Q: A colleague's husband dropped dead last week of an acute myocardial infarction (MI). He was 52, athletic, ate right, had great cholesterol numbers, never smoked, and hardly ever drank alcohol. Is there some way Bill's heart attack could have been predicted?
A: New research is focusing on biomarkers-such as homocysteine-that are independent risk factors for cardiovascular disease (CVD). Although the American Heart Association (AHA) hasn't yet defined an elevated homocysteine level as a major risk factor for CVD, homocysteine screening may one day be as common as cholesterol screening.
Homocysteine is an amino acid synthesized during protein catabolism. High levels of it are toxic to the endothelial lining of arterial walls and can lead to plaque formation and platelet aggregation. One study concluded that in patients who've had an acute MI, elevated homocysteine levels are associated with a higher risk of recurrent coronary events and death, independent of other risk factors. Hyperhomocysteinemia was also found to be associated with a fivefold increase in stroke and an almost threefold increase in risk for Alzheimer's disease.
Factors and conditions that can lead to increased homocysteine levels include organ transplant, renal insufficiency, hypothyroidism, psoriasis, certain malignancies, pernicious anemia, and a rare autosomal recessive disorder (in children). Medications, like phenytoin (Dilantin), carbamazepine (Tegretol), and methotrexate (Trexall, Rheumatrex); the combination of niacin (vitamin B3) and colestipol (Colestid); and estrogen-containing oral contraceptives can also raise homocysteine levels.
A normal homocysteine level is between 4 and 17 micromole/liter (0.54 and 2.3 mg/L) for fasting samples, but it can vary according to age, sex, and body mass. Hyperhomocysteinemia is divided into three classifications: moderate (16 to 30 micromole/liter), intermediate (31 to 100 micromole/liter), and severe (> 100 micromole/liter).
Current research shows that the treatment for hyperhomocysteinemia is quite simple: Consume adequate amounts of vitamins B6 and B12 and folic acid through diet and vitamin supplements. A 2002 clinical study demonstrated that arterial endothelial function improved in subjects within a year of starting folic acid supplementation. In two recent studies, however, no decrease in cardiovascular events or mortality was seen when individuals at high risk for cardiovascular problems took folic acid or B vitamins.
As I said, the AHA doesn't recommend routine testing for homocysteine levels. The test isn't widely available and it may not be reimbursable. However, individuals with a family history of CVD without the established risk factors of high cholesterol, smoking, and hypertension may benefit from having their levels monitored.
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