(Circulation. 1995;92:2058-2065.)
© 1995 American Heart Association, Inc.
Articles |
Rapid Angiographic Progression of Coronary Artery Disease in Patients With Angina Pectoris
The Role of Complex Stenosis Morphology
From the Coronary Artery Disease Research Group, Department of Cardiological Sciences, St George's Hospital Medical School, London, UK.
Correspondence to Dr Juan Carlos Kaski, Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, England.
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Abstract |
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Background Rapid disease progression commonly underlies acute coronary events, and "complex" stenosis morphology may play a role in this phenomenon.
Methods and Results We studied the role of complex stenosis morphology in rapid disease progression in 94 consecutive patients awaiting routine coronary angioplasty. Coronary arteriography was repeated at 8±3 months' follow-up, immediately preceding angioplasty (68 patients) or after an acute coronary event (26 patients). Disease progression of 217 stenoses, of which 79 (36%) were "complex" and 138 (64%) were "smooth," was assessed by computerized angiography. At presentation, 63 patients had stable angina pectoris and 31 had unstable angina that settled rapidly with medical therapy. At follow-up, 23 patients (24%) had progression of preexisting stenoses and 71 (76%) had no progression. Patients with progression were younger (55±12 years) than those without (58±9 years) but did not differ with regard to risk factors, previous myocardial infarction, or severity and extent of coronary disease. Twenty-three lesions (11%) progressed, 15 to total occlusion (11 complex and 4 smooth; 65%). Progression occurred in 17 of the 79 complex stenoses (22%) and in 6 of the 138 smooth lesions (4%) (P=.002). Mean stenosis diameter reduction was also significantly greater in complex than in smooth lesions (11.6% versus 3.9% change; P<.001). Acute coronary events occurred in 57% of patients with progression compared with 18% of those without progression (P<.001) and were more frequent in patients who presented with unstable angina (P=.002).
Conclusions Rapid stenosis progression is not uncommon, and complex stenoses are at risk more than smooth lesions.
Key Words: stenosis • angiography • coronary disease • angina
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Introduction |
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In patients with mild to moderate coronary artery stenosis, disease progression may be slow and evolve gradually over time.1 However, in a substantial proportion of patients, stenosis progression is rapid.1 2 3 4 5 6 7 It has been shown both that coronary stenoses may "grow" rapidly, leading to total vessel occlusion, particularly in patients who develop serious coronary events,4 8 and that new stenoses often develop in segments of coronary arteries that were normal at previous angiography.1 9 Thus, disease progression appears to be neither linear nor predictable.10 11 The unpredictable and episodic nature of disease progression can be explained by rapid stenosis growth due to thrombosis, which occurs as a complication of the basic atherosclerotic process.12 13 Indeed, acute coronary syndromes are most commonly precipitated when mild or moderate coronary stenoses become severely obstructive,9 10 11 and this transformation is usually associated with plaque fissuring, intramural hemorrhage, and occlusive thrombosis.14 15 16 17 In long-term follow-up studies, risk factors and local coronary factors appear to contribute to stenosis progression.1 18 19 20 21 22 Recently, it has been shown that disease progression, whether "silent" or associated with clinical manifestations, is a strong, independent predictor of future coronary events.23
The occurrence of rapid stenosis progression in patients with stable coronary syndromes has not been investigated systematically. In previous studies, intervals between angiograms were usually too long for the assessment of rapid disease progression. Several other limitations of these studies were recently identified.1 Therefore, little is known about the incidence, angiographic characteristics, and clinical significance of rapid disease progression in this setting. In the present study, we took advantage of the current situation in our clinical care system, in which stable angina patients who require routine, nonurgent coronary angioplasty are put on waiting lists. We prospectively assessed the incidence, as well as clinical and angiographic features, associated with rapid disease progression in patients awaiting coronary angioplasty. We focused our attention on the role of angiographically complex stenosis morphology in view of the fact that myocardial infarction and unstable angina are usually associated with "complex" stenoses24 25 and that complicated lesions have been suggested to predict the occurrence of coronary stenosis progression and coronary events in patients with diverse coronary syndromes.26 27 28 29
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Methods |
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Study Patients
We studied 94 individuals from a series of 198 consecutive patients with angina pectoris who underwent coronary arteriography in our unit over a period of 7 months (September 1990 through March 1991) and who were considered candidates for routine coronary angioplasty. After diagnostic arteriography, the 94 patients (77 men and 17 women, aged 58±10 years) were put on a waiting list for angioplasty. All 94 patients were on the waiting list for at least 2 and for up to 12 months from the time of diagnostic coronary arteriography, usually depending on bed and catheter laboratory availability. Of the remaining 104 patients, 93 who underwent angioplasty within 2 months of diagnostic catheterization and 11 whose angiograms were not suitable for computerized analysis were excluded from study. We did not include patients with (1) previous coronary bypass surgery or coronary angioplasty; (2) planned bypass surgery; (3) clinically significant valvular heart disease, serious conduction disturbances, heart failure, or significant arrhythmia; (4) left ventricular aneurysm possibly requiring surgical treatment; (5) significant left main or left main equivalent disease; (6) >80% preseptal left anterior descending coronary stenosis; (7) myocardial infarction within the 12-week period before entry into the study; (8) pharmacological treatment for hyperlipidemia; and (9) time on the waiting list for coronary angioplasty of less than 2 months or more than 12 months.
Clinical features and angiographic
characteristics in the 94 patients
included in the study are shown in Table 1
and Table
2, respectively. We studied type of angina at
presentation, history of myocardial infarction,
conventional risk factors for coronary artery disease (family
history, smoking, hypertension, diabetes mellitus, and plasma
cholesterol), and extent and severity of coronary
artery disease (Tables 1 and 2). At study entry,
63 patients
presented with chronic stable angina pectoris (symptoms stable
for the preceding 6 months) and 31 had unstable angina30
(new onset angina, 3 patients; resting angina, 20 patients; and
crescendo angina, 8 patients), which rapidly settled with conventional
medical therapy in all. During follow-up, all patients received
antianginal medication as prescribed by the treating physician, which
consisted of diverse combinations of calcium antagonists,
nitrates, and ß-blocking agents. Low-dose aspirin (75 to 150
mg/d) was prescribed for every patient when no specific
contraindications existed (4 patients).
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Angiographic Analysis
Coronary Arteriography
Diagnostic coronary arteriography at study
entry was carried out with use of standardized projections, which
were reproduced at the time of the second arteriogram. Patients fasted
and did not smoke in the 12 hours preceding coronary
arteriography. Baseline medical therapy was not discontinued. Nitrates
were administered to all patients to minimize the effects of
coronary vasomotor tone on coronary lumen diameter
size. Sublingual glyceryltrinitrate (0.5 mg) or isosorbide dinitrate (5
mg) was given (2 to 10 minutes before contrast injection) to 63
patients who presented with stable angina.
Intravenous glyceryltrinitrate (100 µg) or isosorbide
dinitrate (1 mg) was administered to all patients who presented
with acute coronary syndromes. After diagnostic
angiography, patients were put on a waiting list for routine
coronary angioplasty and followed up on a regular basis in the
outpatient clinic. All patients gave written informed consent before
study entry. All 94 patients underwent two coronary
arteriograms as part of their clinical evaluation. The first angiogram
was carried out at study entry and the second 8±3 months later,
depending on the dynamics of the waiting list and the patient's
clinical evolution. In 68 patients, who had no change in symptoms and
who did not develop coronary events during follow-up, the
second arteriogram was carried out immediately preceding routine
coronary angioplasty. In the remaining 26 patients, who
developed unstable angina (22 patients) or acute myocardial infarction
(4 patients) during follow-up, coronary arteriography was
carried out 7±6 days after the acute event. At follow-up
angiography, nitrates were administered in identical fashion as during
the first coronary angiogram.
Measurement of Coronary
Artery Diameters
Quantitative assessment. Each pair of
coronary arteriograms was assessed by two experienced
cardiologists blinded to the identity and clinical characteristics of
the patients and to the temporal sequence of the films.
Coronary artery segments were selected between identifiable
branching points. For each segment, measurements were carried out on
end-diastolic frames. Coronary stenoses
were measured where their severity appeared maximal. Coronary
diameters were measured with use of the Coronary Angiography
Analysis System (CAAS) (Pie Data Medical) developed by
Reiber31 and validated by different
authors.23 32 33 Our technique for
measuring
coronary artery diameter using CAAS has been reported in detail
previously.33 34 35 36 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. Seven of the 217 stenoses were located
in coronary arteries less than 1 mm in diameter and were
therefore read visually, as CAAS is less reliable under these
circumstances.23 Orthogonal views were not measured and
averaged because it is accepted that measurements of the views showing
the stenosis at its most severe are sufficient.32
A total of 217 coronary stenoses (
30% diameter
reduction) and 650 angiographically normal segments were
analyzed (6.9 per patient). We studied the reproducibility of
our measurements using this system by calculating the accuracy (defined
as the signed difference between the measured and true value) and the
precision (defined as the standard deviation of these differences) of
the system. Accuracy was 0.08 mm, and precision was 0.10
mm.26 Coronary diameters were measured by two
independent observers, and the angiograms were also
reanalyzed blindly at a later time to ascertain the
interobserver and intraobserver variabilities. Intraobserver variation
(SEE) was 0.09 mm, and interobserver variation was 0.08
mm.
Percentage diameter reduction of a coronary stenosis was calculated on the basis of the diameter of the stenosis at its most severe and diameter of the reference segment (angiographically normal segment proximal to the lesion) measured in millimeters. The following formula was used:
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Qualitative assessment. The morphology of coronary artery stenoses was assessed visually by two experienced cardiologists blinded to the identity and clinical characteristics of the patients and the temporal sequence of the films. Each stenosis was assessed selectively, viewed in two orthogonal projections. Stenoses were classified as "complex" or "smooth" on the basis of visual analysis, but the CAAS-derived symmetry index37 was used to define stenoses as "concentric" (symmetric narrowing of a coronary artery, with an identical or near-identical appearance of the stenosis in orthogonal projections; symmetry index >0.5 to 1.0) or "eccentric" (asymmetric narrowing; index 0.0 to 0.5). Stenoses were classified as complex (eccentric, with overhanging edges, irregular borders, and/or showing ulceration or thrombus)24 25 26 28 or smooth (concentric or eccentric lesions with smooth edges, in the absence of complex features). When discrepancies arose (10 of 217 lesions), the stenoses were classified by consensus.
Stenosis Progression
Accepted
criteria1 38 were used to define
stenosis progression: (1) 20% reduction of minimal
stenosis diameter of a preexisting lesion 30% and (2)
progression of any lesion to a new total coronary occlusion on
restudy.
Stenosis regression was defined as a reduction of
stenosis severity 20% lumen diameter on restudy. A
coronary stenosis was defined as "new" when a
localized narrowing 30% arose in a segment that was angiographically
normal at baseline angiography. In the study, stenosis
progression was defined as "rapid" if it occurred within 1 year
of diagnostic angiography.
Statistical Analysis
Within-lesion differences between first
and repeat
angiograms were compared by use of the paired Student's t
test. Student's t test for unpaired data was used to
compare differences between lesions. Differences in the frequency
distribution of categorical variables between groups were
determined by using Yates' technique (corrected
2 analysis). Differences in reference
diameters between the first and second angiograms were compared by use
of one- or two-sample t tests as appropriate. Data are
presented as mean±1 SD unless otherwise specified.
Significance was defined as P<.05.
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Results |
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Clinical and Angiographic Variables at Study Entry
Sixty-three patients presented with chronic stable angina pectoris and 31 with unstable angina (new onset angina, 3 patients; resting angina, 20 patients; and crescendo angina, 8 patients) that rapidly settled with conventional medical therapy. Patients' age, sex, risk factors, and history of myocardial infarction are summarized in Table 1
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Coronary Stenosis
Severity and
Morphology
In the first coronary angiogram, 46 patients had
one-vessel disease, 36 had two-vessel disease, and 12 had
three-vessel disease (Table 1). Twenty-three vessels in 23
patients were totally occluded, and 267 stenoses 30% were
observed; of these, 217 (2.3 per patient) were suitable for CAAS
analysis. Of the 217 analyzable stenoses, 131 were
30% but <50% and 86 were 50% diameter reduction.
Coronary stenosis diameter reduction (percent) at study
entry, excluding total occlusions (23 arteries) and including all
analyzable stenoses 30%, ranged from 30% to 81% (mean±SD,
46±15%). Absolute stenosis diameter (in millimeters) ranged
from 0.6 to 3.3 (mean±SD, 1.64±0.52 mm) (Table
2). Of the 217
stenoses suitable for analysis, 79 (36%) were complex
and 138 (64%) were smooth.
Coronary Stenosis Progression
Progression of
Preexisting Stenoses
At follow-up, 23 preexisting stenoses (13 of 131
stenoses <50% and 10 of 86 stenoses 50% diameter
reduction; P=NS) had progressed in 23 patients (24%). The
13 stenoses <50% progressed from a mean of 38% to a mean of
71%, and the 10 stenoses 50% progressed from 56% to 100%.
All but one of the 10 lesions 50% that progressed were the lesions
intended for percutaneous transluminal coronary
angioplasty (PTCA). Fifteen of the 23 stenoses (65%) that
progressed developed total occlusion (Figs 1 and
2). Thus, within a year, total occlusion developed in
7% (15 stenoses) of the initial 217 analyzable
stenoses. Changes in minimal stenosis diameter of the
23 stenoses that progressed are presented in Fig 1. At
follow-up angiogram, only one lesion (>50% at study entry) showed
a reduction in coronary diameter (13% change) compared with
baseline (Fig 3).
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Stenosis progression was observed in
17 of the 79 (22%)
complex stenoses and in 6 of the 138 (4%) smooth lesions
(P=.002). Accordingly, total occlusion developed in 11
complex (14%) and 4 smooth (3%) stenoses (P=.003)
(Fig 2).
At study entry, minimal diameter of complex
stenoses was
significantly smaller than that of smooth stenoses (1.51±0.42
mm versus 1.71±0.55 mm) (Table 2). Reduction of lumen
diameter at
follow-up angiogram was significantly (P<.001) larger
in complex (11.6±17.5%) than in smooth lesions (3.9±10.2%) (Fig
3).
Average stenosis severity progressed from 51±11% to 62±20%
in complex stenoses and from 44±15% to 48±14% in smooth
stenoses (P<.001) (Table 2). Change in lumen
diameter of individual complex and smooth stenoses is
presented in Fig 3.
Formation of New Coronary Stenoses
Only three new lesions
developed during follow-up in segments
that were angiographically normal at study entry. None of these
resulted in total coronary occlusion. Severity of the new
stenoses ranged from 31% to 45%.
Coronary Stenosis Progression and Clinical
Presentation at Study Entry
Conventional risk factors were not
significantly different in
patients who showed disease progression compared with patients without
progression (Table 3). However, patients with disease
progression were younger than patients without progression (Table
3).
Thirty-one patients presented with unstable angina, which
settled on medical therapy, and 63 with chronic stable angina pectoris
(Table 1). Seventy-nine stenoses were assessed in patients
who presented with unstable angina: 37 (47%) were complex and
42 (53%) were smooth. In the 63 patients who presented with
chronic stable angina, 138 stenoses were assessed; of these, 42
(30%) were complex and 96 (70%) were smooth. Severity of
coronary stenosis and number of vessels involved were
not significantly different in patients who presented with
stable angina compared with those who presented with unstable
angina (Tables 1 and 2). During follow-up, 17 of
the 31 patients
(55%) who presented with unstable angina developed a new acute
event 7±3 months after study entry (7 had angina at rest, 8 crescendo
angina, and 2 myocardial infarction), whereas only 9 of the 63 patients
(14%) who presented with stable angina developed an acute
coronary syndrome (3 had angina at rest, 4 crescendo angina,
and 2 myocardial infarction) (P=.002; Fig 4).
Eleven complex stenoses (30%) progressed in patients who
presented with unstable angina and six (14%) in patients who
presented with stable angina (P=.1). Four (10%)
smooth lesions progressed in patients with unstable angina and two
(2%) in patients with chronic stable angina (P=.1). Thus,
15 stenoses (11 complex and 4 smooth) progressed in patients
who presented with unstable angina, and 8 stenoses (6
complex and 2 smooth) progressed in patients who presented with
stable angina (P<.01). In the 63 patients with stable
angina at study entry, complex stenoses progressed more than
smooth lesions (10±18% versus 2±6%, respectively,
P=.01). Likewise, complex stenoses progressed more
than smooth lesions in the 31 patients with unstable angina at
presentation (18±15% versus 5±10%, respectively,
P<.01).
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Clinical Coronary Events
The relations between acute events
during follow-up and
clinical and angiographic variables are presented in Table 3.
Twenty-three patients showed stenosis progression during
follow-up. Thirteen of these patients (57%) developed an acute
coronary event. Of the 71 patients who did not show
stenosis progression during follow-up, 13 (18%) had acute
events (11 had unstable angina and 2 developed an acute infarction).
Total coronary occlusion occurred in 15 patients and was
associated with the development of unstable angina in 7 patients and
myocardial infarction in 2 patients. Of the remaining 6 patients with
total coronary occlusion who did not have clinically apparent
events, 3 had visible collaterals at angiography. Both clinical events
and angiographic stenosis progression were associated with
unstable angina and the presence of at least one complex
stenosis at the initial presentation.
Reference Diameters at
First and Second Angiograms
Diameters of stenosis reference segments
for patients
grouped according to stenosis morphology and nitrate therapy at
first and second angiogram are shown in Table 4. Overall
reference diameters were similar at first angiography and at
follow-up (3.16±0.66 versus 3.15±0.66 mm, respectively;
P=.94). Importantly, the reference diameters of patients
receiving oral or intravenous nitrates did not differ at
either angiogram nor was there a change between angiograms
(P=.79). Similarly, no differences were found when diameters
of reference segments of smooth and complex stenoses were
compared at first and second angiograms (P=.56).
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Discussion |
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Our study showed that rapid progression of preexisting stenoses was relatively common in patients with moderate or severe coronary artery disease who were on a waiting list for coronary angioplasty. Indeed, approximately 25% of our patients showed significant stenosis progression while on the waiting list. The incidence of stenosis progression in our study (average follow-up, 8 months) was larger than that reported by the INTACT Study Group1 (average follow-up, 3 years), but this discrepancy may be explained by different patient selection. Although the two studies included clinically stable patients with coronary artery disease, all patients in our study were candidates for coronary revascularization, and a proportion presented with unstable symptoms (which settled promptly on medication), whereas the INTACT study1 included only patients with mild coronary artery disease who did not require myocardial revascularization.
Despite growing interest in rapid disease progression in recent years, the association between angiographic stenosis morphology and rapid stenosis progression has not been systematically investigated in patients with stable angina. In previous studies,1 2 3 4 5 6 8 18 19 20 23 28 39 the interval between initial and follow-up angiograms was longer than 1 year, and follow-up coronary arteriograms were usually dictated by clinical events or were used for diagnostic reasons. Only a few studies had a prospective design and used computerized angiographic analysis.1 23 28 With regard to disease progression, our study provides additional new information of clinical and pathophysiological relevance. We prospectively investigated, using computerized arteriography, consecutive patients with coronary artery disease, representative of the population that undergoes routine coronary angioplasty in a general hospital. Some of our patients had unstable angina at study entry, a syndrome that appears to be associated with stenosis progression,40 but all settled rapidly with medical therapy at study entry and were considered by the treating physician to be suitable candidates for nonurgent revascularization. After diagnostic arteriography, our patients were prospectively put on a waiting list and followed up regularly. The interval between the two angiograms in our study was dictated by the dynamics of the waiting list for the routine revascularization procedure or by coronary events when these developed.
Stenosis Progression
In the present study, only a small
proportion (
10%) of all
analyzable stenoses showed rapid progression. However, the
majority of these lesions progressed to total coronary
occlusion. Stenosis progression was associated with acute
coronary events in 57% of the patients. Interestingly,
however, serious coronary events occurred in only 9 of the 15
patients who developed total coronary occlusions during
follow-up. This finding supports previous observations from our
group36 and others1 that although
stenosis progression is frequently associated with acute
coronary events, it also may occur silently. The presence of
visible collaterals in 3 of the 6 patients who developed
asymptomatic stenosis progression may explain
the phenomenon in these patients. In the remaining 3 patients, who did
not have visible collaterals, the mechanism is speculative. Presence of
nonvisible collateral vessels, gradual stenosis progression,
and myocardial preconditioning may be postulated. A proportion of
patients in our study had coronary events without
stenosis progression. This is not surprising as it is known
that transient dynamic events such as coronary artery spasm or
mild plaque fissuring, with associated thrombosis followed by
spontaneous thrombolysis, frequently take place in patients
with coronary disease.
We observed that patients with disease progression were younger than those without progression. This finding is in agreement with clinical observations by other authors41 and histopathological studies42 43 that have demonstrated that atherosclerotic plaques in young patients with coronary artery disease are characterized by a large amount of lipid-containing foam cells and a relative lack of acellular scar tissue. These observations appear to suggest that atherosclerotic plaques in younger individuals could have developed rapidly, perhaps as a result of plaque disruption.42
In our study, the severity of preexisting
stenoses did not play
a vital role in determining disease progression, as the proportion of
stenoses <50% in diameter and stenoses 50% that
progressed was similar, a finding that confirms results of previous
studies.36 38 Also consistent with previous
observations,1 10 11 total coronary
occlusions in
our study developed not only at the site of severe lesions but also in
segments with mild preexisting stenoses. However, severe
stenoses were more likely to occlude than mild lesions.
In our patients, the development of new angiographically visible stenoses was uncommon. This contrasts with data from the INTACT study,1 in which 144 new stenoses were detected in 230 patients. The longer duration of follow-up in the INTACT study, allowing more time for lesions to develop in normal segments, may explain the different findings.
Role of Angiographic Stenosis Morphology
In a recent
editorial article, Ambrose44 indicated
the need for studies that could provide evidence as to the clinical and
prognostic role of complex lesions. We have obtained relevant
information in this regard. In our study, rapid progression (including
progression to total occlusion) occurred more frequently in complex
stenoses than in smooth stenoses. This observation
expands important findings by Davies et al,45 who found a
strong correlation between qualitative stenosis morphology and
subsequent in-hospital outcome in patients who underwent
thrombolysis. Levin and Fallon27 suggested
that coronary stenoses characterized angiographically
by a "complicated" morphology are probably the "clinically
more dangerous" type. They also give support to angiographic studies
that indicate that lesion roughness is predictive of myocardial
infarction28 and that plaque ulceration identifies
"high-risk" coronary lesions.29 Complex
stenoses occur in patients who develop myocardial infarction
and unstable angina,24 25 and it is established that
acute
ischemic syndromes are most commonly precipitated when mild or
moderate coronary stenoses become severely
obstructive.9 10 17 21 This
transformation is usually
associated with fissuring of the fibrous cap of the
atheroma, intramural hemorrhage, and mural or
occlusive thrombosis, as originally postulated by
Constantinides46 and later elegantly demonstrated by other
authors.12 13 15
Our data show that both complex morphology and unstable angina at presentation are important factors for rapid stenosis progression. In addition, a sizable proportion of stable angina patients in our study showed rapid disease progression. Whether the mechanism responsible for rapid disease progression is the same in patients who present with unstable angina and patients who present with stable angina remains speculative. Both complex plaques and unstable angina appear to arise through plaque disruption and are therefore closely interrelated.14 25 27 Not surprisingly, there was considerable overlap between unstable angina and complexity at presentation and progression in our study. However, we observed that complex lesions progress more than smooth stenoses both in patients presenting with stable angina and in patients presenting with unstable angina. This observation is of considerable importance and indicates that morphological appearance is an independent factor in determining stenosis progression. This is consistent with recent observations by our group in patients with chronic stable angina26 and in patients who stabilized following an unstable episode.47 Our data indicate that in angina patients (particularly, but not exclusively, unstable angina patients) who are considered candidates for routine coronary angioplasty, "active" plaques may exist that may progress rapidly, leading to total vessel occlusion and acute coronary events. The relatively short time in which significant stenosis progression took place in our study suggests that acute changes, rather than slow linear events, occurred at the stenosis site. This is in agreement with current pathophysiological knowledge48 whereby vascular injury and thrombus formation are key events in the origin and progression of coronary disease and in the pathogenesis of acute coronary syndromes.
Limitations of the Study
We are aware that our clinical
findings may not apply where
waiting lists for coronary angioplasty do not exist. However,
our results are of pathophysiological
importance, as they highlight the episodic nature of disease
progression even in stable angina pectoris. Although patients were
prospectively entered in the study, the interval between the two
angiograms varied between patients. This was due to the complex
dynamics of the waiting list, which in our institution includes several
variables, such as bed and catheterization
laboratory availability and patient clinical evolution.
The effect of coronary vasomotor tone is of importance when assessing stenosis progression or regression, and therefore intracoronary nitrates are often given in studies of this nature. Although in the present study we did not use intracoronary nitrates, all our patients received sublingual or intravenous nitrates. Diameters of coronary reference segments were not different in patients who received sublingual compared with those who received intravenous nitrates at either angiogram. Similarly, no differences were found in the diameters of reference segments of the oral and intravenous nitrate–treated patients when the first and second angiograms were compared. This indicates that the vasodilatation achieved during the first and second angiogram was similar and that effects achieved with sublingual and intravenous nitrates were also similar. Thus, it is unlikely that changes in vasomotion could explain our findings.
Qualitative analysis is subjective and partly depends on the experience of the operators, and it is possible that this is reflected in the reproducibility of qualitative analysis in our study. The observations are, however, internally consistent with observations by different observers in a separate population in our institution.26 47
Conclusions
Our results thus suggest that rapid stenosis
progression
is not uncommon in patients with moderate or severe coronary
artery disease who await coronary angioplasty. Stenoses
of complex angiographic morphology are at a higher risk of rapid
progression than smooth lesions. Patients who present with unstable
angina are likely to develop rapid stenosis progression and
further events, even when their symptoms settle rapidly with medical
therapy.
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Acknowledgments |
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Dr L. Chen is supported by an educational grant from the Youde Foundation, St George's Hospital, London, England.
Received February 23, 1995; accepted March 27, 1995.
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