Homocysteine and cardiovascular risk
Keywords:
Atherosclerosis, Cardiovascular disease, Hyperhomocysteinemia, Homocysteine, Nitric oxideAbstract
Numerous epidemiological studies have demonstrated that hyperhomocysteinemia is
a strong and independent risk factor for cardiovascular disease.
Hyperhomocysteinemia can result from a deficiency of the enzymes or vitamin
cofactors required for homocysteine metabolism. Several hypotheses have been
proposed to explain the cellular mechanisms by which hyperhomocysteinemia
promotes cardiovascular disease, including oxidative stress. Conventional risk
factors for cardiovascular disease, including hypercholesterolemia, hypertension,
smoking and diabetes mellitus, account for approximately 50% of all cases.
Evidence now indicates that hyperhomocysteinemia, which occurs in approximately
5 to 7% of the general population, is an important, independent risk factor for
atherosclerosis and thrombotic disease. In Brazil, they are responsible for the
death of 300 thousand people/year and they correspond to 16% of the expenses
of the Unified Healthcare System (SUS). Furthermore, up to 40% of patients
diagnosed with premature coronary artery disease, peripheral vascular disease or
recurrent venous thrombosis have hyperhomocysteinemia. In this review article,
we will summarize the genetic and nutritional factors that induce
hyperhomocysteinemia and further examine the clinical evidence implicating
hyperhomocysteinemia as an independent risk factor for cardiovascular disease.
In addition, potential mechanisms by which homocysteine accelerates
atherosclerosis will be discussed in light of the important findings recently
reported. This study was based on a systematic review of the national and
international literature found in the databases MedLine/PubMed using the key
words: homocysteine, cardiovascular risk, atherosclerosis, free radicals.
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