Inflammation In Blood Vessels Slows Clot-Buster Treatment For Heart Attack

November 09, 1998

DALLAS, Nov. 9 -- Long-lasting inflammation is already thought to precede and help trigger a heart attack, but now research shows that inflammation may also limit the effectiveness of clot-busting treatment, according to a study presented today at the American Heart Association's 71st Scientific Sessions. Agha W. Haider, M.D., Ph.D., the study's lead author, found that individuals with high blood levels of C-reactive protein, a marker of inflammation, have a slow response to clot-busting treatment. Clot-busters, also called thrombolytics, dissolve blood clots that block blood flow to the heart and are frequently the first line of treatment for heart attack.

"The time it takes to open the blood vessels is critical," he says. "The sooner you open the coronary arteries the better it is in terms of patient's making it out of the hospital alive and having fewer complications."

Recent studies have suggested that infections, such as chronic bronchitis, pneumonia or dental infection may increase the risk of heart attack. Such infections may trigger a "protective immune response" that may cause blood vessels to become inflamed and resistant to clot-busting treatment, says Haider.

"We are the first to show that the degree of inflammation can have a significant impact on a person's response to clot-dissolving therapy," says Haider, who is currently conducting research at Boston's Massachusetts Veterans Research Center, which is affiliated with Harvard University Medical School. The study was conducted with colleagues from the Hammersmith Hospital in London.

"This is bad news for individuals in terms of how long it will take to revascularize -- re-open -- their blood vessels and how much damage there will be to the heart as a result of this delayed response to treatment," he says.

The good news is that anti-inflammatory drugs, such as aspirin, could be helpful in speeding the effects of the clot-busting drugs and reducing the amount of damage to the heart, he says. However, this study was not designed to test this question. "Fortunately, most patients already receive aspirin after thrombolytic therapy. Maybe it would be a good idea to use the aspirin earlier during treatment," says Haider. Haider and colleagues studied 24 patients who received thrombolytic therapy after a heart attack.

Coronary angiography -- an X-ray examination of the heart -- was performed 90 minutes after clot-busting treatment to show whether the blood vessels had opened.

Angiography revealed that coronary arteries were still blocked in eight individuals and re-opened in 14 individuals.

Higher C-reactive protein levels indicated a higher level of inflammation. "We found that inflammation impeded response time to clot-dissolving drugs after a heart attack. The higher the degree of inflammation, the longer it took for these patients' arteries to open," says Haider.

Last year Haider presented research suggesting that people with long-term inflammation due to chronic bronchitis were more likely to have had a heart attack by the end of the study.

The study co-authors were Felictia Andreotti, M.D., USIC, in Rome and Graham J. Davies, F.R.C.P., ICSTM, Hammersmith Campus, London.
For more information Nov. 8-11
contact Brian Henry or Carole Bullock
Dallas County Convention Center
(214) 853-8056

American Heart Association

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