Metabolic syndrome is associated with higher wall motion score and larger infarct size after acute myocardial infarction

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.

Incomplete protective effect of coronary collateral circulation for acute myocardial infarction patients

“…Peak serum concentrations of TnI, Myo, and CK-MB were used for estimation of infarction size. [ 10 ] In addition, blood samples were taken from an antecubital vein after a 12-hour fast to measure total cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and fasting plasma glucose levels.…”

“…[ 9 ] Thus, this study sought to explore the clinical significance of CCC for AMI patients under the background of current evidence-based clinical practices in the real world. The main contents of this study include an analysis of basic clinical characteristics, comparisons between CCC and non-CCC subjects for myocardial infarct size as estimated by peak blood concentrations of cardiac-specific enzymes including creatine kinase MB fraction (CK-MB), myoglobin (Myo), and troponin I (TnI), [ 10 ] left ventricular function as gauged by echocardiography, peak value of N-terminal pro-brain natriuretic peptide (NT-proBNP), Killip grades, and the intra-aortic balloon pump (IABP) application rate, death rate, as well as the duration of in-hospital stay. Multiple linear regressions for NT-proBNP and TnI, and Kaplan-Meier curves for 5-years’ main cardiovascular event (MACE) are also analyzed.…”

Metabolic and Biochemical Stressors in Diabetic Cardiomyopathy

“…Studies have confirmed that DCM is not an unusual condition but caused by low-grade non-resolving inflammation, uncontrolled hyperglycemia (glucotoxicity), or hyperlipidemia (lipotoxicity). These factors mainly contribute to metabolic syndrome, leading to cardiac dysfunction and increasing the risk of MI or recurrent MI ( 29 ). Glucotoxicity refers to uncontrolled hyperglycemia and subsequent metabolic changes triggered by excess sugar or carbohydrate ( 30 ).…”

Angiographic severity of coronary artery disease and cardiovascular risk in acute coronary syndrome in patients with metabolic syndrome

“…Atherosclerotic coronary disease, as well as atheromatous plaque progression and rupture with subsequent thrombosis, play a key role in the pathogenesis of acute coronary syndrome (ACS) [1]. The classic risk factors for coronary artery disease (CAD) include age, male sex, sedentary lifestyle, and smoking, but also components of metabolic syndrome (MS) [2,3]. The extent of angiographic lesions, size of infarct, and in-hospital and late prognosis in patients with MS have not been clearly determined.…”

“…The extent of angiographic lesions, size of infarct, and in-hospital and late prognosis in patients with MS have not been clearly determined. There have been only a few studies regarding this issue, with conflicting results [3][4][5][6][7][8]. As part of MS, insulin resistance (IR) is an important risk factor for the development of cardiovascular disorders.…”