Status of Dental Health Could Predict Heart Disease
A method of evaluating dental health could provide important information about a person’s risk of coronary heart disease, said an international group of researchers in a report in this week’s issue of the journal Circulation (Circulation. 2004;109:1095–1100OpenUrl).
In fact, said the research team led by Sok-Ja Janket, DMD, MPH, of Boston University Goldman School of Dental Medicine, their method, called the asymptotic dental score, when combined with measurements of C-reactive protein, high-density lipoprotein, and fibrinogen, equaled or exceeded the Framingham heart score as a predictor.
The researchers decided that by estimating the total production of inflammatory mediators that could be attributed to diseases of the mouth, they might be able to predict coronary heart disease. To do this, they recruited 256 consecutive cardiac patients from the Kuopio University Hospital in Finland. All patients had angiographically confirmed coronary heart disease. A total of 250 controls matched by age, gender, and place of residence were also recruited.
Dental factors that could generate cytokines and other immune mediators were examined. Included in these factors were dental caries, dental status, root remnants, and gingivitis. From these factors, the researchers generated the asymptotic dental score using a variety of statistical analyses based on likelihood ratio. The researchers concluded, “The ADS [asymptotic dental score] may be useful as a prescreening tool for subjects without overt cardiac symptoms to encourage them to seek early cardiac evaluation.”
Others who participated in this study came from Kuopio University Hospital, Kuopio, Finland; Institute of Dentistry, University of Helsinki; Helsinki University Hospital, Helsinki, Finland; National Institute of Neurological Disorders and Stroke; National Institutes of Health, Bethesda, Md; Harvard School of Public Health, Harvard University; and the Veterans Affairs Center for Health Quality, Outcomes, and Economic Research in Bedford, Mass.
More Statins Are Better
Intensive treatment with statins to lower lipid levels in the blood more effectively reduced the rate of atherosclerosis in patients with coronary heart disease than did treating patients more moderately, said researchers in the March 3, 2004, issue of The Journal of the American Medical Association (JAMA. 2004;291:1071–1080OpenUrlCrossRefPubMed).
The researchers participating in the REVERSAL (Reversal of Atherosclerosis in Aggressive Lipid Lowering) study chose 654 study subjects. They were assigned at random to receive 40 g of pravastatin and follow a moderate program designed to reduce low-density lipoprotein cholesterol or to receive 80 mg of atorvastatin and follow an intensive lipoprotein cholesterol–lowering regimen. Of the 654, 502 underwent intravascular ultrasound examinations at the beginning of the study and after 18 months of treatment.
The researchers, led by Steven E. Nissen, MD, of the Cleveland Clinic, found that patients who had moderate levels of cholesterol at the beginning and underwent 18 months of intensive therapy had greater reductions in low-density lipoprotein cholesterol than did those in the group that received the moderate treatment. They also had greater reductions in the marker C-reactive protein and showed statistically significant less progression of atherosclerosis in their coronary arteries than did the patients who followed the moderate treatment regimen.
In the moderate statin group, the volume of plaque buildup increased an average of 2.7%, compared with a 0.4% decrease in the volume of plaque buildup in the intensive treatment group.
In an accompanying editorial (JAMA. 2004;291:1132–1134), Frank M. Sacks, MD, of the Harvard School of Public Health, warned that the price of intensive statin therapy and potential adverse effects should be measured against the positive effects seen in this study. He pointed out that most research had been done using a moderate dose of statins.
“To put maximal statin therapy, such as with 80 mg of atorvastatin or 40 mg of rosuvastatin, on the same footing of clinical confidence requires results from large long-term clinical trials,” he wrote. Such trials are now underway, he said, and any decision about the proper dose of statins to use should await those results.
In addition, he said, “Clinicians must not lose sight of the need to manage other established cardiovascular disease risk factors, including hypertension and atherogenic dyslipidemia, manifested by low levels of high-density lipoprotein cholesterol and high levels of triglycerides.” He also advocated more physician attention to diet and exercise, which might have potent effects on cardiovascular risk.
Gene Therapy Helps Rats With Heart Failure
Delivering a modified form of the phospholamban protein S16EPLN to rat hearts in chronic failure after a heart attack results in increasing the activity of the enzyme SERCA1 in the cells that received the gene modification. This compensated for calcium uptake defects in heart failure, said researchers from the University of California, San Diego, in a report in the March 1, 2004, issue of The Journal of Clinical Investigation (J Clin Invest. 2004;113:727–736OpenUrlCrossRefPubMed).
When rats that had received the gene therapy underwent echocardiography and hemodynamic measurements, they had improvement in overall heart function and contractility. There was less formation of scar tissue. The authors, led by John Ross, Jr, MD, research professor at University of California, San Diego, concluded that the treatment has promise for a novel therapeutic strategy in the treatment of heart failure.
The researchers wrote: “Our findings of enhanced function, reduced remodeling and fibrosis, and lessened heart failure in an animal model relevant to the setting of heart failure in patients after a large acute MI [myocardial infarction] lend support to the potential therapeutic usefulness of this gene transfer approach. In addition, these studies document that the therapeutic effects of PLN [ablated phospholamban] inhibition can be extended to acquired forms of heart failure, suggesting that previous results in some genetic models may be generalizable.”