Dissociation of ST segment elevation and regional wall motion with open-artery, intracoronary Fluosol

Abstract

Intracoronary infusion of oxygenated Fluosol during percutaneous transluminal coronary angioplasty has been shown to reduce chest pain and preserve contractile function. In spite of this evidence for reduced severity of myocardial ischemia, ST elevation is frequently observed on the electrocardiogram. To determine if Fluosol produces ST segment elevation by a mechanism other than myocardial ischemia, closed-chest dogs underwent three interventions: (1) an infusion of oxygenated Fluosol into the unoccluded left anterior descending (LAD) coronary artery; (2) an identical infusion of unoxygenated Ringer's lactate; and (3) a transient occlusion of the LAD coronary artery. Open-artery infusions were chosen to minimize ischemia by permitting antegrade coronary blood flow. ST segments were monitored continuously and contrast left ventriculography was performed to assess regional systolic function. Coronary occlusion for 1 minute resulted in significant ST segment elevation from baseline (0.8 ± 0.2 to 3.2 ± 0.6 mm, p < 0.05) and marked depression in regional ejection fraction (45 ± 7% to −3 ± 4%, p < 0.05). Infusion of Fluosol produced a similar degree of ST segment elevation (0.9 ± 0.3 to 2.8 ± 0.4 mm, p < 0.05), but no change in regional ejection fraction. Ringer's lactate infusion also resulted in ST segment elevation associated with preservation of regional contractility. Because regional systolic function (a sensitive indicator of regional ischemia) was preserved and an open-artery infusion was used, it is concluded that intracoronary infusion of Fluosol causes ST segment elevation by a mechanism other than myocardial ischemia. Thus in the clinical practice of coronary angioplasty, the appearance of ST segment elevation during Fluosol infusion may not necessarily indicate severe myocardial ischemia.