In 2004 a pt with newly diagnosed and untreated pancreatic adenocarcinoma had a syncopal episode. Early in the morning the pt arose and walked to their bathroom. On return to their bedroom they lost consciousness and fell. They woke on the floor approx 1/2 hour later and returned to bed. At 2:00 pm the next day, the pt went to the emergency department. Ekg showed t-wave inversions in leads v1-4. Attempts were made to obtain previous ekgs, but the studies were not available. Cardiac enzymes showed a troponin i of 18. 9ng/ml, a ckmb of 2. 0ng/ml, a total ck of 53 u/l, and a ckmb quotient of 6%. They were admitted with a diagnosis of "syncope and elevated troponin. " a transthoracic echo from the next day showed normal left ventricle with an ef of 68% and no regional wall motion abnormalities. There was moderate pulmonary hypertension with right ventricular hypertrophy, moderate right ventricular dilation, and moderate reduced right ventricular systolic function. Aortic valve sclerosis was also noted. Subsequent troponin levels fell from 18. 9 ng/ml to 17. 4 ng/ml and then to 15. 3 ng/ml. Given the pt's ekg findings, echocardiography finding and normal ckmb, clinicians favored a resolving myocardial infarction. The syncope did not recur during this hosp stay. Clinicians felt that the syncope could have been due to post-myocardial infarction arrhythmia, a vasovagal response, a hypoxic episode, or due to orthostasis. That day the pt was discharged to home. One week later, the pt went to an outpt follow-up visit with their oncologist, the oncologist felt that prior to starting chemotherapy, the pt would need four to six weeks to recover from their possible recent myocardial infarction. The oncologist felt that there was a potential for chemotherapy induced coronary spasm, and he suggested re-evaluation of their coronary status before initiating chemotherapy. No troponin testing was done at this visit. Five days later, the pt returned to the emergency department. Their baseline shortness of breath had worsened. They had gained 6 lb, most likely form increased lower extremity edema. They had developed orthopnea to the point where they could only sleep in a recliner chair. In the emergency department, 1 liter of pleural fluid was removed by thoracentesis. The pt was admitted for worsening hypoxia and pleural effusion. On the day of admission, the pt's troponin level was 162 ng/ml. The pt was started on lovenox, a beta blocker, and aspirin for possible myocardial infarction. The cardiology service evaluated the pt. They felt that the pt's elevated troponin level and cardiac risk factors did suggest the presence of a large myocardial infarction. However, cardiology concluded that the pt's clinical presentation, ckmb enzymes, ekg, echocardiography were not consistent with myocardial infraction. Three repeat troponin levels from the next day were consistently elevated at 162, 153, and 145 ng/ml. The clinicians felt that these troponin values were likely falsely elevated, and notified the lab. Repeat testing of the specimens at different laboratories using different troponin-i assays demonstrated normal values. Repeat testing of the specimens in the lab using scantibodies anti-heterophilic antibody blocking reagent demonstrated normal values. These findings suported cardiology's conclusion that the pt did not have myocardial infarction, and that the pt's elevated troponin level was due to anti-heterophilic antibody interference.