Current opinions about the role of mild hyperhomocysteinaemia as a risk factor of cardiovascular diseases
Authors:
J. Šimon
Authors‘ workplace:
Centrum preventivní kardiologie II. interní kliniky LF UK v Plzni
Published in:
Kardiol Rev Int Med 2009, 11(3): 129-133
Category:
Nontraditional risk factors cardiovascular disease
Overview
Based on the available evidence, hyperhomocysteinaemia is an unquestionable and important risk factor in nearly all atherosclerotic and thrombotic vascular diseases. It is one of the newly classifi ed and researched factors that have been included in the latest Guidelines on cardiovascular diseases prevention in clinical practice. Pathophysiological mechanisms, by which hyperhomocysteinaemia impacts on the process of atherogenesis and thrombogenesis, have largely been explained in experimental and clinical studies. Hyperhomocysteinaemia is highly prevalent in the Czech population, similar to other populations with relatively low dietary folate intake. Replacement of folate alone or in combination with vitamin B12 and pyridoxine represents an inexpensive treatment option for mild hyperhomocysteinaemia and enables near normalization of homocystein levels. Hyperhomocysteinaemia used to be perceived as a causal risk factor and, based on observational studies, substitution with folate and other vitamins involved in methionine cycle had been recommended for many years as primary and secondary prevention of cardiovascular diseases. It was thus rather surprising that a randomised double blind placebo controlled study (NORVIT) confi rmed that substitution with folate and other B-group vitamins, used in secondary prevention, signifi cantly decreased homocysteine levels but had no effect on atherosclerotic vascular disease morbidity and mortality. These results challenged the hypothesis on causality of this risk factor. Consequently, hyperhomocysteinaemia is currently perceived more as a marker than the cause of the disease. Since further pharmacological studies of the effects of vitamin B intervention on mortality and morbidity are currently taking place, we need to wait for defi nitive evidence for causality of this risk factor before vitamin substitution is included in the Guidelines on cardiovascular disease prevention. Routine homocysteine levels’ testing is not currently recommended; it is indicated for the atherothrombotic processes for which clinical explanation of ethiopathogenesis is lacking following standard clinical and biochemical tests.
Keywors:
homocysteine – methionine cycle – vitamin B group – cardiovascular risk
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Cardiology Review
2009 Issue 3
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