(Circulation. 1999;100:e121.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Coronary Pressure
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Nico Pijls and Bernard DeBruyne. 339 pp, illustrated. Dordrect, The Netherlands: Kluwer Academic Publishers; 1997.
To review this important book in proper perspective, a substantive preamble is useful for understanding its major contributions to the pathophysiology of coronary artery stenoses.
Although coronary arteriography is the central diagnostic tool of cardiovascular medicine, the limitations of coronary arteriography need to be recognized and new invasive technologies explored in order to advance our knowledge and improve clinical management of patients.
New knowledge about mechanisms of plaque rupture from heterogeneous diffuse coronary atherosclerosis and benefits of lipid lowering require revisions in our traditional use of cardiac catheterization and coronary arteriography. This new knowledge can be summarized as follows:
1. Eighty-five percent of myocardial infarctions develop at sites of relatively less severely narrowed, lipid-rich plaques that rupture with thrombosis and spasm.
2. Coronary atherosclerosis is diffuse and subject to plaque rupture throughout the length of the epicardial coronary artery.
3. The diagnostic accuracy of coronary arteriography for diffuse coronary atherosclerosis is poor, as low as 10% to 20%, compared with intracoronary ultrasound.
4. Recent trials raise serious questions about the value of arteriographic-based interventions, particularly the lack of improved survival, their failure to reduce myocardial infarctions, or the observed greater mortality and myocardial infarctions in revascularized patients compared with medically treated patients, as reported in the RITA-2, VANQWISH and AVERT Trials, in the Duke clinical database and in the Canadian experience.
5. Vigorous cholesterol lowering markedly reduces cardiac events and mortality more than invasive procedures that do not alter long-term survival or cardiovascular events
Relative to these observations, coronary arteriography is limited by two substantial failures. The first is the continuing visual assessment of stenosis severity despite repeated proof of the gross inaccuracy of this custom, especially when precise quantitative analysis is well-developed and widely available. The second is failure of coronary arteriography to identify and quantify diffuse disease, which accounts for plaque rupture and most coronary events without significant preexisting segmental stenoses.
The fundamental issue is the role of invasive, visually interpreted arteriographic lumenology for the study and management of the diffuse atherosclerotic process in the walls of the coronary arteries. Coronary atherosclerosis is diffuse not discrete. Its progression and outcomes arise from diffuse, continuous processes throughout the coronary tree. Quantifying its severity requires graded, multifaceted, continuous measurements of severity. Its treatment requires graded, multifaceted medical therapy. Revascularization decisions require documentation of lesion-specific physiological severity separate from and greater than the effects of diffuse disease underlying segmental stenoses. The traditional visual, binary thinking process for diagnosis and intervention focused on segmental stenoses and localized mechanical procedures is inappropriate. This new knowledge is the basis for a shift in the practical clinical thinking process for diagnosis and treatment from a binary, segmental, mechanical, viewpoint to a graded, continuous, quantitative orientation toward diffuse atherosclerosis, in which revascularization procedures are based on objective physiological measures of severity that separate segmental from diffuse narrowing.
The errors in visually interpreted coronary arteriogram are well-documented. Experienced arteriographers characteristically overestimate percent diameter narrowing by 30% to 60%. Even when objectively measured, percent diameter narrowing fails to account for the integrated hemodynamic effects of other stenosis dimensions, multiple stenoses in series, diffuse atherosclerotic narrowing, and endothelial-mediated vasomotor dysfunction, all of which have major effects on myocardial perfusion.
The problem of diffuse coronary artery disease is particularly important because it is commonly present but often unrecognized. Compared with intravascular ultrasound, the diagnostic sensitivity of visually interpreted coronary arteriograms for identifying diffuse coronary atherosclerosis ranges from as low as 7% to 43%, with a specificity of 95%. Thus, visual interpretations of coronary arteriograms severely underestimate mild or diffuse coronary atherosclerosis and overestimate severity of stenosis greater than 50% diameter narrowing.
Diffuse coronary disease without segmental narrowing not only
carries a high risk of plaque rupture, but it may also have profound
hemodynamic effects and cause ischemia. For
example, fluid dynamic analysis shows that 3 discrete 30% to
35% diameter stenoses in series have little effect on maximum
coronary flow capacity or coronary flow reserve
normally 
4 times baseline resting flow. However, a diffuse 30% to
35% narrowing along the length of a coronary artery reduces
its flow reserve from a normal of 4 times baseline flow levels to only
1.5 to 2 times baseline flow.
This effect of diffuse disease may be particularly important in determining whether PTCA improves arterial coronary flow capacity. For example, a segmental stenosis of 68% diameter stenosis combined with diffuse 35% diameter narrowing completely eliminates coronary flow reserve. The coronary flow reserve, or ratio of maximum flow to resting baseline flow, is therefore 1.0. Anatomically successful PTCA of the 68% stenosis in this circumstance will improve flow reserve to only 1.6, still severely reduced, due to the residual effects of the diffuse disease remaining after PTCA. However, diffuse regression along the entire length of the artery and only modest regression of the segmental stenoses, as expected after vigorous cholesterol lowering, will increase flow capacity substantially more than by PTCA, while reducing the risk of plaque rupture and coronary events.1
Thus, coronary arteriography as currently used is outmoded and inadequate for determining what stenoses require revascularization procedures, particularly in view of new clinical algorithms based on vigorous lipid and risk factor control as alternatives to invasive procedures for the primary treatment of coronary artery disease. From the perspective of having written the only other textbook on quantifying coronary artery stenosis arteriographically and physiologically,1 I am frequently appalled at the use, even misuse, of coronary arteriograms to justify financially rewarding procedures in patients who would be better served with vigorous medical management.
Standard coronary arteriography, as now visually interpreted in terms of localized percent stenoses, is a poor standard for assessing coronary atherosclerosis and is inferior to functional or physiological measures of severity that reflect the effects of diffuse disease, multiple stenosis, and endothelial mediated vasomotor function.
Intracoronary Doppler and pressure-sensitive guidewires provide measurements of coronary flow velocity and pressure with important insights into the physiological or functional effects of coronary artery disease in humans. The effects of diffuse and/or segmental narrowing on coronary pressure, flow velocity, and coronary flow reserve can be quantitated directly when measurements are made along the length of the artery or distal to stenoses. Distal measurements in the coronary arteries reflect the pressure-flow effects caused by cumulative segmental and diffuse disease proximal to the point of measurements.
For stenoses of intermediate severity, standard measures of arteriographic percent diameter narrowing are of little value in determining their functional severity or physiological significance. In patients with stenoses of intermediate anatomic severity, abnormal coronary flow reserve by distal Doppler wire correlates closely with abnormal stress perfusion defects, and normal coronary reserve correlates with normal stress perfusion images, despite similar arteriographic severity of stenoses in these two group of patients that fails to differentiate between them. The creative work from the laboratory of Morton Kern, and also Patrick Surreys, have confirmed in humans the fundamental concepts of coronary flow reserve as physiological measures of stenosis severity that were initially described experimentally. Furthermore, physiological-functional measures of severity have been shown to be highly effective in differentiating those who need revascularization procedures from those who do not need them independent of arteriographic severity.
The severity of coronary artery stenosis is quantified by the effects of its complete, integrated, geometric dimensions or by the pressure gradient-flow relation reflecting its fluid dynamic effects. Coronary flow reserve is related to or derived from complete geometric anatomy of a stenosis and its fluid dynamic characteristics. Thus, under conditions of maximum coronary vasodilation, flow measurement alone, expressed as coronary flow reserve without knowledge of stenosis geometry or pressure gradient, is a single, simplified, practical, and theoretically complete descriptor of functional severity that is scientifically sound, has been experimentally validated as equivalent to geometric or fluid dynamic analysis, and has been shown to be clinically applicable.
Although the pressure-flow characteristic of coronary artery stenoses have been well-defined, the role of intracoronary pressure measurements alone, analogous to flow reserve, has been missing until recent years. In their book, Coronary Pressure, Nico Pijls and Bernard DeBruyne fill this void by collating their major contributions in our understanding of the effects of coronary artery stenoses on coronary pressure. Their thorough, detailed experimental and clinical investigations complete the theoretical and practical framework of knowledge about the fluid dynamics of coronary artery narrowing which I began 28 years ago. Having worked with the authors and Richard Kirkeeide, my associate, in developing the conceptual basis for their approach, my reviewing this book is particularly rewarding due to its completeness, the symmetry of knowledge, and the fusion of anatomy and physiology of coronary artery narrowing we now have.
There is a direct relation between intracoronary pressure distal to a stenosis and its flow or flow reserve if coronary resistances remain constant as during maximum arteriolar vasodilation. Under these conditions of maximal arteriolar vasodilation, intracoronary pressure measurements distal to a stenosis alone are theoretically related to and experimentally correlate with coronary flow reserve, reflecting functional stenosis severity. The essential concept is that under conditions of maximum arteriolar vasodilation, intracoronary pressure measurements alone, distal to a stenosis, just as flow reserve measurements alone, reflect the integrated geometry and fluid dynamics of a stenotic coronary arterial system. A normal coronary artery or normal reference arterial distribution elsewhere in the heart is not necessary in this approach for determining relative coronary flow reserve based on pressure measurements under conditions of maximal coronary arteriolar vasodilation.
Maximum flow through a stenotic artery compared with maximum flow in an adjacent normal artery is called relative coronary flow reserve. Coronary flow reserve for a stenotic artery may also be expressed as a fraction of its normal expected value in that same artery in the absence of a stenosis, termed fractional flow reserve when derived from pressure measurements as Drs Pijls and DeBruyne have done.
Fractional flow reserve derived from intracoronary pressure measurements under conditions of maximal arteriolar vasodilation may be obtained just distal to a segmental stenosis and/or along the length of a coronary artery. Such measurements indicate the relative contribution to hemodynamic severity of diffuse and segmental coronary artery disease, thereby allowing differentiation of segmental from diffuse coronary disease for deciding on interventional decisions.
This superbly conceived and written book provides the complete theoretical, experimental, and clinical basis for coronary pressure measurements to assess the physiological severity of coronary artery disease. It is a creative synthesis of tremendous scope, from fluid dynamic equations to clinical trials, an example of the best of science in invasive cardiology.
This book is well-organized with a logical sequence from theoretical basis to experimental validation to clinical application. Peer reviewed literature is well integrated into the authors’ work. A chapter on clinical cases nicely illustrates the practical applications. The illustrations, layout and printing are well done, appropriate and easy to read.
I have only two small criticisms, made hesitantly because the book does so much so well. The first concerns the effects of myocardial steal after intravenous (systemic) adenosine or dipyridamole as opposed to subselective intracoronary injection of these vasodilators into the recipient collateralized bed. Although the authors deal with collateral physiology better than most other publications, their approach does not address this issue with the sophistication of which they are capable. The second criticism is their failure to develop how intracoronary pressure measurements continuously along the length of the coronary artery after adenosine or dipyridamole can in principal be used to quantify diffuse coronary artery narrowing separately from single or multiple segmental stenoses. However, by making measurements distal to specific stenoses, they do emphasize how to select specific stenoses for balloon angioplasty. Having discussed these issues with the authors, I suspect that they will fill in the small lacunae with additional reports.
However, more importantly, this book should be read by every cardiovascular physician, particularly invasive cardiologists, as part of their fundamental base of knowledge. No cardiologist can claim the sophistication required of a current or future invasivist without studying this book.
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References |
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TopIntroductionReferences |
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1. Gould LK. Coronary Artery Stenosis and Reversing Atherosclerosis. 2nd ed. London: Arnold Publishers; 1999.
3. The Weatherhead PET Center for Preventing and Reversing Atherosclerosis
4. University of Texas Medical School
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