Published Online
on June 17, 2002

A more recent version of this article appeared on July 2, 2002

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Submitted on February 25, 2002
Revised on April 18, 2002
Accepted on April 18, 2002

Mechanism of Inducible Regional Dysfunction During Dipyridamole Stress

Jian-Ping Bin MD, Elizabeth Le MD, Robert A. Pelberg MD, Matthew P. Coggins MD, Kevin Wei MD, and Sanjiv Kaul MD^*

From the Cardiovascular Imaging Center, the Cardiovascular Division, University of Virginia, Charlottesville.

^* To whom correspondence should be addressed. E-mail: sk{at}virginia.edu.

Background—We hypothesized that increased myocardial oxygen demand resulting from hypotension and reflex tachycardia unmasking a reduced endocardial myocardial blood flow (MBF) reserve is the mechanism of dipyridamole-induced regional dysfunction in chronic coronary artery disease.

Methods and Results—Ameroid constrictors were placed around the proximal coronary arteries and their major branches in 15 dogs to create chronic coronary stenosis. Seven days later, radiolabeled microsphere--derived MBF and 2-dimensional echocardiography--derived percent wall thickening (%WT) were measured at rest and after 0.56 mg/kg dipyridamole. Dipyridamole caused an increase (mean, 21%) in the rate-pressure product secondary to reflex tachycardia resulting from mild systemic hypotension. %WT in myocardial segments with an endocardial MBF reserve (dipyridamole/resting MBF) of 1.5 to 2.5 (n=35) did not change after dipyridamole, whereas it decreased in segments with an endocardial MBF reserve of <1.5 (n=30) and increased in those with an endocardial MBF reserve of 2.5 (n=45) (P<0.05). Most (80%) segments with endocardial MBF reserve of <1.5 and 14% with an endocardial MBF reserve of 1.5 to 2.5 showed inducible dysfunction after dipyridamole, whereas none of the segments with an endocardial MBF reserve of 2.5 showed this finding. A sigmoid relation (y=-6.74/[1+exp (19.9 · [x-1.84])]+1.35 · x, r=0.93, P<0.0001) was noted between endocardial MBF reserve and %WT. In contrast, neither the epicardial MBF reserve nor the endocardial/epicardial MBF ratio during hyperemia was associated with inducible regional dysfunction.

Conclusions—Increased myocardial oxygen demand resulting from hypotension and reflex tachycardia unmasking a reduced endocardial MBF reserve is the primary mechanism of dipyridamole-induced regional dysfunction in chronic coronary artery disease.

Key words: stress • tachycardia • blood flow • myocardium

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