New Definition Of "Myocardial Infarction" May Make Number Of Heart Attack Cases Soar

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: 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 University of Michigan Health System, including Rajendra Mehta, M.D., clinical assistant professor of cardiology in the UMHS Cardiovascular Center, recently completed a study investigating the significance of this change in definition at UMHS. They found that the new definition will mean a significant increase in the number of myocardial infarction cases at U-M, and implies such an increase nationwide. The information was presented today 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." In addition to the far-reaching clinical implications, it's likely that the financial implications also will be great - although those remain unknown.

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/or 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 ECG changes.

"Thus, this is the first definition published that officially includes the use of troponin as a diagnostic marker," Mehta says.

In the U-M 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 had both CKMB and troponin tests performed.

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, M.D., UMHS 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 is also 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 were then divided 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 UMHS, 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 far-reaching, but as yet, unclear.

By identifying patients with an increased cardiac troponin level as having had a heart attack, clinicians will be able to target aggressive, life-saving 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 cost may be greatly offset by the number of lives saved due to preventive care.

"We already know that inadvertent missed diagnoses of heart attack may have grave consequences, including death," Mehta says. "Using troponin levels allows us to identify more high-risk patients and give them the care they need."

Physicians worldwide are becoming aware of the new definition and are incorporating it into their clinical practice, Mehta says. More studies are needed to determine the financial and specific clinical implications.

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