European Heart Journal Advance Access originally published online on January 19, 2009
European Heart Journal 2009 30(3):362-371; doi:10.1093/eurheartj/ehn605
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Prognostic utility of 64-slice computed tomography in patients with suspected but no documented coronary artery disease
1 Department of Cardiovascular Medicine, Desk F 15, Heart and Vascular Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA
2 Imaging Institute, Cleveland Clinic, Cleveland, OH, USA
3 Department of Radiology, University of Florida, Jacksonville, FL, USA
Received 31 July 2008; revised 11 December 2008; accepted 22 December 2008; online publish-ahead-of-print 19 January 2009.
* Corresponding author. Tel: +1 216 445 5250, Fax: +1 216 636 0679, Email: desaim2{at}ccf.org
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Abstract |
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Aims: Although multislice computed tomography (MSCT) detects obstructive coronary artery disease (CAD) with high diagnostic accuracy, there is a paucity of long-term prognostic data. We sought to assess the incremental prognostic value of 64-slice CT in patients with suspected but no documented CAD.
Methods and results: Coronary MSCT was performed on 227 individuals (61% men, mean age 54 ± 12 years, 63% with intermediate pre-test probability) without documented CAD, referred for coronary evaluation. Coronary artery disease by MSCT was categorized as follows: none or mild CAD (<50%, n = 172), 
50% in one vessel (n = 23), two vessels [or in the proximal left anterior descending (LAD), n = 12], and three vessels (or in two vessels including the proximal LAD or left main, n = 20). Baseline risk factors, length of follow-up, and major adverse cardiac events (MACE), including cardiac death, myocardial infarction (MI), and coronary revascularization were recorded. Over a mean follow-up of 2.3 ± 0.8 years, there were 18 MACE [including four hard events (one cardiac death and three MIs)]. Also, patients with one or more vessel obstructive CAD had increased hard events compared with those with less than one-vessel disease (log-rank statistic P-value 0.01). One or more vessel obstructive CAD was a significant predictor of MACE on univariable and multivariable Cox proportional survival analysis [hazard ratios 29.1 (6.7–126.6) and 9.82 (3.58–27.01), respectively, both P < 0.0001]. In 172 patients, with no or mild CAD, there was 99% freedom from MACE during follow-up.
Conclusion: Multislice computed tomography-classified extent of CAD provides incremental prognostic information in patients with suspected but no documented CAD.
Key Words: Multislice computed tomography • Coronary arteries and prognosis
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Background |
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Despite continued advances in management strategies, coronary artery disease (CAD) remains the leading cause of death in the developed world, with continued increases projected in the future.1 In patients presenting with suspected CAD, accurate non-invasive assessment of risk is integral in clinical decision making and guides appropriate patient management. To date, numerous studies have demonstrated the incremental prognostic value of non-invasive stress testing, using either myocardial perfusion scintigraphy or echocardiography, in risk stratification of patients with suspected CAD, particularly those with intermediate pre-test likelihood of CAD.2–8 Similarly, in a primary prevention setting, major advisory bodies recommend the use of a risk-factor algorithm as an initial office-based assessment to further classify coronary heart disease risk.9 However, by one estimate, nearly 40% of US adults would be classified broadly as intermediate risk with this algorithm and may benefit from more precise risk stratification.10 Recent data have demonstrated the incremental prognostic value of coronary calcium scoring in risk stratification, over and above traditional risk factors, in a primary prevention setting.11,12
On the basis of the recently published consensus document, non-invasive coronary angiography using multislice computed tomography (MSCT) is considered appropriate in subjects with intermediate likelihood of CAD, with the goal to exclude the presence of haemodynamically significant luminal stenosis.13 However, MSCT has also shown the ability to accurately detect obstructive CAD and characterize the arterial wall,14–17 potentially allowing additional risk stratification. Early reports have suggested incremental prognostic utility of CAD detected by MSCT in patients with known or suspected CAD.18–20 We sought to assess the prognostic utility of state-of-the-art 64-slice CT coronary angiography in patients with suspected but no previously documented CAD followed for a period of >2 years.
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Methods |
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Study design and patient selection
This was an observational retrospective single-centre study where 227 consecutive subjects, with no prior documented CAD, underwent 64-detector coronary CT angiography between October 2004 and December 2005 at our institution for evaluation of suspected CAD. Patients had suspected cardiac symptoms (typical or atypical chest pain, dyspnoea on exertion, n = 191), or equivocal stress test (n = 36), along with standard cardiac risk factors. Initially, 720 patients who underwent MSCT in that time frame were screened. Patients were excluded if they had the following history: evidence of prior significant CAD (determined as chart documented >30% stenosis in any vessel on prior cardiac catheterization, prior myocardial infarction (MI), prior percutaneous intervention, prior coronary artery bypass grafting, emergent presentation with abnormal cardiac enzymes/dynamic ischaemic electrocardiographic changes, n = 361) or non-coronary indications for MSCT (n = 113). International patients with no social security numbers (n = 19), in whom follow-up could not be ascertained, were excluded from the analysis. This study was approved by the local institutional review board with waiver of individual consent.
The electronic medical record was reviewed by two investigators (T.P.C. and D.N.). Baseline demographic variables, along with family history of premature CAD in first-degree relatives (<55 years in men and <65 years in women), history of diabetes, hyperlipidaemia, hypertension, current smoking, menopausal state, and medication use were extracted, based on physician documented history, documented measurements, and/or use of medications. Laboratory values for lipid parameters, body mass index (kg/m2), and measured values for blood pressure were obtained from the office visit temporally closest to the MSCT examination (generally within 1 month of MSCT examination). Pre-test likelihood of CAD was determined in every patient according to a modification of the Diamond–Forrester method, as published by Morise et al.21 These patients were further categorized into low likelihood (score 0–8), intermediate likelihood (9–15), and high likelihood (>16). Using the Framingham-based Adult Treatment Panel (ATP) III risk assessment tool, an estimate of 10 year risk for coronary heart disease was calculated.9 The 10 year risk estimates were further categorized as low (10 year risk <10%), intermediate (10 year risk 10–20%), or high (10 year risk >20%).
To ascertain follow-up information and screen for occurrence of clinical events, electronic medical records, including clinic visits and telephone interviews, were reviewed. All patients (except for the 19 international patients excluded as discussed earlier) had a follow-up at our institution, with last follow-up on 27 April 2008. The Social Security Death Index was queried to ascertain all-cause mortality. We were able to ascertain the actual cause of death in all cases. Major adverse cardiac events (MACE) were defined as the occurrence of cardiac death, non-fatal MI, or revascularization. Cardiac death was defined as death caused by acute MI, ventricular arrhythmias, or refractory heart failure. Non-fatal MI was defined on the basis of criteria of typical chest pain, elevated cardiac enzyme levels, and typical changes on the electrocardiogram.22 In case of multiple events in a given patient, the first event was included in the analysis.
Multislice computed tomography data acquisition
Multislice computed tomography acquisition technique in our laboratory has been previously described.23 Briefly, MSCT was performed using 64-slice systems (Siemens Sensation 64, Siemens Medical Solutions, Erlangen, Germany or Brilliance 64, Philips Healthcare, Best, The Netherlands) after appropriate use of sublingual nitroglycerin and intravenous beta-blockers. At the time of this study, we routinely used intravenous metoprolol at 5 mg increments every 5 min (up to 30 mg) to bring the heart rate down to 65 beats. Low-osmolar non-ionic contrast agent (90–100 cc Ultravist 370, Berlex, Wayne, NJ, USA) at flow rates between 3.5 and 4.5 mL/s was injected into the antecubital vein using an 18-gauge needle and a power injector (Stellant D, Medrad, Inc., Pittsburgh, PA, USA). Bolus tracking technique was employed to appropriately time the onset of image acquisition. After contrast injection, a retrospective electrocardiographic-gated spiral scan was performed covering the region immediately beneath the aortic arch to the apex of the left ventricle during an inspiratory breath hold of 10–20 s, depending on the particular scanner. The scan parameters were as follows: gantry rotation 330–420 ms, spiral imaging with retrospective electrocardiographic gating and dose modulation (electrocardiographic pulsing), 750–850 mAs, 120 kV, 0.75 mm slice thickness. For all scanners, a multi-segment algorithm was used to reconstruct overlapping images, typically at 75% of the cardiac cycle. If motion artefacts were present, additional reconstructions were made at different points of the R–R interval, as needed. Radiation dose-reducing techniques, i.e. dose modulation, was employed on all scans. Individuals with significant arrhythmia (atrial fibrillation and frequent premature beats) or rapid heart rate (>90 b.p.m.), and contraindications to beta-blockade/calcium channel blockade, were not imaged.
Coronary stenosis and atherosclerotic plaque analysis
Our laboratory has reported the analysis technique previously.23 All studies were interpreted at the time of acquisition by experienced MSCT imagers. Two reviewers (T.P.C. and D.N.) recorded the MSCT interpretations for both, presence of coronary stenosis and coronary plaque. Categorization of significant stenosis (defined as 50% luminal narrowing) was adapted from the previously published Duke criteria and performed as follows24: normal coronaries, non-significant or mild stenosis, significant stenosis in one vessel, stenosis in two vessels or in the proximal left anterior descending (LAD), stenosis in three vessels or in two vessels, including the proximal LAD, or stenosis in the left main. For categorization of plaque, the coronary system was divided into 10 segments: left main and 3 segments (proximal, mid, distal) for the LAD, left circumflex and right coronary arteries, respectively. For each segment, the presence of plaque (resulting in at least 30% reduction in luminal diameter) was recorded as being present or absent and categorized as follows (Figure 1A–C): (i) none, (ii) calcified (composed exclusively of high density material >130 Hounsfield units), (iii) non-calcified (composed exclusively of material having density <130 Hounsfield units), and (iv) mixed (having components of both calcified and non-calcified plaques).16,19 If there were both calcified and non-calcified plaques in one segment, it was classified as a calcified plaque. Coronary plaques were defined as structures >1 mm2 within and/or adjacent to the coronary artery lumen, which could be distinguished clearly from the vessel lumen and the surrounding pericardial tissue, as described previously.25 One coronary plaque was assigned per coronary segment. Minimal luminal irregularities were not classified as plaque. On the basis of these findings, a total plaque score (out of 10) was calculated in each patient. Proximal LAD was defined as extending from the ostium to the take-off of the first diagonal branch. All MSCT reports were independently adjudicated by an experienced reader (M.Y.D.), without concomitant knowledge of clinical data.
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Statistical analysis
Discrete variables are presented as counts and percentages. Continuous data are expressed as mean ± SD or median and inter-quartile range, where appropriate. Continuous variables were compared using Student's t-test (two-sided) or analysis of variance. Categorical variables were analysed using
2 test or Fisher's exact test. To identify the association between clinical (age, gender, diabetes mellitus, hypertension, dyslipidaemia, smoking, family history, aspirin, beta-blockers, statins, body mass index, ATP III risk score, and pre-test likelihood), MSCT variables (total plaque score, type of plaque, presence of proximal plaque, and extent of obstructive CAD), and outcomes, Cox proportional hazard analysis was performed. We defined outcome endpoint as a composite MACE of cardiac death, non-fatal MI, and revascularization. First, univariable analysis of baseline clinical characteristics and MSCT variables was performed to identify potential predictors. The potential predictors that we selected for univariable analysis are associated with cardiovascular outcomes, from a pathophysiological standpoint. To identify independent predictors, we then performed a forward stepwise multivariable analysis of variables with P < 0.10 on univariate analysis. Results of Cox proportional hazard analysis are presented as hazard ratio with 95% confidence intervals. To assess whether proportional hazards assumptions were satisfied, we performed linear regression of Schoenfeld residuals against survival time. Absence of significant correlation (P > 0.05) was taken to signify that proportional hazards assumptions were not violated. Cumulative event rates as a function over time were also obtained by the Kaplan–Meier method. Event curves of MACE and hard cardiac events (defined as cardiac death and non-fatal MI) were compared using log-rank test. Receiver-operating characteristic (ROC) curve analysis was used to calculate area under the curve (AUC) to demonstrate significance of association between plaque score and ATP III risk score. Statistical analyses were performed using JMP software (version 6.0.2, SAS Institute Inc., Cary, NC, USA), Statistica (version 6.1, Statsoft, Tulsa, OK, USA), and SPSS (10.0, SPSS, Chicago, IL, USA). P-values < 0.05 were considered statistically significant. |
Results |
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Patient population
The mean age of the study population (n = 227) was 54 ± 12 years, with majority being white (80%) and male (61%). Forty-nine (22%) patients had low, 143 (63%) had intermediate, and 35 (15%) had high pre-test likelihood of CAD. Also, 166 (73%) patients had low, 56 (25%) had intermediate, and 5 (2%) had high ATP III risk score. There was no correlation between pre-test likelihood and ATP III risk score in the current population (r = 0.20, P = 0.8). Baseline characteristics of the entire study population are provided in Table 1.
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Multislice computed tomography data
The MSCT data for the study population is shown in Table 2. There were 55 patients with obstructive CAD (
50%) in one or more epicardial coronary arteries. The mean total plaque score (out of 10) was 1.9 ± 2.2 (median 1, inter-quartile range 0–3). The radiation dose ranged from 8–12 mSEV in our study population.
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Follow-up data
The mean follow-up for the study population was 2.3 ± 0.8 years (median 2.4 years, inter-quartile range 2.2–2.7 years). Seventy-five (33%) patients underwent invasive angiography and/or functional stress testing. In the follow-up period, there was 1 cardiac death, 3 patients with non-fatal MI, 7 patients with PCI, and 7 with CABG, giving a total of 18 patients with MACE and 4 with hard cardiac events. The decision for revascularization was based on symptoms and/or the presence of ischaemia on concomitant non-invasive testing. No patient had revascularization based solely on MSCT findings. In addition, there were four other deaths in the group, two from cancer, one from stroke, and one in a post-operative setting, judged to be non-cardiac due to pulmonary embolism.
Predictors of major adverse cardiac events and hard events
After ensuring that the proportional hazard assumptions were satisfied, we performed univariable Cox proportional hazard analysis of clinical and MSCT variables to predict MACE, as shown in Table 3. Multivariable analysis of variables with P-value <0.10 in univariable analysis is shown in Table 4. As demonstrated in Table 4, the presence of proximal coronary plaque, extent of coronary plaque, and one or more vessel obstructive CAD were independent predictors of MACE. Subsequently, we generated Kaplan–Meier curves to test the associations between MSCT variables and MACE (Figures 2 and 3) as well as hard events (Figure 4). As demonstrated in Figure 2, patients with no or mild disease had the best freedom from MACE, whereas patients with one or more vessel obstructive CAD had the highest incidence of MACE (log-rank statistic P-value <0.0001). Patients with proximal atherosclerotic coronary plaque (in the left main or proximal LAD) had increased MACE compared with those without (log-rank statistic P-value <0.0001, Figure 3). After exclusion of patients with revascularization, the hard cardiac event rate was significantly higher in patients with one or more vessel obstructive CAD compared with those without (log-rank statistic P-value = 0.01, Figure 4). The presence of proximal atherosclerotic plaque was associated with a trend towards a higher hard cardiac event rate, reaching borderline statistical significance (log-rank statistic P-value = 0.05).
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Incremental value of coronary plaque content over traditional risk assessment
Because majority of the patients (n = 225) had at least a 1 year follow-up, we performed ROC curve analysis to test whether the total plaque score provided incremental value in predicting MACE at 1 year, over and above that provided by ATP III risk score and standard pre-test likelihood prediction models (Figures 5A and B). The AUC for total plaque score predicting MACE at 1 year was significant (0.75, CI 0.62–0.89, P < 0.001). AUC for ATP III predicting MACE was not significant (0.60, CI 0.47–0.73, pv = 0.2). Similarly, AUC for pre-test likelihood predicting MACE at 1 year was not significant (0.47, CI 0.31–0.64, P = 0.7). The difference in AUC between total plaque score and ATP III score was significant (0.15, P-value 0.04). Similarly, the difference in AUC between total plaque score and pre-test likelihood of CAD was significant (0.28, P < 0.01).
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Association of major adverse cardiac events and multislice computed tomography findings
In the current study, there were 172 patients without CAD (n = 96) or mild CAD (n = 76) on MSCT. At 2.3 year follow-up, there were no MACE in the no-CAD group and two MACE (one of which was a hard cardiac event) in the mild CAD group. Hence, in the setting of a low-risk MSCT (mild or no CAD), on Kaplan–Meier survival analysis, there was 1% MACE rate at 2.1 year follow-up (CI 0–2%). On the other hand, there were 20 patients with three-vessel, two-vessel (with proximal LAD), or left main obstructive disease, of whom 11 (45%) had MACE.
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Discussion |
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Our data demonstrate the independent prognostic utility of coronary MSCT in patients with suspected CAD and intermediate pre-test likelihood of significant disease, followed over a mean of 2.3 years. Presence of one or more vessel obstructive CAD was associated with increased rate of hard cardiac events. The prognostic ability of MSCT variables remained significant after correction for traditional risk factors, including age. Extent of coronary atherosclerotic plaque as well as the presence of proximal atherosclerotic plaque was associated with a significantly increased MACE rate. The type of atherosclerotic plaque (calcified, non-calcified, or mixed) was not associated with outcomes. Importantly, we also demonstrated that in symptomatic patients with cardiac risk factors, patients with no CAD on MSCT had a 100% event-free survival over the extent of the follow-up. Finally, we demonstrated that extent of coronary artery plaque, assessed by MSCT, provides incremental value over ATP III risk score in the prediction of MACE in our population.
As this was a relatively low-risk population with no prior documented CAD (as demonstrated by a larger proportion of patients in the low ATP III score category), the major event (cardiac death or non-fatal MI) rate was low at the current duration of follow-up. Hence, along with hard cardiac events, we also used a composite endpoint of cardiac death, MI, and revascularization for outcomes analysis. A longer follow-up is likely necessary to ascertain conclusively the role of MSCT in predicting hard cardiac endpoints.
The current study extends the results of previous descriptions evaluating the prognostic utility of MSCT coronary angiography.18–20 However, there are important differences between the current study and those previous reports. Specifically, our study population was younger without previous documented CAD, including MI or revascularization. Also, all imaging was performed on the current state-of-the-art 64 MSCT. Also, unlike previous reports, the majority of our patients had intermediate likelihood of CAD and had a significantly longer follow-up. Further, unlike the study by Min et al.,18 we documented and used all cardiac endpoints, including cardiac mortality. Also, as expected, the event rate in our study population was lower, despite a longer follow-up, because of the relatively lower cardiac risk at baseline. Our study population is more in line with the current guidelines, which recommend that the appropriate utility of a non-invasive imaging test lies in an intermediate likelihood population.26,27 Indeed, the appropriateness criteria for MSCT coronary angiography, published after these patients were imaged, endorses this utilization.13
In the current clinical paradigm, preliminary evaluation of patients with suspected CAD involves the determination of the pre-test likelihood of disease.21 If the calculated risk is low, no further testing is warranted. On the other end of the risk profile, invasive angiography may be warranted in high-risk patients. However, in routine clinical practice, there are a large proportion of patients who fall in the intermediate-risk category. According to various guidelines, such patients would likely need additional non-invasive testing (including exercise electrocardiography, myocardial perfusion scintigraphy, and/or stress echocardiography) for optimal risk stratification. Multiple reports have demonstrated incremental prognostic value of such testing in the prediction of future events.2–8 Most recently, MSCT coronary angiography has been proposed in lieu of stress testing for risk stratification in intermediate-risk patients with suspected CAD.13 Indeed, MSCT is a highly accurate, non-invasive imaging technique for the diagnosis of CAD; this is particularly so as the high-negative predictive value enables safe and effective exclusion of CAD.14 Similar to previous reports,18,19 patients in the current study with mild or no CAD on MSCT had a very high event-free survival rate.
In our current primary prevention paradigm, traditional risk factor assessment using ATP III risk score is the major method for the stratification of predisposed individuals.9 However, previous reports have demonstrated that traditional risk prediction models could potentially be suboptimal in discerning CAD risk, particularly for younger individuals and women.28–30 Along with the observation that most acute coronary events occur in conjunction with non-stenotic atherosclerotic plaques,31,32 this finding compels us to find additional risk assessment strategies.
In addition to the degree of luminal stenosis, MSCT provides insight into the changes within the arterial wall, in the form of coronary plaque composition and extent (although semi-quantitative at the present time).14–17 The current study demonstrates an incremental prognostic value of the extent of coronary plaque in predicting MACE, over and above ATP III risk score. This finding is similar to previous reports of incremental value of coronary calcium scoring over ATP III risk score.33 Furthermore, emerging literature has demonstrated the potential incremental information about proximal plaques provided non-invasively by MSCT.19 Notably, prior studies have demonstrated that most acute coronary events occur in the proximal portions of the coronaries.34,35 In the current study, we also demonstrate that patients with proximal plaques have a higher event rate compared with those without. The current study also demonstrated that the presence of non-calcified plaque was not predictive of outcomes. It has been suggested previously that in patients presenting with acute coronary syndrome, the site of predominantly non-calcified plaques was the culprit site.36 However, the difference in findings between the two studies can likely be explained by significant differences in risk profile of the study populations (our study comprising a relatively lower risk population).
Strengths and limitations
Our study presents several strengths and limitations. The analysis is strengthened by the relatively large sample size imaged using the state-of-the-art MSCT technology followed over a longer period of time than previously reported. The study population reflects current consensus indications including symptomatic subjects, with intermediate pre-test likelihood/intermediate risk category, which would be deemed clinically appropriate to undergo coronary MSCT. Another issue that needs to be addressed is that of treatment bias. MSCT led to the identification of patients with obstructive CAD, likely resulting in increased revascularization, which constituted the major proportion of the composite MACE endpoint. However, it is worthwhile noting that these patients were undergoing MSCT for symptom evaluation and all decisions regarding revascularization were based on symptoms and/or the presence of concomitant ischaemia on non-invasive testing followed by cardiac catheterization. However, the presence of obstructive CAD on MSCT was associated with hard cardiac events. Multislice computed tomography has a lessened ability to characterize luminal stenosis when calcified plaque is present as a result of ‘blooming’ artefact. Although this limitation may have caused overestimation of coronary stenosis, it should not have impaired our ability to identify plaques per se. From a statistical standpoint, introduction of multiple clinical variables (for Cox analysis) increases type alpha error, i.e. possibility of an arbitrary clinical parameter emerging as independent predictor. However, despite this, in all three models, only individual MSCT parameters emerged as independent predictors.
The radiation associated with coronary MSCT needs to be seriously considered, particularly in younger individuals and women, in the light of recent data demonstrating potentially increased risk of malignancy in such populations.37 However, the use of dose-reduction techniques (e.g. ECG-pulsing during retrospective scanning or prospective axial scanning) can significantly reduce the radiation burden.38–40 For the current study, we uniformly implemented ECG-pulsing during retrospective scanning, which resulted in relatively low radiation dose in our study population. Also, to keep radiation to a minimum, we do not routinely perform calcium scoring or functional assessment on patients undergoing MSCT coronary angiography at our institution.
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Conclusions |
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Non-invasive coronary angiography by 64-slice CT, performed in patients with suspected CAD, the majority of whom had an intermediate pre-test likelihood of disease, provides incremental prognostic value. The presence of one or more vessel obstructive CAD on MSCT is associated with an increased hard cardiac event rate. Also, there is a graded increase in the risk of MACE with increased extent of obstructive CAD seen on MSCT; conversely, patients with no CAD on MSCT had a 100% event-free survival over the extent of the follow-up. In this population with no documented CAD, the extent of coronary artery plaque assessed by MSCT provides incremental value over ATP III risk score in the prediction of MACE.
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Funding |
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The institution and the authors receive modest research support from Siemens Medical Solutions and Philips Healthcare. R.D.W. receives modest research support from Siemens Medical Solutions. S.H. receives research grants (>$10 000) from Siemens Medical Solutions.
Conflict of interest: none declared.
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Acknowledgement |
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The authors would like to acknowledge and thank Ms Marlene Goormastic, MPH, and Ms Kathy Wolski, MPH, for their expert statistical advice during the revision phase of the current manuscript.
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References |
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