(Circulation. 1995;91:2319-2324.)
© 1995 American Heart Association, Inc.
Articles |
Angiographic Stenosis Progression and Coronary Events in Patients With `Stabilized' Unstable Angina
From the Coronary Artery Disease Research Group, Department of Cardiological Sciences, St George's Hospital Medical School, London, England.
Correspondence to Dr Juan Carlos Kaski, Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK.
 |
Abstract |
|---|
 Top Abstract IntroductionMethods Results Discussion References |
|---|
Background Recent studies suggest that angiographically complex coronary stenoses are associated with an adverse short-term outcome. It is not known, however, if this applies to unstable angina patients who stabilize on medical therapy.
Methods and Results We prospectively studied 85 consecutive
patients with unstable angina who stabilized on medical therapy but
were found to require angioplasty for treatment of obstructive coronary
disease. Angiography was carried out at admission, and patients were
restudied 8±4 months (mean±SD) after the first angiogram.
Ischemia-related stenoses were identified and classified as
"complex" (irregular borders, overhanging edges, or thrombus) or
"smooth" (absence of complex features). Stenosis progression
(
20% diameter reduction or new total occlusion) was assessed by
automated edge detection. At initial angiography, there were 198
stenoses (50%, 102), of which 85 (54 complex and 31 smooth) were
ischemia related. At restudy, 21 ischemia-related stenoses and 8
non–ischemia-related stenoses progressed (25% versus 7%,
P=.001). Seventeen of the 21 ischemia-related stenoses that
progressed developed into total occlusion compared with 3 of the 8
non–ischemia-related stenoses (P=.02). Changes in
average
stenosis severity and in absolute stenosis diameter were significantly
larger in ischemia-related stenoses than in non–ischemia-related
stenoses (P=.03). Eighteen (34%) complex stenoses
progressed, compared with 3 (10%) smooth lesions (P=.02).
During follow-up, 1 patient died (myocardial infarction) and 25
patients had nonfatal coronary events that were associated with
progression of ischemia-related stenoses in 14 (56%).
Conclusions In unstable angina patients who stabilize medically, subsequent short-term stenosis progression and coronary events are common. The unstable coronary lesion (particularly complex stenoses) is often not stabilized and will continue to progress over the ensuing months.
Key Words: angina • coronary disease • ischemia • stenosis • angiography
|
Introduction |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Unstable angina is a clinical indicator that coronary disease has progressed.1 Stenosis progression is largely due to plaque rupture and intracoronary thrombosis, which lead to intermittent vessel occlusion.2 3 4 5 6 7 8 Recent studies have also shown that in patients with unstable angina, angiographic stenosis complexity predicts subsequent in-hospital instability.5 8 However, because it is customary in unstable angina to rapidly intervene with percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass surgery (CABG) when significant disease is demonstrated, the natural history of unstable coronary lesions is largely undetermined, and the prognostic implications of angiographic morphology remain speculative in this setting. In particular, it is not known whether complex stenosis morphology is a predictor of poor outcome in patients who present with unstable angina but are stabilized on conventional medical therapy.
Recognition of clinical and angiographic markers of an early unfavorable course may be of value in defining management strategies in unstable angina. In the present study, we prospectively assessed short-term angiographic disease progression and outcome in consecutive patients who presented with unstable angina that stabilized with medical therapy but required elective PTCA for management of obstructive coronary disease.
|
Methods |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Patient Selection
From July 1991 to March 1993, 877 consecutive patients were admitted to our hospital with the diagnosis of unstable angina; of these, 424 underwent coronary angiography during admission. Of the patients who underwent angiography, 322 were either referred for urgent revascularization (PTCA in 126, CABG in 106) or treated conservatively (n=90). One hundred two (24%) were put on a waiting list for elective PTCA and formed the study group. These were patients who stabilized on conventional medication and had angiographically significant stenoses (
50%, 
95%). Inclusion criteria were (1) diagnosis of unstable
angina with transient ischemic ECG changes recorded in the coronary
care or emergency units, (2) rapid stabilization of symptoms and ECG
changes after administration of antianginal agents heparin and aspirin,
(3) angiogram performed after stabilization showing significant
coronary artery disease with a stenosis in at least one major coronary
vessel, and (4) patients who were considered candidates for elective
PTCA by the treating cardiologist and were on a waiting list for this
purpose.
Exclusion criteria were (1) urgent PTCA after diagnostic
angiography,
(2) previous PTCA or bypass surgery, (3) progression to myocardial
infarction during admission (enzyme elevation to twice normal or
presence of new Q waves, or both) or lack of clinical stabilization,
(4) clinically significant valvular heart disease, serious conduction
disturbance, heart failure, or significant arrhythmia, and (5) age 75
years old.
Seventeen (17%) of these 102 patients were subsequently excluded for the following reasons: 6 had poor-quality coronary angiograms that precluded accurate qualitative and quantitative assessment; 2 refused further invasive procedures; and the ischemia-producing artery or ischemia-related stenosis was not identifiable in the remaining 9 patients. Thus, 85 patients constituted the study population.
The clinical criteria for the diagnosis of unstable angina were (1) recent onset of angina at rest or with minimal exertion, (2) rapid and marked deterioration of chronic stable angina, and (3) recurrent episodes of angina at rest. In every patient, medical stabilization of angina was achieved with a standard medical regimen of intravenous nitroglycerin, ß-blocking agents, aspirin, and heparin. After diagnostic arteriography (within 10 days of admission), all 85 patients were put on a waiting list for elective PTCA and followed up regularly. All patients remained on antianginal medication, which was not standardized but left to the discretion of the attending cardiologist.
Angiographic Analysis
Coronary Arteriography
All patients (except 1, who died of acute myocardial infarction
before repeat angiography) underwent two coronary arteriograms as part
of their clinical evaluation. The first was the diagnostic angiogram,
performed at initial admission. The second was performed immediately
before PTCA in 59 patients or soon (8±15 days) after a coronary event
in the remaining 25 patients. Of these, 12 required urgent PTCA and 10
required bypass surgery after the acute events. The time interval
between the diagnostic and follow-up angiograms was 8±4 months
(mean±SD; range, 2 to 14 months).
Quantitative
Assessment
The initial arteriography was carried out using
standardized
projections. Coronary artery stenoses were quantitatively assessed by
two independent observers blinded to the identity and clinical
characteristics of the patients. A stenosis 50% diameter reduction
was considered significant, and a lesion <50% was considered mild. A
segment with a stenosis <25% was interpreted visually and not
included in analysis. Multivessel coronary artery disease was
defined as significant two- or three-vessel disease. The Coronary
Angiography Analysis System (CAAS), Pie Data Medical, developed by
Reiber et al9 and extensively
validated,10 11
was used to measure percent stenosis and absolute minimal stenosis
diameter. Our technique to measure coronary artery diameters using CAAS
has been reported in detail previously.12 13 The stem
of
the Judkins coronary catheter was used for calibration to determine
absolute measurements in millimeters, and correction was made for
radiographic pincushion distortion. For each segment, measurements were
carried out on end-diastolic frames, where severity of the
stenoses appeared maximal. Orthogonal views were not measured and
averaged because it is accepted that measurement of the view showing
the stenosis at its most severe is sufficient.11 Percent
diameter reduction of a coronary stenosis was calculated based on the
diameter of the stenosis at its most severe; the diameter of the
reference segment (an angiographically normal segment proximal to the
lesion) was measured in millimeters. The following formula was used: %
diameter reduction=([diameter of reference segment-diameter
of
stenosis]/diameter of reference segment]x100).
Qualitative Assessment
The morphology of all
coronary artery stenoses 50% was
assessed visually by two experienced observers blinded to the identity
and clinical characteristics of the patients. All significant stenoses
were assessed selectively, viewed in two orthogonal projections, and
classified as "complex" or "smooth." Stenoses
classified as
complex were lesions with overhanging edges, irregular borders, and/or
showing ulceration or thrombus; stenoses classified as smooth were
lesions with smooth edges with no "complex"
features.14 15 Angiographic morphology was scored
independently, and if discrepancies arose, a third observer joined the
judgment, and the stenosis morphology was classified by consensus.
Interobserver agreement of qualitative morphological analyses of all
significant stenoses was 94%. No attempt was made to classify stenoses
<50% (mild stenoses).
Disease Progression
Accepted criteria16 17 were used to define
disease
progression: (1) 20% diameter reduction of a preexisting stenosis or
(2) progression of any lesion to total occlusion at restudy. Regression
was defined as reduction of stenosis severity 20%.
A coronary
stenosis was defined as "new" when a localized
narrowing 30% arose in a segment that was angiographically normal at
baseline angiography.
Ischemia-Related Stenoses
At first angiography, the
ischemia-producing coronary artery was
identified in every patient.4 8 In the 52 patients
with
single-vessel disease, the vessel with a stenosis 50% obstruction
was designated as the ischemia-producing artery. Of the remaining 33
patients with multivessel disease, the ischemia-producing artery was
identified according to transient ST-segment changes on a 12-lead ECG
obtained during angina attacks in 25 patients. In 8 patients, the
ischemia-producing artery could not be defined with certainty from the
ECG. In these patients, the ischemia-producing artery was considered to
be the one supplying the myocardial region that showed reversible
perfusion defects as assessed by thallium scan. In 7 patients (4 with
single-vessel disease and 3 with multivessel disease) with two or more
significant narrowings in the ischemia-producing artery, the most
severe lesion or the lesion that represented the indication
for angioplasty was assumed to be the ischemia-related stenosis.
Coronary Events
Coronary events during follow-up were defined
as (1) worsening
angina or angina at rest that resulted in emergency admission of the
patient to the hospital for stabilization or (2) myocardial infarction
as defined earlier.
Statistical Analysis
Within-lesion differences between first
and repeat angiograms
were compared with use of the paired t test. Student's
t test for unpaired data was used to compare differences
between lesions. Differences in frequency distribution between groups
were determined by using 
2 analysis with
Yates' correction. Data were expressed as mean values±SD unless
specified. Significance was defined as probability less than .05.
|
Results |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Clinical and Angiographic Findings and Disease Progression
Clinical features and angiographic characteristics in the 85 patients included in the study are shown in Table 1
and
Table 2, respectively. One patient died of acute
myocardial infarction before repeat angiography, therefore results on
disease progression refer to the remaining 84 patients. The study group
consisted of 68 men and 17 women with a mean age of 56±10 years
(range, 34 to 72) at initial coronary arteriography. At admission, 19
patients presented with new-onset angina, 29 with crescendo angina,
and 37 with rest angina. At first angiography, 52 patients (61%) had
single-vessel disease and 33 (39%) had multivessel disease. There were
24 totally occluded vessels (in 23 patients) and 198 stenoses (2.6
lesions per patient); of these, 102 were 50% and 96 were <50%
diameter reduction. Mean percent stenosis and absolute stenosis
diameter of all lesions at study entry (excluding the 24 preexisting
total occlusions) ranged from 25% to 83% and 0.56 mm to 3.43 mm
(1.55±0.64 mm), respectively (Table 2).
|
|
At
restudy, 29 preexisting stenoses progressed and six new lesions
(range, 31% to 100%) developed in 28 patients. Three lesions
regressed. Comparison of the profiles of patients with or without
disease progression revealed no significant difference in patient age
or sex, conventional risk factors for coronary artery disease, number
of diseased vessels, history of myocardial infarction, or antianginal
medications (Table 1
). Stenoses 50% progressed more
frequently than
stenoses <50% (23 [23%] versus 6 [6%],
P<.001).
Progression to total occlusion occurred in 18 lesions 50% and in 2
lesions <50% (P=.0006), whereas the number of lesions that
showed nonocclusive progression was similar in lesions 50% and
lesions <50% (5 [5%] versus 4 [4%]). Eighteen of the 23
stenoses 50% and 2 of the 6 stenoses <50% that progressed
developed into total occlusion (P=.1).
Progression of Ischemia-Related Stenoses Versus
Non–Ischemia-Related Stenoses
There were 85 ischemia-related
stenoses and 113
non–ischemia-related stenoses. Of the 85 ischemia-related stenoses, 49
were located in the left anterior descending artery (58%), 19 in the
left circumflex coronary artery (22%), and 17 in the right coronary
artery (20%). At restudy, 21 (25%) ischemia-related stenoses
progressed compared with only 8 (7%) non–ischemia-related stenoses
(P=.001). Of the 21 ischemia-related stenoses that
progressed, 17 developed into total occlusion, whereas only 3 occlusive
events occurred in the 8 non–ischemia-related stenoses that progressed
(P=.02). Changes in stenosis severity and absolute stenosis
diameter were significantly larger in ischemia-related stenoses than in
non–ischemia-related stenoses (P=.03) (Table
2). There
was no correlation between progression of ischemia-related stenoses and
lesion distribution; 12 stenoses progressed in the left anterior
descending artery (25%), 5 in the left circumflex coronary artery
(26%), and 4 in the right coronary artery (24%).
To eliminate the potential impact of inaccuracy of the determination of ischemia-related stenoses in multivessel disease, we assessed progression in the 52 patients with single-vessel disease separately. Disease progression was found in 13 (25%) ischemia-related stenoses and in 4 (7%) non–ischemia-related stenoses (P=.01), which was comparable to the disease progression in the whole group.
Association Between Angiographic Morphology and Stenosis
Progression and Coronary Events
Of the 85 ischemia-related stenoses,
54 (64%) were complex and 31
(36%) were smooth. There were no differences in percent stenosis or
minimal stenosis diameter between complex ischemia-related stenoses and
smooth ischemia-related stenoses at initial angiography (Table
2). Both
percent stenosis and absolute stenosis diameter changed more
significantly in complex ischemia-related stenoses compared with smooth
ischemia-related stenoses (P<.01) (Table 2).
Eighteen
(34%) complex ischemia-related stenoses progressed compared with 3
(10%) smooth ischemia-related stenoses (P=.02). There was
no significant difference in the incidence of coronary events in
patients who had complex ischemia-related stenoses compared with
patients with smooth ischemia-related stenoses at initial angiography
(20 [37%] versus 6 [19%], P=.09).
Relation Between Coronary Events and Disease Progression
Of
the 85 patients, 26 (31%) had coronary events (myocardial
infarction in 5 and unstable angina in 21). Eighteen (72%) of the 25
patients with coronary events (excluding 1 who died of acute myocardial
infarction before repeat angiography) and 10 (17%) of the remaining 59
patients who had no events showed disease progression
(P=.0001). Progression of ischemia-related stenoses was
demonstrated in 14 (56%) of the 25 patients with nonfatal coronary
events. The interval between angiograms was similar in patients with
disease progression or events and patients without progression or
events (8±4 months versus 7±4 months and 7±4 months
versus 8±4
months, respectively). Risk of serious coronary events over time is
presented in Table 3. Neither stenosis progression
nor events were associated with the number of coronary arteries showing
significant narrowing at initial angiography.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
This study was made possible by the relatively long waiting time for PTCA in our institution and provides important information on the natural history of unstable coronary lesions.
Stenosis Progression in Patients With Unstable Angina
Limited
data have shown that a significant number of coronary
artery stenoses progress after a short time in patients with unstable
angina.18 19 20 21 The rate
of progression in patients with
unstable angina has been reported to be 15%, 27%, and 44% at a mean
interval of 2, 4, and 13 months,
respectively.19 20 21 In
addition, occlusive progression was the dominant phenomenon in their
studies. In the present study, disease progression was observed in
33% of our patients at a mean interval of 8 months between angiograms.
Stenoses 50% progressed more frequently and showed a greater
tendency toward total occlusion than mild stenoses, suggesting that
there may be a relation between initial severity of stenosis with
overall and occlusive progression in these patients. The high
prevalence of disease progression and occlusive events found in our
patients is in agreement with previous
reports.19 20 21
Importantly, our data show that although stenosis progression is
largely unpredictable, ischemia-related stenoses patients with unstable
angina are at greater risk for progression, even when patients
stabilize on medication.
Progression of Complex Ischemia-Related Stenoses Versus Smooth
Ischemia-Related Stenoses
Complex stenosis morphology, which commonly
represents
plaque disruption or a partially occlusive thrombus or both, frequently
occurs in patients with unstable
angina.2 3 4 5 6
In our study,
the prevalence of complex stenoses in patients who presented with
unstable angina was comparable to that of previous
studies.4 5 8
Recent studies have shown that in patients with unstable angina, angiographically complex stenoses predict subsequent in-hospital instability.5 8 Furthermore, complex stenoses are also associated with future disease progression22 and myocardial infarction23 independent of the initial clinical presentation. Available evidence, therefore, suggests that complex stenoses may significantly alter the prognosis of the patient. Our study shows that complex ischemia-related stenoses progressed more frequently than smooth ischemia-related stenoses and thus confirms these findings. Progression in our study occurred shortly after the first angiogram, which may suggest that plaque complication may have been responsible.
Recurrent Coronary Events and Stenosis Progression in Unstable
Angina
In patients with unstable angina, frequent recurrent coronary
events have been demonstrated both during
hospitalization8 18 and after hospital
discharge.24 25 Short-term unfavorable outcome
occurred in
31% of our patients after hospital discharge and is comparable to
previous clinical reports.24 25 It is recognized that
unstable angina has a worse short-term prognosis than chronic stable
angina. Rapid thrombotic occlusion,26 increased vascular
tone, dynamic intermittent thrombus formation and lysis, or a
combination of these mechanisms27 have been postulated as
underlying causes for recurrent coronary events in unstable angina
patients. In the present study, we observed that 72% of patients
with coronary events showed disease progression. In particular,
progression of ischemia-related stenoses was found in 56% of the
patients who had coronary events. Although the causes of recurrent
coronary events may be not necessarily the same in all patients, our
study suggests that the association between angiographic complexity and
clinical instability is largely mediated by progression of
ischemia-related stenoses and that local coronary factors may play a
vital role for recurrent coronary events in patients with unstable
angina.
Limitations of the Study
Patients included in this report may
not be representative
of all patients with unstable angina but only of those who stabilize
rapidly on medical therapy and have coronary stenoses that require
PTCA. Prognosis in our patients was worse than that reported by other
authors,18 particularly considering that more than half of
our patients had only single-vessel disease. This may be attributable
to differences in study design and patient population, as the syndrome
of unstable angina encompasses heterogeneous groups of patients and
definitions of unstable angina may vary in different studies.
Our focus in the present study was on angiographic features associated with rapid stenosis progression, but this does not downplay the importance of other factors not considered in our study such as hemostatic variables, plasma lipids, and local macrophage infiltration,28 29 which may enhance thrombogenicity and influence progression of an atherosclerotic plaque. A further limitation of the study is that although our patients were consecutive and prospectively included, the interval between the two angiograms varied between patients. The variable interval was due to the complex dynamics of the waiting list, which was influenced by clinical and administration variables.
The determination of ischemia-related stenoses is problematic, since ST-segment depression may not accurately localize myocardial ischemia. Therefore, in patients with multivessel disease, ischemia-related stenoses as defined in our study may not have necessarily been the culprit for unstable symptoms. However, the similar rate of ischemia-related stenosis progression in patients with single-vessel disease to that of the whole group suggests that possible inaccuracy in judgment of ischemia-related stenoses did not influence our results.
Pathophysiological Significance and Clinical Implications
Coronary atherosclerosis does not progress
linearly.30 31 Coronary thrombosis is regarded as the
final occlusive event in the progression of coronary heart disease. Our
study shows that, in patients with unstable angina, ischemia-related
stenoses are likely to progress to total occlusion. This finding
supports the notion that intermittent coronary occlusion due to plaque
rupture and thrombosis in unstable
angina2 3 4 5 6 7 8
is implicated
with threatened permanent thrombotic occlusion.21 28
Moreover, our observations are also in agreement with recent
experimental studies by Willerson et al,32 which suggested
a strong association between the frequency and severity of platelet
aggregation, thrombosis, and neointimal proliferation after
endothelial injury at the site of experimentally created stenoses.
Willerson et al identified different mechanisms that may contribute to
rapid disease progression and showed the relatively malignant nature of
recurrent platelet aggregation and dislodgment after mechanically
induced endothelial injury.32 These findings also may
explain our observation that even when symptoms are medically
stabilized, the unstable coronary lesion is often not stabilized and
will continue to progress over the ensuing months, with a high risk of
recurrent coronary events.
Although balloon dilatation of unstable coronary stenoses is associated with an increased risk of early and late complications,33 34 35 the relatively common practice in UK centers of adopting a policy of "watchful waiting" in patients with unstable angina who stabilize on medication may not be appropriate. Indeed, this policy resulted in one third of the patients being rehospitalized for a recurrent ischemic event in our study. Although the ideal timing for PTCA in recently stabilized unstable angina is not known,36 it is likely that earlier revascularization is preferable. Our data indicate that the presence of complex stenoses in patients with unstable angina, even in those who improve on medical therapy, calls for more urgent revascularization by means of angioplasty or bypass surgery.
|
Acknowledgments |
|---|
Dr Chen is supported by a grant from the Youde Heart Foundation, St George's Hospital, London, England.
Received October 19, 1994; accepted November 22, 1994.
|
References |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
1. Moise A, Theroux P, Taeymans Y, Descoings B, Lesperance J, Waters DD, Pelletier GB, Pourassa MG. Unstable angina and progression of coronary atherosclerosis. N Engl J Med. 1983;309:685-689. [Abstract]
2. Bresnahan DR, Davis JL, Holmes DR, Smith HC. Angiographic occurrence and clinical correlates of intraluminal coronary artery thrombus: role of unstable angina. J Am Coll Cardiol. 1985;6:285-289. [Abstract]
3. Capone G, Wolf NM, Meyer B, Meister SG. Frequency of intracoronary filling defects by angiography in angina pectoris at rest. Am J Cardiol. 1985;56:403-406. [Medline] [Order article via Infotrieve]
4. Ambrose JA, Winters SL, Stern A, Eng A, Teichholz LE, Gorlin R, Fuster V. Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol. 1985;5:609-616. [Abstract]
5. Williams AE, Freeman MR, Chisholm RJ, Patt NL, Armstrong PW. Angiographic morphology in unstable angina pectoris. Am J Cardiol. 1988;62:1024-1027. [Medline] [Order article via Infotrieve]
6.
Holmes DR Jr, Hartzler GO, Smith HC, Fuster V. Coronary
artery thrombosis in patients with unstable angina. Br Heart
J. 1981;45:411-416.
7.
Wilson R, Holida M, White C. Quantitative angiographic
morphology of coronary stenoses leading to myocardial infarction or
unstable angina. Circulation. 1986;73:286-293.
8. Bugiardini R, Pozzati A, Borghi A, Morgagni GL, Ottani F, Muzi A, Puddu P. Angiographic morphology in unstable angina and its relation to transient myocardial ischemia and hospital outcome. Am J Cardiol. 1991;67:460-464. [Medline] [Order article via Infotrieve]
9. Reiber J, Kooijman CJ, Wijins W, Gerbrands JJ, Schuurbier JCH, den Boer A, Wijins W, Serruys PW. Coronary artery dimensions from cineangiograms: methodology and validation of a computer-assisted analysis procedure. IEEE Trans Med Imag. 1984;MI-3:131-140.
10.
Reiber J, Serruys P, Kooijman C, Wijins W, Slager CJ,
Gerbrands JJ, Schuurbier JCH, den Boer A, Hugenholtz PG. Assessment of
short-, medium-, and long-term variations in arterial dimensions from
computer-assisted quantitation of coronary cineangiograms.
Circulation. 1985;71:280-288.
11. Lespérance J, Hudson G, White C, Laurier J, Waters D. Comparison by quantitative angiographic assessment of coronary stenoses of one view showing the severest narrowing to two orthogonal views. Am J Cardiol. 1989;64:462-465. [Medline] [Order article via Infotrieve]
12. McFadden E, Clarke J, Davies G, Kaski J, Haider A, Maseri A. Effect of intracoronary serotonin on coronary vessel in patients with stable angina and patients with variant angina. N Engl J Med. 1991;324:648-654. [Abstract]
13. Kaski J, Tousoulis D, Pereira W, Crea F, Maseri A. Progression of complex coronary artery stenosis in patients with angina pectoris: its relation to clinical events. Coron Artery Dis. 1992;3:305-312.
14. Ambrose JA, Israel DH. Angiography in unstable angina. Am J Cardiol. 1991;68:78B-84B. [Medline] [Order article via Infotrieve]
15.
Levin D, Gardiner G. Complex and simple coronary artery
stenoses: a new way to interpret coronary angiograms based on
morphologic features of lesions. Radiology. 1987;164:675-680.
16. Ambrose JA, Winters SL, Arora RR, Eng A, Riccio A, Gorlin R, Fuster V. Angiographic evolution of coronary artery morphology in unstable angina. J Am Coll Cardiol. 1986;7:472-478. [Abstract]
17.
Lichtlen P, Nikutta P, Jost S, Deckers J, Wiese B, Rafflenbeul
W, INTACT Study Group. Anatomical progression of coronary artery
disease in humans as seen by prospective, repeated, quantitated
coronary angiography: relation to clinical events and risk factors.
Circulation. 1992;86:828-838.
18. Mulcahy R, Daly L, Graham I, Hickey N, O'Donoghue S, Owens A, Ruane P, Tobin G. Unstable angina: natural history and determinants of prognosis. Am J Cardiol. 1981;48:525-528. [Medline] [Order article via Infotrieve]
19. Kimbiris D, Iskandrian A, Saras H, Goel I, Bemis CE, Segal BL, Mundth E. Rapid progression of coronary stenosis in patients with unstable angina pectoris selected for coronary angioplasty. Cathet Cardiovasc Diagn. 1984;10:101-114. [Medline] [Order article via Infotrieve]
20. Rafflenbeul W, Smith L, Rogers W, Mantle J, Rackley C, Russell R. Quantitative coronary arteriography: coronary anatomy of patients with unstable angina pectoris reexamined 1 year after optional medical therapy. Am J Cardiol. 1979;43:699-707. [Medline] [Order article via Infotrieve]
21. Neill WA, Wharton TR, Fluri-Lundeen J, Cohen IS. Acute coronary insufficiency: coronary occlusion after intermittent ischemic attacks. N Engl J Med. 1980;302:1157-1162. [Abstract]
22. Nagatomo Y, Nakagawa S, Koiwaya Y, Tanaka K. Coronary angiographic ruptured atheromatous plaque as a predictor of future progression of stenosis. Am Heart J. 1990;119:1244-1253.[Medline] [Order article via Infotrieve]
23. Ellis S, Alderman EL, Cain K, Wright A, Bourassa M, Fisher L. Morphology of left anterior descending coronary territory lesions as a predictor of anterior myocardial infarction: a CASS Registry Study. J Am Coll Cardiol. 1989;13:1481-1491. [Abstract]
24. Bertolet BD, Dinerman J, Hartke RJ, Conti CR. Unstable angina: relationship of clinical presentation, coronary artery pathology, and clinical outcome. Clin Cardiol. 1993;16:116-122. [Medline] [Order article via Infotrieve]
25. Pozzati A, Bugiardini R, Borghi A, Ottani F, Muzi A, Morgagni G, Puddu P. Transient ischemia refractory to conventional medical treatment in unstable angina: angiographic correlates and prognostic implications. Eur Heart. 1992;13:360-365.
26. Forrester J. Intimal disruption and coronary thrombosis: its role in the pathogenesis of human coronary disease. Am J Cardiol. 1991;68:69B-77B. [Medline] [Order article via Infotrieve]
27. Maseri A, Crea F. The elusive cause of instability in unstable angina. Am J Cardiol. 1991;68:16B-21B. [Medline] [Order article via Infotrieve]
28. Badimon L, Chesebro JH, Badimon JJ. Thrombus formation on ruptured atherosclerotic plaques and rethrombosis on evolving thrombi. Circulation. 1992;86(suppl III):III-74-III-75.
29.
Phillips NR, Waters D, Havel, RJ. Plasma lipoproteins and
progression of coronary artery disease evaluated by angiography and
clinical events. Circulation. 1993;88:2762-2770.
30.
Bruschke AV, Wijers TS, Kolsters W, Landmann J. The anatomic
evolution of coronary artery disease demonstrated by coronary
arteriography in 256 nonoperated patients.
Circulation. 1981;63:527-536.
31.
Singh R. Progression of coronary athersclerosis: clues
to pathogenesis from serial coronary arteriography. Br Heart
J. 1984;52:451-461.
32.
Willerson JT, Yao SK, McNatt J, Benedict CR, Anderson HV,
Golino P, Murphree SS, Buja LM. Frequency and severity of cyclic flow
alternations and platelet aggregation predict the severity of
neointimal proliferation following experimental coronary
stenosis and endothelial injury. Proc Natl Acad Sci U S A. 1991;88:10624-10628.
33.
Bauters C, Lablanche JM, McFadden EP, Leroy F, Bertrand ME.
Repeat percutaneous coronary angioplasty: clinical and angiographic
follow-up in patients with stable or unstable angina pectoris.
Eur Heart J. 1993;14:235-239.
34. Kamp O, Beatt KJ, De FP, van den Brand M, Suryapranata H, Luijten HE, Serruys PW. Short-, medium-, and long-term follow-up after percutaneous transluminal coronary angioplasty for stable and unstable angina pectoris. Am Heart J. 1989;117:991-996. [Medline] [Order article via Infotrieve]
35.
Rupprecht HJ, Brennecke R, Kottmeyer M, Bernhard G, Erbel R,
Pop T, Meyer J. Short- and long-term outcome after PTCA in patients
with stable and unstable angina. Eur Heart J. 1990;11:964-973.
36. King SB III. Coronary plaque morphology in postinfarction patients: implications for early versus deferred coronary angioplasty. J Am Coll Cardiol. 1990;16:1087-1088.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  F. Otsuka, S. Sugiyama, S. Kojima, H. Maruyoshi, T. Funahashi, K. Matsui, T. Sakamoto, M. Yoshimura, K. Kimura, S. Umemura, et al. Plasma Adiponectin Levels Are Associated With Coronary Lesion Complexity in Men With Coronary Artery Disease J. Am. Coll. Cardiol., September 19, 2006; 48(6): 1155 - 1162. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Rioufol, M. Gilard, G. Finet, I. Ginon, J. Boschat, and X. Andre-Fouet Evolution of Spontaneous Atherosclerotic Plaque Rupture With Medical Therapy: Long-Term Follow-Up With Intravascular Ultrasound Circulation, November 2, 2004; 110(18): 2875 - 2880. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P Avanzas, R Arroyo-Espliguero, J Cosin-Sales, G Aldama, C Pizzi, J Quiles, and J C Kaski Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes Heart, August 1, 2004; 90(8): 847 - 852. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Cosin-Sales, M. Christiansen, P. Kaminski, C. Oxvig, M. T. Overgaard, D. Cole, D. W. Holt, and J. C. Kaski Pregnancy-Associated Plasma Protein A and Its Endogenous Inhibitor, the Proform of Eosinophil Major Basic Protein (proMBP), Are Related to Complex Stenosis Morphology in Patients With Stable Angina Pectoris Circulation, April 13, 2004; 109(14): 1724 - 1728. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Artieda, A. Cenarro, A. Ganan, I. Jerico, C. Gonzalvo, J. M. Casado, I. Vitoria, J. Puzo, M. Pocovi, and F. Civeira Serum Chitotriosidase Activity Is Increased in Subjects With Atherosclerosis Disease Arterioscler. Thromb. Vasc. Biol., September 1, 2003; 23(9): 1645 - 1652. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Rioufol, G. Finet, I. Ginon, X. Andre-Fouet, R. Rossi, E. Vialle, E. Desjoyaux, G. Convert, J.F. Huret, and A. Tabib Multiple Atherosclerotic Plaque Rupture in Acute Coronary Syndrome: A Three-Vessel Intravascular Ultrasound Study Circulation, August 13, 2002; 106(7): 804 - 808. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Goldstein Angiographic plaque complexity: the tip of the unstable plaque iceberg J. Am. Coll. Cardiol., May 1, 2002; 39(9): 1464 - 1467. [Full Text] [PDF]
|
|
|
|
 |
|
 A. G. G. Turpie and E. M. Antman Low-Molecular-Weight Heparins in the Treatment of Acute Coronary Syndromes Arch Intern Med, June 25, 2001; 161(12): 1484 - 1490. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Goldstein, D. Demetriou, C. L. Grines, M. Pica, M. Shoukfeh, and W. W. O'Neill Multiple Complex Coronary Plaques in Patients with Acute Myocardial Infarction N. Engl. J. Med., September 28, 2000; 343(13): 915 - 922. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. T. Roe, R. A. Harrington, D. M. Prosper, K. S. Pieper, D. L. Bhatt, A. M. Lincoff, M. L. Simoons, M. Akkerhuis, E. M. Ohman, M. M. Kitt, et al. Clinical and Therapeutic Profile of Patients Presenting With Acute Coronary Syndromes Who Do Not Have Significant Coronary Artery Disease Circulation, September 5, 2000; 102(10): 1101 - 1106. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.E Bertrand, M.L Simoons, K.A.A Fox, L.C Wallentin, C.W Hamm, E McFadden, P.J de Feyter, G Specchia, and W Ruzyllo Management of acute coronary syndromes: acute coronary syndromes without persistent ST segment elevation. Recommendations of the Task Force of the European Society of Cardiology: Recommendations of the Task Force of the European Society of Cardiology Eur. Heart J., September 1, 2000; 21(17): 1406 - 1432. [PDF]
|
|
|
|
|
|
M Sitges, C Pare, M Azqueta, X Bosch, M VelamazaN, J Magrina, and G Sanz Feasibility and prognostic value of dobutamine-atropine stress echocardiography early in unstable angina Eur. Heart J., July 1, 2000; 21(13): 1063 - 1071. [Abstract] [PDF]
|
|
|
|
|
|
X. Garcia-Moll, F. Coccolo, D. Cole, and J. C. Kaski Serum neopterin and complex stenosis morphology in patients with unstable angina J. Am. Coll. Cardiol., March 15, 2000; 35(4): 956 - 962. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J Davies CORONARY DISEASE: The pathophysiology of acute coronary syndromes Heart, March 1, 2000; 83(3): 361 - 366. [Full Text]
|
|
|
|
|
|
S. M. Zaacks, P. R. Liebson, J. E. Calvin, J. E. Parrillo, and L. W. Klein Unstable angina and non-Q wave myocardial infarction: does the clinical diagnosis have therapeutic implications? J. Am. Coll. Cardiol., January 1, 1999; 33(1): 107 - 118. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J M Mann, J C Kaski, W I Pereira, S Arie, J A Ramires, and F Pileggi Histological patterns of atherosclerotic plaques in unstable angina patients vary according to clinical presentation Heart, July 1, 1998; 80(1): 19 - 22. [Abstract] [Full Text]
|
|
|
|
|
|
M. D. Guazzi, M. Bussotti, L. Grancini, N. De Cesare, M. Guazzi, I. L. Pera, and A. Loaldi Evidence of Multifocal Activity of Coronary Disease in Patients With Acute Myocardial Infarction Circulation, August 19, 1997; 96(4): 1145 - 1151. [Abstract] [Full Text]
|
|
|
|
|
|
C. R. McKenzie, D. R. Abendschein, and P. R. Eisenberg Sustained Inhibition of Whole-Blood Clot Procoagulant Activity by Inhibition of Thrombus-Associated Factor Xa Arterioscler. Thromb. Vasc. Biol., October 1, 1996; 16(10): 1285 - 1291. [Abstract] [Full Text]
|
|
|
|
|
|
P. Zoldhelyi, J. McNatt, X.-M. Xu, D. Loose-Mitchell, R. S. Meidell, F. J. Clubb Jr, L. M. Buja, J. T. Willerson, and K. K. Wu Prevention of Arterial Thrombosis by Adenovirus-Mediated Transfer of Cyclooxygenase Gene Circulation, January 1, 1996; 93(1): 10 - 17. [Abstract] [Full Text]
|
|
|
|
|
|
E. Falk and V. Fuster Angina Pectoris and Disease Progression Circulation, October 15, 1995; 92(8): 2033 - 2035. [Full Text]
|
|
|
|
|
|
J. C. Kaski, M. R. Chester, L. Chen, and D. Katritsis Rapid Angiographic Progression of Coronary Artery Disease in Patients With Angina Pectoris : The Role of Complex Stenosis Morphology Circulation, October 15, 1995; 92(8): 2058 - 2065. [Abstract] [Full Text]
|
|
|
|
|
|
P. Theroux Angiographic and Clinical Progression in Unstable Angina : From Clinical Observations to Clinical Trials Circulation, May 1, 1995; 91(9): 2295 - 2298. [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||