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      Metabolic Syndrome is Associated With Higher Wall Motion Score and Larger Infarct Size After Acute Myocardial Infarction

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          Abstract

          Background:

          Infarct size is an important surrogate end point for early and late mortality after acute myocardial infarction. Despite the high prevalence of metabolic syndrome in patients with atherosclerotic diseases, adequate data are still lacking regarding the extent of myocardial necrosis after acute myocardial infarction in these patients.

          Objectives:

          In the present study we aimed to compare myocardial infarction size in patients with metabolic syndrome to those without metabolic syndrome using peak CK-MB and cardiac troponin I (cTnI) at 72 hours after the onset of symptoms.

          Patients and Methods:

          One-hundred patients with metabolic syndrome (group I) and 100 control subjects without metabolic syndrome (group II) who experienced acute myocardial infarction were included in the study. Diagnosis of metabolic syndrome was based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines published in 2001. Myocardial infarction size was compared between the two groups of patients using peak CK-MB and cTnI level in 72 hours after the onset of symptoms.

          Results:

          Peak CK-MB and cTnI in 72 hours were found to be significantly higher in patients with metabolic syndrome compared with control subjects (both P < 0.001). Patients with metabolic syndrome also had markedly higher wall motion abnormality at 72 hours after the onset of symptoms as assessed by echocardiographically-derived Wall Motion Score Index (WMSI) (P < 0.001). Moreover, statistically significant relationships were found between WMSI and peak CK-MB and also cTnI at 72 hours (Spearman's rho = 0.56, P < 0.001 and Spearman's rho = 0.5, P < 0.001; respectively). However, association between WMSI and left ventricular ejection fraction was insignificant (Spearman's rho = -0.05, P = 0.46).

          Conclusions:

          We showed that patients with metabolic syndrome have larger infarct size compared to control subjects.

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          Most cited references48

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          Cardiovascular morbidity and mortality associated with the metabolic syndrome.

          To estimate the prevalence of and the cardiovascular risk associated with the metabolic syndrome using the new definition proposed by the World Health Organization A total of 4,483 subjects aged 35-70 years participating in a large family study of type 2 diabetes in Finland and Sweden (the Botnia study) were included in the analysis of cardiovascular risk associated with the metabolic syndrome. In subjects who had type 2 diabetes (n = 1,697), impaired fasting glucose (IFG)/impaired glucose tolerance (IGT) (n = 798) or insulin-resistance with normal glucose tolerance (NGT) (n = 1,988), the metabolic syndrome was defined as presence of at least two of the following risk factors: obesity, hypertension, dyslipidemia, or microalbuminuria. Cardiovascular mortality was assessed in 3,606 subjects with a median follow-up of 6.9 years. In women and men, respectively, the metabolic syndrome was seen in 10 and 15% of subjects with NGT, 42 and 64% of those with IFG/IGT, and 78 and 84% of those with type 2 diabetes. The risk for coronary heart disease and stroke was increased threefold in subjects with the syndrome (P < 0.001). Cardiovascular mortality was markedly increased in subjects with the metabolic syndrome (12.0 vs. 2.2%, P < 0.001). Of the individual components of the metabolic syndrome, microalbuminuria conferred the strongest risk of cardiovascular death (RR 2.80; P = 0.002). The WHO definition of the metabolic syndrome identifies subjects with increased cardiovascular morbidity and mortality and offers a tool for comparison of results from diferent studies.
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            Universal definition of myocardial infarction.

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              Hyperinsulinemia as an independent risk factor for ischemic heart disease.

              Prospective studies suggest that hyperinsulinemia may be an important risk factor for ischemic heart disease. However, it has not been determined whether plasma insulin levels are independently related to ischemic heart disease after adjustment for other risk factors, including plasma lipoprotein levels. In 1985 we collected blood samples from 2103 men from suburbs of Quebec City, Canada, who were 45 to 76 years of age and who did not have ischemic heart disease. A first ischemic event (angina pectoris, acute myocardial infarction or death from coronary heart disease) occurred in 114 men (case patients) between 1985 and 1990. Each case patient was matched for age, body-mass index, smoking habits, and alcohol consumption with a control selected from among the 1989 men who remained free of ischemic heart disease during follow-up. After excluding men with diabetes, we compared fasting plasma insulin and lipoprotein concentrations at base line in 91 case patients and 105 controls. Fasting insulin concentrations at base line were 18 percent higher in the case patients than in the controls (P<0.001). Logistic-regression analysis showed that the insulin concentration remained associated with ischemic heart disease (odds ratio for ischemic heart disease with each increase of 1 SD in the insulin concentration, 1.7; 95 percent confidence interval, 1.3 to 2.4) after adjustment for systolic blood pressure, use of medications, and family history of ischemic heart disease. Further adjustment by multivariate analysis for plasma triglyceride, apolipoprotein B, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol concentrations did not significantly diminish the association between the insulin concentration and the risk of ischemic heart disease (odds ratio, 1.6; 95 percent confidence interval, 1.1 to 2.3). High fasting insulin concentrations appear to be an independent predictor of ischemic heart disease in men.
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                Author and article information

                Journal
                Res Cardiovasc Med
                Res Cardiovasc Med
                10.5812/cardiovascmed
                Kowsar
                Research in Cardiovascular Medicine
                Kowsar
                2251-9572
                2251-9580
                20 February 2015
                February 2015
                : 4
                : 1
                : e25018
                Affiliations
                [1 ]Department of Cardiology, Rasoul-e-Akram Hospital, Iran University of Medical Sciences, Tehran, IR Iran
                [2 ]Echocardiography Research Center, Rajaie Cardiovascular, Medical and Research Center, Iran University of Medical Sciences, Tehran, IR Iran
                [3 ]Department of Cardiology, Shahid Beheshti University of Medical Sciences, Tehran, IR Iran
                [4 ]Cardiac Electrophysiology Research Center, Rajaie Cardiovascular, Medical and Research Center, Iran University of Medical Sciences, Tehran, IR Iran
                [5 ]Department of Cardiology, Rajaei Cardiovascular, Medical and Research Center, Iran University of Medical Sciences, Tehran, IR Iran
                Author notes
                [* ]Corresponding author: Mitra Chitsazan, Echocardiography Research Center, Rajaie Cardiovascular, Medical and Research Center, Iran University of Medical Sciences, Tehran, IR Iran. Tel: +98-9122210385, Fax: +98-2122055594, E-mail: mitra.chitsazan66@ 123456yahoo.com
                Article
                10.5812/cardiovascmed.25018
                4350188
                ef662bff-1302-4333-84ed-ce4d8825935c
                Copyright © 2015, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences.

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

                History
                : 30 October 2014
                : 29 December 2014
                Categories
                Research Article

                creatine kinase,echocardiography,myocardial infarction,troponin

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