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Dissociation of ST segment elevation and regional wall motion with open-artery, intracoronary Fluosol
G L Schaer1, M W Krucoff, C Green
1Division of Cardiology, Georgetown University School of Medicine.
Insights
Intracoronary Fluosol infusion during angioplasty causes ST elevation without myocardial ischemia. This finding suggests an alternative mechanism for electrocardiogram changes, distinct from reduced heart muscle function.
Area of Science:
- Cardiology
- Biomedical Engineering
Background:
- Intracoronary Fluosol use in percutaneous transluminal coronary angioplasty (PTCA) reduces chest pain and preserves myocardial function.
- ST segment elevation on ECG is common despite evidence of reduced myocardial ischemia during PTCA with Fluosol.
Purpose of the Study:
- To investigate if Fluosol causes ST segment elevation through a mechanism independent of myocardial ischemia.
- To differentiate the cause of ST elevation during Fluosol infusion from that of actual ischemia.
Main Methods:
- Closed-chest dog model with interventions: oxygenated Fluosol infusion, Ringer's lactate infusion, and transient coronary artery occlusion.
- Open-artery infusions in the left anterior descending (LAD) coronary artery to maintain antegrade flow and minimize ischemia.
- Continuous ST segment monitoring and contrast left ventriculography to assess regional systolic function.
Main Results:
- Coronary occlusion caused significant ST elevation and depressed regional ejection fraction.
- Fluosol infusion induced ST elevation comparable to occlusion but preserved regional ejection fraction.
- Ringer's lactate infusion also caused ST elevation while maintaining regional contractility.
Conclusions:
- Intracoronary Fluosol infusion causes ST segment elevation.
- This ST elevation occurs without a reduction in regional systolic function, indicating it's not due to myocardial ischemia.
- The findings suggest an alternative, non-ischemic mechanism for ST elevation induced by Fluosol during coronary interventions.
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 less than 0.05) and marked depression in regional ejection fraction (45 +/- 7% to -3 +/- 4%, p less than 0.05). Infusion of Fluosol produced a similar degree of ST segment elevation (0.9 +/- 0.3 to 2.8 +/- 0.4 mm, p less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)