Effect of oral nitroglycerin and cold stress on myocardial perfusion in areas subtended by stenosed and nonstenosed coronary arteries.
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.
Bøttcher
Morten
M
Department of Cardiology B, Aarhus University Hospital, Aarhus, Denmark. mboe@dadlnet.dk
Madsen
Mette M
MM
Randsbaek
Flemming
F
Refsgaard
Jens
J
Dørup
Inge
I
Sørensen
Keld
K
Nielsen
Torsten Toftegaard
TT
D000284:Administration, Oral; D000328:Adult; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology; D003080:Cold Temperature; D003326:Coronary Circulation / Q000187:drug effects*; D023921:Coronary Stenosis / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D005996:Nitroglycerin / Q000008:administration & dosage*; D013312:Stress, Physiological / Q000503:physiopathology; D014055:Tomography, Emission-Computed; D014463:Ultrasonography; D014654:Vascular Patency
D005996:Nitroglycerin