© 1999 American Heart Association, Inc.
Original Contribution |
Differential Association of Common Carotid Intima-Media Thickness and Carotid Atherosclerotic Plaques With Parental History of Premature Death From Coronary Heart Disease
The EVA Study
From the National Institute of Health and Medical Research (INSERM), Unit 258 (M.Z., C.B.-K., D.C., P.D.); Centre de Diagnostic et de Prévention Neurovasculaire (P.-J.T.), Paris; and Centre d'examen EVA-INSERM (I.R.), Nantes, France.
Correspondence to Mahmoud Zureik, MD, PhD, INSERM U 258, Hôpital Broussais, 96 rue Didot, 75674 Paris Cedex 14, France. E-mail zureik{at}hbroussais.fr
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Abstract |
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Abstract—Familial aggregation of coronary heart disease (CHD) has been reported in several studies. The specific underlying mechanisms and the relative contribution of atherosclerosis to the subsequent CHD events in subjects with family history are not well established. This study examined the association of parental history of premature death from CHD with ultrasound carotid measurements of atherosclerosis in a population of 1040 subjects aged 59 to 71 years. Ultrasound examination included measurements of intima-media thickness at the common carotid arteries (at sites free of plaques) and assessment of atherosclerotic plaques in the extracranial carotid arteries. Subjects who reported that 1 or both parents had sudden death or died of myocardial infarction before the age of 65 years were considered positive for parental history of premature death from CHD (n=53, 5.1%). The prevalence of atheromatous plaques was higher in subjects with history of premature death from CHD compared with those without history (41.5% versus 20.5%, P<0.001). Age- and sex-adjusted odds ratio of atheromatous plaques associated with parental history of premature death from CHD was 2.85 (95% confidence interval, 1.60 to 5.08; P<0.001). Multivariate adjustment for major known cardiovascular risk factors did not markedly alter the results (odds ratio, 2.70; P<0.002). In contrast, common carotid intima-media thickness was not associated with parental history of premature death from CHD (0.66±0.11 versus 0.66±0.12 mm, P=0.76). These findings were observed in both men and women. In conclusion, parental history of premature death from CHD is strongly associated with carotid plaques. Familial transmission of CHD risk does not seem to be specifically mediated by arterial wall thickening measured at sites free of plaques.
Key Words: carotid arteries • atherosclerosis • coronary disease • ultrasonics • epidemiology
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Introduction |
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Several case-control1 2 3 4 and prospective5 6 7 8 studies have suggested that coronary heart disease (CHD) has a familial pattern. Known cardiovascular risk factors could account only for some, but not all, of the clustering of CHD in families. Inherited susceptibility and/or shared environmental exposures could explain this phenomenon. However, the mechanisms underlying this familial aggregation are unclear, and the relative contribution of atherosclerosis to the subsequent CHD events in subjects with family history is not well established. In some,9 10 11 12 but not all,13 angiography studies, patients with a positive family history of CHD had a more advanced atherosclerotic occlusion and a larger number of affected coronary arteries. In autopsy studies, intimal thickening of the coronary arteries in infancy was associated with grandparents' history of coronary artery disease.14 Also, infants and children whose grandparents originated from geographic areas associated with a high incidence of coronary artery disease have greater thickening of coronary arteries than children whose grandparents come from low-incidence areas.15 16 However, findings of autopsy and angiography studies obtained from highly selected populations and from subjects with advanced atherosclerosis could not be extrapolated to the general population.
In the current epidemiological study, we assess the association of parental history of premature death from CHD with ultrasound carotid measurements of atherosclerosis in a population of 1040 subjects aged 59 to 71 years. In a previous article reporting on this study, we reported that increases in intima-media thickness, as measured in the common carotid arteries (at sites free of any discrete plaque), were related to locally detected atherosclerosis and known risk factors for atherosclerosis.17
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Methods |
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Details of the EVA study have been reported previously.17 Briefly, the EVA study is a longitudinal study of cognitive and vascular aging. The study population was comprised of volunteers aged 59 to 71 years who were recruited from the electoral rolls of the city of Nantes (western France). The study protocol was approved by the Comité d'éthique du Center Hospitalier Universitaire de Kremlin-Bicêtre, and written informed consent was obtained from all participants. During the baseline visit, which took place between June 1991 and July 1993, 1389 subjects were recruited, and high resolution ultrasound examinations of the carotid arteries were performed in 1384 of them. Subjects who were recruited during the training period (between June and December 1991) were considered to have unreliable initial ultrasound examinations on the basis of interreader reproducibility studies and were systematically excluded from statistical analysis (n=235). Furthermore, the current report, based on data provided at baseline visit, was limited to 1040 subjects for whom complete data were available on common carotid intima-media thickness (CCA-IMT), plaque assessment, and/or information about parental history of death.
Ultrasonography
Ultrasound examinations were performed by 4 sonographers using
the Aloka SSD-650, with a transducer frequency of 7.5 MHz. This
system provides an axial resolution of 0.30 mm. Acquisition,
processing, and storage of B-mode images were computer-assisted with
software specially designed for longitudinal studies (EUREQUA,
TSI).18
Details of the protocol have been described elsewhere.17 19 All measurements were made at the time of examination. Briefly, it involved scanning of the common carotid arteries, the carotid bifurcations, and the origin (first 2 cm) of the internal carotid arteries. For all arterial segments, optimal longitudinal and transversal images were stored on an optical disk. The IMT was measured on the far wall of the mid and distal common carotid artery as the distance between the lumen-intima interface and the media-adventitia interface20 using an automated edge-detection algorithm. One transverse and 2 longitudinal measurements of IMT were completed on both the right and left common carotid arteries at a site free of any discrete plaques. The mean of the right and left longitudinal IMT measurements was used in the analysis. Optimal images showing the far wall were stored on an optical disk. On such images, the lumen-intima interface is often more difficult to visualize on the near wall than the media-adventitia interface, and thus, we chose to measure the interadventitial diameter (defined as the distance between both media-adventitia interfaces) rather than the lumen diameter. On each side, the lumen diameter was computed as the interadventitial diameter minus twice the transverse IMT.19 The mean of the right and left lumen diameters was used in the analysis.
Both near and far walls of all arterial segments were
scanned longitudinally and transversally to assess the occurrence of
plaques defined as localized echo structures encroaching into the
vessel lumen. The quantification of plaque thickness was made at the
site of the maximal encroachment perpendicularly to the vessel wall by
measuring the distance between the media-adventitia interface and the
lesion surface facing the lumen. Only lesions for which thickness was
1 mm were considered to be carotid plaques. The sonographer
could be computer-assisted in the identification of interfaces and
placement of electronic calipers by examining the inflections of the
density profile curve taken at the site of plaque. Two
arterial segments were considered on each right and left
side, ie, CCA and carotid bifurcation–origin of the internal carotid
artery. When several plaques were present on the same
arterial segment, the number of plaques was recorded,
but on each arterial segment the description of the plaque
characteristics (thickness, localization, echogenicity, outline
irregularities, and calcifications) was given only for the plaque that
showed the greatest encroachment into the lumen. Reproducibility of the
scanning and reading procedures has been reported
elsewhere.17 18
Medical History and Standard Biological Procedures
All participants were administered a standardized questionnaire
that requested information about demographic background, occupation,
medical history, drug use, and personal habits such as cigarette
consumption. Subjects were classified as ever-smokers or nonsmokers.
Two independent measurements of systolic and
diastolic blood pressure were made with a digital
electronic tensiometer (SP9 Spengler) after a 10-minute rest,
and the mean value was used in the analysis. Self-reported
personal history of myocardial infarction or angina pectoris was also
recorded. Subjects with systolic blood pressure 160
mm Hg or diastolic blood pressure 95 mm Hg or who
were using antihypertensive drugs were considered as hypertensives.
Hypercholesterolemia was defined as total
cholesterol level 7.2 mmol/L (2.80 g/L) or use of
lipid lowering drugs. Subjects who reported medical history of diabetes
or use of antidiabetic drugs or had a fasting plasma glucose level
7.8 mmol/L (1.40 g/L) were considered diabetics (n=67). Body
mass index was computed as weight (in kilograms) divided by height (in
meters squared). Biological procedures for determination of total
cholesterol, high-density lipoprotein
cholesterol, apolipoprotein A-I and B, lipoprotein(a),
triglycerides, and glucose were described
elsewhere.17
Parental History of CHD
Before the B-mode ultrasound examination, subjects were
administered a standardized questionnaire that gave the following
information about each parent: cause of death (cancer, sudden death,
myocardial infarction, stroke, accident, dementia, "aging," and
other causes) and age at death.
For analysis, an age limit of 65 years at death was chosen
a priori to define premature death from CHD. The results of
previous studies have suggested that the increased risk of CHD in
association with family history of CHD is lowered in subjects whose
parents or relatives died of CHD at a late age.21 22 A
posteriori, we found that parental history of late death from CHD (65
years) was not related to either cardiovascular risk
factors or to B-ultrasound carotid measurements (data not shown); as a
consequence, subjects with parental history of late death from CHD were
classified with those with no parental history of premature death from
CHD.
At inclusion, 31 fathers and 157 mothers were still alive. Before the age of 65 years, 350 fathers and 194 mothers had died. Of them, 19.1% of fathers and 30.9% of mothers had died of cancer; 5.7% and 3.6%, respectively, had died as sudden death; 5.1% and 3.6%, respectively, had died of myocardial infarction; and 70.1% and 60.3%, respectively, had died from other causes. Subjects who reported that 1 or both parents had died of myocardial infarction or sudden death before the age of 65 years were considered as positive for parental history of premature death from CHD, and those who reported that neither parent had died of CHD before the age of 65 years were coded as negative. No attempt was made to validate the parental history of premature death from CHD in parents.
Statistical Analysis
Standard procedures from the Statistical Analysis System
(SAS Corp) were used for univariate and
multivariate analyses. Differences in mean
value of CCA-IMT and in prevalence of plaques according to parental
history of premature death from CHD were reported by gender and tested
by t test and 
2 analysis.
Differences in cardiovascular risk factors according to
parental history of premature death from CHD were adjusted for gender
and tested by ANCOVA for quantitative variables and by
Mantel-Haenszel 2 test for qualitative
variables. The associations of intima-media thickness and
prevalence of plaques with family history of premature death from CHD,
independently of other risk factors, were examined by ANCOVA and
logistic regression models in which family history and other risk
factors were introduced as independent variables. When
systolic blood pressure (or diastolic blood
pressure), lipids, and plasma glucose levels were introduced in the
models as continuous variables, adjustment for treatments for the
corresponding related diseases (hypertension,
hypercholesterolemia, and diabetes) were
systematically performed.
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Results |
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Of the 1040 participants included in this study, 53 (5.1%) had a parental history of premature death from CHD. Thirty-eight (3.7%) reported a paternal history of premature death from CHD, and 17 (1.6%) reported a maternal history of premature death from CHD. Two subjects had both paternal and maternal histories.
When compared with subjects without history of premature death
from CHD, those with positive history tended to have higher
sex-adjusted values of systolic blood pressure, total
cholesterol, low-density lipoprotein
cholesterol, triglycerides, apolipoprotein B,
and blood glucose (Table 1
). The
differences reached statistical significance only for total
cholesterol and apolipoprotein B. Personal history of CHD,
hypertension, hypercholesterolemia, and
diabetes also tended to be more frequent among subjects with a parental
history of premature death from CHD (Table 1), but none of these
differences reached statistical significance (borderline for
hypercholesterolemia).
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The prevalence of atheromatous plaques in the common
carotid, carotid bifurcations, and internal carotid arteries was higher
in subjects with history of premature death from CHD compared with
those without history of premature death from CHD (Table 2). In contrast, the mean intima-media
thickness and the mean lumen diameter of the common carotid arteries
were similar in the 2 groups. These findings were observed in both men
and women (Table 2).
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Age- and sex-adjusted odds ratio of atheromatous
plaques associated with parental history of premature death from CHD
was 2.85 (95% confidence interval, 1.60 to 5.08; P<0.001).
Even after adjustment for age, sex, body mass index, smoking,
hypertension, hypercholesterolemia, diabetes,
and CHD, the odds ratio did not markedly change and remained highly
significant (Table 3). Further adjustment
for intima-media thickness yielded very close results (Table 3).
In the multivariate analysis, substitution of
systolic blood pressure (or diastolic blood
pressure), total cholesterol (or high-density lipoprotein
and low-density lipoprotein cholesterol), and blood glucose
levels for hypertension, hypercholesterolemia,
and diabetes, respectively, did not alter the results (data not shown).
These results indicate that the association of plaque with parental
history of premature death from CHD was only modestly modified when
traditional cardiovascular risk factors were taken into
account.
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When we defined the atheromatous plaques as a wall
thickness 1.5 mm instead of 1 mm, the prevalence of
plaques remains markedly higher in subjects with history of premature
death of CHD compared with those without history (32.1% versus 16.1%,
P<0.003). Age- and sex-adjusted odds ratio of
atheromatous plaques associated with parental history
of premature death from CHD was 2.76 (95% confidence interval, 1.55 to
5.23; P<0.001).
After exclusion of subjects who had a personal history of CHD at
inclusion and/or those who were being treated for hypertension,
hypercholesterolemia, or diabetes, similar
patterns of results were observed (Table 3
).
In contrast, multivariate analysis confirmed
the lack of association between intima-media thickness and parental
history of premature death from CHD. Further adjustment for carotid
plaques did not change this result (Table 3).
When CCA-IMT was used as categorical variable (divided into tertiles according to sex-specific values), the frequency of positive parental history of premature death from CHD was 4.6% in tertile 1, 5.8% in tertile 2, and 4.5% in tertile 3 (P=0.65). The positive association between carotid plaques and parental history was observed within each tertile of CCA-IMT (data not shown).
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Discussion |
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In the current study performed in a large population of relatively aged subjects, we found that parental history of premature death from CHD was associated with the presence of plaques in the extracranial carotid arteries.
Few studies have assessed the relationship between B-mode ultrasound carotid measurements of atherosclerosis and family history of CHD. In the Cardiovascular Health Study,23 subclinical atherosclerosis, evaluated by the results of a resting ECG, echocardiogram, carotid artery sonography, ankle-brachial blood pressure measures, history of disease, cardiovascular surgery, and selective symptomatology, was more prevalent in elderly subjects with family history of myocardial infarction in first degree relatives aged <65 years. The results of the associations between family history and B-ultrasound carotid measurements were not reported separately from the other manifestations of subclinical atherosclerosis. In a Finnish study,24 the severity of carotid atherosclerosis, recorded in 4 graded categories (no atherosclerotic lesion, intimal-medial thickening, nonstenotic plaque, and any degree of stenosis), was not associated with family history of ischemic heart disease. Our results, strengthening the findings of the Cardiovascular Health Study and those of the autopsy and angiography studies, suggest that familial aggregation of CHD could be, at least partly, mediated by the atherogenic process per se.
Familial aggregation, of CHD and of many of its risk factors such as hypertension, diabetes, triglycerides, and total cholesterol, has been reported in several studies.25 26 27 The specific mechanisms are not completely known, and it is not clear whether the clustering of CHD could be explained totally by clustering of higher levels of these known risk factors and/or by some unidentified familial factors (genetic and environmental predispositions).
In the current study, subjects with positive parental history of premature death from CHD, in accordance with previous reports,6 7 28 29 tend to have an unfavorable cardiovascular risk profile (higher prevalence of hypercholesterolemia, hypertension, diabetes, etc). This may offer 1 possible explanation of the association between parental history of premature death from CHD and carotid plaques. However, our results suggest that other possibly heritable factors could also be important determinants of atheromatous plaque formation.
Surprisingly, CCA-IMT was not associated with parental history of premature death from CHD. Several hypotheses could be formulated to explain the differential association of parental history with carotid plaques and CCA-IMT.
Thickening of the intima-media at the common carotid is generally considered to be an early marker of generalized atherosclerosis because of its association with the main cardiovascular risk factors,30 31 32 33 34 35 the presence of other localizations of atherosclerosis,36 37 38 39 and an increased risk of CHD and stroke.40 41 However, its pathophysiological significance with regard to the atherosclerotic process is questionable. First, the interpretation of results provided by ongoing studies is largely dependent on the methodology used to assess the intima-media thickness, especially on the site of measurement and the inclusion or not of atherosclerotic plaques in the measurement interval.30 31 32 33 34 35 Second, because of the inability of B-mode ultrasonography to differentiate the intimal from the medial layer, the anatomic structure involved in the arterial wall thickening cannot be determined. Third, IMT below certain levels may not reflect atherosclerosis but may merely be an adaptative intimal thickening to physiological variations in shear and tensile forces along the length of arteries.42 43 A recent report from the Rotterdam study suggests that CCA-IMT <1.1 mm might not represent local atherosclerosis but might reflect an adaptative response to altered flow, lumen diameter, shear stress, and pressure.44
Another explanation of the differential association of parental history of CHD with carotid plaques and CCA-IMT is that plaques (localized thickening) and IMT (diffuse thickening) are 2 related, but not identical, components of the atherosclerosis development.17 In this case, some heritable factors might be specifically involved in plaque formation but not in diffuse intima-media thickening. Whatever the explanation, our results reinforce the concept that plaques and IMT should be differentiated from each other and analyzed separately.45
Our liberal definition of plaque as a thickness of 1 mm could
not explain the differential association of parental history with
carotid plaques and CCA-IMT. In fact, reanalysis of our data
using a more restrictive definition of plaque thickness (1.5 mm)
showed a strong association between parental history of premature death
of CHD and carotid plaques. This more restrictive definition of plaque
could not markedly modify the results of CCA-IMT because only 4 of the
20 subjects initially considered to have plaque in the common carotid
arteries had plaque thickness values between 1 and 1.5 mm and
because these 4 subjects had no parental history of premature death of
CHD.
Survival and self-selection biases could have occurred in this study performed in an elderly population of volunteers with a low prevalence of carotid plaques. Subjects with positive familial history of CHD might die at an earlier age or might have clinically manifested cardiovascular diseases. This could partly explain the lack of association between CCA-IMT and parental history of premature death from CHD if older survivors with positive familial history have lower values of CCA-IMT. However, the rate of premature death from CHD observed is comparable to those having parental history of earlier myocardial infarction (aged <60 years) reported in a population of French middle-aged working men.46
Another potential limitation of this study is the possible misclassification of subjects according to parental history of premature death from CHD. Inaccurate reported family history of CHD has been previously mentioned.47 48
On the one hand, subjects who had a personal history of CHD or who were treated for a related disease, such as hypertension, hypercholesterolemia, or diabetes could be more prone to report a positive parental history of premature death from CHD. This could be explained for by at least 2 reasons: first, because there is a familial aggregation of this disease, and second, because these subjects could be more concerned and less likely to omit a parental history. The exclusion of subjects who had a personal history of CHD and/or of those treated with hypertensive, hypolipidemic, or antidiabetic drugs is likely to reduce this bias considerably46 and, in fact, yielded similar results as those observed in all subjects.
On the other hand, positive history of premature death from CHD was not validated by hospital or family doctor records. Because the B-mode ultrasound examination was performed after the collection of data concerning the family history of CHD, differential misclassification of parental history of CHD according to the presence of plaques and/or CCA-IMT is unlikely (parental history was assessed before ultrasound examination). Undifferential misclassification could only lead to an underestimation of the true association between family history and carotid plaques. The association between family history of premature death from CHD and CCA-IMT could have been diluted because of the undifferential misclassification. However, there was acceptable power to detect small differences in CCA-IMT in spite of the potential misclassification bias. Assuming48 that 3.5% of parental histories were false-negative (underreporting) and 28% were false-positive (overreporting) and assuming that the mean values (and standard deviations) of CCA-IMT of the false-negative and false-positive subjects are, respectively, similar to those of the true negative and true positive subjects, our study provided 76% and 61% power to detect true differences in CCA-IMT of 0.05 and 0.04 mm, respectively. Nevertheless, the limitation due to the crude assessment of parental history in this study should be kept in mind.
In conclusion, parental history of premature death of CHD was strongly associated with carotid plaques in both men and women. Familial transmission of CHD risk does not seem to be specifically mediated by arterial wall thickening measured at sites free of plaques. Investigation of possibly heritable factors related to the pathogenesis of atherosclerotic plaques would lead to a better understanding of the familial aggregation of CHD.
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Acknowledgments |
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The EVA study is organized under an agreement between INSERM and the Merck, Sharp and Dohme-Chibret Company. We thank the ultrasound physicians, Drs J.M. Fève, C. Leroux, and C. Magne. We acknowledge C. Delanoe and S. Bachelier for their secretarial and technical assistance at the EVA Center.
Received April 16, 1998; accepted July 17, 1998.
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