Catheterization and Cardiovascular Diagnosis 29:93-98 (1 993) zy Editorial Caveat Emptor: zyxw A Clinician’s Guide to Physiologic Significance of Arterial Assessing Stenoses Robert F. Wilson, MD, and David D. Laxson, MD INTRODUCTION A zyxwvutsrqpo burgeoning number of methods have been devel- oped recently to assess the zyxwvutsrq physiologic significance of coronary stenoses. Their application in decisionmaking for patients with coronary artery syndromes has been applauded by coronary physiologists but viewed with skepticism by many clinicians. What is meant by the physiologic significance of a coronary lesion and what is the evidence that determination of this entity can im- prove decisionmaking? Which of the tools developed to assess physiologic abnormalities are useful, and when? A SHORT PRIMER IN CORONARY HEMODYNAMICS Over the last 40 years our understanding of coronary artery hemodynamics has been expanded greatly [ 1,2]. We know that the arteries visible on the angiogram are conduit vessels under normal circumstances they provide almost no resistance to blood flow. In contrast, the mi- crocirculation (vessels less than 400 pm in diameter) regulates perfusion by causing wide changes in resis- tance (Fig. 1). The microcirculation is composed of ar- teriolar “resistance” vessels and smaller vessels at the capillary level. The muscular arterioles autoregulate blood flow to each myocyte by constricting or dilating in response to a variety of stimuli. When the arterioles are dilated maximally, total coronary resistance decreases by 3.5- to 6-f0ld, enough to meet the most extreme meta- bolic demand (exercise typically causes a 2- to 4-fold increase in blood flow) [3,4]. As a stenosis develops in an epicardial artery, the mi- crocirculation dilates to compensate for the additional resistance imparted by the stenosis. The blood pressure distal to the stenosis falls. Capillary perfusion is main- tained because the pressure drop across the stenosis is compensated for by the reduction is pressure head across the arteriolar bed. This normalizes total coronary resis- tance and preserves basal blood flow. zyxwvuts A physiologically the significant stenosis is one that zyxw is severe enough to cause compensatory arteriolar dilation. The clinical impor- tance of compensatory arteriolar dilation is that resting blood flow is maintained, but the degree to which blood flow can increase further is diminished because the ar- teriolar bed is already partially dilated at rest. Failure of blood flow the rise sufficiently to match metabolic de- mand leads to stress-induced ischemia. In dogs with normal coronary arteries, compensatory arteriolar dilation is not engaged until about 75% of the lumenal area is obstructed 151. When >90% of the epi- cardial lumen cross-sectional area is occluded, resting blood flow begins to fall because microcirculatory va- sodilation is exhausted. Humans with minimal athero- sclerosis behave like the dog; compensatory arteriolar dilation is engaged starting at about 70% area stenosis (45 -50% diameter stenosis) and increases progressively as the stenosis becomes more severe [6,7]. In patients with more widespread atherosclerosis, le- sions of 50% area stenosis or less may be “physiologi- cally significant” and cause arteriolar dilation [8,9]. This shift occurs because diffuse arterial narrowing of the ‘‘normal’’ portion of the artery makes focal narrow- ings appear less severe [lo]. The presence of undetected (and often undetectable) diffuse atherosclerosis is the reason that simple angiography frequently does not per- mit an accurate assessment of the significance of a focal coronary lesion 11 1,121. This important deficiency has led to the plethora of new methods (and businesses) for assessing the physiologic impact of coronary stenoses. From the Cardiovascular Division of the Department of Medicine, University of Minnesota, Minneapolis. Received December 31, 1992; revision accepted February 4, 1993. Address reprint requests to Robert F. Wilson, Box 508 UMHC, 420 Delaware Street, S.E., Minneapolis, MN 55455. 0 1993 Wiley-Liss, Inc.