Related Experiment Videos
Myocardial thallium-201 kinetics in normal and ischemic myocardium
Insights
Thallium-201 myocardial uptake and redistribution depend on blood flow. Reduced blood flow slows thallium washout from heart cells, explaining delayed redistribution in chronic perfusion issues.
Area of Science:
- Cardiology
- Nuclear Medicine
- Physiology
Background:
- Myocardial uptake of thallium-201 (Tl-201) is influenced by blood flow.
- Delayed redistribution of Tl-201 after altered myocardial perfusion is a known phenomenon.
- Net Tl-201 accumulation depends on extraction and efflux rates.
Purpose of the Study:
- To quantify myocardial extraction and intrinsic efflux of Tl-201.
- To assess these parameters at normal and reduced myocardial blood flow.
- To elucidate the mechanisms of Tl-201 redistribution.
Main Methods:
- Experiments conducted on anesthetized dogs.
- Measurement of myocardial extraction fraction at varying coronary perfusion pressures.
- Assessment of intrinsic Tl-201 washout kinetics in the absence of systemic recirculation.
Main Results:
- Myocardial extraction fraction was high (82%) at normal flow and did not significantly change with reduced pressure.
- Intrinsic Tl-201 washout had a slow component (T 1/2 = 54 min) at normal flow.
- Washout slowed significantly at reduced perfusion pressures (T 1/2 = 300 min below 60 mm Hg).
- A rapid washout component (T 1/2 = 2.5 min) likely represents interstitial Tl-201.
Conclusions:
- Myocardial redistribution of Tl-201 is primarily due to slower intrinsic cellular washout at reduced perfusion levels.
- Increased myocardial extraction efficiency does not explain redistribution in chronic reduced perfusion.
- Intrinsic cellular efflux is the key determinant of Tl-201 redistribution patterns.
Abstract:
The initial myocardial uptake of thallium-201 depends on myocardial blood flow distribution. The phenomenon of delayed thallium redistribution after transiently or chronically altered myocardial perfusion has been described. The net myocardial accumulation of thallium-201 after injection depends upon the net balance between continuing myocardial extraction from low levels of recirculating thallium in the blood compartment and the net rate of efflux of thallium from the myocardium into the extracardiac blood pool. These experiments were designed to measure separately the myocardial extraction and intrinsic myocardial efflux of thallium-201 at normal and at reduced rates of myocardial blood flow. The average myocardial extraction fraction at normal blood flow in 10 anesthetized dogs was 82 +/- 6% (+/- SD) at normal coronary arterial perfusion pressures and increased insignificantly, to 85 +/- 7%, at coronary perfusion pressures of 10--35 mm Hg. At normal coronary arterial perfusion pressures in 12 additional dogs, the intrinsic thallium washout in the absence of systemic recirculation had a half-time (T 1/2) of 54 +/- 7 minutes. The intrinsic cellular washout rate began to increase as distal perfusion pressures fell below 60 mm Hg and increased markedly to a T 1/2 of 300 minutes at perfusion pressures of 25--30 mm Hg. A second, more rapid component of intrinsic thallium washout (T 1/2 2.5 minutes) representing approximately 7% of the total initially extracted myocardial thallium was observed. The faster washout component is presumed to be due to washout of interstitial thallium unextracted by myocardial cells, whereas the slower component is presumed due to intracellular washout. The net clearance time of thallium measured after i.v. injection is much longer than the intrinsic myocardial cellular washout rate because of continuous replacement of myocardial thallium from systemic recirculation. Myocardial redistribution of thallium-201 in states of chronically reduced perfusion cannot be the result of increased myocardial extraction efficiency, but rather, is the result of the slower intrinsic cellular washout rate at reduced perfusion levels.