The University Record, April 2, 2001

New definition may increase number of heart attack cases

By Valerie Gliem
Health System Public Relations

Kelly Saran (left), clinical nurse, and Rajendra Mehta, clinical assistant professor of internal medicine, look over charts in the U-M Cardiovascular Center. Photo by Martin Vloet, U-M Photo Services
One of the most compelling questions regarding the November 2000 hospitalization of Vice President Dick Cheney was whether or not he’d had a heart attack.

At first, the answer was no. Then, a check of Cheney’s enzyme levels showed he had, in fact, suffered his fourth heart attack.

Why the confusion? It may have been due to the fact that, for the past several years, physicians have been working to pin down the best set of criteria for determining whether a patient has had a heart attack, also known as a myocardial infarction.

In September 2000, a new, widely accepted definition of myocardial infarction was introduced—a definition developed by a joint committee of the European Heart Society and the American College of Cardiology. The most significant change is that the definition adds cardiac troponin, an enzyme found only in heart muscle tissue, to the measures already used to determine whether or not a myocardial infarction has occurred.

Researchers at the Health System, including Rajendra Mehta, clinical assistant professor of cardiology in the Cardiovascular Center, recently completed a study investigating the significance of this change in definition. They found that the new definition will mean a significant increase in the number of myocardial infarction cases at the U-M, and they expect a similar increase nationwide. The information was presented recently at the 50th annual Scientific Session of the American College of Cardiology.

“In the United States, nearly a million heart attacks are diagnosed annually,” Mehta says. “These data suggest that under the new criteria, 250,000 more will be diagnosed each year. These myocardial infarctions would have been missed by the old criteria.”

There have been many proposed criteria for the diagnosis of myocardial infarction. Prior to 2000, the most commonly used were those published by the World Health Organization in 1979, which state that a myocardial infarction has occurred when two of the following three criteria are met: symptoms consistent with ischemia, or decreased blood flow to the heart; changes in an electrocardiogram; and elevated enzymes—most commonly, one called CKMB.

But the new guidelines, published in 2000, require that elevated enzymes, which can include CKMB or troponin, be one of the criteria in addition to either ischemic symptoms or electrocardiogram changes.

In the study, all patients admitted to U-M hospitals from May 1, 1999, to Jan. 1, 2000, with suspected acute coronary syndrome were entered in a database. There were 493 patients included, all of whom underwent both CKMB and troponin tests.

CKMB is the creatine phosphokinase that is found in the heart muscle. Troponin is an enzyme found in muscle tissue. Specifically, cardiac troponin is found in myocardial cells in the heart. Both enzymes are vitally important in muscle contraction, and many physicians routinely measure CKMB and troponin to evaluate ischemic heart disease.

“When a myocardial infarction occurs, heart muscle dies, and in the process, the muscle leaks intracellular components such as CKMB and troponin into the surrounding tissues,” says Mark Meier, resident physician and a study researcher.

Cardiac troponin is a more sensitive marker of myocardial damage, because the troponins are more abundant in the myocardial cells than CKMB, says Meier. Cardiac troponin also is more specific, because unlike CKMB, it is not found in other tissues and is not present in the blood in normal individuals.

After identifying the 493 patients, the researchers looked more closely at the 305 patients whose enzyme levels were elevated. They then divided the patients into two groups. Group A contained patients with a positive CKMB test. Because all of these patients were admitted with symptoms, everyone in Group A would be diagnosed with myocardial infarction, according to the World Health Organization criteria from 1979.

Group B patients had a normal CKMB level but elevated troponin. Those patients would not have been diagnosed with myocardial infarction based on the World Health Organization criteria of 1979 but would be considered heart attack patients under the European Heart Society/American College of Cardiology standards of 2000.

Because the troponin test is more sensitive and picks up even slight muscle damage, using troponin levels detects patients who have had a less severe heart attack.

The results showed that, at the U-M, including troponin in the diagnostic criteria will result in a 26 percent increase in the number of myocardial infarctions diagnosed each year.

“It may also mean that the criteria may select for a clinically less complicated patient population,” Meier says. “Patients in Group B had fewer in-hospital complications such as arrhythmias and heart failure. In addition, they needed fewer angioplasties and bypass surgeries.” However, during six months of follow up, their complication rate reached or exceeded that of patients diagnosed with the old criteria.

The results suggest that the clinical and financial implications are potentially far-reaching. By identifying patients with an increased cardiac troponin level as having had a heart attack, clinicians will be able to employ aggressive, lifesaving strategies that are known to improve both short- and long-term survival.

So, although the cost of the blood test for troponin is added to patient care costs, this expense may be offset by the number of lives saved due to preventive care.

Other project researchers were: Kim Eagle, Albion Walter Hewlett Professor of Internal Medicine, chief of the Division of Cardiology and co-director of the Cardiovascular Center; Eva Kline-Rogers, nurse practitioner and outcomes research coordinator; Jeanna V. Cooper, research associate, Department of Internal Medicine; and Wisam H. Al-Badr, research associate.