Study finds elevated homocysteine more than doubled heart attack risk in high risk patients
A report scheduled to be published in 2007 appearing early online in the journal Cardiology revealed that having an above average total homocysteine level increases the risk of a coronary event among men and women with atherosclerosis by a factor of 2.5.
The current study involved participants in the Benzafibrate Infarction Prevention Study which evaluated the effect of benzafibrate for secondary prevention of coronary events in 3,090 men and women with chronic heart disease, defined as a history of heart attack or angina. Dr Moti Haim, of the Rabin Medical Center in Petah Tikva and his colleagues in Israel matched 69 subjects who experienced fatal or nonfatal heart attack, or sudden death with an equal number of participants who remained free of recurrent coronary events or stroke throughout the 4.7 to 7.6 year follow-up period. Blood samples were analyzed at the beginning of the study for lipids, fibrinogen, blood chemistry and other factors, and total homocysteine concentrations were measured in frozen serum samples obtained at the beginning of the study.
The median total homocysteine among individuals with recurrent coronary events was 15.2 micromoles per liter compared to 12.9 micromoles per liter in the control group, with a median of differences between the matched pairs of subjects of 3.95 micromoles per liter. Individuals whose homocysteine levels were in the top one-third of participants experienced a 2.5 times greater risk of a coronary event or sudden death than those whose values were in the lowest third.
“In the present study, we provided evidence that in patients with preexisting vascular disease, there is an association between total homocysteine concentration and incidence of coronary events, which is independent of traditional risk factors and inflammatory markers,” the authors write. They note that not all studies have found the same association, and hypothesize that elevated homocysteine could be a strong predictor of coronary events in high risk patients but not low risk ones. Furthermore, they could not conclude whether homocysteine was a causative factor or bystander marker of cardiovascular risk. “If total homocysteine level is causally related to CHD risk, then our findings suggest that patients with preexisting vascular disease may have a greater potential benefit from interventions that lower homocysteine concentrations,” they observe.
The evidence is clear that having an elevated homocysteine level is an independent risk factor for heart disease. One large study conducted among physicians who had no history of heart disease showed that having a highly elevated homocysteine level was associated with a more than 3-fold increase in the risk of heart attack over a 5-year period (Stampfer MJ et al 1992).
It is important to begin your homocysteine-lowering program by working with a qualified physician and taking the necessary blood tests to evaluate your risk. To help lower your homocysteine level, the Life Extension Foundation suggests:
CDP choline—250 to 500 mg daily. Alternatively, you can use 1 to 3 teaspoons of liquid choline chloride daily mixed with 2 ounces of juice, 1 tablespoon of pure lecithin granules daily, or 250 mg of a-GPC daily.
Homocysteine has been shown to be an independent risk factor for the premature development of coronary artery disease and thrombosis. This test is intended for use in screening individuals who may be at risk for heart disease and stroke. Studies have shown that even moderate levels of homocysteine pose an increased risk for arteriosclerosis compared with the lowest 20th percentile (<7.2 mcmol/L) of population controls.
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