LETTERS TO THE EDITOR
Reply
Carlo Caiati, MDa and
Sabino Iliceto, MDa
a Department of Cardiovascular and Neurological Science, Ospedale S. Giovanni di Dio, via Ospedale 46, 09124 Cagliari, Italy
Drs. Kaufmann and Jenni pointed out that a reason for the error in assessing coronary flow reserve with this novel Doppler method with adenosine (1) could be both the flow-mediated dilation of the epicardial vessel during hyperemia and the hyperemia-induced variation of blood flow velocity profile. In addition, they observed a large discrepancy between the contrast infusion modalities used in this recent study and those used in our previous studies.
Regarding the first point, the published data are controversial and scanty. In fact, an animal study using intravascular echocardiography has shown no variation of epicardial coronary vessel size during intracoronary adenosine (2). In another human study conducted in patients with and without left main coronary artery disease, intravenous adenosine did not increase the angiographic lumen diameter in the mid and distal segments (control 3.39 ± 0.85 vs. 3.35 ± 0.98 mm after adenosine; percent change –1 ± 12%) as compared with the proximal epicardial vessel diameter (control 3.72 ± 0.99 vs. 3.72 ± 0.86 mm after adenosine; percent change 1 ± 6%) (3).
Flow-mediated dilation, if any, should not always take place. Flow-mediated vasodilation is, in fact, impaired both in patients without increment of flow (in which, of course, no shear stress can be exerted on the coronary endothelium) and in patients with no flow-limiting atherosclerosis (4). Therefore, in our study, flow-mediated vasodilation, if any, should have affected the assessment of coronary flow reserve only in patients with preserved capacity to increase flow (no flow-limiting stenosis) and, at the same time, without overt atherosclerosis of the left anterior descending coronary artery. This refers to only a small percentage of group 1 in our series. In addition, the data cited by Kaufmann et al. refer mostly to studies in which an intracoronary bolus of adenosine or papaverine was administered. In contrast, in our study, intravenous adenosine was used. It can be hypothesized that a vasodilator agent administered through the intravenous route can have less effect on the conductance vessel (only an indirect effect, if any, through increment of flow), as compared with the intracoronary route (direct effect of bolus and indirect flow-mediated action) (5). A major impact of flow-mediated dilation could be hypothesized in studies in which endothelial dysfunction in the absence of coronary artery disease has to be evaluated. Further studies are needed to shed more light on this issue.
Regarding their second point, the hyperemia-induced blood flow velocity profile variation is a minor limitation (relatively small source of error, 12%) of any Doppler method that affects not only our new noninvasive method but also the intracoronary Doppler flow wire method.
Regarding their third point, a careful reading of the Methods sections of this recent study and previous reports would have avoided any confusion. In fact, there is no contradiction with the previous experience, because, as correctly specified, only the concentration of the agent (300 mg/ml) was the same as that in the previous experience. The modality of administration, however, has changed radically. Now we use, as reported (1), an infusion through a pump with an infusion rate of 1 ml/min, where in the past, we manually injected contrast as a bolus (at  2 ml/s). The advantage of this new modality has been addressed in a recent paper of ours (6).
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References
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- Caiati C, Zedda N, Montaldo C, Montisci R, Iliceto S. Contrast-enhanced transthoracic second harmonic echo Doppler with adenosine: a noninvasive, rapid and effective method for coronary flow reserve assessment. J Am Coll Cardiol. 1999;34:122–130[Abstract/Free Full Text]
- Sudhir K, MacGregor JS, Barbant SD, et al. Assessment of coronary conductance and resistance vessel reactivity in response to nitroglycerin, ergonovine and adenosine: in vivo studies with simultaneous intravascular two-dimensional and Doppler ultrasound. J Am Coll Cardiol. 1993;21:1261–1268[Abstract]
- Kern MJ, Deligonul U, Tatineni S, Serota H, Aguirre F, Hilton TC. Intravenous adenosine: continuous infusion and low dose bolus administration for determination of coronary vasodilator reserve in patients with and without coronary artery disease. J Am Coll Cardiol. 1991;18:718–729[Abstract]
- Cox DA, Vita JA, Treasure CB, et al. Atherosclerosis impairs flow-mediated dilation of coronary arteries in humans. Circulation. 1989;80:458–465[Abstract/Free Full Text]
- Rose GA, Mathier MA, Kusshwaha SS, Semigran MJ. Adenosine causes flow-mediated epicardial vessel dilation in humans. (abstr)J Am Coll Cardiol. 1995;25(Suppl):336A
- Caiati C, Montaldo C, Zedda N, Bina A, Iliceto S. New noninvasive method for coronary flow reserve assessment: contrast-enhanced transthoracic second harmonic echo Doppler. Circulation. 1999;99:771–778[Abstract/Free Full Text]
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References