BACKGROUND: Maximal hyperemia is a critical prerequisite for correct fractional flow reserve (FFR) measurements. Continuous administration of adenosine by femoral venous access is considered the gold-standard. However, antecubital venous access is used as an alternative route of administration due to the increasing popularity of radial versus femoral access for coronary catheterization. Because of a potentially larger cross sectional venous area in the arm-theoretically associated with slower flow velocities-and the extremely short half-life of adenosine, there are concerns whether this route of administration is truly equivalent to the femoral route. METHODS: Fifty randomly selected patients with coronary artery disease were included. FFR was measured with a pressure monitoring wire and the recording was digitally stored. Hyperemia was successively induced by adenosine via the antecubital vein at a dose of 140 microg kg(-1) min(-1) (A140), via the antecubital vein at a dose of 170 microg kg(-1) min(-1) (A170), and via the femoral vein at a dose of 140 microg kg(-1) min(-1) (F140). RESULTS: Induction of hyperemia by A140 yielded significantly lower hyperemic responses than compared with A170 (P = 0.038) and F140 (P = 0.005). No significant difference was seen between adenosine administration by A170 versus F140. Hyperemic stimulation by A140 underestimated lesion severity near the ischemic threshold of FFR more frequently than the other modalities. There were no differences in side-effects between any of the dosages and routes of administration. CONCLUSIONS: The intravenous application of adenosine via antecubital venous access is feasible but slightly less effective than the femoral approach. In this setting, an antecubital dosage of 170 microg kg(-1) min(-1) is comparable to the standard dosage of 140 microg kg(-1) min(-1) in the femoral vein. In some patients, this regimen might prevent an underestimation of lesion severity.
BACKGROUND: Maximal hyperemia is a critical prerequisite for correct fractional flow reserve (FFR) measurements. Continuous administration of adenosine by femoral venous access is considered the gold-standard. However, antecubital venous access is used as an alternative route of administration due to the increasing popularity of radial versus femoral access for coronary catheterization. Because of a potentially larger cross sectional venous area in the arm-theoretically associated with slower flow velocities-and the extremely short half-life of adenosine, there are concerns whether this route of administration is truly equivalent to the femoral route. METHODS: Fifty randomly selected patients with coronary artery disease were included. FFR was measured with a pressure monitoring wire and the recording was digitally stored. Hyperemia was successively induced by adenosine via the antecubital vein at a dose of 140 microg kg(-1) min(-1) (A140), via the antecubital vein at a dose of 170 microg kg(-1) min(-1) (A170), and via the femoral vein at a dose of 140 microg kg(-1) min(-1) (F140). RESULTS: Induction of hyperemia by A140 yielded significantly lower hyperemic responses than compared with A170 (P = 0.038) and F140 (P = 0.005). No significant difference was seen between adenosine administration by A170 versus F140. Hyperemic stimulation by A140 underestimated lesion severity near the ischemic threshold of FFR more frequently than the other modalities. There were no differences in side-effects between any of the dosages and routes of administration. CONCLUSIONS: The intravenous application of adenosine via antecubital venous access is feasible but slightly less effective than the femoral approach. In this setting, an antecubital dosage of 170 microg kg(-1) min(-1) is comparable to the standard dosage of 140 microg kg(-1) min(-1) in the femoral vein. In some patients, this regimen might prevent an underestimation of lesion severity.
Authors: Gianni Casella; Marcus Leibig; Thomas M Schiele; Reiner Schrepf; Victoria Seelig; Hans-Ulrich Stempfle; Petra Erdin; Johannes Rieber; Andreas König; Uwe Siebert; Volker Klauss Journal: Am Heart J Date: 2004-10 Impact factor: 4.749
Authors: Morton J Kern; Amir Lerman; Jan-Willen Bech; Bernard De Bruyne; Eric Eeckhout; William F Fearon; Stuart T Higano; Michael J Lim; Martijn Meuwissen; Jan J Piek; Nico H J Pijls; Maria Siebes; Jos A E Spaan Journal: Circulation Date: 2006-08-28 Impact factor: 29.690
Authors: Nico H J Pijls; Pepijn van Schaardenburgh; Ganesh Manoharan; Eric Boersma; Jan-Willem Bech; Marcel van't Veer; Frits Bär; Jan Hoorntje; Jacques Koolen; William Wijns; Bernard de Bruyne Journal: J Am Coll Cardiol Date: 2007-05-17 Impact factor: 24.094
Authors: A Jeremias; S D Filardo; R J Whitbourn; R S Kernoff; A C Yeung; P J Fitzgerald; P G Yock Journal: Circulation Date: 2000-01-25 Impact factor: 29.690
Authors: Sigmund Silber; Per Albertsson; Francisco F Avilés; Paolo G Camici; Antonio Colombo; Christian Hamm; Erik Jørgensen; Jean Marco; Jan-Erik Nordrehaug; Witold Ruzyllo; Philip Urban; Gregg W Stone; William Wijns Journal: Eur Heart J Date: 2005-03-15 Impact factor: 29.983
Authors: Theodoros D Karamitsos; Ntobeko A B Ntusi; Jane M Francis; Cameron J Holloway; Saul G Myerson; Stefan Neubauer Journal: J Cardiovasc Magn Reson Date: 2010-11-16 Impact factor: 5.364