Abstracts of Posters Presented at the International Anesthesia Research Society; 72nd Clinical and Scientific Congress; Orlando, FL; March 7-11, 1998: Cardiovascular Anesthesia
INTRODUCTION: Perioperative myocardial infarctions (PMI) are often difficult to diagnose because  perioperative myocardial ischemic episodes are often clinically silent, and may occur even without hemodynamic changes;  nonspecific ECG changes often occur postoperatively;  CPK isoenzymes (iso) can be elevated after orthopedic surgery without evidence of cardiac damage. Since cardiac Troponin I (TropI) is the only known molecular marker for myocardial damage not expressed in regenerating muscles, we chose to assess its usefulness in diagnosing PMI in the setting of orthopedic surgery.
METHODS: 85 patients, most with risk factors for ischemic heart disease were assessed for PMI. The operative procedures included total hip arthroplasty (36), total knee arthroplasty (34), posterior spine fusion (7), and others (8). Three blood samples for CPK-MB and TropI levels were drawn at 8 hr. intervals postoperatively. A 12 lead ECG was performed upon entry to PACU and daily x2. A CPK-MB index >3, and a TropI level of > 1.2 ng/ml were considered positive for an MI.
RESULTS: Seven (7/85) had elevated CPK-MB and TropI levels postoperatively. Five of these patients had ECG changes, one had angina without ECG changes, and one patient's ECG showing an old anterolateral wall MI was unchanged. TropI levels peaked within 16 hrs. except in patient #2 where it continued to rise. She experienced cardiogenic shock. Three (3/85) patients had elevated CPK-MB levels but normal TropI, and an unchanged ECG. They all did well clinically, ECG changes correlated better with elevated TropI levels than with elevated CPK-MB index. Of the 7 patients with a PMI by both assays, two had cardiac symptoms. No patients with cardiac Sx had a normal TropI level.
CONCLUSIONS: CPK-MB can often be elevated post orthopedic surgery especially in the setting of spine surgery as reported by others. This study shows TropI to be a good marker of myocardial injury in this patient population, and may help to identify the source of elevated CPK postop. It appears to be as sensitive, and more specific than CPK-MB, with each one of these markers being more specific and sensitive than ECG changes alone, or cardiac Sx. The significance of an elevated MB index in the setting of low total CPK is of questionable clinical significance. A concomitant rise in TropI level however supports the diagnosis of an MI, as in some of our patients. The lack of cardiac Sx, a normal TropI level, and an unchanged ECG together negate the possibility of an MI when CPR isos are positive as in our three patients. Although further studies are warranted, a persistant rise of TropI post infarction may be a poor prognostic indicator in patients experiencing an MI. (Table 1)
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