Background Angiographic studies of the regression of coronaryartery disease are invasive and costly, and they permit onlylimited assessment of changes in the extent of atheroscleroticdisease. Electron-beam computed tomography (CT) is noninvasiveand inexpensive. The entire coronary-artery tree can be studiedduring a single imaging session, and the volume of coronarycalcification as quantified with this technique correlates closelywith the total burden of atherosclerotic plaque.
Methods We conducted a retrospective study of 149 patients (61percent men and 39 percent women; age range, 32 to 75 years)with no history of coronary artery disease who were referredby their primary care physicians for screening electron-beamCT. All patients underwent base-line scanning and follow-upassessment after a minimum of 12 months (range, 12 to 15), anda volumetric calcium score was calculated as an estimate ofthe total burden of plaque. Treatment with 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase inhibitors was begun at the discretionof the referring physician. Serial measurements of low-densitylipoprotein (LDL) cholesterol were obtained, and the changein the calcium-volume score was correlated with average LDLcholesterol levels.
Results One hundred five patients (70 percent) received treatmentwith HMG-CoA reductase inhibitors, and 44 patients (30 percent)did not. At follow-up, a net reduction in the calcium-volumescore was observed only in the 65 treated patients whose finalLDL cholesterol levels were less than 120 mg per deciliter (3.10mmol per liter) (mean [±SD] change in the score, –7±23percent; P=0.01). Untreated patients had an average LDL cholesterollevel of at least 120 mg per deciliter and at the time of follow-uphad a significant net increase in mean calcium-volume score(mean change, +52±36 percent; P<0.001). The 40 treatedpatients who had average LDL cholesterol levels of at least120 mg per deciliter had a measurable increase in mean calcium-volumescore (mean change, +25±22 percent, P<0.001), althoughit was smaller than the increase in the untreated patients.
Conclusions The extent to which the volume of atheroscleroticplaque decreased, stabilized, or increased was directly relatedto treatment with HMG-CoA reductase inhibitors and the resultingserum LDL cholesterol levels. These changes can be determinednoninvasively by electron-beam CT and quantified with use ofa calcium-volume score.
Both primary prevention and secondary prevention of coronaryartery disease are being widely investigated.1,2 Preventivecardiology would benefit from the introduction of noninvasivetechniques that accurately quantify the extent of coronary atherosclerosis.The studies conducted to date on the regression of coronaryartery disease have used arteriographic techniques.3,4,5,6,7,8,9,10These methods are invasive and costly, and they require lengthyand elaborate analysis by expert investigators. Furthermore,long follow-up times are necessary to detect small changes inthe minimal luminal diameter at the level of focal stenoses.However, small gains in luminal diameter have been shown tocorrespond to substantial clinical benefits.11 Electron-beamcomputed tomography (CT) can rapidly and noninvasively quantifythe extent of coronary-artery calcification within the entirecoronary-artery tree, closely approximating the total plaqueburden as measured at autopsy.12,13,14,15,16,17,18,19
One of the most appealing features of electron-beam CT is thepotential to detect the progression or regression of coronaryatherosclerotic disease noninvasively. However, the reportedlylimited reproducibility of the traditional calcium score hashampered the application of electron-beam CT to this field.20,21,22,23,24To circumvent this problem, we developed a novel calcium-volumescore with a high degree of reproducibility between scans.25This score represents the volume of plaque and is based on theassumption that aging plaques may become smaller in volume whilebecoming denser.21,26,27 The score has a wide range of valuesand varies according to age, sex, and other factors. In thisretrospective study, we sought to test the hypothesis that thereis a relation between treatment with 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase inhibitors and the change incoronary-plaque volume, as assessed by electron-beam CT, overthe course of one year.
Methods
Patients
We reviewed the medical records of 195 consecutive asymptomaticpatients, with no history of coronary artery disease, who werereferred by their primary care physicians for sequential electron-beamscanning procedures at intervals of 12 to 15 months. All informationon risk factors for coronary artery disease was obtained byreview of the patients' medical records. The patients in thisobservational study either were not receiving any lipid-loweringtherapy or were receiving HMG-CoA reductase inhibitors as theironly lipid-lowering medications. In every case, the choice whetherto begin lipid-lowering therapy was made by the referring physician.Serial measurements of low-density lipoprotein (LDL) cholesterolwere obtained throughout the study, and the values were averaged.Forty-six patients were excluded from the study: 30 (15 percent)because of inadequate image quality and 16 (8 percent) becausethey had an initial calcium-volume score below 30. The studygroup was composed of the remaining 149 patients. The studyprotocol was approved by the institutional review board of theElectron Beam Tomography Research Foundation.
Imaging Procedures
All patients underwent imaging with an Imatron C-100 scanner(Imatron, South San Francisco, Calif.). Imaging was performedwith a 100-msec scanning time and a single-slice thickness of3 mm. A total of 40 slices were obtained during two breath-holdingperiods. Tomographic imaging was electrocardiographically triggeredat 80 percent of the RR interval. All areas of calcificationwithin the borders of a coronary artery with a minimal opticaldensity of 130 Hounsfield units were computed. A calcified coronaryplaque was considered present if at least four consecutive pixelswith signal density of at least 130 Hounsfield units were measured(an area equivalent to 2.24 mm2). The acquired images were reviewedat a NetraMD workstation (ScImage, Los Altos, Calif.). Patientswere included in this study only if complete data were availablefrom their scans, without misregistration of slices due to artifactsof motion, respiration, or asynchronous electrocardiographictriggering. To ensure the continuity and consistency of theinterpretation of scores, a single expert investigator, unawareof the patients' clinical status and the temporal sequence ofthe studies, reviewed all the scans.
Calculation of Calcium-Volume Scores
The traditional calcium score is calculated by multiplying thearea of a calcified plaque by a signal-density cofactor. Whenlipid-lowering agents reduce the soft lipid core of a calcifiedplaque, the density of the plaque and its calcium score increase,whereas its volume may decrease. Therefore, in this study weused a novel scoring system to calculate the volume of a plaqueaccording to the principle of isotropic interpolation.25,28,29,30Our software allowed us to slice the volume lying between twoimaging planes into several sections. The density of each sectionwas then determined relative to that of the original imagingplanes by a process of mathematical interpolation. The processwas repeated at high speed in all three spatial orthogonal directions,and the volume of a calcified plaque was calculated.25 The finalscore is presented as a whole number to facilitate comparisonwith the traditional calcium score, although it is actuallya volume measured in fractions of cubic millimeters (valuesin cubic millimeters were multiplied by 1000 to generate wholenumbers). In an earlier study, we assessed the variability ofthe calcium-volume score between scans and compared it withthe variability of the traditional score.25 The reproducibilityof the interpolated volume score was consistently superior tothat of the traditional score, and the accuracy of the newerscoring system was significantly greater than that of the latter(P<0.001), with an overall 39.5 percent reduction in error.The median interscan variability of the calcium-volume scorewas 8.9 percent for all scoring levels (5.8 percent when thescore was 30 or more). To ensure maximal accuracy in our analysisof changes in calcium-volume scores over time, we included inthis study only patients with an initial calcium-volume scoreof at least 30. Since the variability of the traditional calciumscore is too great,20,21,22,23,24,25 we decided not to use thistraditional score.
Statistical Analysis
In this retrospective analysis, patients were classified intothree groups. Group 1 consisted of patients who were not treatedwith HMG-CoA reductase inhibitors. Groups 2 and 3 consistedof treated patients. In group 2 the average levels of LDL cholesterolwere at least 120 mg per deciliter (3.10 mmol per liter), andin group 3 they were less than 120 mg per deciliter. Withineach group, the change in the calcium-volume score from baseline to follow-up was expressed in both absolute and relativeterms. Standard summary statistics, including mean and medianof changes in the score, were used to document the results ineach group, and the paired t-test was used to determine thesignificance of the difference in the average changes withineach group. The sign test was used to construct confidence intervals.Comparisons of mean relative changes in the calcium-volume scorebetween groups were made with the two-sample t-test. A two-samplez test was used to document the significance of the differencebetween groups in the proportion of patients for whom a changein calcium-volume score was found. Regression analysis was usedto summarize the relation between the relative change in thecalcium-volume score and the average LDL cholesterol level intreated patients. Confidence intervals around the fitted regressionline were calculated.
Residual plots and the runs test31 were used to confirm thatthere were no violations of the basic assumptions of regressionanalysis. Patients were matched in order to compare the relativechange in the calcium-volume score among groups of patientsafter correction for differences in the base-line calcium-volumescore and the average LDL cholesterol level. Finally, an analysisof covariance was conducted in two cohorts of patients selectedfrom the subgroups of treated and untreated patients definedaccording to LDL cholesterol level. These analyses were performedto adjust for the possible influence of differences in base-linecalcium-volume scores on final scores. P values of less than0.05 (two-tailed) were considered to indicate significance.All values are expressed as means ±SD.
Results
The base-line clinical characteristics of the study patientsare presented in Table 1. Among the 149 patients, 61 percentof whom were men (age range, 32 to 75 years), 105 (70 percent)received treatment with HMG-CoA reductase inhibitors and 44(30 percent) did not. The average interval between the initialand follow-up scans was 13.7±0.6 months (range, 12 to15 months).
Table 1. Clinical Characteristics of the Patients.
Changes in Calcium-Volume Scores in Relation to LDL Cholesterol Levels
Figure 1 shows a scatter plot of the percent change in the calcium-volumescore at one year in relation to the average LDL cholesterollevel for each patient. The mean LDL cholesterol level was 114±23mg per deciliter (2.95±0.59 mmol per liter) for treatedpatients and 147±22 mg per deciliter (3.80±0.57mmol per liter) for untreated patients (P<0.001). The averagechange in the calcium-volume score for the treated group wasan increase of 5±28 percent, as compared with 52±36percent for untreated patients (P<0.001). All untreated patientshad an increase in score. We found no differences in the degreeof change in the calcium-volume score over time between menand women, although the numbers may have been too small to demonstratea sex difference.
Figure 1. Scatter Plot of the Percent Change in the Calcium-Volume Score at One Year in Relation to the Average LDL Cholesterol Level for All Patients.
All untreated patients (group 1) and treated patients with average LDL cholesterol levels of at least 120 mg per deciliter (group 2) had increased scores, whereas 63 percent of treated patients with average LDL cholesterol levels below 120 mg per deciliter (group 3) had decreased scores. To convert values for cholesterol to millimoles per liter, multiply by 0.02586.
All patients with a net decrease in the score were treated patientswith average LDL cholesterol levels of less than 120 mg perdeciliter. Starting from this observation, we proceeded to analyzeour data for changes in the mean calcium-volume scores in thethree groups of patients. Figure 2 shows a plot of the percentchange in the calcium-volume score at one year in relation tothe average LDL cholesterol level for patients treated withHMG-CoA reductase inhibitors (groups 2 and 3). In this analysisthe regression was significant (both the constant and the slopecoefficient were significantly different from zero, P<0.001)and showed a good linear relation (r=0.5). In a similar regressionanalysis conducted for the untreated patients, the relationwas not linear. Residual analysis supported the basic assumptionsof this regression model.
Figure 2. Regression Analysis of the Percent Change in the Calcium-Volume Score in Relation to the Average LDL Cholesterol Level in Treated Patients at One Year.
CI denotes confidence interval. To convert values for cholesterol to millimoles per liter, multiply by 0.02586.
Patients with Average LDL Cholesterol Levels of at Least 120 mg per Deciliter
In the 44 untreated patients (group 1), the average LDL cholesterollevel was 147±22 mg per deciliter, and in the 40 treatedpatients whose LDL cholesterol levels remained at least 120mg per deciliter (group 2), the average LDL cholesterol levelwas 139±18 mg per deciliter (3.59±0.47 mmol perliter). In both groups there was a significant increase in thecalcium-volume score (Figure 3). In group 1 the mean calcium-volumescore was 479±629 at base line and 646±762 atfollow-up; the mean increase per patient was 167±179(P<0.001). In group 2 the mean calcium-volume score was 1017±2062at base line and 1254±2483 at follow-up; the mean increaseper patient was 237±502 (P=0.005). The mean percent changesin calcium-volume score were 52±36 percent in group 1and 25±22 percent in group 2 (P<0.001 for the differencein change between the groups). Thus, the percent increase inthe calcium-volume score was significantly greater in untreatedpatients than in treated patients whose average LDL cholesterollevels were 120 mg per deciliter or more.
Figure 3. Initial Values (Open Bars) and Final Values (Solid Bars) for the Calcium-Volume Score in Relation to the Average LDL Cholesterol Level and Treatment Status.
Patients in group 1 were not treated with HMG-CoA reductase inhibitors; patients in group 2 were treated and had average LDL cholesterol levels of at least 120 mg per deciliter; patients in group 3 were treated and had average LDL cholesterol levels below 120 mg per deciliter. P values are for comparisons of initial and final values within groups.
Patients with Average LDL Cholesterol Levels Below 120 mg per Deciliter
Among the 65 treated patients in group 3, the average LDL cholesterollevel was 100±17 mg per deciliter (2.59±0.44 mmolper liter). The average calcium-volume score in this group was980±1611 at base line and 956±1700 at follow-up;the average change per patient was a decrease of 23±261(P not significant). The mean relative change in the calcium-volumescore was a significant decrease of 7±23 percent (P=0.01).Sixty-three percent of the patients in this group had a netdecrease in the calcium-volume score, but the remaining 37 percenthad a net increase, despite medical treatment. On the otherhand, no patient in either group 1 or 2 had regression of disease.Thus, patients whose LDL cholesterol levels had been reducedto below 120 mg per deciliter were much more likely to havea decreased calcium-volume score than patients who had receivedno treatment or whose LDL cholesterol levels had remained ator above 120 mg per deciliter despite treatment (P<0.001for the two-sample test for the proportion in group 3 vs. theproportions in groups 1 and 2). Among patients whose calcium-volumescores decreased, the mean percent change in score was –21±17percent and the median change was –17 percent.
Matching of Patients
The average base-line calcium-volume score of the untreatedpatients was considerably lower than that of the patients inthe two treated groups (Figure 3). Because of concern that thisdifference might have affected the rates of change in the absolutescore over time, we matched 24 patients from each group whohad similar initial calcium-volume scores (within 15 percent)and assessed the percent change in the score between base lineand follow-up (Figure 4). The mean changes were +57±37percent for group 1, +26±23 percent for group 2, and–2±22 percent for group 3 (P<0.001 by one-wayanalysis of variance for the overall comparison of the meanpercent changes). These results were similar to the overallresults of the comparison of the three groups. An analysis ofcovariance, in which the initial score was taken as the covariate,confirmed the results for matched pairs (mean changes, +52±28percent for group 1, +25±29 percent for group 2, and–7±30 percent for group 3; P<0.001 for all comparisons).Thus, the initial calcium-volume score had no influence on therate of growth of calcified plaques.
Figure 4. Initial Values (Open Bars) and Final Values (Solid Bars) for the Calcium-Volume Score in Patients Matched for Initial Score in Relation to the Average LDL Cholesterol Level and Treatment Status.
Patients in group 1 were not treated with HMG-CoA reductase inhibitors; patients in group 2 were treated and had average LDL cholesterol levels of at least 120 mg per deciliter; patients in group 3 were treated and had average LDL cholesterol levels below 120 mg per deciliter. P values are for comparisons of initial and final values within groups.
Further subgroup analysis addressed the interesting questionof whether HMG-CoA reductase inhibitors have an effect on theevolution of atherosclerotic coronary artery disease beyondtheir ability to reduce absolute levels of LDL cholesterol.In this analysis, we matched 28 patients each from the treatedand untreated groups with similar average levels (within 3 percent)of LDL cholesterol. The mean LDL cholesterol levels were 141mg per deciliter (3.66 mmol per liter) for the treated groupand 140 mg per deciliter (3.62 mmol per liter) for the untreatedgroup; the median was 140 mg per deciliter for both groups.The calcium-volume score increased by a mean of 50±37percent in the untreated group and 26±22 percent in thetreated group (P<0.001). This difference represented a 48percent lower rate of increase in the calcium-volume score fortreated as compared with untreated patients, although both groupsof patients had similar final LDL cholesterol levels. In ananalysis of covariance conducted to ensure that the observeddifference in the percent increase in calcium-volume score hadnot been influenced by the initial difference in calcium-volumescore, the reduction in the rate of increase was 45 percent,which was still significant (P<0.05).
Discussion
In this retrospective study we demonstrated that treatment withHMG-CoA reductase inhibitors can reduce the volume of calcifiedplaque in the coronary arteries and that these changes can bequantified reliably and noninvasively by electron-beam CT.
To date, studies of the regression of coronary artery diseasehave used quantitative coronary angiography and have requireda follow-up of several years to demonstrate small reductionsin luminal stenosis.3,4,5,6,7,8,9,10 Angiographic studies areinvasive, costly, and time consuming. Although these techniquespermit the assessment of disease regression at the level ofmeasurable focal stenoses, they do not provide information onthe effects of therapy on the total burden of coronary-arteryplaque. Furthermore, the arterial remodeling that is known tooccur in vessels affected by an atherosclerotic process is verylikely to affect the reliability of serial angiographic studiesof luminal stenosis after medical interventions.32,33,34 Incontrast, electron-beam CT is a rapid, noninvasive method thatcan be used to study the entire coronary-artery tree, and itis considerably less expensive than angiography.
It is now recognized that deposition of calcium in the coronaryarteries is an active process that may be a response to damagecaused by several types of noxious stimuli.35 Furthermore, thereis a direct correlation between the extent of coronary calcificationand the total burden of atherosclerotic plaque.16,18,19 Schmermundet al. have recently shown that electron-beam CT is similarto coronary angiography in measuring the effects of severalknown risk factors on coronary atherosclerosis.36 These findingssuggest that it may be appropriate to use this new techniqueto assess the extent of disease and the benefits of therapy.
Our analysis showed that the rate of change in the volume ofcalcified coronary plaque, as determined by electron-beam CT,was significantly lower in treated than in untreated patients.Furthermore, this difference appeared to be related to the levelof LDL cholesterol after treatment. Our study also demonstratedthat follow-up times can be much shorter with this techniquethan when angiography is used to assess the effects of medicaltherapy on atherosclerotic disease.
Stabilization of and decreases in plaque volume were found tobegin at an LDL cholesterol level of less than 120 mg per deciliter.However, lipid-lowering therapy was effective in slowing increasesin plaque volume at any level of LDL cholesterol. Treated patientsin whom LDL cholesterol levels failed to drop below 120 mg perdeciliter still had a slower progression of disease than untreatedpatients — even among patients matched with respect tothe average LDL cholesterol level. This finding indicates thattreatment at any level may produce a substantial slowing ofthe natural growth of coronary-artery plaque. In an analysisof data from the West of Scotland Coronary Prevention Study,outcomes were compared between patients in the treatment groupand those in the placebo group who had the same final LDL cholesterollevel.37 Patients in the placebo group had a higher rate ofcoronary events than the pravastatin-treated patients. Theseintriguing observations appear to confirm that even when notused aggressively, therapy with HMG-CoA reductase inhibitorsmay beneficially influence the course of coronary artery disease.
Thirty-seven percent of treated patients who had average LDLcholesterol levels below 120 mg per deciliter had increasesin plaque volume despite adequate therapy. This supports thehypothesis that other factors besides LDL cholesterol are involvedin the progression of atherosclerotic disease. Some lipoproteinsthat are unaffected or only slightly affected by treatment withHMG-CoA reductase inhibitors, such as small, dense LDLs, Lp(a),and intermediate-density lipoproteins, or the presence of alow level of high-density lipoprotein cholesterol may contributeto the progression of the disease.38,39,40 Furthermore, factorsother than lipoprotein, such as homocysteine, fibrinogen, C-reactiveprotein, and various infectious agents, may also play an importantpart in the initiation and continued progression of atherosclerosis.38,41,42,43,44,45,46,47,48,49,50Future studies of the regression of coronary artery diseasein patients treated with lipid-lowering agents will continueto investigate the contribution of all such factors.
Patients who did not receive treatment with HMG-CoA reductaseinhibitors had lower initial calcium-volume scores than treatedpatients. This difference may have been due to physicians' biastoward treating patients with higher scores because of an assumptionthat a smaller amount of coronary calcification indicates lessimportant atherosclerotic disease. However, since untreatedpatients uniformly had a more rapid, uninterrupted increasein plaque volume, such an assumption may not have been justified.
Limitations of the Study
Since various HMG-CoA reductase inhibitors were used at differentdoses, treatment could have had diverse effects on the progressionof calcium-volume scores. An LDL cholesterol level of 120 mgper deciliter was arbitrarily selected as a cutoff point foranalysis of change in calcium-volume scores, and it does notnecessarily constitute a reference level for future studies.During the follow-up period, we did not assess the effect ofthe modification of any risk factor for coronary artery diseaseother than LDL cholesterol, although the base-line characteristicswere similar in all groups of patients. Finally, this was apilot study with the limitations inherent in a small sample.
Clinical Implications
Our study, like many others, has shown that HMG-CoA reductaseinhibitors have beneficial effects on the natural course ofcoronary artery disease and that with adequate technique, electron-beamCT is an accurate method of documenting the evolution of calcifiedcoronary plaque. The accuracy of this technique is such thateven short-term follow-up may be sufficient to indicate thedirection of the effect of treatment on the disease. The useof electron-beam CT as a diagnostic tool in preventive cardiologymay make possible a new form of secondary prevention directedat asymptomatic patients with coronary calcifications.
Supported in part by the Dean's Fund for Faculty Research, OwenGraduate School of Management, Vanderbilt University.
Drs. Callister and Russo own publicly traded shares in Imatron,which manufactures the electron-beam computed tomographic scannersused for cardiac imaging in this study.
Source Information
From the Electron Beam Tomography Research Foundation (T.Q.C., P.R., N.J.L., D.J.R.) and Vanderbilt University (B.C.), both in Nashville. Presented in part at the 70th Scientific Sessions of the American Heart Association, Orlando, Fla., November 9–12, 1997.
Address reprint requests to Dr. Raggi at the EBT Research Foundation, 64 Valleybrook Dr., Hendersonville, TN 37075.
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