Effects of nitroglycerin by technetium-99m sestamibi tomoscintigraphy on resting regional myocardial hypoperfusion in stable patients with healed myocardial infarction

Abstract

Myocardial sestamibi uptake reflects regional flow distribution and cellular integrity; however, some segments showing reduced tracer uptake at rest may consist of viable, although hypoperfused, myocardium. It is speculated that the administration of nitroglycerin (NTG) before the sestamibi injection would improve the tracer uptake in resting hypoperfused regions. Thirty-six stable patients with previous myocardial infarction (56 ± 2 years; mean ejection fraction 42 ± 2%), in whom perfusion defects could be seen at resting sestamibi tomography, repeated the scintigraphic study 2 to 6 days later, receiving NTG (0.3 to 0.6 mg sublingually) before the tracer injection. The size of the tracer uptake defect was quantified from circumferential profiles in 3 short-axis slices by integrating the area below the lower normal limit (mean — 2 SD). After NTG, the mean perfusion defect significantly decreased (from 6,324 ± 619 to 5,365 ± 516, p < 0.01). The defect was reduced beyond the reproducibility limits in 20 patients (56%, group 1) and was unchanged or increased in 16 (44%, group 2). The resting sestamibi defect size was comparable between the 2 groups. The average percent reduction of the perfusion defect after NTG was 29 ± 4% (range 7 to 74). The perfusion defects that improved after NTG were associated with a less severe 2-dimensional echocardiographic regional wall motion score (2.1 ± 0.1 vs 2.8 ± 0.1 in segments showing fixed defect, p < 0.001), a lower rate of patency (37% vs 83%, p < 0.05), and a worse grade of the sestamibi defect-related vessel flow according to the Thrombolysis in Myocardial Infarction trial (1.2 ± 0.3 vs 2.4 ± 0.3, p < 0.05). After NTG, changes in regional myocardial flow distribution may occur in a sizable number of stable patients with healed myocardial infarction, as reflected by their improved sestamibi uptake in areas showing resting perfusion defects in the absence of symptoms of myocardial ischemia.