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Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-2857
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The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 10 3766-3772
Copyright © 2006 by The Endocrine Society

Acromegaly and Coronary Disease: An Integrated Evaluation of Conventional Coronary Risk Factors and Coronary Calcifications Detected by Computed Tomography

Salvatore Cannavo, Barbara Almoto, Giovanni Cavalli, Stefano Squadrito, Giovanni Romanello, Maria Teresa Vigo, Francesco Fiumara, Salvatore Benvenga and Francesco Trimarchi

Sezione di Endocrinologia (S.C., B.A., S.S., G.R., M.T.V., S.B., F.T.) e Unità Coronarica (G.C.), Dipartimento Clinico Sperimentale di Medicina e Farmacologia, University of Messina, 98125 Messina, Italy; and Centro di Diagnostica per Immagini (F.F.), Santa Teresa di Riva, 98028 Messina, Italy

Address all correspondence and requests for reprints to: Salvatore Cannavò, M.D., Sezione di Endocrinologia, Pad. H, piano 4 Azienda Ospedaliera Universitaria Policlinico "G. Martino," Via Consolare Valeria, 1, 98125 Messina, Italy. E-mail: cannavos{at}unime.it.


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Discussion
 References
 
Context: Coronary atherosclerosis in acromegaly was not extensively investigated in the literature until now. At autopsy, it was demonstrated in about 20% of patients with long-lasting disease, and myocardial infarction was reported as cause of death in a quarter of acromegalics.

Objective: The objective of the study was to evaluate coronary atherosclerosis in a cohort of acromegalics with controlled or uncontrolled disease.

Design: Coronary risk was evaluated by the Framingham algorithm, according to the Framingham score (FS). Patients were stratified into low (<6%), intermediate (6–20%), and high (>20%) midterm risk. Coronary calcium deposits were detected by multidetector computed tomography and measured by the Agatston algorithm. Coronary artery calcium [Agatston score (AS)] was quantified at the level of left main artery, left anterior descendent artery, left circumflex artery, right coronary artery, and posterior descendent artery. Total AS values in healthy persons are less than 50 (aged < 60 yr) and less than 300 (age ≥ 60 yr).

Patients: Thirty-nine patients (12 males and 27 females, aged 53.0 ± 2.1 yr) were evaluated. In each patient, the mean of at least four determinations of serum IGF-I, assayed during the last 2 yr before study, was normalized for the age-matched normal range, and the result was presented as SD value (IGF-I SD). On the basis of serum IGF-I SD, acromegaly was considered controlled (≤1.9 SD; n = 24) or uncontrolled (≥ 2.0 SD; n = 15).

Results: The FS was intermediate in 12 and high in two acromegalics. Overall, the FS was not correlated with serum GH values and IGF-I SD. Mean FS was not significantly different between patients with controlled and uncontrolled acromegaly. Total AS was increased in nine patients, most frequently in left anterior descendent, left circumflex, and left main arteries. In these nine patients, mean AS was similar in individuals with controlled and those with uncontrolled acromegaly, and the rate of 17% patients with controlled disease having increased AS was not statistically different from the rate of 33% uncontrolled acromegalics. Total AS was increased in six of 12 males and in three of 27 females ({chi}2 7.1, P < 0.01). Overall, total AS correlated with FS (r2 = 0.4, P < 0.0002) but not age, body mass index, disease duration, indexed left ventricular mass, serum cholesterol, triglycerides, GH, or IGF-I levels. Increased AS was more frequently observed in acromegalics with diabetes mellitus ({chi}2 = 5.2, P < 0.05) or hypertension ({chi}2 = 9.8, P < 0.002) but not in smokers ({chi}2 = 1.34, P = NS). Seven of nine patients with coronary calcium deposits had a FS greater than 6%. In six of 13 patients with FS greater than 6%, multidetector computed tomography did not demonstrate coronary calcifications.

Conclusions: In our study, the integrated evaluation of FS and AS showed that 41% of acromegalics are at risk for coronary atherosclerosis and that coronary calcifications were evident in about half of them despite the fact that myocardial infarction was not more frequent in acromegalic patients than the general population. Moreover, the control of acromegaly did not influence significantly the extent of coronary atherosclerosis.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Discussion
 References
 
ACROMEGALY IS A rare disease almost always due to a GH-secreting pituitary adenoma (1), and it is characterized by increased serum GH and IGF-I levels. Typical signs and symptoms of disease are frequently associated with metabolic and cardiovascular complications, such as obesity, hypertriglyceridemia, diabetes mellitus, and hypertension, which confer an increased risk for atherosclerosis. However, data about atherosclerosis in acromegalic patients are scanty and controversial. Analysis of determinants of mortality outcome indicates that cerebrovascular and cardiovascular events are very frequent, representing the first cause of death in young patients (2). However, ultrasonographic evaluation of carotid arteries showed a significant increase of intima-media thickness (IMT) in some studies only (3, 4). On the other hand, the prevalence of myocardial infarction is similar to that observed in the general population (5), and autoptic studies demonstrated that gross atherosclerotic alterations of the coronary arteries are detectable only in patients with long-term acromegaly (6).

In the general population, coronary risk is currently calculated by algorithms, i.e. the Framingham scheme, that are based on the analysis of conventional risk factors, such as sex, age, left ventricular mass, hypertension, smoking habit, diabetes mellitus, and lipid status. Computed tomography (CT) was recently introduced in cardiology to evaluate coronary atherosclerosis, particularly to identify coronary calcifications. Two types of CT scanners are currently used: the electron-beam CT and the more recent multidetector CT (MDCT) (7). The electron-beam CT generates a rotating x-ray beam by reflecting a rapidly undulating electron beam onto a stationary tungsten target under the patient table; the MDCT generates a beam by mechanically rotating an x-ray tube around the patient and is characterized by a high spatial and temporal resolution.

The aim of our study was to investigate whether acromegalic patients are at risk for coronary disease, based on the controlled or uncontrolled status of acromegaly. For this purpose, we evaluated coronary ischemic risk, using the Framingham algorithm, and the presence of coronary calcifications, using MDCT.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Discussion
 References
 
Patients

The study was carried out in 39 acromegalic patients (12 men and 27 women), aged 22–72 yr (mean ± SE, 53.0 ± 2.1 yr). Five patients were untreated because they were just diagnosed, 29 were previously surgically treated, nine underwent radiotherapy (which was {gamma}-knife in three cases), and 30 were on medical treatment. Of these 30 patients, 27 were treated with somatostatin analogs (octreotide LAR 20 or 30 mg or lanreotide 60 mg, im every 28 d) and three with pegvisomant (10–15 mg daily, sc) (Table 1Go). In each patient, the duration of acromegaly was estimated from the lag time between the onset of symptoms and signs of disease and the date when treatment was proven to be effective (group of controlled patients) or the date of enrollment in this study (group of uncontrolled patients). Body mass index (BMI), smoking habit, supine systolic and diastolic blood pressure, baseline serum glucose, cholesterol (total and high-density lipoprotein), and triglyceride levels were evaluated in each patient. These parameters and age were used to calculate the risk to undergo myocardial infarction within the next 10 yr, according to the Framingham risk scoring (FS). On the basis of this score, patients were stratified into low (<6%), intermediate (6–20%), and high (>20%) midterm risk (8). All patients gave their informed consent to be enrolled in the study.


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  		TABLE 1. Previous therapies in 39 patients with controlled or with uncontrolled acromegaly

 
Cardiac evaluation

Cardiovascular evaluation was performed preliminarily by electrocardiography and echocardiography: the left ventricular mass was indexed (LVMi) for the body surface. LVMi was increased when greater than 135 g/m2 (men) or greater than 110 g/m2 (women). Patients were imaged on an eight-slice MDCT scanner (LightSpeed Ultra, implemented with the software SmartScore, General Electric Medical Systems, Fairfield, CT) with electrocardiogram triggering during a single inspiratory breath hold of 12-sec duration, using sequential data acquisition. The unenhanced CT scans were analyzed for the quantification of coronary artery calcium, using the Agatston algorithm (9), in the following coronaries: left main artery (LMA), left anterior descendent artery (LAD), left circumflex artery (LCA), right coronary artery (RCA), and posterior descendent artery (PDA). The Agatston score (AS) quantifies the deposits of calcium in the intima-media of coronary arteries (10). The AS was calculated by multiplying the sum of the areas (in square millimeters) of each calcific lesion with a weighted CT attenuation score, which is dependent on the maximal CT attenuation (in Hounsfield units) within the lesion. Depending on the age of healthy subjects, the normal value of AS is less than 50 (<60 yr) and less than 300 (≥60 yr) (9).

In 34 of 39 patients, contrast-enhanced MDCT scan was used to evaluate the presence of calcified and noncalcified plaques, aneurysm, or stenosis of the vessel lumen. In the other five patients, MDCT was performed only without contrast enhancement because these patients were affected by chronic renal insufficiency (n = 1), had experienced allergic reactions (n = 2), or refused their consent to the injection of iodinated contrast agents (n = 2).

Control group

In 55 nonacromegalic volunteers (41 men and 14 women, aged 61.0 ± 1.4 yr) FS and AS were evaluated in accordance with the protocol used for acromegalic patients. Framingham evaluation showed a low, intermediate, or high risk in 28, 14, and 13 cases, respectively. A history of myocardial infarction or angina pectoris had been reported by 16 subjects with intermediate or high FS. None of them was affected by endocrine diseases.

Hormone assays

Serum GH and IGF-I levels were measured in duplicate, by chemiluminescent immunoassay (Diagnostic Products Corp., Los Angeles, CA). The sensitivity thresholds for GH and IGF-I values were 0.04 and 6 ng/ml, respectively. The intra- or the interassay coefficients of variation, for all assays, were less than 5% and less than 10%, respectively. The range of normality for serum IGF-I levels was derived from 485 healthy subjects. Serum IGF-I normal values for subjects aged 21–35, 36–50, and 51–75 yr are 115–358, 94–284, and 64–238 ng/ml, respectively. In each patient, we calculated the mean of at least four determinations of serum IGF-I, assayed during the last 2 yr before the study. To normalize IGF-I levels in patients of different ages, these levels are presented as SD from the mean of the age-matched normal subjects (IGF-I SD). On the basis of serum IGF-I SD, acromegaly was considered controlled (≤1.9 SD) or uncontrolled (≥2.0 SD). Controlled patients, but not patients treated with pegvisomant, and two uncontrolled acromegalics had serum GH levels less than 1 ng/ml during oral glucose tolerance test (glucose 75 g, per os).

Statistical analysis

Data are expressed as mean ± SE. Statistical difference between two means was evaluated with the Student’s t test for unpaired data, whereas the difference between proportions was evaluated using the {chi}2 test. Statistical evaluation of AS values was performed after their logarithmic transformation (AS-log10). Linear regression test was used to correlate both cardiovascular risk (expressed as FS) and calcium deposits (expressed as AS) each together and with serum GH levels and IGF-I SD.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Discussion
 References
 
In the 39 patients, serum GH and IGF-I averaged 3.2 ± 0.6 ng/ml and 1.8 ± 0.6 SD, respectively. Acromegaly was considered controlled in 24 of the 39 patients (seven men and 17 women) and uncontrolled in the remaining 15 patients (five men and 10 women). The two groups were comparable for sex, age, and disease duration (12.3 ± 6.3 vs. 9.5 ± 4.4 yr, P = NS). Baseline serum GH and IGF-I levels were significantly lower in patients with controlled acromegaly than in those with uncontrolled disease (GH: 1.2 ± 0.5 vs. 5.3 ± 1.4 ng/ml, P < 0.05; IGF-I SD: 0.1 ± 0.2 vs. 5.2 ± 1.4 SD, P < 0.002). LVMi was increased in 14 patients (36%, six men and eight women), seven with controlled and seven with uncontrolled disease. The mean BMI of the 39 patients was 29.8 ± 1.0, BMI was 24.9 or less in 10 patients, 25.0–29.9 in 11, 30.0–34.9 in another 11, 35.0–39.9 in four, and greater than 40.0 in three. Myocardial infarction had occurred in three patients (8%) before enrollment in this study. In these three patients, IGF-I SD was normal (n = 2) or increased (n = 1).

The evaluation of the coronary risk by the Framingham algorithm showed that FS was not correlated with serum GH values (r2 = 0.2, P = NS) or IGF-I SD (r2 = 0.1, P = NS), and mean FS was not significantly higher in uncontrolled vs. controlled patients (11.0 ± 5.1 vs. 4.3 ± 0.9%, P = NS). An intermediate or high FS risk was calculated in 12 patients (six controlled and six uncontrolled) and two patients (one controlled and one uncontrolled), respectively (Table 2Go). The rate of patients with an intermediate or high FS risk having uncontrolled acromegaly was not statistically higher than those having controlled disease (47 vs. 29%, {chi}2 = 1.2, P = NS). A FS greater than 6% was calculated in nine of 12 males and five of 27 females ({chi}2 = 11.5, P < 0.0001). In the three patients with past history of myocardial infarction, the midterm risk for new coronary ischemic events was low, intermediate, or high in one patient each.


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  		TABLE 2. FS was calculated in each acromegalic patient on the basis of age, sex, BMI, smoke habit, supine systolic and diastolic blood pressure, baseline glycemia, and serum total and high-density lipoprotein cholesterol and triglyceride levels

 
Total AS was increased in nine patients (no. 1, 2, 7, 8, 10–13, and 15 in Table 3Go) and in men more frequently than women (50 vs. 11%, {chi}2 = 7.1, P < 0.01). These nine patients included the three with previous myocardial infarction (no. 1, 2, and 12 in Table 3Go). In these patients, mean AS-log10 was not significantly higher in those uncontrolled, compared with controlled ones (2.7 ± 0.2 vs. 2.2 ± 0.4, P = NS). Moreover, the rate of patients having increased AS was not statistically different between controlled (17%) and uncontrolled (33%) acromegalics ({chi}2 = 1.4, P = NS). The AS was increased in the LAD in eight of the nine patients, LCA in seven, LMA in six, RCA in four, and PDA in one case. In all the other cases, calcified plaques were not detected (AS = 0). Overall, total AS was positively correlated with the FS (r2 = 0.4, P < 0.01) (Fig. 1Go) but not with LVMi, serum cholesterol, triglycerides, GH or IGF-I levels. Moreover, coronary calcium deposits were associated with the occurrence of diabetes mellitus ({chi}2 = 5.2, P < 0.05) or hypertension ({chi}2 = 9.8, P = 0.002) but not smoking habit. In the 55 nonacromegalic subjects (controls), AS was positively correlated with FS (r2 = 0.6, P < 0.0001).


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  		TABLE 3. Acromegalic patients (stratified on the basis of the control of the disease) who were at increased coronary risk based on intermediate/high FS and/or increased coronary calcium deposits, as assessed by AS

 

Figure 1
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  		FIG. 1. Correlation between FS and AS in 39 acromegalics patients.

 
The combined evaluation of FS and AS in our patients demonstrated that eight controlled patients (33%) and eight uncontrolled patients (53%) had FS greater than 6% and/or increased AS ({chi}2 = 1.5, P = NS) (Table 3Go). The rate of patients with coronary calcium deposits, as evaluated by AS, was significantly higher in patients with intermediate or high FS, compared with those with low FS (50 vs. 9%, {chi}2 = 8.9, P < 0.005). In accordance, the rate of patients with FS greater than 6% was higher in patients with coronary calcium deposits (78%), compared with those with AS = 0 (23%) ({chi}2 = 8.9, P < 0.005). MDCT did not confirm abnormal calcium deposits in coronary vessels in 50% of patients with intermediate or high FS risk (Table 4Go). The prevalence of intermediate or high risk, evaluated by FS, was significantly increased in patients with more prolonged active acromegaly (≥10 yr) in comparison with those with less prolonged disease (<10 yr) (55 vs. 16%, {chi}2 = 6.5, P < 0.01). However, the prevalence of coronary calcium deposits, evaluated by AS, was not significantly different in the two groups (35 vs. 10%, {chi}2 = 3.3, P = NS) (Fig. 2Go). The integrated evaluation of FS and AS in patients grouped for age demonstrated that all five acromegalics younger than 40 yr had FS less than 6% and AS = 0, five of 21 patients 40–60 yr showed FS 6–20% and/or increased AS (both FS and AS were increased in three patients, and FS or AS alone was increased in one patient each), whereas 11 of 13 patients older than 60 yr had intermediate (nine cases) or high (two cases) FS but coronary calcium deposits in only five of 13 ({chi}2 = 5.8, P < 0.02). The prevalence of increased AS was not significantly different between the group 40–60 yr and the group older than 60 yr (19 vs. 38%, {chi}2 = 1.5, P = NS). Acromegaly was controlled in 60% of the group younger than 40 yr, 62% of group 40–60 yr, and 54% of the group older than 60 yr (Fig. 2Go). When AS was normalized for FS, the prevalence of coronary calcification was similar between controlled and uncontrolled acromegalics (FS ≤ 6%: {chi}2 = 0.3, P = NS; FS > 6%: {chi}2 = 0.3, P = NS). Moreover, the prevalence of increased FS (>6%) or increased AS was not significantly different between obese (BMI ≥ 30; 47% had increased FS and 21% had increased AS) and nonobese (BMI ≤ 29.9; 25% had increased FS and 25% had increased AS) acromegalics (Fig. 2Go).


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  		TABLE 4. Integrated evaluation of FS and AS in patients with controlled and uncontrolled acromegaly

 

Figure 2
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  		FIG. 2. Relationship between duration of active acromegaly, age of patients, or obesity and increased coronary risk evaluated by FS (in the left side) or AS (in the right side). The upper panel shows the prevalence of patients with intermediate or high FS ({Uparrow}FS) or increased AS ({Uparrow}AS) in the group with more (≥10 yr) or less prolonged (<10 yr) duration of acromegaly. The middle panel shows the prevalence of patients with intermediate or high FS ({Uparrow}FS) or increased AS ({Uparrow}AS), grossly grouped for age (<40 yr, 40–60 yr, or >60 yr of age). The lower panel shows the prevalence of patients with intermediate or high FS ({Uparrow}FS) or increased AS ({Uparrow}AS), grossly grouped for BMI (≤29.9 or ≥30).

 
The contrast-enhanced MDCT confirmed the presence of calcified plaques in the patients with high AS (Fig. 3Go) and detected aneurysms of the LMA or RCA in two patients with controlled acromegaly, who had FS greater than 6% and AS = 0.


Figure 3
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  		FIG. 3. Volume rendering (A) and multiintensity projection (B) of the heart in one illustrative patient with increased AS (patient 1 in Table 3Go). The white arrows show calcified plaques of the left main coronary artery (a), RCA (b), and LAD coronary artery (c).

 

   Discussion
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
References
 
The relationship between atherosclerosis and GH/IGF-I excess is controversial. Acromegaly is often complicated by metabolic abnormalities, which increase the atherosclerotic risk. Some studies suggest that GH influences the endothelium either directly via endothelial IGF-I synthesis or indirectly through hypertension, abnormalities of body composition, and lipid metabolism (11). In accordance with this evidence, some authors demonstrated that the IMT of common carotids is increased in acromegalic patients, but it decreases slightly when acromegaly is effectively controlled by somatostatin analogs (3). In contrast, other authors (4) did not find the above increase of IMT, and they concluded that the low extent of atherosclerosis in their acromegalic patients was due to an IGF-I-mediated protection.

Coronary atherosclerosis in acromegaly has been poorly investigated until now. Autopsy studies demonstrated coronary atherosclerosis in 19% of patients with long-lasting acromegaly (6), with myocardial infarction being the cause of death in 23% of acromegalics patients (12). However, this last study was done in a Finnish population, which is known to have a high incidence of cardiovascular events independently of acromegaly. From the epidemiological database of the Istituto Superiore di Sanità, a branch of the Italian Department of Health, during the period 1982–2002, the annual incidence of fatal myocardial infarction in Sicilian men or women was 1.4 or 0.5 for 100,000 inhabitants in the group younger than 30 yr old, 44.6 or 9.6 in the group 30–60 yr old, and 367 or 142 in the group older than 60 yr (13). Another epidemiological study reports that in the 35- to 75-yr-old Italian population, about half of the coronary ischemic events are fatal (14). In a cohort of 67 acromegalics we have been following up from January 1985 through February 2006, myocardial infarction occurred in four (6%, three men and one woman) and at an age of 43–60 yr. However, myocardial infarction was fatal only in one of the three men (data not shown). Such low rates of morbidity and mortality might be due to the fact that our 67 patients were very strictly controlled, and in most cases, they were effectively treated not only for acromegaly but also for its complications. Moreover, the majority of them complied with recommended healthier lifestyle changes.

Atherosclerosis results in the deposition of calcium within the walls of arteries. In the early stages of the atherosclerotic process, calcium deposits are very small and difficult to detect by conventional x-ray imaging. Over the past few years, CT technology has advanced to the point that detection of minimal calcium deposits can be accomplished quite easily. CT scanning, therefore, affords an opportunity to detect coronary atherosclerosis at an early stage, well before clinical manifestations of coronary disease. Indeed, coronary calcium score correlates with the total atherosclerotic plaque burden (15, 16), and it is considered a surrogate marker for coronary atherosclerosis (8). Coronary CT without contrast enhancement is a noninvasive, economic, and repeatable technique to detect and quantify coronary calcification. Compared with other techniques, as the gold standard conventional angiography, coronary CT can be used in asymptomatic patients to evaluate the risk of future ischemic coronary events and to follow it up. However, MDCT does not have enough spatial and temporal resolution to show clearly all the coronary segments and detect calcium deposits in the coronary microcirculation.

In the present study, the coronary risk of our 39 acromegalics, evaluated by the Framingham algorithm, was intermediate or high in 31 or 5% of patients, respectively. FS is currently used in the asymptomatic subjects to evaluate the midterm risk (10 yr) to develop a cardiac event (17). In our patients, FS was not correlated with serum GH values or IGF-I SD. Although the mean FS was higher in uncontrolled patients than controlled patients, the difference was not significant. As in the general population, in acromegalics the female gender conferred a protective effect because the coronary risk was increased in 18% of women, compared with 75% of men.

MDCT demonstrated calcium deposits in 23% of patients, most frequently in LAD, LCA, and LMA. AS correlated positively with FS, and 78% of patients with increased AS had intermediate or high coronary risk, as assessed by FS. On the other hand, only 50% of patients with intermediate or high FS had increased AS, namely coronary calcium deposits detected by MDCT. Thus, approximately half of acromegalics with increased coronary risk, calculated from conventional factors, do not have coronary calcifications, which are a mirror of early coronary atherosclerosis (8, 18, 19, 20). It is noteworthy that AS was unrelated with serum GH or IGF-I SD. Similar to FS, both mean AS and prevalence of increased AS were higher in uncontrolled patients than controlled patients, but differences were not statistically significant. Also similar to FS, increased AS was significantly more frequent in men than women. Concordance between AS and FS was partial in the group of acromegalics with previous myocardial infarction because three of three had increased AS but two of three had intermediate or high risk by FS. This partial discrepancy is due to the reversibility of the conditions that contribute to the conventional calculation of coronary risk (20). In fact, changes in BMI or serum cholesterol or triglycerides levels can modify the FS, regardless of coronary calcifications.

In our study, risk for ischemic events evaluated by FS, but not coronary calcium deposits measured by AS, increased more frequently in patients with longer duration of active disease. Accordingly, in the group of patients older than 60 yr, who had the highest potential risk of myocardial infarction, 85% had an intermediate or high FS risk, but only 38% had increased AS. Moreover, the prevalence of increased AS was not significantly different between the group 40–60 yr old and the group older than 60 yr. Our results indicate that calcium deposits do not progress in acromegaly as in the general population and are consistent with the study of Otsuki et al. (4). This study (4) found no difference of carotid IMT between acromegalic patients and controls, suggesting an IGF-I-mediated protection. Our data on the presence of coronary calcifications in patients normalized for FS value, being unrelated to the activity of acromegaly, suggest that coronary atherosclerosis is not influenced by the control of acromegaly and that systemic complications, which occur more frequently in uncontrolled patients, do not exert a strong pathogenetic role on coronary disease.

Contrast-enhanced CT, performed in 87% of our acromegalics, confirmed the presence of calcified plaques in the patients with high AS and detected aneurysms of the LMA or RCA in two patients with controlled acromegaly. Previous studies also demonstrated that luminal stenosis, aneurysms, and noncalcified plaques, demonstrated by MDCT, can be vulnerable sites of rupture or erosion (21).

In conclusion, the combined evaluation of Framingham scoring and AS based on coronary imaging by MDCT demonstrates that 41% of acromegalics are at risk for coronary atherosclerosis and that calcified plaques are detectable in about half of this risk group. Control of acromegaly did not influence significantly the extent of coronary atherosclerosis. However, these data need to be further confirmed prospectively in a larger acromegalic cohort.


   Footnotes
 
First Published Online July 11, 2006

Abbreviations: AS, Agatston score; BMI, body mass index; CT, computed tomography; FS, Framingham score; IMT, intima-media thickness; LAD, left anterior descendent artery; LCA, left circumflex artery; LMA, left main artery; LVMi, indexed left ventricular mass; MDCT, multidetector CT; PDA, posterior descendent artery; RCA, right coronary artery.

Received January 3, 2006.

Accepted July 5, 2006.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 References
 

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