Physical obstruction and coronary vasoconstriction mediated by adrenergic stress are
believed to be responsible for episodes of myocardial hypoperfusion and angina. Nitroglycerin
relieves symptoms by reducing preload and dilating epicardial vessels. The net perfusion
change and relation to stenosis severity of nitroglycerin and adrenergic stress have
been debated. This study aimed to evaluate whether oral nitroglycerin and adrenergic
stress alters perfusion in myocardial segments subtended by stenosed and nonstenosed
coronary arteries. Myocardial perfusion was quantified (using N-13-ammonia positron
emission tomography [PET]) at rest, after oral nitroglycerin 400 microg, and after
cold stress in 25 patients with coronary artery disease (62 +/- 9 years, 21 men) and
in 30 controls (34 +/- 9 years, 22 men). Myocardial perfusion was quantified in areas
supplied by stenosed (>70%) and nonstenosed (<30%) coronary arteries. The cold pressor
test did not significantly alter myocardial perfusion in any of the groups. However,
when normalized for rate-pressure product, the response in stenosed areas showed a
significantly more pronounced reduction compared with nonstenosed areas (0.78 +/-
0.18 vs 0.64 +/- 0.19 ml/g/min, p <0.005 and 0.86 +/- 0.19 vs 0.73 +/- 0.24 ml/g/min,
p <0.05, p <0.05) for intergroup comparison. In both stenosed areas and nonstenosed
areas nitroglycerin increased perfusion (0.51 +/- 0.14 vs 0.60 +/- 0.17 ml/g/min,
p <0.05 and 0.56 +/- 0.14 vs 0.61 +/- 0.17 ml/g/min, p <0.05). Nitroglycerin did not
alter myocardial perfusion in the control group. There was a negative correlation
between the cold pressor test response and stenosis severity (r(2) = 0.17, p <0.046),
whereas this was not the case for nitroglycerin. In patients with coronary artery
disease, myocardial segments supplied by stenosed coronary arteries showed an altered
perfusion response to adrenergic stress. Oral nitroglycerin increased myocardial perfusion
irrespective of the presence of a stenosis.