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Published Online
on June 6, 2002

Arteriosclerosis, Thrombosis, and Vascular Biology. 2002
Published online before print June 6, 2002, doi: 10.1161/01.ATV.0000024569.80106.B4
A more recent version of this article appeared on August 1, 2002
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Submitted on April 16, 2002
Accepted on May 10, 2002

Coronary Flow Velocity and Disturbed Flow Predict Adverse Clinical Outcome After Coronary Angioplasty

Scott Kinlay *; Jasmine Grewal ; Deborah Manuelin ; James C. Fang ; Andrew P. Selwyn ; John A. Bittl ; and Peter Ganz

From the Cardiovascular Division, Brigham and Women's Hospital, Boston, Mass.

* To whom correspondence should be addressed. E-mail: skinlay{at}massmed.org.

Objective—Laminar flow becomes disturbed at high velocities, reducing shear stress and augmenting vascular inflammation and proliferation, processes that are pivotal in restenosis and atherogenesis. We hypothesized that disturbed blood flow after coronary angioplasty is associated with adverse long-term clinical outcome.

Methods and Results—The cineangiograms from 97 patients undergoing laser-assisted coronary angioplasty were analyzed. Coronary blood flow velocity, the residual lesion dimensions, and the Reynolds number (an index of disturbed flow) were measured by using a frame-counting technique and quantitative coronary angiography. Cox proportional hazards were used to assess the relative risk of adverse events (target-vessel revascularization, myocardial infarction, or death) over a mean 2.5 years after the index procedure. There were 41 adverse events during 245 patient years of follow-up (17% per year of follow-up). The risk of an adverse event was increased for patients with a high flow velocity (>250 mm/s; relative risk 2.5, 95% CI 1.3 to 4.7) or a high Reynolds number (>200) at the stenosis inlet (relative risk 2.1, 95% CI 1.1 to 4.1) at the end of the procedure. Adjustment for other factors did not alter these results.

Conclusions—High Reynolds numbers, indicating disturbed blood flow after coronary angioplasty, increase the risk of adverse clinical events, potentially through shear-stress--related molecular mechanisms that promote restenosis and atherogenesis.




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