(Circulation. 1997;96:1461-1469.)
© 1997 American Heart Association, Inc.
Articles |
Coronary Artery Calcium in Acute Coronary Syndromes
A Comparative Study of Electron-Beam Computed Tomography, Coronary Angiography, and Intracoronary Ultrasound in Survivors of Acute Myocardial Infarction and Unstable Angina
From the Department of Cardiology, University Clinic Essen (Germany) (A.S., D.B., G.G., J.G., M.H., R.E.); the Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Foundation, Rochester, Minn (A.S., J.R.); the Institute for Diagnostic and Interventional Radiology, University Witten/Herdecke, Mülheim an der Ruhr, Germany (R.S.); and the Institute for Development and Research of Microtechnology, University of Bochum (Germany) (D.G.).
Correspondence to Axel Schmermund, MD, Mayo Clinic and Foundation, Cardiovascular Diseases, E 16-B Mayo, 200 First St SW, Rochester, MN 55905. E-mail schmermund.axel{at}mayo.edu
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Abstract |
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Background Quantification of coronary artery calcified plaques by electron-beam CT (EBCT) may predict cardiovascular events. However, whereas advanced coronary atherosclerotic plaques can be identified, mildly stenotic lipid-rich (soft) plaques may be difficult to detect. The value of EBCT in a subgroup of patients has therefore been questioned. To investigate this, we evaluated patients with acute coronary syndromes by EBCT and compared the results with coronary angiography and, in patients with an indeterminate angiogram, intracoronary ultrasound (ICUS).
Methods and Results EBCT was performed in 118 consecutive
patients (57±11 years of age) with previous myocardial infarction
(n=101) or unstable angina (n=17). A standard protocol requiring a CT
density >130 Hounsfield units in an area 
1.03 mm2
was used for the definition of coronary artery calcium. We
found that 110 patients had moderate to severe coronary artery
disease by coronary angiography, and 8 had either mildly
stenotic plaques at a single site (4 patients, confirmed by
ICUS) or nonatherosclerotic causes of the unstable coronary
syndrome (4 patients). One hundred and five of the 110 patients (96%)
with moderate to severe angiographic disease but only 1 of the 8 other
patients (13%) had a positive EBCT. Patients with acute
coronary syndromes and negative EBCTs were significantly
younger than patients with positive EBCTs (46±12 versus 58±10 years,
P<.001), and a higher percentage was actively smoking
(100% of the smokers versus 46%, P<.05).
Conclusions The vast majority of patients with acute coronary syndromes and at least moderate angiographic disease have identifiable coronary calcium by EBCT. Those patients with negative EBCTs have minimal or no atherosclerotic plaque formation. They are younger and tend to be active cigarette smokers.
Key Words: angina • calcium • coronary disease • imaging • myocardial infarction
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Introduction |
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Coronary artery calcium is almost invariably associated with coronary atherosclerotic plaque formation.1 EBCT allows accurate quantification of coronary artery calcium2 3 and has therefore been investigated as a tool for noninvasive detection of CAD.4 5
Coronary artery calcium area has been demonstrated to be linearly related to histological plaque area and to quantify overall coronary plaque volume.6 The anatomic extent of angiographic disease is clearly an important determinant of prognosis.7 In most patients, a mixture of fibrous (presumably advanced, more mineralized, and stable) and lipid-rich (potentially unstable) plaques is observed.8 Thus, the more often the fibrous plaques are seen that can be detected by EBCT, the more often soft, vulnerable plaques may be associated.8 9 The prognostic value of EBCT calcium scanning in symptomatic and asymptomatic subjects has been pointed out in two recently published studies.10 11 Specifically, subjects with little or no coronary artery calcium detected by EBCT were reported to have a very small chance of developing clinically manifest coronary syndromes over the course of 1 to 2 years compared with subjects with high calcium burdens.
Although unstable angina and MI usually result from extensive atherosclerotic disease, the individual lesions causing the event are often only mildly stenotic,12 and in some young survivors of MI, focal disease with a small overall coronary plaque burden can be observed.13 Yet only a certain "threshold" of atherosclerotic plaque volume seems to be associated with coronary artery calcium detected by EBCT.6 Endothelial dysfunction may contribute to lesion vulnerability even in early plaque formation, and oxidative stress induces an enhanced inflammatory response and monocyte infiltration that further renders lesions unstable.14 Additionally, arterial thrombosis and coronary spasm represent mechanisms not specifically linked to atherosclerosis that may nevertheless cause acute coronary syndromes.
Because of the above-noted points, a serious question has arisen as to the absence of coronary artery calcium in a subgroup of patients presenting with acute coronary syndromes.15 However, this has not been specifically examined. The purpose of the present study was to evaluate the detection of calcified atherosclerotic plaques by EBCT in patients with acute coronary syndromes. We compared EBCT to coronary angiography in survivors of acute MI or unstable angina. ICUS was used to corroborate our findings in patients with indeterminate angiograms.
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Methods |
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Patients
Between April 1994 and August 1996, 118 consecutive patients (97 men, 21 women; mean age, 57±11 years), all of whom underwent coronary angiography, gave informed consent to undergo an EBCT examination for the assessment of coronary artery calcium. One hundred one patients had a previous index MI (84 men, 17 women; mean age, 57±11 years), and 17 patients had a previous first episode of unstable angina (13 men, 4 women; mean age, 55±10 years). Most of these patients were referred by their physicians or other medical centers for further diagnosis and/or treatment at the University Clinic Essen.
MI was diagnosed according to World Health Organization criteria.16 Q-wave MI was present in 72 of the 101 patients with MI (71%). Patients with coronary atherectomy, rotablation, stent implantation, or coronary artery bypass surgery before the EBCT examination were excluded from the study. For the purposes of this study, unstable angina was defined as definite angina at rest or new-onset angina within a week of presentation.17 In addition to the history and symptoms reported by the patient, documentation of ST-T changes in the ECG and a creatine kinase elevation less than twice the upper normal limit was obtained. In all patients, coronary angiography was performed for the clinical evaluation of CAD. In 13 patients with indeterminate angiograms, an additional ICUS examination was undertaken for further classification of the patient.18 EBCT scans were performed within 18 months (176±90 days) after the acute coronary syndrome.
Electron-Beam Computed Tomography
Nonenhanced EBCT scans were performed with an Evolution scanner
(Siemens) in the high-resolution single-slice mode with an image
acquisition time of 100 milliseconds and a section thickness of 3
mm. The use of a 26-cm2 field of view and a 512x512
reconstruction matrix yielded a pixel area of 0.258
mm2. Patients were positioned supine, and after
localization of the main pulmonary artery, contiguous slices
down to the apex of the heart were obtained with ECG-gated triggering
at 80% of the RR interval.
Coronary foci with a CT density 130 HU and an area of four or
more adjacent pixels (1.03 mm2) were determined to
represent coronary artery calcium. This protocol is
widely used.5 The tomograms of all patients without
coronary artery calcium detected with this protocol were also
analyzed for the presence of coronary foci with a lower
minimum lesion area of two or more adjacent pixels (0.52
mm2).
In the presence of EBCT coronary artery calcium, a lesion score
was calculated by multiplying the area of the hyperattenuating focus in
square millimeters by a "density factor" as described by Agatston
et al.19 The density factor was determined from the peak
density within the hyperattenuating focus. The threshold was set at 130
HU: 1=130 to 199 HU, 2=200 to 299 HU, 3=300 to 399 HU, 4400 HU.
Calcific lesions were assigned to the distribution of the major
coronary arteries, and a total calcium score was calculated as
the sum of all lesion scores.
Coronary Angiography
Selective coronary angiography was performed by the
Judkins technique in each patient with a minimum of two biplane
projections for the left coronary artery system and one
biplane projection for the right coronary artery by use of
a HICOR System (Siemens). For lumen opacification only non-ionic
contrast medium was used. Luminal narrowing of equal or more than 50%
was defined as significant stenosis. Off-line quantitative
coronary angiography (MEDIS, Reiber) was used to confirm
categorization of lesions and to characterize the culprit lesion in the
event-related coronary artery in patients with no detectable
coronary artery calcium.20 Patients with
significant stenoses (>50% diameter reduction) in one or at
least two major vessels were defined as having one-vessel or
multivessel coronary artery disease, respectively. Patients
with significant stenoses and those with intermediate (30%
to 50% luminal diameter) stenoses at more than one site in the
coronary system were classified as having moderate to severe
atherosclerotic disease. Two patients, one with occlusive
arterial thrombosis and one with spontaneous
coronary dissection, were considered not to have significant
angiographic disease because there were no stenoses. However,
the cause of acute MI was clearly visualized by coronary
angiography, so the angiogram was considered positive for the
sensitivity calculations.
Intracoronary Ultrasound
ICUS was performed after the coronary angiogram in 13
patients with no apparent or only mild angiographic disease. Catheters
with 20- to 30-MHz transducers (Boston Scientific Corp) guided by a
0.014-in floppy guide wire (ACS) and connected to a console (Hewlett
Packard) were used. The imaging catheter was positioned under
fluoroscopic guidance into the distal segment of the respective
coronary artery. The catheter was then pulled back manually to
the proximal part of the respective coronary artery in 3- to
4-mm steps. Each position of the ultrasound catheter was marked
separately, and a short fluoroscopic sequence was filmed concomitantly.
All segments with signs of arteriosclerosis were
marked. Finally, the ultrasound catheter was reinserted to the distal
position, and a slow, continuous pullback registration (1 mm/s)
was obtained. All data were stored continuously on a videotape system
(Super VHS, Sony) for playback and off-line analysis.
Coronary artery sections were considered normal when the criteria proposed by Nissen et al21 and Ge et al22 were met. Plaques were defined as echo-dense structures with a sharp demarcation within the vessel lumen separated by an echo-lucent zone from the adjacent structures. Plaques were categorized as eccentric only if an arc of disease-free arterial wall was seen within the lesion.23 The presence of calcium was diagnosed when echoes brighter than the reference adventitia with acoustic shadowing of deeper arterial structures were observed.24 The minimal luminal diameter, corresponding vessel diameter, and external and internal elastic membrane cross-sectional areas were measured at end diastole.22 The plaque cross-sectional area was calculated by subtracting the internal elastic membrane (lumen) from the external elastic membrane cross-sectional area. Luminal diameter stenosis and area stenosis were calculated.
Statistical Analysis
Values are reported as mean±SD if not indicated otherwise.
Characteristics of patients with and without coronary artery
calcium detected by EBCT were compared by use of an unpaired
t test for age distribution and 
2 and
Fisher's exact test for categorical variables. Receiver-operating
characteristic curve analysis was performed to establish the
relationship between the definition of calcium quantities by EBCT and
the angiographic definition of significant disease. Sensitivity as the
dependent y variable was plotted as a function of
1-specificity as the x variable (equivalent to the
false-positive rate) to determine individual
{x,y} pairs with different calcium scores. A
value of P<.05 was considered significant for all
statistical evaluations. The analyses were performed with the
SigmaStat for Windows 1.0 (Jandel Corp) and True Epistat 5.10 (Epistat
Services) software systems.
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Results |
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Of the 118 patients with acute coronary syndromes, 106 (90%) had positive EBCTs, ie, a calcium score >0. No coronary artery calcium was seen in 12 patients (10%), 9 patients with MI who were 46±12 years (23 to 67 years) of age, and 3 patients with unstable angina who were 46±15 years (32 to 61 years) of age (Table 1
). The mean total EBCT score in the 106
patients with positive EBCTs was 427.0±516.2 (2.58 to 3099.3). It was
significantly higher in 92 patients with MI than in 14 patients with
unstable angina: 460.2±528.7 versus 197.0±248.2 (P<.01).
When an altered scoring protocol with a minimum lesion area of two
pixels (0.52 mm2) instead of four pixels (1.03
mm2) was used to define coronary artery calcium, a
score >0 was seen in 5 of 12 patients (42%) who had negative EBCTs
with the standard protocol.
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Coronary Anatomy as Defined by
Arteriography
Of the 118 patients with acute coronary syndromes, 105
(89.0%) had significant angiographic disease: 103 patients (87%) with
significant stenoses and 2 patients (2%) with no
stenoses but arterial thrombotic occlusion (1
patient) and coronary dissection (1 patient). Nine patients
(8%) had intermediate 30% to 50% diameter stenoses, 2 of
whom had a single intermediate stenosis in an otherwise
normal-appearing coronary system (confirmed by ICUS). Normal
coronary angiograms or only minor wall irregularities were
observed in 4 of 118 patients (3%). Of these patients, 2 had focal
plaque formation visualized only by ICUS, whereas the other 2 had no
plaques as determined by ICUS but had myocardial bridging (1 patient)
and arterial spasm (1 patient). Thus, angiographically
moderate to severe coronary atherosclerosis was
found in 110 patients. In 8 patients, mild plaque formation at a single
site (4 patients) or nonatherosclerotic mechanisms of acute
ischemia (4 patients) were seen.
EBCT With Respect to Coronary Anatomy
Positive EBCTs were observed in 105 of the 110 patients (96%)
with moderate to severe coronary
atherosclerosis and in 1 of the other 8 patients (13%;
P<.001). With regard to the detection of plaques in the
whole patient population, the presence of calcium by EBCT showed a
sensitivity comparable to the presence of significant angiographic
stenoses: 90% and 87%, respectively. Using a calcium score
>0 as the cutoff point, sensitivity and specificity of EBCT to
diagnose significant angiographic stenoses or any angiographic
stenoses 30% were 95% and 47% (significant
stenoses) or 95% and 100% (stenoses 30%),
respectively. Positive and negative predictive values were 93% and
58% (significant stenoses) or 100% and 50% (stenoses
30%), respectively. Receiver-operating characteristic curve
analysis of coronary calcium scores for the detection
of significant angiographic CAD yielded an area under the curve of
0.90±0.03 (mean±SEM; P<.0001). The best values for
sensitivity and specificity, 91% and 73%, respectively, were obtained
at a cutoff score of 10.30 (Fig 1).
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Table 2 gives the distribution of
significant angiographic CAD and angiographic multivessel disease in
patients with positive and negative EBCTs. Mild or no angiographic
stenoses were seen in 1 of 106 patients (1%) with positive
EBCTs but in 7 of 12 patients (58%) with negative EBCTs (including 1
patient with arterial thrombotic occlusion and 1 with
coronary dissection; P<.001). Table 3 describes the angiographic findings in
the 12 patients with negative EBCTs. Fig 2 shows three angiograms of patients with
negative EBCTs.
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Characteristics of Patients With Negative EBCTs
Patients with negative EBCTs were 12 years younger than patients
with positive EBCTs (P<.001; Table 2
). Mean and median ages
were 46 and 44 years, respectively, and 8 of the 12 patients (67%)
were <50 years of age, whereas only 22 of 106 patients (21%) with
positive EBCTs were <50 years of age. The distribution of sex and most
coronary risk factors was comparable in both groups (Table 2).
However, although there was no difference in the overall percentage of
past or present smokers, all 7 smokers with negative EBCTs were
active smokers at the time of the unstable event, whereas this was true
for only 31 of the 67 smokers (46%) with positive EBCTs
(P<.05).
The percentage of patients with unstable angina rather than MI did not
differ in patients with positive and negative EBCTs: 13% (14 of 106
patients) versus 25% (3 of 12 patients; P=NS). Furthermore,
the prevalence of Q-wave MI among patients with MI did not differ in
patients with positive and negative EBCTs: 72% (66 of 92 patients)
versus 67% (6 of 9 patients; P=NS). At the time of the EBCT
examination, 2 of 12 patients (17%) with negative EBCTs had developed
small left ventricular aneurysms with
well-preserved overall left ventricular function after MI
(Table 1).
ICUS Characteristics of Patients With Negative EBCTs
ICUS was performed in 8 of 12 patients (67%) with negative EBCTs
and in 5 of 106 patients (5%) with positive EBCTs. Except for one
lesion with a diameter stenosis slightly >50% (54.5%), there
were no significant stenoses in these patients. In 1 of the 8
patients with negative EBCTs, ICUS was performed only after directional
coronary atherectomy. In 4 of these 8 patients (50%),
eccentric plaques of a soft texture were documented (Fig 3c). The typical ultrasonic pattern of
calcification was not seen in patients with negative EBCTs, but in 4 of
5 patients with positive EBCTs (Fig 3a). All plaques observed in
patients with negative EBCTs had an arc of disease-free
arterial wall within the lesion (ie, eccentric lesion; Fig 3c), whereas some degree of concentricity was seen in all plaques in
the 5 patients with positive EBCTs (Fig 3a). Plaque area in the 4
patients with negative EBCTs who had plaques and were examined before
any intervention was 6.6±2.5 mm2 (3.2 to 9.3
mm2), and area stenosis was 51.8±11.2
mm2 (39.9 to 65.5 mm2). In 1 of these
patients, a tear in the middle of a plaque with an echo-lucent core
indicated plaque rupture (Fig 3d1 and 3d2).
Systolic and diastolic movement of the fibrous cap
could be observed (Table 4).
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In 3 patients with a negative EBCT, small intima lesions with an
area 
1 mm2 and otherwise normal vessel walls
were seen using ICUS. One patient had acute thrombotic occlusion of the
proximal LAD. This occurred in a very large vessel segment with stasis
of blood. Another of these patients showed catheter-induced
coronary spasm directly distal to myocardial bridging in the
mid LAD. In this and in another patient with myocardial bridging (Fig. 3b1 and 3b2), the intimal lesions were
identified just proximal to the intramyocardial vessel segment (Table 4).
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Discussion |
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The present study is the first investigation of EBCT calcium scans with regard to coronary artery anatomy in patients with unstable coronary syndromes. EBCT reliably identified coronary calcific plaques in those patients with moderate to severe coronary atherosclerotic disease. Negative calcium scans were seen in 10% of the patients. These patients were characterized by several attributes.
Low Atherosclerotic Plaque Burden in Patients With Negative
EBCTs
In most patients with negative EBCTs, the acute coronary
syndrome was considered to be caused either by mechanisms other than
atherosclerosis (4 patients) or by focal
atherosclerotic plaque formation (3 patients). Whereas patients with a
positive EBCT had mostly significant angiographic and multivessel
disease, significant angiographic stenoses were observed in
only 5 of 12 patients with negative EBCTs, and only 1 patient had
multivessel disease. ICUS in 8 patients with negative EBCTs revealed
either no apparent atherosclerotic disease or soft plaques with a
disease-free arc of the arterial wall and no ultrasonic
calcification, characteristics that are found in early and
angiographically silent coronary
atherosclerosis.18 22 The percentage of
patients with negative EBCTs reflects the difficulty to detect plaques
in these patients rather than in those with more extensive angiographic
disease. One patient had an isolated unstable plaque with ruptured
fibrous cap. Interestingly, a follow-up EBCT examination 9 months later
still did not detect any coronary artery calcium, although
plaque healing had been demonstrated with ICUS 2 months after the
unstable coronary event in this patient.25
Histopathological ex vivo2 6 and ICUS in vivo studies26 have shown that coronary artery segments with little atherosclerotic plaque burden may not be detected by EBCT. Although frequently only mildly to moderately stenotic lipid-rich plaques cause unstable coronary syndromes,12 most patients with acute coronary syndromes have angiographic multivessel disease.13 Autopsy examination of patients with fatal acute coronary events usually reveals extensive coronary atherosclerosis.27 In this regard, the population examined in the present study may not have been representative of a broader general population with acute coronary syndromes. It was a referral population, and some patients were explicitly referred to our department for further evaluation of angiographically indeterminate or minimal lesions by intracoronary two-dimensional and Doppler ultrasound techniques.18
Generally, plaque rupture and, as blood components are exposed to tissue factors in the lesion, thrombus deposition are considered the most common mechanisms of unstable coronary syndromes.28 The severity and duration of ischemia depend on the extent of thrombus formation in the diseased vessel. Although endothelial dysfunction, vasospasm, thrombosis, and atherosclerosis are all interrelated, it is now well established that coronary vasospasm and arterial thrombosis occasionally occur in the absence of atherosclerotic lesions.29 A variety of physical and chemical toxins may lead to a loss of endothelial vasodilatory and antithrombotic properties.28 Endothelial integrity is compromised not only in advanced atherosclerosis30 but also in apparently normal coronary arteries in the presence of risk factors.31
Younger Age in Patients With Negative EBCTs
In the present study, patients with negative EBCTs were
significantly younger than patients with positive EBCTs, and 8 of 12
patients (67%) were <50 years of age. The appearance of calcium
deposits is related to the natural history of atherosclerotic lesions,
representing an active rather than a degenerative
process.32 In lesions seen in adolescents, calcium is
first detected intracellularly.33 Extracellular calcium
appears in preatheromatous lesions usually found in middle-aged
adults. Concerning lesion morphology, calcium deposits are more often
observed in type Vb/VII lesions than in type III and IV lesions and
thus are less often found in early stages of coronary
atherosclerosis.33 34 Plaques of <50%
area stenosis are frequently not calcified.2 As
coronary plaque burden increases with age, the amount of
calcification also increases.35 In general, the
sensitivity of EBCT calcium scanning for the detection of significant
CAD is best in patients >50 years of age.5
Smoking in Patients With Negative EBCTs
Of the 12 patients with negative EBCTs in the present study, 7
were active smokers at the time of the coronary event. Smoking
was, together with hypercholesterolemia, the
most common coronary risk factor in this group. In two studies
evaluating risk factor correlates of EBCT coronary artery
calcium, smoking was reported to be associated with an increased
prevalence and extent of coronary
calcification.36 37 However, these studies comprised
heterogeneous groups of symptomatic and
asymptomatic patients and did not differentiate between
past and active smoking.
Smoking is a well-known risk factor for cardiovascular events. It exerts a deleterious effect on the vascular endothelium and causes direct vasoconstriction of both coronary epicardial and resistance vessels.38 39 Platelet aggregation and fibrinogen levels are increased, resulting in an enhanced risk of thrombosis even in the absence of severe atherosclerotic disease.40 In an ICUS study of target lesions in patients with stable and unstable angina, plaques in 37 of 52 smokers (71%) and in 46 of 94 nonsmokers (49%) were classified as soft rather than hard plaques (P=.01, univariate analysis).41 However, this difference was not significant in a multivariate analysis. In a pathological study of carotid plaques obtained at endarterectomy, smoking was found to be associated with a significantly increased frequency of mural plaque thrombosis.42
Study Limitations
The issue of repeatability and variability of EBCT scans was not
addressed in the present study, although it plays an important
role, especially in the range of CT density values in proximity to the
threshold of 130 HU. Variation of scores may depend on breathing,
improper ECG gating, imaging artifacts, and the size and localization
of calcific deposits in the arterial tree.43
However, the EBCT protocol in the present study (CT density
threshold=130 HU in an area 1.03 mm2)19
is the one most widely used,5 and it was our intention to
evaluate the EBCT protocol of most laboratories for the assessment of
coronary artery calcium. In the present study, a minimum
pixel area that was decreased from 1.03 to 0.52 mm2
identified coronary calcium in only 5 of 12 patients (42%)
with negative standard EBCTs, and only 1 of the 8 patients <50 years
was among them.
There is no generally accepted exact definition of moderate or severe coronary atherosclerosis in a coronary angiogram. There is no typical angiographic pattern of vulnerable plaques,44 and accordingly angiography does not allow the identification of individual plaques at risk. Yet despite its well-known limitations, coronary angiography is considered the standard method of evaluating coronary anatomy. We classified patients as having moderate to severe atherosclerosis in the presence of one or more angiographically significant stenosis or two or more intermediate stenoses in an otherwise normal-appearing arteriogram. Patients with only wall irregularities or a single intermediate stenosis were considered to have mild atherosclerotic disease, and this is certainly not inconsequential.
ICUS was performed to obtain additional information in patients with indeterminate arteriograms. Thus, few patients underwent an ICUS examination, and our data do not allow us to make general conclusions concerning the dominant plaque morphology in our patients. This did not, however, compromise the outcome of our study with respect to its purpose, which was to evaluate the detection of calcified plaques by EBCT in patients with acute coronary syndromes.
Clinical Implications
The identification of patients at risk for atherosclerotic
coronary events is of paramount importance because aggressive
treatment of risk factors allows physicians to substantially lower the
rate of events in these patients.45 In this setting, EBCT
is a diagnostic modality of great interest because it is
noninvasive, can be performed easily, and allows direct visualization
of the coronary arteries. The present study demonstrates
that EBCT identifies calcified plaques in the vast majority of patients
with vulnerable atherosclerotic plaques. The excellent results reported
in the first prognostic studies using EBCT10 11 are thus
confirmed and further elucidated. On the other hand, patients with low
coronary plaque burden or mechanisms of unstable events that
are not specifically related to atherosclerosis may be
missed by EBCT calcium scanning. This may be of concern, particularly
in younger age groups and active smokers. The prognostic implication of
negative EBCTs in these patients remains to be established. In two
patients with negative EBCTs in the present study who had left
ventricular aneurysms, overall left
ventricular size and function were well preserved.
Currently, EBCT seems a very promising method to identify patients at
risk for future atherosclerosis-related
coronary unstable events.
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Acknowledgments |
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Dr Schmermund was supported in part by a grant from the German Research Association (Deutsche Forschungsgemeinschaft, Schm 1233/1-1).
Received February 18, 1997; accepted March 30, 1997.
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