(Circulation. 1995;92:2333-2342.)
© 1995 American Heart Association, Inc.
Articles |
Our Preoccupation With Coronary Luminology
The Dissociation Between Clinical and Angiographic Findings in Ischemic Heart Disease
From the Department of Cardiology and the Joseph J. Jacobs Center for Thrombosis and Vascular Biology, Cleveland Clinic Foundation, Cleveland, Ohio.
Correspondence to Eric J. Topol, MD, Department of Cardiology, Cleveland Clinic Foundation, 9500 Euclid Ave, Desk F25, Cleveland, Ohio 44195. E-mail internettopole@ccsmtp.ccf.org.
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Abstract |
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 Top Abstract IntroductionLimitations of Angiography Clinical Investigation Mechanisms and Implications References |
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Abstract Nearly 40 years after its invention, the angiogram is still considered by most physicians to be the "gold standard" for defining coronary anatomy. Careful investigations have revealed many deficiencies inherent in this approach. The purpose of this article is to outline the evidence that our current preoccupation with coronary "luminology" may be misguided and to propose a rational paradigm for future practice and investigation. Angiography depicts coronary anatomy from a planar two-dimensional silhouette of the lumen. Angiography is limited in resolution to four or five line pairs per millimeter. Confounding factors include vessel tortuosity, overlap of structures, and the effects of lumen shape. After intervention, a hazy, broadened silhouette may overestimate the actual gain in lumen size. Studies show marked disparity between the apparent severity of lesions and their physiological effects. After myocardial infarction, cardiologists too often do not make an attempt to demonstrate the physiological significance of the stenosis before performing percutaneous coronary revascularization. Similarly, the allure of a better, more gratifying angiogram with new interventional devices appears to be a dominant factor in their popularity. Interventional cardiologists should be aware that techniques yielding marked angiographic benefit may also generate important but unrecognized hazards. The dissociation between the angiogram and clinical outcome should influence future research efforts. Our review of the literature indicates that we may benefit from shifting the current focus and preoccupation with coronary luminology to achieving the desired clinical end point: promoting survival and long-term freedom from myocardial infarction and the disabling symptoms of coronary heart disease.
Key Words: angiography • myocardial infarction • atherosclerosis • revascularization • angioplasty
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Introduction |
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TopAbstractIntroductionLimitations of Angiography Clinical Investigation Mechanisms and Implications References |
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In 1957, Sones performed the first selective coronary angiogram, offering the first opportunity to visualize atherosclerotic coronary disease in vivo and heralding a new subspecialty of cardiovascular medicine.1 Today, nearly 40 years later, the angiogram is still considered the "gold standard" for definition of coronary anatomy. Cardiologists have increasingly relied on coronary angiography to guide both clinical practice and research, with more than a million procedures now performed annually in the United States.2 In recent years, many research studies, particularly in thrombolysis and intervention, have used computerized measurement techniques, a process known as quantitative coronary angiography. This practice has created an entirely new jargon with terms such as minimal luminal diameter, acute gain, late loss, and relative gain.3 4 5 Such indexes are now universally used to appraise new revascularization devices and evaluate treatments aimed at limiting restenosis.
Coronary angiography has had a profound impact on the diagnosis and management of ischemic heart disease, setting up the potential for both surgical and percutaneous coronary revascularization and the foundation for contemporary myocardial reperfusion therapy. The enormity of the significance of coronary angiography and how it has completely revamped cardiovascular medicine in the past four decades cannot be adequately emphasized. Although the value of coronary angiography remains unquestioned, radiographic imaging depicts the coronary artery as a simple two-dimensional projection of the lumen. Unfortunately, the silhouette or "luminogram" is a relatively poor representation of coronary anatomy and a limited standard on which to base therapeutic decisions. The purpose of this article is to outline the evidence that our current preoccupation with coronary luminology may be significantly misguided and to propose a rational paradigm for future clinical practice and investigation.
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Limitations of Angiography |
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TopAbstractIntroductionLimitations of Angiography Clinical Investigation Mechanisms and Implications References |
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As early as the 1960s, investigators began questioning the accuracy and reproducibility of coronary angiography.1 6 7 8 9 10 11 12 13 Initial studies established that visual interpretation exhibited clinically significant intraobserver and interobserver variability, with differences in the estimation of stenosis severity approaching 50%.6 7 Comparative studies reported major discrepancies between the apparent angiographic severity of lesions and postmortem histology,8 9 10 11 12 13 with angiography significantly underestimating the extent of atherosclerosis. More recently, using functional testing, investigators have focused on the discordance between angiographic lesion severity and the physiological effects of the stenosis.14 15
Observer Variability and Comparisons With Histology
Angiography depicts intricate coronary cross-sectional
anatomy from a planar two-dimensional silhouette of the
contrast-filled vessel lumen. However, both necropsy studies and
intravascular ultrasonography demonstrate that coronary lesions
are often complex, with markedly distorted or eccentric luminal shapes.
For a complicated coronary lesion, any arbitrary angle of view
may significantly misrepresent the extent of narrowing (Fig
1A
). Theoretically, two orthogonal angiograms should
accurately reflect the severity of most lesions. However, adequate
orthogonal views are frequently unobtainable because of
foreshortening, overlapping side branches, or disease at bifurcation
sites. Even when unlimited projections are available, the
angiographic silhouette cannot accurately depict certain complex
luminal shapes (Fig 1B).
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After intervention, the
limitations of projection imaging are
particularly problematic. Necropsy and intravascular
ultrasound studies demonstrate that mechanical interventions exaggerate
the extent of luminal eccentricity by fracturing or dissecting the
atheroma.16 The angiographic appearance of the
complex postinterventional vessel often consists of an enlarged,
although frequently "hazy," lumen. After extensive plaque
fracture, the hazy, broadened angiographic silhouette may overestimate
the true gain in lumen size (Fig 2). It is more
difficult for a computer program to accurately measure the angiographic
dimensions of the hazy, dissected luminogram to calculate the residual
diameter. Yet, this is precisely how most clinical studies in the 1990s
assess the efficacy of new interventional devices.
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The traditional
method for characterizing angiographic lesion severity
relies on measurement of the percent stenosis. This process
requires comparison of dimensions within both the lesion and an
adjacent, uninvolved "normal" reference segment. However,
necropsy studies demonstrate that coronary disease is
frequently diffuse and contains no truly normal
segment.9 10 12 In the presence of
diffuse disease,
calculation of the angiographic percent stenosis will
predictably underestimate disease severity (Fig 3). In
extreme circumstances, diffuse, concentric, and symmetrical disease
involving the entire vessel will result in the angiographic appearance
of a small but normal artery.
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Angiography is often confounded by the
phenomenon of coronary
"remodeling," first described in 1987 by Glagov et
al17 (Fig 4). The remodeling process is
observed histologically as the outward displacement of
the external vessel wall overlying the atheroma. The
adventitial enlargement opposes luminal encroachment, thereby
concealing the presence of disease. Although remodeled lesions do not
restrict blood flow, clinical studies have demonstrated that these
low-grade lesions represent the most important source for
acute coronary syndromes.18 Recently, we reported
that such atheromas are virtually always present in
ergonovine-positive patients with a "normal"
angiogram.19
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Physical Limits of Angiography
The resolution of modern
angiographic equipment is surprisingly
modest.20 The best image intensifiers can resolve only
about four or five line pairs per millimeter, often somewhat less with
aging equipment. Prudence limits radiation doses to about 25 µR per
frame, exacerbating an image flaw known as "quantum statistical
noise." Quantum noise is an unyielding source of image degradation
that can be attenuated only by increasing radiation doses to
unacceptable levels. Because of these limits, structural features
smaller than about 0.2 mm are invisible to the angiographer. Notably,
important features fall within this size limit, including
intracoronary thrombi and small focal calcifications.
Angiographic resolution is further degraded by rapid coronary artery motion.20 The velocity of the right coronary artery can reach 50 mm/s. Although pulse-mode radiation "freezes" coronary motion, the shortness of each pulse is limited by thermal loading of the x-ray tube and the need for a small "focal spot." Adequate exposure in a large patient typically yields pulse durations of 4 to 7 ms, which may rise to 10 ms for compound angles. A coronary artery moving at 50 mm/s will produce a motion blur of 0.50 mm during a 10-ms pulse width. This indistinct border confounds the usual measures of stenosis severity.
Complexity of Coronary Anatomy
Coronary arteries
characteristically follow a serpiginous
path with complex curvatures, sharp bends, and unpredictable twists and
turns. Angiography depicts lesions in tortuous vessels correctly only
when the x-ray beam is orthogonal to the vessel. Optimal
angiography requires two "triple orthogonal views," defined as a
pair of projections orthogonal both to each other and to the
vessel.21 However, the angiographer possesses no certain
means to achieve orthogonality. Accordingly, current practice typically
consists of imaging at a variety of angles to find the optimal
projection: one that yields the "minimum" diameter.
Unfortunately, this empirical process is limited by factors including
toxicity of contrast agents, radiation exposure, and operator patience.
Experienced angiographers are aware that, despite meticulous imaging in
multiple views, some lesions may be evident only in a few frames.
The
left main coronary artery (LMCA) represents a
particularly troublesome site for angiographic
imaging.11 22 23 The LMCA is often short
and overlaps
other structures, providing a limited opportunity to identify a normal
reference segment (Fig 5). Detection of ostial LMCA
disease is confounded by the tendency for catheters to "seat"
beyond the lesion, requiring reflux of contrast into the aorta for
adequate visualization. Unfortunately, refluxing contrast fills the
aortic cusp, which may obscure the lesion. The distal LMCA is often
obscured by the confluence of shadows from the overlapping left
anterior descending, left circumflex, and ramus medianus arteries.
Other coronary bifurcations present comparable
difficulties, because superimposition of the parent and daughter often
partially obscures the bifurcation (Fig 6). Almost
diabolically, atherosclerosis exhibits a predilection
for bifurcation sites. Thus, the segments most difficult to image are
often the sites with the most significant disease.
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Problem of Coronary Flow Reserve
In chronic ischemic coronary
disease, symptoms
result principally from the ability of stenoses to blunt
increases in blood flow in response to metabolic demands.
This phenomenon, originally described by Gould et al in the
1970s,24 is commonly called coronary flow reserve
(CFR).24 25 Determination of CFR requires measurement
of
blood flow at rest and after induction of reactive hyperemia,
usually by administration of a coronary vasodilator. Animal and
human studies have documented that a normal CFR, in the absence of
epicardial stenoses, should exceed 
5:1 (ratio of
hyperemic to basal flow). Several methods for measurement of
CFR in patients were developed during the 1980s and 1990s, including
intracoronary Doppler flow probes, digital angiography,
and quantitative positron emission
tomography.14 15 25 26
Each of these approaches has documented major discrepancies between the
apparent angiographic severity of coronary lesions and their
physiological effects. Animal studies demonstrate
that flow reserve remains normal (typically a 5:1 to 7:1 ratio) until
the stenosis severity approaches 75%. Between 75% and 95%,
CFR falls progressively to reach values approaching a 1:1 ratio.
Accordingly, the angiographic differences between moderate and severe
lesions may be only a few tenths of a millimeter. Such differences are
difficult to discern, given the limitations in angiographic resolution,
the confounding effects of projection angles, the irregularity of
luminal shape, and the impact of diffuse disease. Other factors further
weaken the correlation between angiography and flow reserve, including
the presence of ventricular hypertrophy, the
metabolic state of the myocardium, and
microvascular disease. Thus, the epicardial stenosis
represents only one factor responsible for a reduction in flow
reserve in patients with clinical symptoms. Accordingly, a
stenosis incapable of producing angina in one patient may
result in severe functional limitation in another.
Quantitative Angiography: The Emperor Without
Clothes
Originally described by Brown et al27 in the late
1970s, quantitative coronary angiography (QCA) was intended to
replace the "eyeball" interpretation of the angiogram with an
objective, computer-based method. Proponents believed that the
failings of the angiogram originated principally from arbitrary, visual
inspection. Initial studies demonstrated that computerized
determination of vessel borders was highly reproducible, enabling
serial measurements of angiograms without significant intraobserver or
interobserver variability. Accordingly, QCA gradually became the
standard for evaluating the effects of thrombolysis, new
interventional devices, and regression or progression of
atherosclerosis. A whole new industry developed, fueled
by clinical trials, in which self-described "core
laboratories" measured luminograms at $100 to $400 per patient and
reported the luminal size in hundredths of a millimeter.
Eventually,
the proponents of QCA confused reproducibility with
accuracy. In reality, QCA possesses virtually all of the limitations of
conventional interpretation methods. No matter how precisely measured,
the luminogram of a complex, cloverleaf–shaped lesion or the
silhouette of dissected, "hazy" atheroma poorly
represents the actual lumen size (Figs 1
and 2).
Intraluminal
filling defects from thrombus (Fig 7, left) or the
absence of a disease-free reference segment (Fig 7, right)
confound
the analysis. QCA cannot distinguish the relative narrowing of
a diffusely diseased vessel or accurately quantify LMCA or bifurcation
lesions with overlapping contrast-containing structures (Figs 3 through
6).
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Published studies showing the excellent reproducibility of QCA bear little resemblance to the clinical situation.28 Generally, these validation studies presented the computer operator with carefully chosen, optimally opacified frames from preselected projections. The performance of QCA in clinical practice is confounded by a staggering array of variables. A recent analysis by Keane et al29 of 10 core QCA laboratories showed marked variability between laboratories for the straightforward quantification of phantom stenoses. Previously, we reported that when observers were permitted to select from available projections and frames, the variability of computer-analyzed angiography approached that of visual inspection.28 Many experienced angiographers believe that visual assessment of stenoses should always be performed on moving images to integrate the interpretation over many frames. No quantitative angiographic program can perform this function.
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Clinical Investigation |
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TopAbstractIntroductionLimitations of Angiography Clinical Investigation Mechanisms and Implications References |
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The described theoretical and practical limitations of angiography have been confirmed through clinical trials of thrombolysis, angioplasty devices, and restenosis. Studies demonstrate that angiography cannot predict which patients will require angioplasty after thrombolysis,30 31 32 33 34 35 36 cannot reliably identify the patients who benefit from new interventional devices, and cannot identify those patients likely to undergo plaque rupture. These studies must remind us of the hazards of formulating clinical decisions principally or solely on the basis of the angiographic appearance of lesions.
Acute Myocardial Infarction: The Oculostenotic
Reflex
The first randomized trials in interventional
cardiology were performed in the setting of acute
myocardial infarction. The Thrombolysis and Angioplasty in
Myocardial Infarction (TAMI-1) trial, published in 1987, demonstrated
that angioplasty was unnecessary and potentially deleterious after
successful thrombolysis.30 Subsequent trials
corroborated this finding, confirming that the severity of the residual
stenosis after thrombolysis poorly predicts
recurrent ischemia or
reocclusion.31 32 33 34 35 36
A vivid
demonstration of this dissociation occurs with the
"no-reflow" phenomenon, in which the epicardial lumen appears
adequate but contrast echocardiography shows no
tissue perfusion.37 Accordingly, before the residual
stenosis in an infarct vessel is addressed, there should be
demonstration of either spontaneous or provocable signs of
ischemia.30 31 32 33 34 35 36
However, nearly a decade later,
this finding has not been fully integrated into clinical practice.
The term "oculostenotic" reflex was coined to denote what appears to be an irresistible temptation among some invasive cardiologists to perform angioplasty on any significant residual stenosis after thrombolysis.38 Although this approach is not supported by the American College of Cardiology and American Heart Association guidelines,39 the ritual of reflex angioplasty is exercised thousands of times each year. Systematic functional assessment in patients after successful reperfusion suggests that fewer than half will have objective evidence of provocable ischemia.40 Importantly, a randomized trial of patients with a negative functional test but a significant infarct vessel stenosis demonstrated worse outcome in the group assigned to angioplasty.41
However, despite data to contrary, it remains the overriding belief of some invasive cardiologists that the residual stenosis must be alleviated to favorably affect the prognosis. Recent data from the GUSTO trial (United States patients) and a National Registry of Myocardial Infarction indicate that more than 40% of patients undergo angioplasty after receiving thrombolytic therapy.42 43 Unfortunately, in a large number of these patients, functional assessment is not performed. A large insurance claims database revealed that, in the late 1980s, only 9% of patients with recent myocardial infarction underwent exercise testing before coronary intervention.44
Directional Atherectomy: Angiographic Gratification
Introduced in the United States in late 1990, directional
coronary atherectomy (DCA) generated considerable excitement
for its potential to remove (debulk) coronary
atheromata.45 Registry data, which led to
commercial approval, supported a high procedural success rate, with a
complication rate similar to that of historical balloon angioplasty
controls.46 DCA quickly became popular, constituting
nearly 15% of the procedures performed in the United States in 1992.
However, in 1993, the results of the Coronary Angioplasty
Versus Excisional Atherectomy Trial (CAVEAT) yielded surprising
results.47 Compared with balloon angioplasty, atherectomy
induced more significant complications, particularly non–Q-wave
infarction (twofold risk) and abrupt vessel closure. At 6 months, there
were higher rates of death and nonfatal myocardial infarction, and at 1
year, a persistently higher mortality rate in patients assigned to
atherectomy.47 48 There was no reduction in repeat
revascularization and minimal evidence of reduced
angiographic restenosis.
Taken as a whole, these findings provide little support for widespread application of directional atherectomy. However, in the United States, the overall use of directional atherectomy was 15% of percutaneous coronary revascularization procedures before this trial and remained 15% in 1994. Thus, negative data from a large, multicenter effort, conducted by experienced operators, had little to no effect on the frequency of use of atherectomy. Although other explanations are possible, the dominant factor sustaining the use of this procedure appears to be "angiographic gratification," the allure of a better, more gratifying angiographic image after atherectomy. Early in the development of directional atherectomy, studies showed that debulking of plaque resulted in improved luminal caliber compared with balloon dilatation.49 This difference in lumen size between atherectomy and angioplasty was validated in the CAVEAT and Canadian Coronary Atherectomy Trial (CCAT).47 50
On the basis of lumen size data in atherectomy patients and related findings from nonrandomized balloon angioplasty registries, the "bigger is better" paradigm was introduced. This concept refers to the theory that a larger luminogram attained by intervention will invariably result in better angiographic and clinical outcomes.4 5 However, for DCA, the bigger is better hypothesis remains unproven, and a randomized trial of balloon versus optimal atherectomy (BOAT) is currently in progress. Nevertheless, in CAVEAT, the angiographic outcome at 6 months was marginally improved, but paradoxically, death and non–Q-wave myocardial infarction were increased in patients with a larger lumen achieved via atherectomy.47 Recently, proponents of a bigger luminogram have focused so narrowly on lumen size that clinical end points may be disregarded. This phenomenon is exemplified by a recent matched-pair study of patients undergoing atherectomy or angioplasty in which the authors failed to report on any clinical outcomes.51 Interestingly, the inattention to atherectomy-related complications appears confined to the United States; outside this country, fewer than 3% of patients having percutaneous interventions undergo directional atherectomy.
Stents: A Critical Reappraisal
In contrast to atherectomy,
two randomized comparisons with
balloon angioplasty demonstrated that the Palmaz-Schatz
coronary stent reduced angiographic
restenosis.52 53 Like DCA, the cardinal
feature stimulating the growth of stenting is greater improvement in
the coronary luminogram. Compared with balloon angioplasty,
patients randomized to stenting had a 30% greater improvement in
initial lumen caliber, although there was attrition of the benefit over
time. Unlike atherectomy, angiographic gratification, in the case of
stenting, appears to be associated with enhanced durability and reduced
recurrence rates. However, the margin of benefit appeared to
narrow after a protocol-mandated angiogram after 6
months.52 53 54 Stents were commercially
approved for
elective coronary revascularization in
August 1994, and their use has catapulted rapidly, with estimates that
by 1996, nearly 50% of interventions will involve stenting rather than
balloon angioplasty.53A
Superficially, these trials support the concept that bigger is better, but disquieting concerns remain. At 6 months, luminal diameter showed a relatively small, and in one trial statistically insignificant, advantage for stenting.52 The stent trials reported increased complications and costs, thus exchanging a slightly more gratifying luminogram for potentially serious immediate risks of hemorrhage and prolonged hospitalization.52 53 54 To avoid intensive anticoagulation, research is presently directed toward optimization of deployment via high-pressure inflations, ultrasound guidance, or both.55 56 57 However, the long-term risks of a permanent endovascular prosthesis remain unknown in patients with de novo lesions. Of potentially greater concern, the desire to optimize the lumen size has increased application of stenting in patient groups not yet fully studied or approved by the Food and Drug Administration. These include patients with restenosis or saphenous vein graft disease. While coronary stenting for a variety of patient and lesion subsets may indeed prove beneficial, it remains unwarranted to extrapolate excessively from short-term angiographic studies in patients with new native-vessel lesions.
Restenosis Trials
Critical review of pharmacological and
device trials to reduce
restenosis reveals marked differences between the
angiographic and clinical results (Table
1).47 52 53 58 59 60 61
In CAVEAT,47
compared with balloon angioplasty, atherectomy patients showed
the same extent of diameter improvement as produced by stenting in the
BENESTENT trial. However, only the latter trial demonstrated a
significant difference in clinical outcome. In a study of nitric oxide
donors,58 angiographic measurements showed less
restenosis at 6-month follow-up but no change in the
need for repeat revascularization. A trial of
angiopeptin,59 a somatostatin-like growth factor
inhibitor, showed no measurable angiographic benefit but
significant improvement in clinical results. Directional atherectomy in
saphenous vein graft disease61 produced angiographic
benefits similar to those of CAVEAT but a significant reduction of
repeat revascularization at 6
months.47 61 These trials dramatically exemplify the
lack
of correlation between the luminogram and clinical results.
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Atherosclerosis Regression and Plaque
Rupture
Atherosclerosis regression studies provide a
salient example of the dissociation between angiography and clinical
outcomes. Nine multicenter, randomized lipid-lowering trials using
both angiographic and clinical assessment showed a negligible
improvement of luminal caliber, typically an absolute difference of
only 1% to 3%. Yet these same studies yielded a staggering 25% to
75% reduction in acute events, including myocardial
infarction.62 63 64 Thus, the differences
between
angiographic and clinical end points exceed an order of
magnitude. Although in the 1960s and 1970s most authorities
believed that the tightest stenoses would most likely progress
to occlusion, subsequent clinical studies have established that acute
syndromes are most commonly produced by rupture of minor
plaques.65 66 67 Thus, it appears that
the benefits of
lipid-lowering therapy are derived by stabilization of these
low-grade, lipid-rich plaques, not changes in angiographic
lumen size.
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Mechanisms and Implications |
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TopAbstractIntroductionLimitations of Angiography Clinical Investigation Mechanisms and Implications References |
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What are the explanations for the apparent dissociation between angiographic and clinical outcomes in thrombolytic and interventional trials? A full understanding remains uncertain, but several factors appear important, including the requirement for repeat coronary angiography in asymptomatic patients, potentially triggering an oculostenotic reflex. Other factors include injury to the microcirculation or myocardial damage, which may reduce the clinical significance of a flow-limiting stenosis supplying an infarcted segment. Alternatively, partial or complete denervation may suppress symptoms.68
Insights From Intravascular Ultrasound
Coronary intravascular
ultrasound provides valuable
insights into the mechanisms underlying the dissociation between
angiographic and clinical outcomes. Studies have compared ultrasound
and angiographic dimensions in vivo, examining truly normal vessels,
arteries with angiographically occult disease, and coronary
lesions before and after intervention.69 These comparisons
show that the two imaging modalities correlate closely in undiseased
vessels with a nearly circular lumen shape. However, as the lumen
becomes progressively more irregular, the correlation between a
silhouette imaging method (angiography) and a tomographic modality
(ultrasound) diverges significantly.70 71 These
differences are most profound in imaging of postinterventional arteries
with a dissected atheroma or otherwise distorted luminal
shape. In such vessels, the reported correlation between angiography
and ultrasound lumen size is
r=.30.72 73
Fundamentally, angiography cannot accurately depict the true size of
the complex luminal shapes commonly encountered after
interventions.
The disparity between angiographic and ultrasound
dimensions after
interventions creates important paradoxes. A "suboptimal"
angiographic silhouette may result from an intervention that yields a
relatively round and smooth but moderate-sized lumen (Fig 8,
left). However, this modest lumen may have a
cross-sectional area that is actually larger than a vessel with a
"better" angiographic result in which the lumen gain was derived
from complex cracks or splits in the atheroma (Fig 8,
right). A recent analysis of patients undergoing balloon
angioplasty, directional atherectomy, or rotational ablation confirmed
this phenomenon.74 The disparity between angiographic and
ultrasound lumen sizes varied considerably for different interventional
devices and paralleled the degree of irregularity of lumen
shape. Importantly, a complex or irregular lumen will produce greater
flow resistance than a circular lumen, which may explain why some
patients have continued symptoms despite an optimal angiographic result
(Fig 8).
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Other phenomena observed by intravascular
ultrasound may help explain
the results of several of the cited clinical trials. The lumen shape by
ultrasound after directional atherectomy is surprisingly irregular,
with deep cuts or grooves in the plaque or fronds of material extending
into the lumen (Fig 9).75 76 These
surface
irregularities are invisible to the angiographer but may facilitate
thrombus formation or embolization, which may explain the high
incidence of acute events after DCA. Ultrasound also shows many
casualties of the dogmatic "bigger is better" philosophy. Fig
10 shows two examples of deep and extensive injury
arising from overly aggressive attempts to enlarge the lumen with
directional atherectomy. Although unproven, it is possible that such
severely injured arteries will be maximally stimulated to develop
severe neointimal hyperplasia.
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Intravascular ultrasound provides a useful perspective on the inability of angiography to predict untoward clinical events. Ultrasound commonly reveals atherosclerosis at coronary sites without any disease apparent by angiography.71 Because low-grade plaques are clearly implicated in acute coronary events, the extent of unrecognized atherosclerosis may determine the prognosis, not the degree of enlargement on the luminogram at the interventional site.
Laboratory Surrogates in Clinical
Cardiology
On the basis of the findings of clinical trials and
intravascular
ultrasound, we can now add angiography to the list of
diagnostic procedures in which surrogate end points have
failed to predict clinical outcome (Table 2). Examples
include suppression of premature ventricular contractions
with antiarrhythmic agents,77 improving the
hemodynamics in heart failure to promote
longevity,78 and using the activated partial
thromboplastin time to ensure optimal anticoagulation in
thrombolysis.79 In each of these cases, use of
a laboratory surrogate seemed intuitively reasonable but was
subsequently proved by randomized trials to be incorrect and dangerous.
In each case, the false impressions arising from overinterpretation of
a laboratory test or measurement generated a therapeutic backfire, in
which mortality was paradoxically increased. These observations
emphasize the importance of avoiding the precocious reliance on any
untested laboratory parameter as a true surrogate for
clinical outcome. For example, if a larger coronary lumen after
stenting correlates with improved long-term clinical outcomes, this
finding does not necessarily translate to rotational ablation or
directional atherectomy.
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Effects on Clinical Investigation
The dissociation between
the angiogram and clinical outcome should
influence future research efforts. Clinical trials must be large enough
to retain the statistical power to differentiate clinical outcomes, not
only a surrogate end point such as angiographic lumen size. Ideally,
important clinical trials should incorporate a mechanistic substudy to
determine the linkage between clinical and laboratory end points. This
approach aided the Global Utilization of Streptokinase and Tissue
Plasminogen Activator in Occluded
Coronary Arteries (GUSTO-I) trial, in which an angiographic
substudy in 2431 of the 41 021 enrolled patients demonstrated the
pivotal relationship between the 90-minute patency and 30-day
mortality.80 81 82 Similarly, restenosis
trials
currently evaluating platelet glycoprotein IIb/IIIa
inhibitors will include a 6-month angiogram in 900 of the
4000 to 5000 patients.83 The design of these substudies
preempts the possibility that follow-up angiography per se will
drive repeat revascularization procedures but
permits objective validation of angiographic indexes of the clinical
outcomes.
In addition to closely tracking clinical end points, future trials of restenosis and new interventional devices should not rely exclusively on measurements obtained from an angiographic silhouette.84 85 Intravascular ultrasound dimensions are frequently divergent from quantitative angiographic measurements, whereas the tomographic perspective of ultrasound provides unique insights into the mechanism, shape, and extent of lumen enlargement. Ultrasound has important limitations, too, including its inability to characterize thrombus, artifactual distension of the lumen via the catheter, lack of accessibility for distal lesions and tortuous vessels, nonuniform rotational distortion, nonorthogonal positioning, and cost. Nevertheless, future trials of restenosis and new revascularization devices should consider the use of ultrasound or a suitable alternative that provides full interrogation of the diseased vessel wall. Similarly, trials of atherosclerosis regression should include assessment of the vessel wall to identify not just the magnitude but also the mechanism by which the tested agent reduces the frequency of clinical events.84 85
Implications for Clinical Practice
Examples demonstrate that
miscues can arise when clinicians and
investigators rely excessively on angiography for clinical
decision-making. How should we incorporate this knowledge into
clinical practice? Procedures should not be performed solely to improve
the luminal appearance—so-called coronary
"cosmetology." Operators should exercise restraint in selecting
specific devices because they provide a more gratifying angiogram,
particularly if there is no clear documentation of a clinical
advantage. Interventional cardiologists need to be aware that
techniques yielding marked angiographic benefit may also generate
important but initially unrecognized hazards. This appreciation of the
limitations and boundaries of angiographic data may help switch our
focus from the current preoccupation with coronary luminology
to that of achieving the desired clinical end point promoting survival
and long-term freedom from myocardial infarction and the disabling
symptoms of ischemic heart disease.
Received February 13, 1995; revision received April 19, 1995; accepted May 10, 1995.
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