Abstract
Cardiovascular diseases are commonly related to classical risk factors, but other risk markers have been identified, including homocysteine. Homocysteine is a sulphurated amino acid which derives from methionine. The causes of hyperhomocysteinemia are multifactorial, such as genetic defects, pathophysiological conditions, lifestyle and drugs-related. Hyperhomocysteinemia favors atherothrombosis through endothelial dysfunction, enhancement of inflammation and thrombophilic profile. A number of clinical and laboratory trials exist regarding the association between homocysteine levels and an increased risk of cardiovascular disease. However, the lack of homogeneity in the data, together with the high number of factors capable of influencing homocysteine plasma levels, and the disappointing results of therapeutic trials do not permit us at present to consider homocysteine as an independent and major risk factor for cardiovascular disease.
MeSH terms
-
Cardiovascular Diseases / blood
-
Cardiovascular Diseases / epidemiology
-
Cardiovascular Diseases / etiology*
-
Cardiovascular Diseases / prevention & control
-
Folic Acid / therapeutic use
-
Follow-Up Studies
-
Homocysteine / analysis
-
Homocysteine / physiology*
-
Homocystinuria / complications
-
Humans
-
Hyperhomocysteinemia / complications*
-
Hyperhomocysteinemia / diagnosis
-
Hyperhomocysteinemia / drug therapy
-
Hyperhomocysteinemia / epidemiology
-
Hyperhomocysteinemia / genetics
-
Methionine / metabolism
-
Methylation
-
Methylenetetrahydrofolate Reductase (NADPH2) / deficiency
-
Methylenetetrahydrofolate Reductase (NADPH2) / genetics
-
Methylenetetrahydrofolate Reductase (NADPH2) / physiology
-
Prospective Studies
-
Randomized Controlled Trials as Topic
-
Retrospective Studies
-
Risk Factors
-
Vitamin B 12 / therapeutic use
-
Vitamin B 6 / therapeutic use
Substances
-
Homocysteine
-
Vitamin B 6
-
Folic Acid
-
Methionine
-
Methylenetetrahydrofolate Reductase (NADPH2)
-
Vitamin B 12