Effect of phentolamine on the hyperemic response to adenosine in patients with microvascular disease.
For accurate measurement of the fractional flow reserve (FFR) of the myocardium, the presence of maximum hyperemia is of paramount importance. It has been suggested that the hyperemic effect of the conventionally used hyperemic stimulus, adenosine, could be submaximal in patients who have microvascular dysfunction and that adding alpha-blocking agents could augment the hyperemic response in these patients. We studied the effect of the nonselective alpha-blocking agent phentolamine, which was administered in addition to adenosine after achieving hyperemia, in patients who had microvascular disease and those who did not. Thirty patients who were referred for percutaneous coronary intervention were selected. Of these 30 patients, 15 had strong indications for microvascular disease and 15 did not. FFR was measured using intracoronary adenosine, intravenous adenosine, and intracoronary papaverine before and after intracoronary administration of the nonselective alpha blocker phentolamine. In patients who did not have microvascular disease, no differences in hyperemic response to adenosine were noted, whether or not alpha blockade was given before adenosine administration; FFR levels before and after phentolamine were 0.76 and 0.75, respectively, using intracoronary adenosine (p = 0.10) and 0.75 and 0.74, respectively, using intravenous adenosine (p = 0.20). In contrast, in patients who had microvascular disease, some increase in hyperemic response was observed after administration of phentolamine; FFR levels decreased from 0.74 to 0.70 using intracoronary adenosine (p = 0.003) and from 0.75 to 0.72 using intravenous adenosine (p = 0.04). Although statistically significant, the observed further decrease in microvascular resistance after addition of phentolamine was small and did not affect clinical decision making in any patient. In conclusion, when measuring FFR, routinely adding an alpha-blocking agent to adenosine does not affect clinical decision making.
Aarnoudse
Wilbert
W
Department of Cardiology, Catharina Hospital, Eindhoven, The Netherlands.
Geven
Maartje
M
Barbato
Emanuele
E
Botman
Kees-joost
KJ
De Bruyne
Bernard
B
Pijls
Nico H J
NH
D000241:Adenosine / Q000008:administration & dosage; D000317:Adrenergic alpha-Antagonists / Q000008:administration & dosage; D001783:Blood Flow Velocity / Q000187:drug effects; D017023:Coronary Angiography; D023921:Coronary Stenosis / Q000175:diagnosis / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006940:Hyperemia / Q000139:chemically induced* / Q000503:physiopathology; D007269:Injections, Intra-Arterial; D007275:Injections, Intravenous; D008297:Male; D008833:Microcirculation / Q000187:drug effects* / Q000502:physiology; D008875:Middle Aged; D010208:Papaverine / Q000008:administration & dosage; D010646:Phentolamine / Q000008:administration & dosage; D015203:Reproducibility of Results; D012720:Severity of Illness Index; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000008:administration & dosage
D000317:Adrenergic alpha-Antagonists; D014665:Vasodilator Agents; D010208:Papaverine; D000241:Adenosine; D010646:Phentolamine