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Rare heart problem decreases in clot-busting era


The incidence of cardiac tamponade, an infrequent but potentially fatal event following a heart attack, has not increased despite the widespread use of clot-busting and blood-thinning medications, according to an new analysis by Duke Clinical Research Institute investigators. Since bleeding is the major side effect of such medications, researchers said concerns with increased rates of tamponade existed.

Cardiac tamponade occurs when fluids or blood fill the pericardium, the tough sac enclosing the heart. After an acute heart attack, heart muscle can rupture leading to bleeding into the pericardial sac. Fluids filling the pericardium can cause a rapid drop in blood pressure, leading to loss of consciousness or death. Often a medical emergency, physicians quickly treat it puncturing the pericardium and draining the accumulated fluid.

Prior to widespread use of clot-busting, or fibrinolytic, drugs in the early 1990s, between 4 and 8 percent of acute heart attack patients suffered from cardiac rupture and tamponade.

In their analysis of more than 100,000 patients worldwide, the Duke researchers found that 0.85 percent of acute heart attack patients suffered from tamponade while in the hospital. Duke cardiologist Manesh R. Patel, M.D., presented the results of the analysis Nov. 9, 2004, at the American Heart Association’s annual scientific sessions in New Orleans. "The rates of tamponade in our population of clinical trial patients is similar to if not lower that reported in the pre-fibrinolytic era, and it supports the conclusion that the rate is not significantly higher with these therapies, as was once the general concern," Patel said.

While the researchers found a low incidence of tamponade in general, they cautioned that physicians should still pay close attention to their acute heart attacks patients, since their analysis showed that treatment delays increased the likelihood of cardiac tamponade occurring. "Even though less than 1 percent of patients who undergo fibrinolytic therapy will suffer from cardiac tamponade, it is still a catastrophic event and potentially life-threatening," Patel said. "The time from symptom onset to treatment strongly predicts the development of tamponade, which underscores the need for continuing efforts to rapidly treat patients having an acute heart attack."

For their analysis, the Duke pooled the clinical data from seven multi-center international trials designed to evaluate different fibrinolytic agents from 1990-2002. Out of the population of 102,060 acute heart attack patients who were enrolled in the trials, 865, or 0.85 percent, developed cardiac tamponade during their hospitalization.

On average, the patients who suffered cardiac tamponade tended to be older (71.9 vs. 61.6 years old); were more likely to be female (54 percent vs. 25.1 percent), and were more likely to have suffered an attack on the front wall of the heart (61.9 percent vs. 41.5 percent). Additionally, the researchers found that tamponade patients waited longer – 3.5 hours vs. 2.8 hours – before the initiation of fibrinolytic therapy. "Knowing which patients are more at risk for cardiac tamponade should make it easier for physicians to prevent it from happening," Patel continued. "The strongest predictor that physicians can affect was how long it took for fibrinolytic treatment to begin. The key is providing blood flow to the infarcted heart as soon as possible."

Patel recommends that patients who are at increased risk for tamponade should undergo routine cardiac ultrasound to detect any signs of fluid accumulation in the pericardium. To help physicians, Patel is developing a "nomogram," or health care flow chart, in which physicians taking care of heart attack patients can enter different patient characteristics into an algorithm that can quickly identify patients at the highest risk for tamponade.

Tamponade is also common in patients who suffer from cancer or kidney disease. In these patients, like the heart attack patients, the accumulating fluid in the pericardium puts pressure on the heart, preventing it from filling to capacity with blood. Since too little blood leaves the heart, the body’s tissue are starved of oxygen. That initiates a chain of events that can lead to unconsciousness and death.

The seven clinical trials from which data was drawn were GUSTO-I, GUSTO-IIb, GUSTO-III, ASSENT-II and ASSENT-III, ASSENT-III Plus and Hero-2. Patel’s analysis of the data was supported by the Duke Clinical Research Institute.

Richard Merritt | EurekAlert!
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