Abstract
Platelets are key players in the thrombotic processes. The alterations of platelet function due to the occurrence of metabolic disorders contribute to an increased trend to thrombus formation and arterial occlusion, thus playing a major role in the increased risk of atherothrombotic events in patients with cardiometabolic risk factors. Several lines of evidence strongly correlate metabolic disorders such as obesity, a classical condition of insulin resistance, dyslipidemia, and impaired glucose homeostasis with cardiovascular diseases. The presence of these clinical features together with hypertension and disturbed microhemorrheology are responsible for the prothrombotic tendency due, at least partially, to platelet hyperaggregability and hyperactivation. A number of clinical platelet markers are elevated in obese and type 2 diabetes (T2DM) patients, including the mean platelet volume, circulating levels of platelet microparticles, oxidation products, platelet-derived soluble P-selectin and CD40L, thus contributing to an intersection between obesity, inflammation, and thrombosis. In subjects with insulin resistance and T2DM some defects depend on a reduced sensitivity to mediators—such as nitric oxide and prostacyclin—playing a physiological role in the control of platelet aggregability. Furthermore, other alterations occur only in relation to hyperglycemia. In this review, the main cardiometabolic risk factors, all components of metabolic syndrome involved in the prothrombotic tendency, will be taken into account considering some of the mechanisms involved in the alterations of platelet function resulting in platelet hyperactivation.
Highlights
Several lines of evidence suggest a strong correlation between metabolic disorders and hemodynamic such as obesity, dyslipidemia, diabetes, hypertension, and cardiovascular (CV) diseases (CVD), with endothelial dysfunction as the initial step toward atherothrombosis (Figure 1)
The presence of a clustering of three or more risk factors in the same individual, including abdominal obesity, atherogenic dyslipidemia, high systolic and diastolic blood pressures, and impaired glucose tolerance has been defined by World Health Organization (WHO) as metabolic syndrome (MS) [11], though there is some minor variation in the definition by other health care organizations
According to the National Cholesterol Education Program (NCEP)’s Adult Treatment Panel (ATP) III criteria [19], MS is recognized as a condition related to CVD occurring if the patient has three or more of the following: (1) central obesity characterized by waist circumference >102 cm in men and >88 cm in women; (2) fasting blood TGs ≥150 mg/dL and high-density lipoprotein cholesterol (HDL) ≤40 mg/dL in men or ≤50 mg/dL in women; (3) fasting glucose ≥100 mg/dL; and (4) systolic blood pressure ≥130 mmHg and/or diastolic blood pressure ≥85 mmHg
Summary
Several lines of evidence suggest a strong correlation between metabolic disorders and hemodynamic such as obesity, dyslipidemia, diabetes, hypertension, and cardiovascular (CV) diseases (CVD), with endothelial dysfunction as the initial step toward atherothrombosis (Figure 1). The presence of a clustering of three or more risk factors in the same individual, including abdominal obesity, atherogenic dyslipidemia, high systolic and diastolic blood pressures, and impaired glucose tolerance has been defined by World Health Organization (WHO) as metabolic syndrome (MS) [11], though there is some minor variation in the definition by other health care organizations. Each of these cardiometabolic disorders contributes to alter hemostatic balance leading to a prothrombotic phenotype [12]. This review will focus on the role of obesity on prothrombotic tendency in patients affected by MS, being adipocytes able to produce and/or release hormones which deeply influence hemostatic balance, platelet function, pro-inflammatory state and oxidative stress
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