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Circulation. 2006;113:2679-2682
doi: 10.1161/CIRCULATIONAHA.106.632687
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(Circulation. 2006;113:2679-2682.)
© 2006 American Heart Association, Inc.


Editorial

Cardiology Is Flow

Yoram Richter, PhD; Elazer R. Edelman, MD, PhD

From BIOrest Ltd, Tel-Aviv, Israel (Y.R.); and the Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Boston, and Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, Mass (E.R.E.).

Correspondence to Dr Yoram Richter, BIOrest Ltd, POB 58187, Tel-Aviv 61581 Israel (e-mail yrichter@biorest.co.il), or Dr Elazer Edelman, Department of Medicine, Brigham and Women’s Hospital, 75 Francis St, Boston MA 02115 (e-mail ere@mit.edu).


Key Words: Editorials • angiography • angioplasty • atherosclerosis • blood flow • diagnosis • hemodynamics


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 

Panta rhei. (Everything flows).1

Cardiology is about flow. The primary purpose of the cardiovascular system is to drive, control, and maintain blood flow to all parts of the body. Flow dictates the form and function of the heart and blood vessels through ontogenic and phylogenic development, the structural and functional consequence of repair, and in its end stages, remodeling and response to failure. Flow should therefore be a primary focus by which we explain where lesions form, why they degrade and decompensate, and how we grade the extent of restoration of function after vascular intervention. Yet this is not the case. Flow is not a standard part of our clinical lexicon. Few reliable and consistent means of measuring flow exist. Despite early use of surrogate flow markers (eg, TIMI frame count), we do not quantify flow restoration after interventions. Moreover, there is simply no agreement as to the aspect or degree of flow that is most important in lesion development or functional recovery.

Article p 2744


*    Flow and Atherogenesis
 
The nonhomogeneous nature of atherosclerosis has been appreciated since the earliest days of research in the field.2 Certain arterial segments develop profound lesions, whereas adjacent regions seem completely spared. Neither properties of blood nor local cellular and molecular biological events can vary significantly on such length scales to explain such spatial heterogeneity. Local flow properties can change on these scales (Figure 1), and alterations in local flow pattern—for example, the intricate vectorial description of fluid speed and direction across the entire cross . . . [Full Text of this Article]




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