Summary: Unexpected or bizarre new electrocardiographic changes should alert the physician to the possibility of lead transposition and, if in doubt, the electrocardiogram should be repeated. The classic form of limb lead transposition leading to the appearance of dextrocardia is well recognized. We report a patient with myocardial infarction where lead transposition led to a diagnosis of reinfarction and to the inappropriate use of thrombolytic therapy.
Key words: myocardial infarction, electrocardiogram, reinfarction
Case ReportA 59-year-old man with a history of angina pectoris presented with the symptoms of a myocardial infarction. On admission he was hemodynamically stable with a pulse of 52 beats/min and a blood pressure of 150/80 mmHg. There were no clinical or radiological signs of heart failure. The initial electrocardiogram showed first-degree atrioventricular block, left-axis deviation, and an acute inferoposterior myocardial infarction. The infarction was subsequently confirmed by an increase in enzyme levels.He was given oral aspirin, 150 mg, and streptokinase, I .5 megaunits infused intravenously over 1 hour. Over the next few hours, his chest pain worsened and an intravenous infusion of isosorbide dinitrate, 2-10 mg/h, was started.Twelve hours after admission, despite the isosorbide dini- trate infusion the pain persisted. Examination showed no new clinical findings. Repeat electrocardiogram showed an evolving inferoposterior myocardial infarction ( Fig. 1) but no new changes. The pain resolved with oral indomethacin, 50 mg, and the nitrate infusion was stopped. Twenty four hours after admission, at 2.00 a.m., the patient awoke with further severe chest pain.He was perspiring and in distress, with an irregular pulse and hypotension (blood pressure was 95/60/mmHg). There were no new murmurs. A repeat chest radiograph showed mild pulmonary edema. Oxygen and intravenous frusemide, 50 mg, were administered. A third electraardiogram (Fig. 2) showing a marked axis change to -15 degrees, the disappearance of ST elevation in leads I1 and 111, absent complexes in aVR and aVF, and Q waves in V , .6 suggested a developing anteroseptal myocardial infarction.The bizarre nature of the electrocardiogram was noted, but in the context of the patient's symptoms and clinical condition it was interpreted as a further episode of infarction in a different cardiac territory. Further thrombolytic therapy in the form of intravenous tissue plasminogen activator, 100 mg, was given over 3 hours. The chest settled and his subsequent progress was unremarkable. A fourth electrocardiogram showed no evidence of the anteroseptal myocardial infarction, and was the same as shown in Figure I . The patient was discharged home eight days after admission.
