(Circulation. 1998;98:824-825.)
© 1998 American Heart Association, Inc.
Adenosine-Induced Preconditioning of Human Myocardium?
Christian Seiler, MD;
; Michael Billinger, MD
University Hospital, Cardiology,
Bern, Switzerland
To the Editor:
Although the article by Leesar and coworkers in the June 3, 1997,
issue of Circulation1 concludes that
"adenosine preconditions human myocardium," in
our opinion their investigation in 30 patients undergoing balloon
angioplasty (PTCA) and pretreatment with normal saline or
adenosine (2 mg/min for 10 minutes) merely allows them to
reiterate their introductory statement that "to the best of our
knowledge, evidence that adenosine can precondition human
myocardium in vivo is still lacking." First of all, the
fact that there have been recent studies demonstrating reduced signs of
myocardial ischemia during repeated balloon inflations does not
necessarily suggest the existence of ischemic preconditioning
in the conventional, ie, biochemical, sense. As long as the
contribution of the gradual opening of collateral channels with
successive balloon occlusions is not accounted for in the observed
phenomenon of attenuated myocardial ischemia, ischemic
"preconditioning" may be not a biochemical but a biophysical
process of collateral recruitment due to the temporally increasing
effect of a pressure gradient across the anastomoses between the
nonstenotic donor vessel and the occluded recipient vessel.
Hence, the finding that such a thing as ischemic
preconditioning, in the normally used sense of the word, exists in
humans is very controversial and is inversely associated with whether
or not the authors accounted for collaterals.2
Second, and considering the effects of adenosine on the
resistance and conductance vessels of the coronary circulation,
it is similarly disputable whether there is such a thing as
adenosine-induced preconditioning or whether the phenomenon of
mitigated myocardial . . . [Full Text of this Article]
Roberto Bolli, ;
MD Massoud Leesar;
MD Mirza Ahmed;
MD Marcus Stoddard;
; MD John Broadbent, MD
Division of Cardiology,
University of Louisville Health Sciences Center,
Louisville, Ky
This article has been cited by other articles:

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