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J Am Coll Cardiol, 2006; 48:312-318, doi:10.1016/j.jacc.2006.02.064 (Published online 22 June 2006).
© 2006 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: CARDIAC IMAGING

Prevalence of Noncalcified Coronary Plaques by 64-Slice Computed Tomography in Patients With an Intermediate Risk for Significant Coronary Artery Disease

Jörg Hausleiter, MD*,*, Tanja Meyer, MD{dagger}, Martin Hadamitzky, MD*, Adnan Kastrati, MD*, Stefan Martinoff, MD{dagger} and Albert Schömig, MD*

* Klinik für Herz- und Kreislauferkrankungen, Klinik an der TU München, Munich, Germany.
{dagger} Institut für Radiologie und Nuklearmedizin, Deutsches Herzzentrum München; Klinik an der TU München, Munich, Germany.

Manuscript received August 31, 2005; revised manuscript received January 20, 2006, accepted February 14, 2006.

* Reprint requests and correspondence: Dr. Jörg Hausleiter, Deutsches Herzzentrum, Lazarettstrasse 36, 80636 München, Germany. (Email: hausleiter{at}dhm.mhn.de).


   Abstract
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 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES: In this prospective study, we investigated the prevalence and characteristics of clearly discernible noncalcified coronary plaques in a patient population with suspected significant coronary artery disease (CAD) by using 64-slice computed tomography (CT).

BACKGROUND: The assessment of noncalcified coronary plaques by noninvasive strategies may be important to improve cardiovascular risk stratification.

METHODS: To rule out significant stenosis, high-resolution 64-slice coronary CT (0.6-mm collimation, 330-ms gantry rotation time) was performed in 161 consecutive patients with an intermediate risk for having CAD. Computed tomography data sets were evaluated for presence of coronary calcifications, noncalcified plaques, and/or lumen narrowing.

RESULTS: Noncalcified coronary plaques were detected in 48 (29.8%) of 161 enrolled patients. Although noncalcified plaques together with coronary calcifications were present in 38 of 161 (23.6%) patients, the prevalence of noncalcified plaques as the only manifestation of CAD was 6.2% (10 of 161 patients). Patients with noncalcified plaques were characterized by significantly higher total cholesterol, low-density lipoprotein, and C-reactive protein levels as well as a trend for more diabetes mellitus. The majority of noncalcified plaques resulted in lumen narrowing of <50%. Of the remaining 113 patients, CAD and coronary calcifications were ruled out in 53 of 161 (32.9%) patients, whereas 60 of 161 (37.3%) patients presented with calcifications in the absence of noncalcified plaque.

CONCLUSIONS: With the use of 64-slice CT, clearly discernible noncalcified atherosclerotic coronary plaques can be detected in a large group of patients with an intermediate risk for having CAD. The assessment of these plaques by CT angiography may allow for improved cardiovascular risk stratification.

Abbreviations and Acronyms
  ASE = Agatston score equivalent
  CAD = coronary artery disease
  CRP = C-reactive protein
  CT = computed tomography
  IQR = interquartile range
  LDL = low-density lipoprotein
  MSCT = multislice computed tomography
  PROCAM = Prospective Cardiovascular Münster score

Acute coronary syndromes, including sudden coronary death, frequently are caused by plaque erosion, ulceration, or rupture. The term "vulnerable plaque" has been introduced to define plaques susceptible to such ischemic complications (1). A large number of vulnerable plaques are predominantly noncalcified and nonstenotic and similar to type IV atherosclerotic lesions described in the American Heart Association classification (2). Type IV lesions are characterized by extracellular lipid accumulations also known as lipid cores. These lipid cores dramatically increase intimal wall shear stress compared with fibrous tissue and calcifications (3), rendering lipid-rich atherosclerotic plaques by far more unstable and vulnerable to sudden rupture than other types of lesions. The detection of such vulnerable plaques remains a difficult task; invasive techniques, among others intravascular ultrasound (4), optical coherence tomography (5), plaque thermography (6), and angioscopy (7), have been used to describe markers of plaque vulnerability. Noninvasive imaging techniques such as high-resolution computed tomography are considered as promising new methodologies with the potential to detect vulnerable patients.

Recent reports have demonstrated the ability of contrast-enhanced multislice computed tomography (MSCT) to detect noncalcified atherosclerotic plaque (8–11). However, the prevalence of noncalcified plaque detected by 64-slice computed tomography (CT) has never been systematically evaluated. Therefore, we prospectively studied the prevalence and characteristics of noncalcified plaque visualized with an enhanced spatial resolution of 64-slice CT in patients with suspected coronary artery disease (CAD).


   Methods
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Results
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Patients.   From October 2004 through January 2005, 161 consecutive patients with an intermediate risk for having CAD were referred to our interdisciplinary cardioradiologic MSCT laboratory. The intermediate risk for having significant CAD was defined as: 1) chest pain or dyspnea in the presence of negative stress tests; 2) the absence of chest pain but positive stress tests; or 3) the absence of chest pain and of positive stress tests but intermittent arrhythmias. Intermittent arrhythmias were defined as exercise-induced premature ventricular complexes during bicycle stress testing, short runs of nonsustained ventricular tachycardias during Holter electrocardiography (ECG) monitoring (e.g., ≥3 consecutive beats), or intermittent atrial arrhythmias with increasing frequency within the last year. Patients were excluded who had: 1) known CAD; 2) chest pain in combination with positive tests for myocardial ischemia; or 3) arrhythmias that did not allow ECG-triggering of the MSCT scan. All study related data, including patient history, current medication, and laboratory results, as well as MSCT related data and results were collected prospectively in a dedicated coronary MSCT reporting system with the use of Oracle database. The global risk of myocardial infarction was estimated with the use of the Prospective Cardiovascular Münster (PROCAM) study scoring system (12).

MSCT.   Patients with a heart rate >60 beats/min received metoprolol 5 to 20 mg intravenously before the MSCT scan (Sensation 64 Cardiac, Siemens Medical Solutions, Erlangen, Germany). Coronary vasodilatation was achieved by the administration of nitroglycerin 0.8 mg sublingually before the scan to obtain a maximum opacification of the coronary arteries. A native scan without contrast dye was performed to determine the total calcium burden of the coronary tree (sequential scan with 32 x 0.6-mm collimation, tube current 60 mAs at 120 kV). Contrast-enhanced CT angiography data were acquired with the use of a spiral scan with 32 x 0.6-mm collimation, 330-ms gantry rotation, pitch of 0.2, and tube voltage at 120 kV. A total of 64 overlapping 0.6-mm slices per rotation were acquired with the use of a focal spot periodically moving in the longitudinal direction (z-flying focal spot) (13). This sampling scheme results in an improved spatial resolution which is identical to that of a 64 x 0.3-mm detector (0.4 x 0.4 x 0.4-mm isotropic resolution). Tube current was modulated according to the ECG, with a maximum current of 850 to 950 mAs during a time period of approximately 330 ms centered at 375 ms before the next R-wave and reduction by 80% during the remaining cardiac cycle (14). In our cardiovascular MSCT research laboratory, the estimated effective dose associated with cardiac 64-slice CT angiography was estimated to be 11.0 ± 4.1 mSv. Contrast agent (60 to 80 ml; 350 mg iodine/ml) was injected intravenously (4.5 to 5.0 ml/s). Transaxial images were reconstructed using an ECG-gated half-scan reconstruction algorithm (temporal resolution 164 ms) and kernel B30f. In case of a heart rate of >65 beats/min, a bisegmental reconstruction algorithm is applied that uses data obtained from two consecutive heartbeats, reducing the effective reconstruction interval per heart cycle down to 83 ms, depending on the heart rate. The position of the reconstruction window within the cardiac cycle was individually optimized to minimize motion artifacts.

MSCT image interpretation.   Vessel wall calcifications were quantified on a separate workstation (Wizard, Siemens Medical Solutions), based on the standard built-in algorithm using an Agatston score equivalent (ASE) adapted for MSCT. Two reviewers independently evaluated the contrast-enhanced MSCT scans by assessment of the axial slices, of multiplanar reformations and of three thin-slab maximum intensity projections. Orientated along the heart axis, the thin-slab (5-mm thickness, 1-mm increment) maximum intensity projections were reconstructed perpendicular to each other. The coronary artery tree was segmented according to modified American Heart Association classification (15) and the segments were investigated for lumen narrowing. Segments were graded as small (diameter <1.5mm), normal appearing (stenosis grade 0% to 24%), slightly narrowed (stenosis grade 25% to 49%), moderately narrowed (stenosis grade 50% to 74%), and severely narrowed (stenosis grade ≥75%).

The presence of noncalcified atherosclerotic plaque tissue was defined as any discernible structure in the coronary artery wall with a CT density less than the contrast-enhanced coronary lumen but greater than the surrounding connective tissue. For the determination of plaque density values, the respective coronary segment was rendered and displayed in orthogonal views (0.6-mm thick slices) according to the vessel axis. Measurements were obtained from manually traced regions of interests encompassing the noncalcified plaque proportions. These tracings were drawn as large as possible but avoiding the borders of adjacent structures to limit the effect of interpolation and partial volume on the measurements. Calcified plaque components of mixed plaques (combined noncalcified and calcified plaque tissues) were excluded from the assessment of the noncalcified plaque density. Standard display settings were used for the evaluation of the contrast-enhanced MSCT scans (window width 800 Hounsfield units [HU]; window center 250 HU).

Invasive coronary angiography.   Invasive coronary angiograms were evaluated by two independent and experienced investigators cardiologist that were unaware of the results of the CT examination. Stenosis severity in each coronary segment was classified according to the maximal luminal diameter stenosis present in each segment. Lesions were examined in orthogonal views, and stenosis severity was visually determined using a similar grading system as with MSCT image interpretation.

Statistical analysis.   Continuous variables are expressed as median (interquartile range [IQR]) and compared by means of Mann-Whitney U test; discrete variables are expressed as counts or percentages and compared with chi-square or the Fisher exact test (whenever an expected cell value was <5). Statistical significance was accepted for p < 0.05.


   Results
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 Abstract
 Methods
 Results
Discussion
 References
 
A coronary MSCT investigation was performed in 161 patients. A dose of 15 mg (IQR 10, 20) of metoprolol was administered in 124 (77.0%) patients to lower the heart rate, which resulted in a mean heart rate of 57 beats/min (IQR 53, 81) beats/min during scanning.

No coronary calcifications were present in 63 of 161 (39%) patients, whereas calcified plaques were determined in 98 of 161 (61%) patients (Fig. 1). Subsequent contrast-enhanced coronary CT angiography revealed the presence of noncalcified plaques in 10 (16%) of the 63 patients who had no coronary calcifications. In these patients, noncalcified plaques were the only manifestation of CAD. The overall prevalence of patients with noncalcified plaques as the only manifestation of CAD was 6.2% (10 of 161 patients). In patients with coronary calcifications, additional noncalcified plaques were detected in 38 of 98 (39%) patients, whereas 60 of 98 (61%) patients were free of noncalcified plaques by CT angiography. In summary, CAD because of the presence of calcified or noncalcified plaques, was detected in a total of 108 patients. Table 1 summarizes the characteristics of patients with and without CAD. Patients without CAD were significantly younger and presented with a lower cardiovascular risk profile, resulting in a lower 10-year risk for a cardiovascular event by the PROCAM score. Accordingly, less cardiovascular medications were taken by patients without CAD.


Figure 1
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  		Figure 1 Prevalence of calcified and noncalcified plaques in the study group. CAD = coronary artery disease; CT = computed tomography.

 

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  		Table 1. Clinical Characteristics of Patients With and Without Coronary Artery Disease
 
Noncalcified plaques, alone or in combination with calcifications, were observed in 48 (44%) of 108 patients with CAD (30% of all 161 studied patients). Patients with noncalcified plaques were characterized by significantly higher total cholesterol and low-density lipoprotein (LDL) levels as well as a trend of having more diabetes mellitus. Furthermore, the inflammatory marker C-reactive protein (CRP) was significantly increased in patients with noncalcified plaques. In contrast, patients with noncalcified plaques did not differ with respect to most traditional cardiovascular risk factors, including age, gender, body mass index, arterial hypertension, smoking as well as the estimated 10-year cardiovascular risk by the PROCAM score. Although there were no differences in the rates of beta-blockers, angiotensin-converting enzyme inhibitors, diuretics as well as Ca2+-antagonists, the use of statins was significantly lower in patients with noncalcified plaques. Table 2 summarizes the clinical characteristics of patients with and without the presence of noncalcified plaques in more detail. The MSCT investigation revealed that patients with noncalcified plaques tend to have fewer coronary calcifications than patients without noncalcified plaques (ASE: 80 [IQR 9, 246] vs. 170 [IQR 17, 554] for patients with vs. without noncalcified plaques; p = 0.12). Figure 2 presents a CT angiogram in a 52-year-old male patient who presented with chest pain. A large noncalcified plaque is visualized in the proximal left anterior descending coronary artery, which was the only manifestation of CAD in this patient.


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  		Table 2. Clinical Characteristics of Patients With and Without Noncalcified Plaques
 

Figure 2
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  		Figure 2 Coronary computed tomography angiogram in a 52-year-old male patient who presented with chest pain. In the long-axis reconstruction (left), a large nonstenotic and noncalcified plaque is visualized in the proximal left anterior descending (LAD) coronary artery, which was the only manifestation of coronary artery disease in this patient. In the cross-sectional image of the LAD (right), the noncalcified plaque can be clearly depicted from the contrast-filled lumen and the surrounding connective tissue. The density measurements within the plaque revealed a predominantly lipid-rich plaque with 28 HU.

 
Noncalcified coronary plaques were identified in a total of 77 coronary segments (1.6 ± 1.1 segments per patient, range 1 to 5). A total of 34 of 77 (44%) segments revealed completely noncalcified plaques whereas 43 of 77 (56%) segments had mixed plaques with calcified and noncalcified components. The majority of these plaques (68%) resulted in a lumen narrowing of <50% with a predominant location in the left anterior descending coronary artery in 51% (39 of 77 noncalcified plaques). The median density values of the noncalcified plaques were 68 HU (IQR 51 to 87 HU).

Invasive coronary angiography was performed in 23 patients with noncalcified plaques by CT angiography. A total of 40 noncalcified plaques were present in these patients. One-half of these plaques resulted in minor wall irregularities with a maximum stenosis grade of 25% by invasive angiography. Nonsignificant stenosis with lumen narrowing between 25% and 50% were observed in additional nine noncalcified plaques. The remaining 11 noncalcified plaques resulted in high-grade lumen narrowing and were treated by using percutaneous coronary intervention.


   Discussion
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 Methods
 Results
 Discussion
References
 
Lipid-rich coronary plaques have been associated with an increased vulnerability for sudden plaque rupture, leading to acute ischemic coronary syndromes. The ability to detect these plaques at early stages by a noninvasive methodology would probably improve risk stratification of these patients. This prospective study indicates that such noncalcified coronary plaques, alone or in combination with calcifications, can be detected in a high proportion of patients investigated by 64-slice CT angiography for suspected CAD. These patients were characterized by higher total cholesterol, LDL, and CRP levels and by a trend of having more diabetes mellitus. Furthermore, this study demonstrates that noncalcified coronary plaques were the only manifestation of CAD in 6% of the study population (or in 16% of patients with a negative score for coronary calcifications).

The identification of patients at increased risk for an ischemic and potentially fatal cardiac event is a difficult task in cardiovascular medicine. Despite extensive studies and development of several risk prediction models, traditional cardiovascular risk factors fail to predict development of CAD in a large group of patients (16). A stepwise approach for risk stratification has been proposed recently. The proposed noninvasive tools range from self-questionnaire to molecular plaque imaging. Multislice computed tomography angiography has been introduced as noninvasive technique for the reliable detection of coronary stenosis in addition to the quantification of calcified plaque burden (17,18). With the improved spatial resolution, CT angiography also allows for the detection of noncalcified coronary plaques. Compared with intravascular ultrasound, the sensitivity and specificity of 16-slice CT for the detection of noncalcified plaques, alone or in combination with calcified plaques, has been described at approximately 78% and 87% to 92%, respectively (10,11). Coronary plaques not detected by 16-slice CT had a smaller plaque thickness and were located in smaller coronary arteries (10). With the enhanced spatial resolution of approximately 0.4 mm with 64-slice CT technology a further improvement in noncalcified plaque detection could be expected.

In the current study, we studied the prevalence of noncalcified plaques in a population of consecutive patients with suspected CAD by 64-slice CT angiography. This patient population is believed to have the largest benefit of noninvasive MSCT angiography (17,18). In the current study, the MSCT findings allowed for a separation of the population into three groups: 1) CAD was ruled out in approximately one-third of studied patients; 2) CAD with coronary stenosis and/or calcifications but without noncalcified plaques was present in another third of investigated patients; and 3) approximately one-third of patients presented with noncalcified plaques alone or in combination with coronary calcifications. In this study, noncalcified plaques were defined as clearly discernible structures with density values less than the contrast-enhanced lumen but greater than the surrounding connective tissue. Diffuse noncalcified plaques, which may result in blurred contours of the contrast-enhanced lumen, and small noncalcified plaques, were not included in this analysis. Therefore, the presence of noncalcified plaques will be underestimated compared with histologic postmortem studies. Of interest, patients with noncalcified plaques had higher total cholesterol, LDL, as well as CRP levels. The significantly higher CRP values in patients with noncalcified plaque are of particular interest. No association between CRP and the calcified plaque burden was found in the SIRCA (Study of Inherited Risk of Coronary Atherosclerosis) (19). In contrast, our study demonstrates that elevated CRP values correlate with earlier noncalcified stages of atherosclerotic plaque development. This finding supports the association of the inflammatory burden with increased cardiovascular risk (20).

The definition of clearly discernible noncalcified plaques may allow for the improved detection of patients at higher risk for subsequent cardiovascular ischemic events. In fact, in this population with suspected CAD, noncalcified plaques were the only manifestation of CAD in 10 (6.2%) of 161 studied patients; when related to patients in whom no calcifications were detectable by CT, the frequency of noncalcified plaques as the only manifestation of CAD was considerably higher (10 of 63 [16%] patients). The assessment of traditional cardiovascular risk factors in combination with CT scanning for coronary calcifications may have failed to identify this patient population with a potentially higher cardiovascular risk. Therefore, noncalcified plaque detection by coronary CT angiography may have an additive prognostic value, particularly in patients with an ASE of 0. The absence of coronary calcifications has been described in 0.7% male patients with significant coronary stenosis (21) and in 4% patients suffering from an unheralded myocardial infarction (22). Although the precise mechanisms and the composition of plaques causing a myocardial infarction are largely unknown, it is hypothesized that predominantly lipid-rich coronary plaques are more rupture-prone than fibrous-rich plaques. In the current study we identified a total of 77 noncalcified plaques (or 1.6 plaques/patients) with a median plaque density of 68 HU (IQR 51 to 87 HU). Although the accuracy of the assessment of plaque densities may be influenced by several factors, among others, the precise definition of noncalcified plaque contours, the intraluminal attenuation of contrast dye, as well as the used convolution kernel, these results suggest that a large number of detected noncalcified plaques may contain more hypodense structures such as lipid accumulations. However, further studies are needed to validate CT modalities for the assessment of coronary plaque composition before a clear differentiation into lipid- or fibrous-rich plaques is possible.

Clearly, the risk for ischemic events in patients with noncalcified plaques as well as the additive value of noncalcified plaque detection over traditional calcium scoring is currently not known. Therefore, long-term follow-up studies in larger populations are needed to further investigate the impact of noncalcified plaque detection by MSCT on cardiovascular events on top of the traditional assessments of cardiovascular risk factors and coronary calcifications. Furthermore, strategies for the prevention of cardiovascular events in patients with detected noncalcified plaques remain to be evaluated. The visualization of noncalcified plaque by MSCT is limited by plaque and vessel size; therefore, smaller plaques predominantly located in smaller coronary arteries will no be accurately identified by currently available CT scanner generations. Finally, the possible benefits of noncalcified plaque detection by CT angiographies need to be weighed against the potential hazards associated with the radiation dose delivered to the chest.

In conclusion, high-resolution 64-slice CT angiography allows for the detection of discernible noncalcified coronary plaques in a large group of patients with suspected CAD. These findings may improve risk stratification of patients susceptible for an ischemic cardiovascular event. However, further data on the prognostic impact of these noncalcified plaques are needed before their assessment by coronary CT angiography can be recommended for clinical decision making and risk stratification.


   Acknowledgments
 
The authors are indebted to the medical and technical staff members of the computed tomography laboratories for their invaluable contribution and in particular to Mrs. U. Lang, C. Schwarzer, and B. Child (all RT) for their expert technical assistance.


   References
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 Discussion
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A. N. DeMaria, O. Ben-Yehuda, G. K. Feld, G. S. Ginsburg, B. H. Greenberg, W. Y.W. Lew, J. A.C. Lima, A. S. Maisel, J. Narula, D. J. Sahn, et al.
Highlights of the Year in JACC 2006
J. Am. Coll. Cardiol., January 30, 2007; 49(4): 509 - 527.
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M. J. Budoff
Prevalence of Soft Plaque Detection With Computed Tomography
J. Am. Coll. Cardiol., July 18, 2006; 48(2): 319 - 321.
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