Macrovascular complications of metabolic syndrome: An early intervention is imperative

Alexander Tenenbaum*, Michael Motro, Ehud Schwammenthal, Enrique Z. Fisman

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review


The metabolic syndrome is a widespread clinical condition and an important cluster of atherothrombotic disease risk factors. The inclusion of this syndrome in the recently published Adult Treatment Panel III (ATP III) guidelines focused the attention of the physicians on this entity. Abdominal obesity, PPAR modulation, insulin resistance (with or without glucose intolerance), atherogenic dyslipidemia, elevated blood pressure, prothrombotic and proinflammatory states are the principal factors of this multifaceted syndrome. There are two major pathways of metabolic syndrome progress: (1) With preserved pancreatic beta cells function and insulin hypersecretion, which can recompense for insulin resistance. This pathway leads mostly to the macrovascular complications of metabolic syndrome. (2) With substantial injure of pancreatic beta cells leading to gradually reduced insulin secretion and to hyperglycemia (e.g. overt type 2 diabetes). This pathway leads to both microvascular and macrovascular complications. Because macrovascular complications of insulin resistance state precede the onset of hyperglycemia, early intervention in patients with metabolic syndrome is particularly important. Since central obesity (accompanied by insulin resistance even in the absence of hyperglycemia) is the key factor leading to development of metabolic syndrome and its future macrovascular complications, we assume that next logical step is the recognition of central obesity itself as a major risk factor for cardiovascular diseases.

Original languageEnglish
Pages (from-to)167-172
Number of pages6
JournalInternational Journal of Cardiology
Issue number2
StatePublished - Nov 2004


  • Diabetes mellitus
  • Insulin resistance
  • Metabolic syndrome
  • Obesity
  • Peroxisome proliferator-activated receptors (PPAR)


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