma levels of certain markers of oxidative stress and anti oxidant activity were measured in all the subjects. Malonaldehyde (MDA) and nitrite (NO2) were measured as markers of free radical mediated endothelial injury, and superoxide dismutase (SOD) enzyme as an indicator of antioxidant activity. RESULTS: It was found that the plasma levels of MDA and nitrite were significantly elevated in the patients of acute myocardial infarction compared to the control group (7.29 +/- 3.28 v/s 4.57 +/- 0.63 nmol/ml and 12.85 +/- 8.71 v/s 0.97 +/- 0.25 microM respectively), thereby indicating that oxygen free radicals cause endothelial damage in them. The superoxide dismutase levels were also found to be elevated in these patients (5.57 +/- 1.47 v/s 3.91 +/- 0.66 U/ml). CONCLUSION: These results indicate that acute myocardial infarction is a state of enhanced free radical activity, which causes endothelial damage. The elevated SOD levels may imply that the body attempts to combat this oxidative stress by raising it's level of anti-oxidants.