© 2001 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Natural History and Topographic Pattern of Progression of Coronary Calcification in Symptomatic Patients
An Electron-Beam CT Study
From the Department of Cardiology (A.S., D.B., S.M., R.E.), University Clinic Essen, Essen, Germany; the Institute for MicroTherapy (P.K., D.G.), Bochum, Germany; the Institute for Diagnostic and Interventional Radiology (H.P., R.S.), Mülheim, Germany; and the Department of Radiology and MicroTherapy (P.K., H.P., D.G., R.S.), University Witten/Herdecke, Witten, Germany.
Correspondence to Dr Axel Schmermund, Department of Cardiology, University Clinic Essen, Hufelandstraße 55, D-45122 Essen, Germany. E-mail Axel.Schmermund{at}uni-essen.de
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract—Electron-beam CT may assess the progression of coronary atherosclerosis by visualizing changes in calcification. The present investigation analyzes (1) the rate of progression of calcification in symptomatic patients, (2) the topographic pattern, and (3) the influence of baseline plaque burden and risk factors. Progression of calcification during a mean (median) interval of 18 (15) months was measured in 102 symptomatic outpatients (aged 59±9 years, 80% male) with calcification. In 4 patient groups with a baseline total score (Agatston criteria) of 1 to 30, >30 to 100, >100 to 400, and >400, the median was 3.1, 26.1, 58.9, and 109.7, respectively, for absolute annual progression of the score (P<0.05) and 57%, 49%, 32%, and 15%, respectively, for relative progression (P<0.05). On the coronary segmental level, changes were largely restricted to typical predilection sites of coronary atherosclerosis. The presence of angiographically defined coronary narrowing influenced absolute, but not relative, progression. Of the risk factors, only low density lipoprotein cholesterol levels showed a trend, although not significant, for predicting progression. These data indicate that baseline plaque burden determines the rate of progression of calcification. This appears to be a coronary systemic process, reflecting the natural history of coronary atherosclerosis.
Key Words: progression • coronary atherosclerosis • calcium • electron-beam CT • coronary artery disease
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Electron-beam CT (EBCT) has been used in serial studies to determine the progression of coronary calcified plaque disease.1 2 3 4 5 6 The natural rate of progression of calcification has been described in healthy subjects in a community setting.4 It has been suggested that in asymptomatic high-risk patients, the influence of treating elevated lipid levels on the progression of coronary atherosclerotic disease can be evaluated by use of EBCT.3 5 If these reports are taken into consideration, EBCT may be of value in assessing the treatment of symptomatic patients. However, little is known about the rate of progression to be expected in symptomatic patients with modern pharmacological therapy. The progression of calcification may vary substantially between patients with or without established coronary artery disease (CAD) and may depend on the baseline amount of calcification.6
As calcification develops, the pattern of distribution among the major coronary arteries and the coronary segments has not been clarified. Only the changes in the overall amount of calcification have previously been reported. It was the aim of the present investigation (1) to analyze the rate of progression of calcification in symptomatic patients with modern treatment, (2) to establish the topographic pattern of progression, and (3) to determine the relationship of EBCT-derived and angiographic coronary findings and of risk factors with the rate of progression.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Patients
Outpatients followed in the Cardiology Department of the University Clinic Essen because of known or suspected CAD were considered for this investigation. Patients were included in a consecutive manner between January 1997 and December 1999 if they were males aged
40 years or
females aged 45 years and if the scanner at a remote site was
available. Exclusion criteria were body weight >300 pounds, possible
or confirmed pregnancy, prior coronary stent implantation,
plaque-debulking coronary interventions or bypass surgery, and
arrhythmias interfering with the ability to perform ECG-gated
triggering. Patients with previous percutaneous
coronary angioplasty were accepted if the intervention was
performed before and not during the follow-up period. It has been
suggested that angioplasty does not alter EBCT calcium
measurements.7 A total of 111
patients were included in the study. The minimum interval between the 2
studies was 6 months. The mean±SD interval was 18.2±11.6 months
(median was 15 months, and 25th and 75th percentiles were 9 and 25
months, respectively). Cardiovascular risk factors and medication use were regularly recorded during the follow-up period at 3- to 6-month intervals. Laboratory measurements were performed as reported previously.8 The mean value of several measurements was calculated.
Electron-Beam CT
Nonenhanced EBCT scans were performed with a Siemens
Evolution scanner (Imatron Inc) in the single-slice mode with an image
acquisition time of 100 ms and a section thickness of 3 mm, as
described
previously.8 9 10 11
A 26-cm2 field of view was used. Contiguous
slices down to the apex of the heart were obtained.
For each study, including separate analyses of the
major coronary arteries and 12 coronary segments as
described below, a calcium score was determined by using the methods of
Agatston et al.12 The calcium
score is the product of the area of coronary artery calcium
(at least 4 contiguous pixels with a CT density 130 Hounsfield units)
and a factor rated 1 through 4 dictated by the maximum CT density
within that lesion. Calcified lesions were encircled manually by a
physician and were included in the analysis only if they were
strictly in the trajectory of the coronary arteries. All
studies were analyzed in this same fashion with the use of the
original software provided with the scanner console. Because it has
been suggested that for serial EBCT studies, the area of calcification
provides for better
reproducibility,2 calcium
areas, which represent an inherent component of the Agatston
score, were also computed for the major coronary arteries and
the overall amount of calcification.
In our laboratory, scan-to-scan reproducibility was tested in 40 patients as part of a multicenter validation study that was independent of the present series.13 The median variability between 2 scans performed minutes apart in the same patient (only in patients with positive calcium scores) was 10% for the Agatston score and 8% for the calcium area and was not statistically different. In the present investigation, reproducibility was not as much a concern as in studies analyzing individual changes, because calcification was analyzed in groups of patients. Therefore and because calcium scores (which are more familiar to physicians than calcium areas) are usually reported,14 the present investigation gives calcium scores for the detailed analysis of 12 coronary segments.
On the basis of the coronary segmental classification proposed by the American Heart Association,15 12 major coronary segments were analyzed separately. For convenience, these segments can be assumed to correspond largely to the proximal, mid, and distal portions of the right coronary artery (RCA) and the right posterior descending coronary artery (RPD, segments 1 to 4 according to the American Heart Association); the left main stem (segment 5); the proximal, mid, and distal left anterior descending coronary artery (LAD) and first diagonal branch (segments 6 to 9); and the proximal, mid, and distal left circumflex coronary artery (LCx, segments 11, 13, and 15). We10 11 and others16 have previously described the application of this segmental model to EBCT images. Only 12 of the 15 segments specified in the American Heart Association classification were considered because only they could be assessed reliably.
Statistical Analysis
The changes in coronary calcium area and
score values between the 2 scans were annualized. Absolute changes in
area and score were calculated as
follows:
 | (1) |
 | (2) |
To analyze the influence of different baseline total
calcium scores on parameters of the progression of
calcification, patients were classified into 4 groups according to
suggestions by Rumberger et
al.17 Total calcium score cut
points of 30, 100, and 400 were used. Patients with a positive score of
30 had minimal coronary calcified
atherosclerosis, whereas the extent and severity of the
disease increased in patients with scores between 30 and 100, between
100 and 400, and >400. In modification of the suggestions by Rumberger
et al, we used 30 instead of 10 as the cut point for minimal
atherosclerosis because of the potential for artifacts
confusing the topographic analysis in the very low score range.
In recent reports, calcium scores >30 generally had an interscan
variability
<10%.2 13 18
Usually, the median of calcium area and score values and their changes were computed. However, because most segmental calcium score values were 0, the 75th percentile was given for segmental calcium score values. A 2-tailed value of P<0.05 was considered to indicate a significant difference.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Patient Demographics
Characteristics of the 111 patients are listed in Table 1
. Cardiovascular risk factors were
highly prevalent among the patients, and multiple medications were used
during the follow-up period. A positive total calcium score was found
at baseline in 103 patients (93%) and at follow-up in 102 patients
(92%). In 8 patients (7%), no calcium was detected at either of both
examinations, and in 1 patient (1%), a positive total calcium score
(2.6) was observed at baseline but not at follow-up. At baseline, the
mean and median values were 434.3 and 134.1, respectively, for the
coronary calcium score and 130.6
mm2 and 46.2
mm2, respectively, for the coronary
calcium area. At follow up, these values were 527.5 and 206.1,
respectively, for the calcium score and 143.6
mm2 and 58.5
mm2, respectively, for the calcium area. The
detailed values for each major coronary artery are listed in
Table I (please see online data supplement at
http://atvb.ahajournals.org). Most patients had a baseline total
calcium score >100 in this symptomatic population.
Figure 1 shows that at baseline, calcification was seen most
frequently in the proximal LAD, followed by the proximal LCx. Whereas
in the left coronary system, the presence and the amount of
calcification were much more prominent in the proximal coronary
segments, the distribution was more even in the
RCA.
|
|
Progression of Coronary
Calcification
For the analysis of progression, only the 102
patients with a positive total score at follow-up were considered. The
baseline total calcium score was 1 to 30 in 18 (18%) patients, >30 to
100 in 21 (21%) patients, >100 to 400 in 31 (30%) patients, and
>400 in 32 (31%) patients. Within all subgroups, calcium score and
area were greater at follow-up than at baseline, and this was
significant for the 3 groups with scores ranging between 1 and 400
(Table 2). The absolute annual progression was significantly
less in the lowest total calcium score group compared with the other
groups, as shown in
Figure 2. The relative progression of calcification (calcium
area and score) was greater in the lower than in the higher total
calcium score groups, but the difference was much less pronounced than
for the absolute values.
|
|
P<0.05 vs >400. B, Percent changes. *P<0.05 vs >400.
In the total group of 102 patients, mean and median
relative annual progression of the total score was 51% and 32%,
respectively, and mean and median relative annual progression of the
total area was 42% and 27%, respectively (Table
II; please see online
data supplement at http://atvb.ahajournals.org). In the subgroups with
baseline scores of 1 to 30, >30 to 100, >100 to 400, and >400,
median relative annual progression of the calcium score was 57%, 49%,
32%, and 15%, respectively, and that of the calcium area was 36%,
39%, 27%, and 13%, respectively
(Figure 2 and online Table II).
Overall regression of calcification was measured in 15 (15%) of 102 patients. The percentage of patients with regression was quite evenly distributed among the 4 baseline score subgroups, ie, 3 of 18 (17%, lowest baseline score group), 2 of 21 (10%), 4 of 31 (13%), and 6 of 32 (19%, highest baseline score group).
Coronary angiographic status was known in 85 (83%)
patients. At least 1 vessel showed luminal diameter obstruction 50%
in 52 (61%) patients (partly treated by angioplasty, as shown in
Table 1). The median baseline total coronary
calcium score in these patients was 353.8, which was significantly
greater than that in patients without angiographically obstructive CAD
(median 97.8, P<0.001 by
Mann-Whitney test). The median absolute annual progression of the total
calcium area and score was significantly greater in patients with
versus patients without obstructive CAD: 15.6 and 43.8, respectively,
versus 6.9 and 26.3, respectively
(P=0.03 and
P=0.04, respectively). However,
the relative annual progression was similar in the 2 patient groups.
The median values of relative area and score progression were 20.3%
and 26.6%, respectively, in patients with obstructive CAD and 27.4%
and 26.0%, respectively, in patients without obstructive CAD
(P>0.8).
Topographic Pattern of Progression of
Calcification
As shown in
Figure 2 (and shown in online Table II), the changes in
areas and scores in the major coronary arteries were very
comparable, suggesting that the CT density of the lesions changed in
the same direction and with the same magnitude as the lesion area. The
difference in the rate of progression between the vessels did not reach
significance.
Figure 3 shows the topography of progression of the
segmental calcium scores. Clearly, those segments with the highest
initial (baseline) calcium burden also displayed the greatest increase
in calcification. Analysis according to the baseline total
calcium score subgroups revealed that in the lower score subgroups, the
most prominently calcified segments also displayed the greatest rate of
progression. With higher total calcium scores, there appeared to be a
shift toward greater relative progression in those segments that were
less prominently calcified at baseline.
|
Topographic Pattern of Progression According to
Overall Changes in Calcification
To analyze the topography of progression
according to the overall change in total calcium score, patients were
classified into quartiles of relative total calcium score change. The
changes in the major coronary artery scores paralleled the
overall calcium score changes. The progression of calcification was
evenly distributed among the major coronary arteries (online
Table II).
The changes in segmental calcium scores,
demon-strated in Figure I (please see online data supplement
athttp://atvb.ahajournals.org), also paralleled the overall
changes. The proximal left coronary segments and the RCA
segments (more evenly distributed) displayed an increasing progression
in scores with an increasing progression of total calcium
scores.
Factors Influencing the Rate of
Progression
Baseline overall coronary plaque burden (ie,
calcium scores and areas) was an independent predictor of absolute and
relative overall changes in calcium score
(P<0.05, respectively, linear
regression analysis). However, as judged by the
r2
values, only 
5% to 10% of the variability in progression was
explained by baseline calcium score or area. As described above,
angiographic status predicted only absolute, but not relative,
progression of calcification.
Of the risk factors listed in
Table 1, only LDL cholesterol demonstrated a
tendency, although not significant, for increased values in patients
with greater progression of calcium area. LDL cholesterol
in patients with relative progression above the median was 142±44
mg/dL (median, 139 mg/dL) versus 130±33 mg/dL (median, 128 mg/dL) in
patients with relative progression below the median
(P=0.1). Use of lipid-lowering
medication was 80% in patients with regression of calcification versus
62% in the other patients
(P=0.3). Use of lipid-lowering
medications was also not different among the 4 baseline score
subgroups, ie, 13 of 18 (72%, lowest baseline score group), 11 of 21
(52%), 22 of 31 (71%), and 20 of 32 (63%, highest baseline score
group).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The present data provide information on the rate of absolute and relative annual progression of calcification in symptomatic patients with risk factors and modern medical therapy (online Table
II). Several observations deserve to be noted. It
appears clinically relevant that opposite trends in absolute and
relative (percent) measures of progression were seen
(Figure 2). Patients with extensive calcification had the
greatest absolute rate of progression, indicating an enhanced activity
of atherosclerotic plaque disease despite medical therapy. This
underscores the need to account for the initial extent of
calcification. However, angiographically proven obstructive CAD per se
did not appear to accelerate the progression of
calcification.
Further observations pertain to the pathophysiology and
natural history of calcifying atherosclerosis. Changes
in calcium area and score were very consistent and indicated
that calcified lesion density progressed along with lesion area (online
Table II,
Figure 2). There were no significant differences in the rate
of progression of calcification between the major coronary
arteries (LAD, LCx, and RCA). It appears only consequential that the
most consistent and greatest progression of calcification was
observed in the segments with the most prominent initial involvement.
Consistent with previous pathological and angiographic studies
on the natural history of
atherosclerosis,19 20
the rate of progression of calcification was greatest in the proximal
left coronary system and showed a more even distribution from
proximal to distal in the RCA
(Figure 3).
Greater relative progression of overall calcification was a result of uniformly greater relative progression of calcification in the coronary segments involved. Thus, the development or stabilization of calcified atherosclerotic disease occurred simultaneously at different predilection sites in the coronary tree.19 20 This uniform pattern of change suggests that the development of calcified plaque disease is a coronary systemic process.
Rate of Progression of Calcification
The overall mean relative progression of calcification
observed in patients with positive calcium scores was 51% for total
calcium scores and 42% for total calcium areas. The median values were
32% and 27%, respectively.
Most previous reports on the rate of progression of calcification examined only asymptomatic patients. Maher et al4 reported a mean annual progression of coronary calcium scores in healthy adults (aged 46±7 years) of 24%. In asymptomatic patients with several risk factors, Budoff et al5 observed a mean annual progression of 33%, which was lower in patients on lipid-lowering therapy than in the total group. These 2 reports included patients with negative EBCTs.
Callister et al2 assessed the progression of a volumetric score essentially computed on the basis of calcium areas. In asymptomatic high-risk individuals, they observed a mean and median relative annual change of the volumetric score of 52% and 44%, respectively. Expanding on that work, they subsequently reported that successful pharmacological LDL cholesterol reduction led to a significant mitigation of progression of the volumetric score.3 In untreated patients with a mean LDL cholesterol level of 147 mg/dL, the mean annual progression was 52%. In patients treated pharmacologically but whose LDL cholesterol level remained >120 mg/dL (at a mean value of 139 mg/dL), mean annual progression was 25%. In patients with LDL cholesterol values <120 mg/dL, on average a 7% regression of the volumetric score was observed.3
In an early careful study, Janowitz et al6 compared the progression of total calcium area in 10 patients with angiographically proven CAD with that in 10 asymptomatic patients and found a significant difference of 48% versus 22%, respectively. This difference was not reproduced in our present series of 85 patients who underwent coronary angiography. This may partly be due to different patient characteristics apart from the angiographic data, inasmuch as we examined a selected referral population treated with modern pharmacological therapy. We believe that in stable angina pectoris, it is unlikely that luminal obstruction per se predicts accelerated progression of CAD. Rather, it would indicate an angiographically appreciable advanced stage of coronary atherosclerotic plaque disease and thus increased susceptibility to further endothelial injury and progression of disease in the absence of adequate treatment.
Regression of Calcification
It is yet unclear whether regression of calcification,
observed in 15 (15%) patients in the present investigation, is
more than simply a phenomenon within the range of interscan
reproducibility. Callister et
al3 found regression of the
volumetric score in 63% of 65 patients with low LDL
cholesterol levels. A possible explanation for regression
of calcification has been derived from an animal model in rhesus
monkeys, who after 3.7 years on a low cholesterol
regression diet showed a slightly decreased area of calcified lesions,
perhaps as a result of shrinkage and increased density of the
lesions.21 The median changes
of calcium areas and scores in patients with regression of
calcification in the present investigation generally went in the
same direction. It remains unresolved whether, indeed, "lesion
consolidation" with decreased calcium area and increased density may
account for the regression of calcification in some
patients.
Topographic Pattern of Progression of
Calcification
The topographic pattern of progression as reflected in
the analysis of 12 coronary segments paralleled the
overall changes in calcification seen with different baseline total
calcium scores as well as with varying overall changes, ranging from
regression of scores to annual progression >60%. Changes were seen
predominantly at the typical predilection sites of
atherosclerosis in the proximal left coronary
segments.19 20 Of
note, the distribution of disease progression was much more even in the
RCA, with substantial progression found in the distal segments of that
vessel. Accordingly, for studies of the progression of coronary
calcification, it is likely useful to obtain sections through the
cardiac apex instead of a limited set including only the proximal
cardiac
structures.22
Risk Factor Influences
Risk factor influences were moderate, and only LDL
cholesterol appeared to modify the rate of progression.
However, this did not achieve significance. The use of lipid-lowering
drugs did not differ between patients with higher versus lower baseline
amounts of calcification and thus cannot explain the different rates of
progression between these groups.
Study Limitations
It has been mentioned that a recently validated
volumetric calcium score appears to offer advantages for serial EBCT
studies because of significantly improved reproducibility compared with
the Agatston
score,2 3 which is
presently the most widely
used.14 For the present
investigation, volumetric calcium scoring, which depends on
3D-rendering capabilities, was not available. However, the calcium area
has also been reported to yield improved reproducibility, because as
with the volumetric score, calcium area does not take an arbitrarily
assigned density factor into account. We computed calcium area and
score (Agatston score) for the major coronary arteries and the
complete coronary tree, which enabled us to compare the changes
in both parameters.
It should be noted that recently published
studies13 18 have
demonstrated a better reproducibility of the EBCT-derived Agatston
score than earlier
studies.22 23 24
This is partly due to improvements in the technique with the new
scanner generation. For example, scanning can presently be
completed in 1 breath-holding as opposed to the 2 breath-holdings
required when the older EBCT scanners were used. The more recent
publications have reported a median variability of the Agatston score
10%, which is clearly less than the median progression of 32%
observed in the present investigation. These reassuring data
notwithstanding, small amounts of calcium, especially on the segmental
level, can certainly yield measurements with substantial
variability.24 However, it
should be noted that in the present investigation, groups of
patients were analyzed. The consistent increase in
calcium scores between the baseline and the follow-up scan in subgroups
of patients and in the coronary segments indicates that our
results are meaningful.
Because a selected referral population was examined, our data cannot be extrapolated without much caution to other symptomatic populations. Especially, ethnic groups other than whites (which made up the present population) may show different rates of disease progression. Our results are in agreement with previous reports also derived from predominantly white patients.2 3 4 5 Pathological investigations have demonstrated an impressive consistency in the predilection sites and axial distribution of coronary atherosclerosis among various ethnic groups and in both sexes.19 Hence, there is no reason to believe that the topographic pattern of disease progression would differ in other patient populations.
Conclusions
The present data appear to provide a useful basis
for interpretation of the progression of calcified plaque disease in
symptomatic patients with modern therapy. Patients with
extensive calcification had the greatest absolute rate of progression,
indicating an enhanced activity of atherosclerotic plaque disease
despite medical therapy. Therefore, it appears critical to account for
the initial extent of calcification. The topographic pattern of
progression of calcification revealed uniform changes at the
predilection sites of coronary atherosclerosis,
consistent with the natural history of the disease. These
uniform changes indicate that the mechanisms that influence disease
progression affect the coronary tree in a systemic
fashion.
Received June 1, 2000; accepted August 14, 2000.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Braun J, Oldendorf M, Moshage W, Heidler R, Zeitler E, Luft FC. Electron beam computed tomography in the evaluation of cardiac calcifications in chronic dialysis patients. Am J Kidney Dis. 1996;27:394–401.[Medline] [Order article via Infotrieve]
2.
Callister TQ, Cooil
B, Raya SP, Lippolis NJ, Russo DJ, Raggi P. Coronary artery
disease: improved reproducibility of calcium screening with an
electron-beam CT volumetric method.
Radiology. 1998;208:807–814.
3.
Callister TQ, Raggi
P, Cooil B, Lippolis NJ, Russo DJ. Effect of HMG-CoA reductase
inhibitors on coronary artery disease as assessed
by electron-beam computed tomography.
N Engl J Med. 1998;339:1972–1978.
4. Maher JE, Bielak LF, Raz JA, Sheedy PF II, Schwartz RS, Peyser PA. Progression of coronary artery calcification: a pilot study. Mayo Clin Proc. 1999;74:347–355.[Abstract]
5. Budoff MJ, Lane KL, Bakhsheshi H, Mao S, Grassmann BO, Friedman BC, Brundage BH. Rates of progression of coronary calcium by electron beam tomography. Am J Cardiol. 2000;86:8–11.[Medline] [Order article via Infotrieve]
6. Janowitz WR, Agatston AS, Viamonte M Jr. Comparison of serial quantitative evaluation of calcified coronary plaque by ultrafast computed tomography in persons with and without obstructive coronary artery disease. Am J Cardiol. 1991;68:1–6.[Medline] [Order article via Infotrieve]
7. Stanford W, Travis ME, Thompson BH, Reiners TJ, Hasson RR, Winniford MD. Electron-beam computed tomographic detection of coronary calcification in patients undergoing percutaneous transluminal coronary angioplasty: predictability of restenosis: a preliminary report. Am J Card Imaging. 1995;9:257–260.[Medline] [Order article via Infotrieve]
8.
Schmermund A,
Baumgart D, Görge G, Grönemeyer D, Seibel R, Bailey K, Rumberger
JA, Paar D, Erbel R. Measuring the effect of risk factors on
coronary atherosclerosis: coronary
calcium score vs. angiographic disease severity.
J Am Coll Cardiol. 1998;31:1267–1273.
9.
Schmermund A,
Baumgart D, Görge G, Seibel R, Grönemeyer D, Ge J, Haude M,
Rumberger JA, Erbel R. 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.
Circulation. 1997;96:1461–1469.
10. Baumgart D, Schmermund A, Görge G, Haude M, Ge J, Adamzik M, Sehnert C, Altmaier K, Grönemeyer D, Seibel R, et al. Comparison of electron beam computed tomography with intracoronary ultrasound and coronary angiography for the detection of coronary atherosclerosis. J Am Coll Cardiol. 1997;30:57–64.[Abstract]
11. Schmermund A, Baumgart D, Adamzik M, Ge J, Grönemeyer D, Seibel R, Sehnert C, Görge G, Haude M, Erbel R. Comparison of electron-beam computed tomography and intracoronary ultrasound in detecting calcified and non-calcified plaques in patients with acute coronary syndromes and no or minimal to moderate angiographic coronary artery disease. Am J Cardiol. 1998;81:141–146.[Medline] [Order article via Infotrieve]
12. Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M Jr, Detrano R. Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol. 1990;15:827–832.[Abstract]
13. Achenbach S, Ropers D, Möhlenkamp S, Schmermund A, Nossen J, Muschiol G, Groth J, Kusus M, Regenfus M, Daniel WG, et al. Variability of repeated coronary artery calcium measurements by electron beam tomography. Am J Cardiol. In press.
14.
Wexler L, Brundage
B, Crouse J, Detrano R, Fuster V, Maddahi J, Rumberger J, Stanford W,
White R, Taubert K. Coronary artery calcium: pathophysiology,
epidemiology, imaging methods, and clinical
implications: a statement for health professionals from the American
Heart Association. Circulation. 1996;94:1175–1192.
15. Austen WG, Edwards JE, Frye RL, Gensini GG, Gott VL, Griffith LS, McGoon DC, Murphy ML, Roe BB. A reporting system on patients evaluated for coronary artery disease: Report of the Ad Hoc Committee for Grading of Coronary Artery Disease, Council on Cardiovascular Surgery, American Heart Association. Circulation. 1975;51(suppl):5–40.
16. Kajinami K, Seki H, Takekoshi N, Mabuchi H. Coronary calcium and coronary atherosclerosis: site by site comparative morphologic study of electron beam computed tomography and coronary angiography. J Am Coll Cardiol. 1997;29:1549–1556.[Abstract]
17. Rumberger JA, Brundage BH, Rader DJ, Kondos G. Electron beam computed tomographic coronary calcium scanning: a review and guidelines for use in asymptomatic persons. Mayo Clin Proc. 1999;74:243–252.[Abstract]
18. Adamzik M, Schmermund A, Reed JE, Adamzik S, Behrenbeck T, Sheedy PF II. Comparison of two different software systems for electron-beam CT-derived quantification of coronary calcification. Invest Radiol. 1999;34:767–773.[Medline] [Order article via Infotrieve]
19. Montenegro MR, Eggen DA. Topography of atherosclerosis in the coronary arteries. Lab Invest. 1968;18:586–593.[Medline] [Order article via Infotrieve]
20. Halon DA, Sapoznikov D, Lewis BS, Gotsman MS. Localization of lesions in the coronary circulation. Am J Cardiol. 1983;52:921–926.[Medline] [Order article via Infotrieve]
21.
Strong JP,
Bhattacharyya AK, Eggen DA, Malcom GT, Newman WP III, Restrepo C.
Long-term induction and regression of diet-induced atherosclerotic
lesions in rhesus monkeys, I: morphological and chemical evidence for
regression of lesions in the aorta and carotid and
peripheral arteries.
Arterioscler Thromb. 1994;14:958–965.
22. Wang S, Detrano RC, Secci A, Tang W, Doherty TM, Puentes G, Wong N, Brundage BH. Detection of coronary calcification with electron-beam computed tomography: evaluation of interexamination reproducibility and comparison of three image-acquisition protocols. Am Heart J. 1996;132:550–558.[Medline] [Order article via Infotrieve]
23. Devries S, Wolfkiel C, Shah V, Chomka E, Rich S. Reproducibility of the measurement of coronary calcium with ultrafast computed tomography. Am J Cardiol. 1995;75:973–975.[Medline] [Order article via Infotrieve]
24.
Bielak LF,
Kaufmann RB, Moll PP, McCollough CH, Schwartz RS, Sheedy PF. Small
lesions in the heart identified at electron beam CT: calcification or
noise? Radiology. 1994;192:631–636.
This article has been cited by other articles:
 |
|
 |
|
  L. L. Demer and Y. Tintut Vascular Calcification: Pathobiology of a Multifaceted Disease Circulation, June 3, 2008; 117(22): 2938 - 2948. [Full Text] [PDF]
|
|
|
|
 |
|
 E. R. Brown, R. A. Kronmal, D. A. Bluemke, A. D. Guerci, J. J. Carr, J. Goldin, and R. Detrano Coronary Calcium Coverage Score: Determination, Correlates, and Predictive Accuracy in the Multi-Ethnic Study of Atherosclerosis Radiology, June 1, 2008; 247(3): 669 - 675. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Wexler What Is the Value of Measuring Coronary Artery Calcification? Radiology, January 1, 2008; 246(1): 1 - 2. [Full Text] [PDF]
|
|
|
|
 |
|
 T. Schlosser, P. Hunold, T. Voigtlander, A. Schmermund, and J. Barkhausen Coronary Artery Calcium Scoring: Influence of Reconstruction Interval and Reconstruction Increment Using 64-MDCT Am. J. Roentgenol., April 1, 2007; 188(4): 1063 - 1068. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Muntner, E. Ferramosca, A. Bellasi, G. A. Block, and P. Raggi Development of a cardiovascular calcification index using simple imaging tools in haemodialysis patients Nephrol. Dial. Transplant., February 1, 2007; 22(2): 508 - 514. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Greenland, R. O. Bonow, B. H. Brundage, M. J. Budoff, M. J. Eisenberg, S. M. Grundy, M. S. Lauer, W. S. Post, P. Raggi, R. F. Redberg, et al. ACCF/AHA 2007 Clinical Expert Consensus Document on Coronary Artery Calcium Scoring By Computed Tomography in Global Cardiovascular Risk Assessment and in Evaluation of Patients With Chest Pain: A Report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography) Developed in Collaboration With the Society of Atherosclerosis Imaging and Prevention and the Society of Cardiovascular Computed Tomography J. Am. Coll. Cardiol., January 23, 2007; 49(3): 378 - 402. [Full Text] [PDF]
|
|
|
|
|
|
A. Schmermund, S. Achenbach, T. Budde, Y. Buziashvili, A. Forster, G. Friedrich, M. Henein, G. Kerkhoff, F. Knollmann, V. Kukharchuk, et al. Effect of Intensive Versus Standard Lipid-Lowering Treatment With Atorvastatin on the Progression of Calcified Coronary Atherosclerosis Over 12 Months: A Multicenter, Randomized, Double-Blind Trial Circulation, January 24, 2006; 113(3): 427 - 437. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Y. Qunibi Reducing the Burden of Cardiovascular Calcification in Patients with Chronic Kidney Disease J. Am. Soc. Nephrol., November 1, 2005; 16(11_suppl_2): S95 - S102. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. T. Bloomgarden Inflammation, Atherosclerosis, and Aspects of Insulin Action Diabetes Care, September 1, 2005; 28(9): 2312 - 2319. [Full Text] [PDF]
|
|
|
|
|
|
A. E. Cassidy, L. F. Bielak, Y. Zhou, P. F. Sheedy II, S. T. Turner, J. F. Breen, P. A. Araoz, I. J. Kullo, X. Lin, and P. A. Peyser Progression of Subclinical Coronary Atherosclerosis: Does Obesity Make a Difference? Circulation, April 19, 2005; 111(15): 1877 - 1882. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Giachelli Vascular Calcification Mechanisms J. Am. Soc. Nephrol., December 1, 2004; 15(12): 2959 - 2964. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. R. Folsom, G. W. Evans, J. J. Carr, A. E. Stillman, and Atherosclerosis Risk in Communities (ARIC) Study I Association of Traditional and Nontraditional Cardiovascular Risk Factors with Coronary Artery Calcification Angiology, November 1, 2004; 55(6): 613 - 623. [Abstract] [PDF]
|
|
|
|
|
|
A. R. Folsom, G. W. Evans, J. J. Carr, A. E. Stillman, and Atherosclerosis Risk in Communities (ARIC) Study I Association of Traditional and Nontraditional Cardiovascular Risk Factors with Coronary Artery Calcification Angiology, November 1, 2004; 55(6): 613 - 623. [Abstract] [PDF]
|
|
|
|
|
|
T. Schlosser, P. Hunold, A. Schmermund, H. Kuhl, K.-U. Waltering, J. F. Debatin, and J. Barkhausen Coronary Artery Calcium Score: Influence of Reconstruction Interval at 16-Detector Row CT with Retrospective Electrocardiographic Gating Radiology, November 1, 2004; 233(2): 586 - 589. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Shemesh, N. Koren-Morag, S. Apter, J. Rozenman, B. A. Kirwan, Y. Itzchak, and M. Motro Accelerated Progression of Coronary Calcification: Four-year Follow-up in Patients with Stable Coronary Artery Disease Radiology, October 1, 2004; 233(1): 201 - 209. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. M. Chertow, P. Raggi, S. Chasan-Taber, J. Bommer, H. Holzer, and S. K. Burke Determinants of progressive vascular calcification in haemodialysis patients Nephrol. Dial. Transplant., June 1, 2004; 19(6): 1489 - 1496. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Raggi, L. J. Shaw, D. S. Berman, and T. Q. Callister Prognostic value of coronary artery calcium screening in subjects with and without diabetes J. Am. Coll. Cardiol., May 5, 2004; 43(9): 1663 - 1669. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Budoff Tracking Progression of Heart Disease with Cardiac Computed Tomography Journal of Cardiovascular Pharmacology and Therapeutics, April 1, 2004; 9(2): 75 - 82. [Abstract] [PDF]
|
|
|
|
 |
|
 R. S. Farivar and L. H. Cohn Hypercholesterolemia is a risk factor for bioprosthetic valve calcification and explantation J. Thorac. Cardiovasc. Surg., October 1, 2003; 126(4): 969 - 975. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. A. Steitz, M. Y. Speer, M. D. McKee, L. Liaw, M. Almeida, H. Yang, and C. M. Giachelli Osteopontin Inhibits Mineral Deposition and Promotes Regression of Ectopic Calcification Am. J. Pathol., December 1, 2002; 161(6): 2035 - 2046. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Vliegenthart, M. Oudkerk, B. Song, D.A.M. van der Kuip, A. Hofman, and J.C.M. Witteman Coronary calcification detected by electron-beam computed tomography and myocardial infarction. The Rotterdam Coronary Calcification Study Eur. Heart J., October 2, 2002; 23(20): 1596 - 1603. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Achenbach, D. Ropers, K. Pohle, A. Leber, C. Thilo, A. Knez, T. Menendez, R. Maeffert, M. Kusus, M. Regenfus, et al. Influence of Lipid-Lowering Therapy on the Progression of Coronary Artery Calcification: A Prospective Evaluation Circulation, August 27, 2002; 106(9): 1077 - 1082. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. L. Demer Cholesterol in Vascular and Valvular Calcification Circulation, October 16, 2001; 104(16): 1881 - 1883. [Full Text] [PDF]
|
|
|
|
|
|
A. Schmermund and R. Erbel Unstable Coronary Plaque and Its Relation to Coronary Calcium Circulation, October 2, 2001; 104(14): 1682 - 1687. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||