Correlation between Metabolic Syndrome and its components with myocardial dysfunction in ICU

Abstract

Metabolic syndrome (MetS) is a multiplex risk factor that arises from insulin resistance accompanying abnormal adipose deposition and function. It is a risk factor for coronary heart disease, as well as for diabetes, fatty liver, and several cancers. Clinical manifestations of metabolic syndrome include the following:  Hypertension  Hyperglycemia  Hypertriglyceridemia  Reduced high-density lipoprotein cholesterol (HDL-C)  Abdominal obesity  Chest pains or shortness of breath: Suggesting the rise of cardiovascular and other complications  Acanthosis nigricans, hirsutism, peripheral neuropathy, and retinopathy: In patients with insulin resistance and hyperglycemia or with diabetes mellitus  Xanthomas or xanthelasmas: In patients with severe dyslipidemia MetS has been shown to associate with almost a 2 fold increase in CVD risk. MetS is composed of several factors contributing to CVD, namely hypertension, hyperlipidemia, obesity, procoagulability, and hyperglycemia. Among these factors, hyperlipidemia, procoagulability, and hyperglycemia are directly the result of hepatic insulin resistance. It has been well known for a long time that prolonged exposure to hyperglycemia has a major effect on the pathogenesis of atherosclerosis. Hyperglycemia induces a series of alterations at the molecular and cellular levels that potentially accelerate the atherosclerotic process. Non-enzymatic glycosylation of proteins and lipoproteins in the arterial wall is one of the mechanisms that change the normal function of proteins, leading to interference with receptor recognition, changing enzymatic activity, and disruption of molecular conformation. A second proposed mechanism is PKC activation following exposure to high glucose. Following PKC activation, transforming growth factor-ß (TGF-ß) expression increases. This factor plays an important role in regulating extracellular matrix production by activating gene expression of proteoglycans and collagen. Finally, an increase in oxidative stress by hyperglycemia can promote atherosclerosis by activating PKC.