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Published online before print December 26, 2002, 10.1148/radiol.2262011903
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(Radiology 2003;226:483-488.)
© RSNA, 2003

Cardiac Imaging

Coronary Calcification Compared in Patients with Acute versus in Those with Chronic Coronary Events by Using Dual-Sector Spiral CT1

Joseph Shemesh, MD, Sara Apter, MD, Yacov Itzchak, MD and Michael Motro, MD

1 From the Cardiac Rehabilitation Institute (J.S., M.M.) and Department of Diagnostic Imaging (S.A., Y.I.), Chaim Sheba Medical Center, Sackler Faculty of Medicine, Tel-Hashomer, 52621, Israel. From the 2001 RSNA scientific assembly. Received November 27, 2001; revision requested January 4, 2002; final revision received June 7; accepted July 3. Address correspondence to J.S. (e-mail: dshemesh@netvision.net.il).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To compare underlying calcific atherosclerotic lesions in acute versus chronic coronary events in patients with hypertension by using dual-sector spiral computed tomography (CT).

MATERIALS AND METHODS: Eight hundred eighty-four calcific lesions were analyzed in a cohort of 50 patients (39 men, 11 women; age range, 55–79 years; mean age, 66 years ± 6 [SD]) with hypertension who sustained a coronary event during 3-year follow-up. All underwent dual-sector spiral CT within 12 months before the event. Twenty-nine patients had an acute event (acute group): acute myocardial infarction, 20; unstable angina pectoris, six; acute ischemia, two; sudden death, one. Twenty-one patients had chronic manifestations of obstructive coronary disease (chronic group): severe stable angina, five; angiographically identified disease, 12; disease requiring angioplasty, two; and disease requiring bypass surgery, two. To examine differences between the two study groups, the {chi}2 or Fisher exact test was applied to categorical parameters and the two-sample t test or Wilcoxon rank sum test to quantitative parameters.

RESULTS: High prevalence of coronary calcium (total coronary calcium score [TCS] >0) was observed in both groups: 93% (27 of 29) in the acute and 95% (20 of 21) in the chronic group. There were 518 lesions in the chronic and 366 in the acute group, with a median number of 35 and nine lesions per patient, respectively (P < .001). The median TCS was 906 for the chronic and 63 for the acute group (P < .01).

CONCLUSION: A mild degree of calcification characterizes patients with acute coronary events, while diffuse high-attenuation calcific plaques are associated with chronic coronary events.

© RSNA, 2003

Index terms: Coronary vessels, calcification, 54.812 • Coronary vessels, CT, 54.12115 • Coronary vessels, diseases, 54.76 • Heart, diseases, 518.76


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Coronary arterial calcium (CAC), an unequivocal marker of coronary atherosclerosis (1,2), can be detected and measured with dual-sector spiral computed tomography (CT) (3,4). Although CAC correlates highly with plaque burden, its relationship to plaque instability is unclear. A large variation in the degree of calcification within the vulnerable plaque is demonstrated on postmortem radiographs of coronary arteries (5). Calcium characteristics of culprit coronary arteries (ie, the vessels causing the coronary events) in patients with acute coronary events studied by means of intravascular ultrasonography (US) (6,7), dual-sector spiral CT (8), and electron-beam CT (9–11) suggest that mildly to moderately calcified segments are the most likely to rupture. However, some researchers (9,12,13) believe that high-degree rather than milder forms of calcification are more related to acute coronary events. Whether the amount and pattern of calcium has any stabilizing role, or whether these factors destabilize the coronary plaques, is unclear. The purpose of our study was to compare underlying calcific atherosclerotic lesions in acute versus chronic coronary events in patients with hypertension by using dual-sector spiral CT.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Patients were selected from among the 547 participants of the International Nifedipine Study: Intervention as a Goal in Hypertension Treatment (INSIGHT) calcification study at our institution. This study was designed to compare the effect of a calcium channel blocker (Nifedipine Gastro-Intestinal Therapeutic System [GITS]; Bayer, Leverkusen, Germany) versus that of a diuretic on the progression of CAC in patients who have hypertension and are at high risk for experiencing a future acute coronary event (14). The main inclusion criteria in the INSIGHT protocol were hypertension and age of 50–80 years. Participants were also required to have at least one of the following: diabetes mellitus; smoking; positive family history of coronary arterial disease at age less than 50 years; left ventricular hypertrophy; or documented coronary arterial disease, defined as a history of myocardial infarction, coronary angioplasty, bypass surgery, or presence of obstructive lesion of 50% or more of the lumen in at least one epicardial coronary artery.

All patients underwent baseline dual-sector spiral CT and were followed up for 3 years with annual scanning. During the 3-year follow-up, 50 patients (39 men, 11 women; age range, 55–79 years; mean age, 66 years ± 6 [SD]) sustained a coronary event; all underwent dual-sector spiral CT within 12 months prior to the event, and all were included in the study. We analyzed 884 calcific lesions in this group.

Patients were divided into two groups: acute and chronic. Twenty-nine had an acute event: acute myocardial infarction, 20; unstable angina pectoris, six; acute ischemia, two; and sudden death, one. Twenty-one patients had chronic manifestations of obstructive coronary disease (ie, a chronic event): severe stable angina, five; angiographically identified disease, 12; disease requiring angioplasty, two; and disease requiring bypass surgery, two. All calcific lesions were analyzed, and the calcium characteristics were compared between the study groups. Institutional review board approval was obtained, and written informed consent was obtained separately from each participant, for both the main INSIGHT study and for the secondary calcification study.

CT Protocol
Dual-sector spiral CT studies were performed (CT Twin scanner; Philips, Cleveland, Ohio). With the patient supine, a posteroanterior scout image of the chest was obtained. A spiral scanning length of 8–11 cm was chosen to start at the carina and extend caudally through the coronary arteries. During spiral scanning with the tube rotating at one revolution per second and the table moving at 5 mm/sec, images were acquired with a nominal section thickness of 2.5 mm (effective section thickness, 3.2 mm), without electrocardiographic gating, and with 120 kVp and 240 mAs. The reconstruction increment was 1.5 mm. Calcified plaques were scored on contiguous sections, starting with the most cephalic section in which a coronary artery was seen—usually the left anterior descending artery—and continuing to a longitudinal distance of 6 cm. Calcified plaques caudal to this location were not scored.

Quantification of Coronary Calcium
A previously published protocol was used (3). All images were transferred to a workstation (MX View; Philips), and all pixels of 90 HU or more were highlighted in color. Use of the 90-HU threshold instead of the traditional 130-HU threshold with this spiral ungated technique yielded a better sensitivity with equal specificity, as compared with those yielded by angiographic methods of investigating obstructive coronary disease (3,4). An observer with 9 years of experience (J.S.) circled all highlighted lesions within the coronary arteries.

Scoring was performed (J.S.) with software at the workstation. To be counted, a lesion had to have an area of 0.5 mm2 or greater. The program calculated and recorded the area in square millimeters for each lesion. A score for each region of interest was calculated automatically by multiplying the attenuation factor by the area. The attenuation factor was derived as follows: for CT values of 90–199 HU, the factor was 1; for CT values of 200–299 HU, the factor was 2; for CT values of 300–399 HU, the factor was 3; and for CT values greater than 399 HU, the factor was 4. The total coronary calcium score (TCS) was determined by multiplying the area of each lesion by the attenuation factor and summing the lesion scores for all sections.

Estimation of Extent of CAC
The following parameters were used to evaluate the extent of calcium: number of coronary vessels with calcification, total number of calcific lesions, the area and attenuation of each lesion, total area of calcium per patient, and the TCS of each patient. Diffuse calcific lesions were arbitrarily defined as lesions with an area greater than 20 mm2.

Statistical Methods
To examine the differences between the two study groups, the {chi}2 or the Fisher exact test was applied to categorical parameters, and the two-sample t test or the Wilcoxon rank sum test was applied to quantitative parameters. All tests were two tailed, and a P value <= .05 was considered to indicate a statistically significant difference. The data were analyzed by using commercially available statistical software (SAS; SAS Institute, Cary, NC).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Patient clinical characteristics are shown in Table 1. The mean age was equal in both groups (66 years ± 6). The percentage of patients with clinically documented coronary arterial disease was higher in the chronic group (52% [11 of 21]) than in the acute group (38% [11 of 29], P = .310). The percentage of patients with diabetes was higher in the acute group (38% [11 of 29]) than in the chronic group (19% [four of 21], P = .215).


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  		TABLE 1. Clinical Characteristics of Study Groups

 
Calcium characteristics in both groups are given in Table 2. High prevalence of CAC (TCS > 0) was observed in both groups: acute, 93% (27 of 29), and chronic, 95% (20 of 21). Number of lesions, number of vessels with CAC, total calcific area, attenuation of the lesions, and TCS were all significantly higher in the chronic group than in the acute group (Table 2). Seventy-six percent (22 of 29) of the patients in the acute group, as compared with 19% (four of 21, P < .001) in the chronic group, had CAC within the lowest attenuation range (90–199 HU). In sharp contrast, 71% (15 of 21) of the patients in the chronic group, as compared with only 17% (five of 29, P < .001) in the acute group, had CAC within the highest attenuation range (>399 HU).


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  		TABLE 2. Calcium Characteristics for each Study Group

 
Three-vessel calcifications were found in 81% (17 of 21) of the patients in the chronic group but in only 31% (nine of 29, P < .001) of the patients in the acute group. Median TCS was 906 (interquartile range, 287–1,176) in the chronic group versus 63 (interquartile range, 17–180) in the acute group (P < .01) (Fig 1). Diffuse calcific lesions (area >20 mm2) were twice as prevalent in the chronic group (23% [121 of 518]) as in the acute group (14% [47 of 366], P = .001). Also, the mean area of the lesions was higher in the chronic group than in the acute group (16 mm2 ± 24 versus 10 mm2 ± 13, P < .001). An example of diffuse calcification is shown in Figure 2, and a minimally calcific lesion in a patient who sustained an acute myocardial infarction is shown in Figure 3.



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  		Figure 1. Bar graphs show characteristics of calcium in patients with acute and in those with chronic events. As compared with findings in the acute group, a sharp difference, with a significantly greater number of lesions per patient, greater total calcium area, and higher total calcium score, is clearly seen in the chronic group. Q = quartile.

 


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  		Figure 2. Transverse CT scan shows diffuse calcification of the left anterior descending coronary artery (LAD) in a 69-year-old patient who had hypertension and positive thallium stress test results that led to coronary angiography. Triple-vessel obstruction was found, and the patient underwent coronary bypass surgery. The CAC score in the left anterior descending coronary artery was 710, and the total calcium score was 2,115.

 


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  		Figure 3. Transverse CT scan shows a mildly calcific lesion in the left anterior descending coronary artery (LAD) in a 59-year-old patient who had hypertension and hypercholesterolemia and who sustained acute myocardial infarction. To enable identification of the minimally calcific lesion within the region of interest (a), automatic highlighting of the calcification was used, which colored the calcification gray. This patient’s TCS was 27.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The main finding of this study is that the coronary arteries of patients who sustained acute coronary events contained mild to moderate amounts of calcification, in sharp contrast to the high grade of calcification observed in the coronary arteries of patients who had chronic coronary events. Chronic obstructive coronary arterial disease clinically manifests as angina pectoris, positive stress test results, and positive thallium and echocardiographic stress test results. These are all consequences of flow-limiting obstructive lesions and lead the clinician to perform elective coronary angiography. When indicated, one of the revascularization procedures, angioplasty or bypass surgery, is performed.

Chronic coronary events are the consequences of complex obstructive atherosclerotic lesions. These lesions are frequently characterized by advanced calcification (15,16), which increases with the overall plaque burden. The same dual-sector spiral CT technique has been used to demonstrate that mean TCS increases in parallel with the number of obstructed vessels seen at angiography—from 15 in normal coronary arteries to 830 in triple-vessel disease (3). In another study (17) in which dual-sector spiral CT was used, patients with typical stable angina pectoris had a much higher median TCS than did subjects without symptoms: 248 versus 38 in men and 156 versus 11 in women.

Detrano et al (18) demonstrated that subjects with risk factors but no ischemic symptoms had a mean TCS of 44. Much higher scores (mean, 335) were observed in patients who had symptoms and were undergoing clinically indicated coronary angiography (19), and a mean TCS of 491 was reported in patients with angiographic evidence of left main– or three-vessel coronary disease (20). The results of our study can be used to confirm that coronary vessels in patients who underwent elective coronary angiography, angioplasty, or bypass surgery and those with severe stable angina pectoris have advanced calcification; 81% (17 of 21) of such patients in this study had three-vessel calcification, half had a total calcific area greater than 339 mm2 and a TCS above 906, and 71% (15 of 21) had lesions with the highest attenuation range (>399 HU).

Our CT results suggest that calcification is a feature of advanced obstructive coronary atherosclerosis. Hence, it cannot be said that calcium per se contributes to the development of acute coronary syndromes. In fact, calcium is found infrequently in the culprit lesions of ruptured plaques (21). Postmortem study results (22–24) demonstrated that vulnerable plaques typically contain a large amount of lipids with a thin fibrous cap. The large lipid core in thin-cap fibroatheroma is soft and bears the circumferential stresses less well than do the fibrous components of the arterial wall (21,23,25). In a series of cases of sudden coronary death, more than 50% of thin-cap fibroatheromas showed a lack of calcification or only speckled calcification on postmortem radiographs of coronary arteries (26).

Huang et al (27), after performing large-strain finite-element analysis, suggested that, in contrast to the destabilizing effect of the lipid core, calcium is a stabilizing force that is similar to fibrous plaque. In another study, Cheng et al (25) demonstrated, by means of analysis of the biomechanical properties of atherosclerotic plaques, that calcified lesions are more resistant to rupture than are noncalcified plaques. Kragel et al (28), in a postmortem study of 27 hearts, found that ruptured plaques tended to contain more lipids and less fibrous tissue and calcium than did those that had not ruptured. Similar findings were also observed in peripheral arteries: Johnson et al (29), in a prospective study of patients with carotid arterial atherosclerosis but without symptoms, showed that patients with US-detectable carotid calcium were much less likely to have cerebral events with symptoms than were those with no detectable carotid calcium, despite the same severity of stenosis.

The results of our study support these observations and can be used to confirm that stable, stenotic, atherosclerotic arteries are more heavily calcified than are those containing unstable plaques. Total calcium scores in the patients with acute coronary events in our study did not exceed 491, a score that corresponds to the 33rd percentile of TCS in the chronic group. Moreover, half of these patients had a TCS of less than 63 (ie, very mild total calcification and mild CAC), and 75% had a TCS of less than 180.

These results can be used to confirm findings of a previous study (8) in which the characteristics of coronary calcium in patients with stable angina were compared with those with first acute myocardial infarction by using dual-sector spiral CT with a scanning protocol similar to that used in our study. In this study, the same pattern of mild calcifications was found in the 73 culprit arteries in the patients with acute myocardial infarction: 16 (22%) had no calcium detected, 30 (41%) had mild lesions (defined as an area <5 mm2), and another 20 (27%) had moderate calcific lesions (area of 5–20 mm2). These findings correspond to the lesion frequency found in the acute group in our study: 47% (171 of 366) of the lesions were mild, and 40% (148 of 366) were moderate.

Figure 1 summarizes the sharp differences in the extent and pattern of CAC in the patients in the chronic group, as compared with those in the acute group. The median total calcified area in the chronic group, at 339 mm2, was 10 times higher than the 33 mm2 in those who sustained an acute event. A sharp difference was also observed regarding the attenuation of the calcifications: While the majority of the patients (15 of 21) in the chronic group had lesions with the highest attenuation factor (>399 HU), most of the patients (22 of 29) in the acute group had lesions with the lowest attenuation factor (<200 HU). An example image in a patient who underwent coronary angiography because of ischemic changes at thallium stress testing and who had typical diffuse calcification is shown in Figure 2; an example image in a patient who had mild calcification and sustained acute myocardial infarction is shown in Figure 3.

Our results can be further used to confirm the findings of several previous studies; Beckman et al (6) used intravascular US to address the question of whether plaque calcification is a protective or malignant process in the setting of existent coronary atherosclerosis. The investigators quantified the amount of calcium present in the culprit lesions in patients with coronary disease with symptoms and correlated the findings with acuteness of symptom presentation and clinical stability. The maximal arc of calcium decreased progressively from patients with stable angina (91° ± 10) to those with unstable angina (59° ± 80) and to those with myocardial infarction (49° ± 11, P = .014). The authors concluded that acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses, as compared with findings in patients with stable angina.

In another report, African Americans (30) with similar risk-factor profiles had less CAC yet more coronary events than did white subjects. Secci et al (31) followed 326 adults who were at high risk and had a mean age similar to that of the patients in our study (66 years ± 8) for 32 months ± 4 after electron-beam CT for coronary calcium. Five coronary deaths and six infarctions occurred, but they were not significantly more frequent in the higher quartiles for TCS. The authors concluded that their results clearly showed that patients with little or no CAC can die of myocardial infarction. Furthermore, these investigators found an association between higher levels of calcium and revascularization and suggested that the stability of calcified lesions led to more stable and less catastrophic coronary events. The results of our study strengthen this hypothesis.

However, debate exists about the relationship between CAC and the likelihood of plaque rupture. In one autopsy study (13) of 90 hearts from patients who had died of coronary disease, 94% of all ruptured plaques contained calcium. This probably reflects the high calcium burden in patients with known coronary arterial disease. The authors of this study further found that a moderate amount of calcium is the best marker for plaque instability; this is in accordance with our findings. In another study, Mascola et al (12) compared CAC seen at electron-beam CT in 120 culprit arteries in acute myocardial infarction with that in 240 nonculprit arteries; they found that calcifications occurred more heavily in the culprit vessels. They did not mention whether only first myocardial infarction was included, so the high degree of calcification may reflect preexisting chronic coronary arterial disease.

The main clinical application of our study is the contribution to the better understanding of CAC characteristics and their potential as predictors of ischemic coronary events. Although interventional procedures are usually associated with a greater amount of CAC, many acute events occur against a background of minor or mild calcifications. This should draw attention to the possible importance of minor amounts of CAC in the selection of higher-risk patients for intensive primary prevention measures.

This study had some limitations. Since the electrocardiographic gating technique was not available at the time we began the study, we used a nongated dual–detector technique. This technique has since been replaced by the use of faster electrocardiographically gated multi–detector row spiral techniques. According to our scanning protocol, only the caudal 6 cm of the coronary tree was scored for two reasons: to reduce motion artifacts, which are more frequent in the caudal part of the heart, and because coronary calcifications start in the proximal part of the heart and, in most cases, are situated in the proximal 3–6 cm. However, despite these limitations, the clinical accuracy of the nongated procedure, its reproducibility (4), and its usefulness in tracking the progression of calcific coronary atherosclerosis (32,33) have been shown to be adequate.

Because of the relatively small number of patients in our study, we could not evaluate the effect of risk factors on calcium characteristics and events. This study was not designed to address this question. Further studies with larger populations should be conducted to clarify this important issue, as well as to confirm the predictive value of mild calcifications, particularly in patients without symptoms.


   ACKNOWLEDGMENTS
 
The authors acknowledge Gil Harrari, MSc, for his statistical support in the data processing of this study.


   FOOTNOTES
 
Abbreviations: CAC = coronary arterial calcium, INSIGHT = International Nifedipine Study: Intervention as a Goal in Hypertension Treatment, TCS = total coronary calcium score

Author contributions: Guarantor of integrity of entire study, J.S.; study concepts, J.S., M.M.; study design, J.S.; literature research, S.A.; clinical studies, J.S.; data acquisition and analysis/interpretation, J.S.; statistical analysis, J.S.; manuscript preparation, S.A.; manuscript definition of intellectual content, J.S., Y.I., M.M.; manuscript editing, M.M., Y.I.; manuscript revision/review and final version approval, M.M.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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CT of Coronary Artery Disease
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J. Golledge, M. McCann, S. Mangan, A. Lam, and M. Karan
Osteoprotegerin and Osteopontin Are Expressed at High Concentrations Within Symptomatic Carotid Atherosclerosis
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