ATP III Calls for More Intensive Low-Density Lipoprotein Lowering in Target Groups
The Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) follows the path set by the two previous reports but calls for intensified lipid lowering in certain groups of adults classified as high-risk. If there is a single characteristic of this report, it is that it individualizes therapy as much as possible in a recommendation for an entire population. The report, printed in its entirety, makes up the majority of this week’s double issue of Circulation (Circulation. 2002;107:3143–3420).
The first step is risk assessment, beginning with full lipoprotein analysis with a measurement of LDL cholesterol and identifying of factors that increase risk. Individuals with multiple risk factors are at increased risk of disease, and the report specifically targets those with diabetes.
The report identifies an optimal LDL cholesterol level as <100 mg/dl and defines low HDL as <40 mg/dl. Triglyceride cut points are also lowered to identify areas of moderate elevations.
The report recommends the use of plant stanols/sterol and viscous or soluble fiber as therapeutic dietary options to enhance the lowering of LDL cholesterol. It also recommends treatment beyond LDL lowering for people whose triglycerides are at ≥200 mg/dl.
Its focus, however, is on the relationship between risk factors and LDL and HDL cholesterol levels. The risk factors affect the treatment to modify LDL levels and sets targets for the LDL levels in relationship to the number of risk factors an individual has.
Is Mercury-Containing Fish a Cardiovascular Risk Factor? Yes or No—Take Your Pick
In a successive set of reports in The New England Journal of Medicine, two groups reached opposite conclusions about whether consuming fish contaminated with mercury raises the risk of cardiovascular disease (N Engl J Med. 2002;347:1747–1754; N Engl J Med. 2002;347:1755–1760).
Mercury is known to cause neurologic and kidney damage when consumed at high levels. However, the consequences of lower levels of exposure are poorly understood.
To determine that, researchers led by Eliseo Guallar, MD, from the Johns Hopkins Medical Institutions in Baltimore, Md, measured levels of a type of Ω-3 fatty acid in fat tissue and mercury levels in toenail clippings from 684 men who had previously had a myocardial infarction. They compared their readings to those taken from 724 men with no heart attack history.
Mercury levels were 15% higher in the men who had had heart attacks than it was in the controls. When they adjusted statistics for mercury levels, high Ω-3 fatty acid levels were found to be protective against heart attack. They suggested, however, that current government warnings that pregnant women or women of child-bearing potential avoid fish that have high levels of mercury might be extended to the general adult population.”
However, the second study by Kazuko Yoshizawa, MD, from the Harvard School of Public Health, found no association between heart disease and mercury. His group measured the levels of mercury from the toenail clippings of 33 737 male health professionals between the ages of 40 and 75. At 5-year follow-up, the researchers found that there were 470 cases of heart disease among the men in the group.
They found that levels of mercury were significantly associated with fish consumption and that dentists had the highest mercury levels. However, their study found no correlation between the amount of mercury in the toenail clippings and the risk of heart disease.
The studies, of course, were performed in very different ways and on different groups of people, and they demonstrate the need for a large, well-controlled population-based study to discover whether the link between mercury and heart disease truly exists.
Polymorphisms of 3 Genes May Predict Myocardial Infarction
Three genes—connexin 37, plasminogen activator inhibitor type 1, and stromelysin-1—and their variants may be a key to predicting a genetic risk of myocardial infarction, according to researchers led by Yoshiji Yamada, MD, PhD, of the Department of Gene Therapy at Gifu International Institute of Biotechnology in Japan, in a report in the December 12, 2002, issue of The New England Journal of Medicine (N Engl J Med. 2002;347:1916–1923).
The researchers used a fluorescence or colorimetry-based allele-specific DNA-primer-probe assay system to determine the genotypes of 112 polymorphisms of 71 candidate genes in 2819 unrelated Japanese patients who had suffered a myocardial infarction. They compared the results with those of 2242 unrelated control patients from Japan.
In an accompanying editorial (N Engl J Med. 2002;347:1963–1965), Ron J.G. Peters, MD, and S. Matthijs Boeckholdt of the Academic Medical Center in Amsterdam, the Netherlands, wrote, “The study by Yamada et al is noteworthy because of its large size and because of the two-step analysis. . . . This approach decreases the likelihood that the findings result from the play of chance.”
They said the findings should be used as a springboard to further research aimed at determining the underlying mechanism of disease and warned that the research, although important, cannot be used to make primary prevention recommendations at this time.