title: Pharmacologic stress-induced regional myocardial blood flow heterogeneity and left ventricular wall thickening abnormality: comparison of intravenous adenosine with dipyridamole in a model of critical coronary stenosis.
abstract: Variations in reported sensitivity of myocardial perfusion scans or wall motion abnormalities during pharmacologic stress with intravenous adenosine and dipyridamole may be caused by differences in myocardial oxygen demand or myocardial blood flow redistribution induced by each agent. To investigate the physiologic correlates of functional abnormalities during pharmacologic stress testing, regional myocardial blood flow (radiolabeled microsphere technique) and left ventricular segmental wall thickening (quantitative two-dimensional echocardiography) were measured in 9 dogs with an open chest model of critical stenosis of the left circumflex coronary artery. Data were obtained at baseline and peak drug infusion for intravenous adenosine (0.42 mg/kg over a 3-minute period) and for intravenous dipyridamole (0.56 mg/kg over a 4-minute period). Adenosine and dipyridamole induced regional flow abnormality in 7 (77%) of 9 dogs. Myocardial segments with decreased endocardial/epicardial flow ratio were similar for both agents (2.9 +/- 1.8 vs 2.7 +/- 1.3, p = [NS]). Segments with myocardial flow heterogeneity (ratio of endocardial flow to control left anterior descending/left circumflex endocardial flow) were similar for both agents (2.7 +/- 0.9 vs 2.3 +/- 1.0, p = NS). Adenosine-induced wall thickening abnormality (77% vs 55% with dipyridamole) correlated with regional flow abnormality. Significantly lower mean arterial pressure (53 +/- 1.7 mm Hg vs 64 +/- 1.9 mm Hg, p < 0.01) and more prolonged drug effect (18 +/- 6.4 min vs 3 +/- 1.4 min, p < 0.001) were seen for dipyridamole compared with adenosine. Adenosine induces regional flow abnormality similar to dipyridamole but with less hemodynamic perturbation, and adenosine-induced wall thickening abnormality more closely parallels regional flow abnormality.
authors.affiliation: Department of Internal Medicine, Morehouse School of Medicine, Atlanta, GA 30310, USA.
authors.forename: E O
authors.initials: EO
authors.lastname: Ofili
authors.forename: F A
authors.initials: FA
authors.lastname: Dressler
authors.forename: J A
authors.initials: JA
authors.lastname: St Vrain
authors.forename: H
authors.initials: H
authors.lastname: Goodgold
authors.forename: J
authors.initials: J
authors.lastname: Standeven
authors.forename: B
authors.initials: B
authors.lastname: Chandel
authors.forename: R
authors.initials: R
authors.lastname: Gentilcore
authors.forename: L
authors.initials: L
authors.lastname: McBride
authors.forename: R
authors.initials: R
authors.lastname: Castello
authors.forename: M
authors.initials: M
authors.lastname: Kern
authors.forename: A J
authors.initials: AJ
authors.lastname: Labovitz
mesh_terms: D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D015986:Confounding Factors, Epidemiologic; D003326:Coronary Circulation / Q000187:drug effects*; D004176:Dipyridamole / Q000494:pharmacology*; D004285:Dogs; D006352:Heart Ventricles / Q000187:drug effects* / Q000473:pathology; D006439:Hemodynamics / Q000187:drug effects; D007262:Infusions, Intravenous; D008297:Male; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D014665:Vasodilator Agents; D004176:Dipyridamole; D000241:Adenosine