ISSN 0326-646X





Sumario Vol. 42 - Nº 3 Julio - Septiembre 2013

Mechanisms of Cardiovascular
Risk in Metabolic Syndrome

Pedro E. Miguel-Soca.

Universidad de Ciencias Médicas.
Ave. Lenin No.4, esquina Aguilera. (80100) Holguín, Cuba.
E mail

Recibido 31-JUL-2013 – ACEPTADO 09-AGOSTO-2013.

The author declares not having a conflict of interest.

Rev Fed Arg Cardiol. 2013; 42(3): 166-167


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The prevalence of obesity in teenagers is increasingly higher and consequently, the associated risk of developing metabolic syndrome (MS). The prevalence of MS using criteria from the IDF (International Diabetes Federation) in teenagers in schools from the province of Salta, Argentina [1], was 4.1%, similar to the one reported in other studies, with predominance in young people with overweight and obesity. See the paper published in Rev Fed Arg Cardiol 2013; 42 (2) 119-126.

The molecular mechanisms involved in the risk of developing ischemic heart disease deserve a special consideration. A key trait of metabolic syndrome is the resistance to insulin, particularly significant in the visceral adipose tissue of the patients with abdominal obesity. In such conditions, an increase of the arrival of fatty acids to the liver occurs through the portal pathway, and subsequently the synthesis of triglycerides (TG) in this organ with two immediate consequences: the deposit of TG with hepatic steatosis and the increase of release into the blood of lipoproteins of very low density (VLDL), which causes hypertriglyceridemia [2]. Another factor that favors hypertriglyceridemia is a lower activity of the lipase of lipoproteins, an endothelial enzyme depending on insulin, which is in charge of degrading VLDL and chylomicrons (they transport TG from the diet). In the mentioned investigation [1], 9.2% of teenagers presented hypertriglyceridemia, one of the diagnostic criteria of MS.

Hypertriglyceridemia has repercussions on the pattern of lipoproteins by favoring the activity of the protein carrier of cholesterol esters that exchanges lipids between VLDL and the lipoproteins of high density (HDL), which enriches HDL cholesterol with TG, making it more susceptible to the degradation of liver lipase with reduction of the blood concentrations [2]. The role of HDL cholesterol in the reverse transport of cholesterol, the only way the organism has of removing the excess of cholesterol from tissue and arterial walls by biliary excretion, explains at least in part, the greater risk of ischemic heart disease in patients with MS. It is remarkable that Gotthelf [1] found 26.5% of low HDL cholesterol in Argentine students, a percentage that is higher in adults.

In conditions of resistance to insulin, VLDL get richer in cholesterol esters, which makes them more atherogenic and low density lipoproteins (LDL) become small and dense, also more atherogenic by its capacity of infiltrating the arterial intima, to oxidize more easily and be uptaken by macrophage receptors, which favors the formation of foam cells and atherosclerosis, another condition that increases cardiovascular risk in patients with MS [2].

Another contributing factor to the cardiovascular risk of the patients with MS is the increase of blood pressure accompanying resistance to insulin. People with MS also present leptin resistance, which leads to hyperleptinemia [3]. Leptin is a protein produced in white adipose tissue that mediates sympathetic hyperactivity in obese individuals; these actions of leptin over the sympathetic nervous system are preserved, which favors sympathetic overstimulation at renal level, of lumbar nerves and brown fat. In such context, sympathetic hyperactivity would generate left ventricular hypertrophy per se, and would stimulate the renin-angiotensin-aldosterone system (RAAS) activity, capable of increasing the levels of blood pressure, altering peripheral resistance to insulin and generating myocardial trophic effects [3].

In patients with MS, a chronic inflammatory state of low intensity is generated, which facilitates the process of atherosclerosis and its sequels, such as ischemic heart disease. The increase of visceral adipose tissue increases the synthesis of proinflammatory cytokines, such as interleukins 6 (IL-6) and the tumor necrosis factoralpha (TNF-α) that intervene in this inflammatory process [2].

Besides environmental factors related with unhealthy lifestyles, in obesity and MS genetic factors also participate, representing 40-90% of individual variability of body mass index [4]. As an example, the gene associated to obesity and fat mass (FTO), located in chromosome 16q12.2, is related to obesity in cross-sectional studies and it has been suggested that its alleles of risk of adiposity predispose to cardiovascular events in populations in high risk [4].

Finally, the topic approached by Gotthelf [1] is interesting, with a great impact on medical practice, and in spite of the controversial aspects, her investigation may have implications on prevention, early diagnosis and the timely management of MS and associated co-morbidities [5].




  1. Gotthelf SJ. Prevalencia de síndrome metabólico según definición de la International Diabetes Federation (IDF) en adolescentes escolarizados de la provincia de Salta, Argentina. Rev Fed Arg Cardiol 2013; 42: 119-26.
  2. Miguel-Soca PE, Escofet Niño S. Predictores del grosor íntima-media carotídeo. Rev Esp Cardiol 2013; 66: 326-7.
  3. Piskorz D, Citta L, Citta N, et al. El descenso de la presión arterial no se asocia con regresión de la hipertrofia ventricular izquierda en pacientes hipertensos con síndrome metabólico. Rev Fed Arg Cardiol 2008; 37: 238-44.
  4. Miguel-Soca P, Cruz-Lage L, Edwards-Scringer I. Genes de la obesidad monogénica. An Sist Sanit Navar 2013; 36: 125-7.
  5. Salazar M. Síndrome metabólico. ¿Debemos abandonar la percepción clínica? Rev Fed Arg Cardiol 2011; 40 (2): 99-101.

Publication: September 2013

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