(Circulation. 1998;97:2281-2282.)
© 1998 American Heart Association, Inc.
Intracoronary Doppler and Collateral Resistance
Christian Seiler, MD, FACC
Cardiology,
University Hospital Bern,
Bern, Switzerland
To the Editor:
In the July 1, 1997, issue of Circulation, Piek and
coworkers1 provided very interesting
intracoronary data on the pharmacological responsiveness of the
human coronary collateral circulation. In 38 patients with
1-vessel coronary artery disease and visible (n=24) or
recruitable (n=14) collaterals, a collateral flow index, indices for
collateral resistance, and index for the resistance in the vascular bed
downstream of the collateral receiving artery were investigated
regarding their response to intracoronary adenosine or
nitroglycerin injected into the collateral donor
artery. The authors found that spontaneously visible and recruitable
collaterals substantially differed in their response to
intracoronary adenosine or
nitroglycerin in that the former were able to decrease
their resistance and thus increase the flow through it, whereas the
latter were unable to do so. Although the direct study of collateral
hemodynamics in humans is very important because almost
no data exist in this area of research, the mentioned results of the
present study have to be taken cautiously for some methodological
reasons.
1. The authors' assertion is incorrect that they obtained collateral
flow by measuring diastolic occlusive time velocity
integral (dVi, cm). In fact they determined just an index for
collateral flow that did not account for the influence of changes in
the caliber of coronary collaterals, which may develop during
pharmacological stress.
2. More importantly, an analysis of combined
intracoronary Doppler- and pressure-derived collateral
indices in our laboratory2 has indicated that the
calculation of a collateral index using just diastolic
integrated velocity signals does not yield accurate results
when compared with pressure-derived, intracoronary,
ECG-validated values (n=21 patients with bidirectional flow velocity
signals). In our opinion, flow velocity signals have to be added over
the entire cardiac cycle irrespective of their direction in order to
provide correct results of collateral flow
indices.2 Intuitively, this makes sense, since
coronary epicardial flow indicated by the velocity signal will
finally reach the myocardial bed irrespective of the direction it has
taken at the time of its detection upstream. Systolic velocity
signals originating from increased epicardial backward or forward flow
due to enhanced myocardial wall stress can be recognized easily by
their high pitch, high peak velocity, and high acoustic intensity onset
and their short duration. These signals should not be accounted for in
the computation of collateral flow indices. However, all other flow
velocity signals during systole should be used in the calculation of
Doppler indices of collateral flow.
3. As a minor point, it has to emphasized that Equation 3 in the
appendix of the article is given incorrectly. It should probably read
Pw=dVi*R4 (and not Pw+dVi*R4).
View this table:
[in this window]
[in a new window]
|
Table 1. Effect of Adenosine and Nitroglycerin on Resistance
Calculations Using Total Blood Flow Velocity Integral in Patients With
Recruitable Collateral Vessels (Group 1) and Patients With
Spontaneously Visible Collateral Vessels (Group
2)
|
|
References
1.
Piek JJ, van Liebergen AM, Koch KT, de Winter
RJ, Peters RJG, David GK. Pharmacological modulation of the human
collateral vascular resistance in acute and chronic coronary
occlusion assessed by intracoronary blood flow velocity
analysis in an angioplasty model. Circulation. 1997;96:106–115.[Abstract/Free Full Text]
2.
Seiler C, Fleisch M, Meier B. Intracoronary occlusive
pressure compared with velocity measurements for the assessments of
collaterals. Eur Heart J. 1997;18(suppl):240.
Abstract.
Response
Jan J. Piek, MD;
; Rob A. M. van Liebergen, MD
Department of Cardiology,
Academic Medical Center,
Amsterdam, Netherlands
Only a limited number of studies have been conducted on the
hemodynamics of the coronary collateral
circulation in humans. Consequently, the data reported in our
article1 require confirmation by other
investigators. The critical comments by Seiler are well appreciated and
may stimulate further research on this topic of interest. The comments
raised are addressed in numerical order.
1. The currently available technical equipment in interventional
cardiology hampers the assessment of collateral
vascular resistance in an angioplasty model by measurement of
collateral volume flow. This requires a simultaneous
assessment of both collateral blood flow velocity and the diameter of
the arterial segment. It is correct that collateral flow
was estimated in the study as an index using the diastolic
blood flow velocity integral. The selective administration of
vasodilators (adenosine or nitroglycerin) in
the donor coronary artery may induce vasodilation of the
recipient coronary artery.2 This
indicates that the observed changes in collateral blood flow velocity
after the administration of vasodilators in patients with spontaneously
visible collateral vessels are rather an underestimation of the true
alterations in volume flow and hence of the collateral vascular
resistance. On the other hand, our conclusion that recruitable
collateral vessels, in general, do not respond to vasodilators may be
incorrect due to this phenomenon. These methodological drawbacks were
addressed in the limitations section of the article.
2. The use of the diastolic blood flow velocity integral
for the calculation of the collateral vascular resistance was based on
the consideration that systolic blood flow velocity signals can
be generated by myocardial contraction even in the absence of
recruitable collateral vessels.
The interpretation of these systolic signals is rather
undefined, taking into account the limited number of studies performed
on this subject.3 4 The diastolic
blood flow velocity integral as an index of collateral flow is
arbitrary.
Table 2 of the original article depicts the alterations in the
coronary blood flow velocity after the administration of
vasodilators using the diastolic blood flow velocity
integral as well as the total blood flow velocity integral.
Bidirectional signals were added for the calculation of this total
blood flow velocity integral. That table shows that the blood flow
velocity alterations are not different using the diastolic
or total blood flow velocity integrals.
For completeness, we have calculated the changes in collateral
vascular resistance based on the total blood flow velocity integral
rather than the diastolic velocity integral. Again, the
following Table
shows that this
collateral flow index does not yield different conclusions, with the
exception of the effect of nitroglycerin on the
peripheral vascular resistance index of the recipient
coronary artery, which shows a trend toward
significance.
3. The authors apologize for the incorrect Equation 3 (Pw+dVi*R4) in
the appendix that should read as: Pw=dVi*R4.
References
1.
Piek JJ, van Liebergen RAM, Koch KT, de Winter RJ,
Peters RJG, David GK. Pharmacological modulation of the human
collateral vascular resistance in acute and chronic coronary
occlusion assessed by intracoronary blood flow velocity
analysis in an angioplasty model. Circulation. 1997;96:106–115.
2.
Fujita M, Yamanishi K, Inoko M, Miwa K. Preferential
dilation of recipient coronary arteries of the collateral
circulation by intracoronary administration of
nitroglycerin. J Am Coll Cardiol. 1994;24:631–635.[Abstract]
3.
Yamada T, Okamoto M, Sueda T, Hashimoto M, Kajiyama G.
Relation between collateral flow assessed by Doppler guide wire and
angiographic collateral grades. Am Heart J. 1995;130:32–37.[Medline]
[Order article via Infotrieve]
4.
Tron C, Donohue TJ, Bach RG, Wolford T, Caracciolo EA,
Aguirre FV, Khoury A, Kern MJ. Differential characterization of human
coronary collateral blood flow velocity. Am Heart
J. 1996;132:508–515.[Medline]
[Order article via Infotrieve]
