Gout Increases Heart Attack Risk, According to Study
Gout Increases Heart Attack Risk, According to Study
Gout, also referred to as gouty arthritis, is a significant independent risk factor for heart attack, according to a study from the University of Pittsburgh School of Medicine. The study was published in the August 2006 issue of Arthritis & Rheumatism. The study focused on 12,866 study participants (men) who were enrolled in the Multiple Risk Factor Intervention Trial (MRFIT) for a mean of 6.5 years.
5,337 men had hyperuricemia at beginning of the study.
1,123 men developed gouty arthritis during the study.
There was no statistical difference between groups over cholesterol levels, use of aspirin, family history of heart attack, or diabetes mellitus.
The gout group was found to more likely use diuretics and alcohol, and have elevated blood pressure, age, blood glucose, and body mass index.
More smokers were found in the group without gout.
During the study, 1,108 heart attacks occurred in the gout group (10.5 percent) and 990 heart attacks occurred in the group without gout (8.43 percent). 246 of the 1,108 heart attacks were fatal. The connection between gout and risk of heart attack was also obvious among those who did not use alcohol, diuretics, or aspirin as well as those who did not have metabolic syndrome, diabetes mellitus, or obesity. This was the first study, among men with no prior history of coronary artery disease, that revealed gout is a significant risk factor for heart attack.
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An Update on Gout Disease
Gout is one of the most painful rheumatic conditions. For many people, the first gout attack occurs in the big toe, but many other joints can be affected by gout disease. In 2002, there were nearly 4 million outpatient visits in the United States related to gout. According to a report in the September 15, 2007 issue of American Family Physician (AFP), even though gout is well-understood and easily diagnosed, the quality of treatment may be less than optimal for up to half of patients with gout.
Gout develops from an accumulation of excess uric acid in the body which causes monosodium urate crystal deposition in the joints. Excess uric acid can result from increased uric acid production or decreased elimination of uric acid from the body. Certain purine-rich foods can cause an increase in uric acid levels. Some medications also can cause increased uric acid levels.
First-line treatment for acute gout is nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids depending on other conditions the patient may have. Colchicine is considered second-line therapy. For chronic gout, allopurinol is the most common treatment. There are also new therapeutic options for gout in development. The AFP update on gout points out that Febuxostat, a nonpurine xanthine oxidase antagonist and Puricase (PEG-uricase), a pegylated uricase enzyme are in clinical trials and perhaps will lead to more treatment options for gout in the future.
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