(Hypertension. 1996;27:949-954.)
© 1996 American Heart Association, Inc.
Articles |
Hypertension Promotes Coronary Calcium Deposit in Asymptomatic Men
From the Centre de Médecine Préventive Cardiovasculaire, INSERM, and Département de Radiologie (M.C.P.), Hôpital Broussais, Paris, France.
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Abstract |
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Abstract Despite its important role in coronary disease, coronary atherosclerosis has been poorly investigated in uncomplicated hypertension. Therefore, we evaluated the presence and amount (score) of coronary calcium with ultrafast computed tomography in 73 pairs of age-matched asymptomatic hypertensive or normotensive men. We also estimated the extent of peripheral atherosclerosis as the number of arterial sites (carotid, aortic, femoral) with echographic plaque. Compared with normotensive men, hypertensive men had more frequent coronary calcium (63% versus 47%), a higher calcium score (57±111 versus 18±38), and an odds ratio of calcium deposit of 1.95 (with confidence intervals [CI] 95%, 1.01 to 3.79) for any score and of 2.38 (95% CI, 1.02 to 5.52) or 4.84 (95% CI, 1.53 to 15.3) for scores above 50 or 100, respectively. Hypertensive men showed correlations of calcium score with age and hypertension duration but not with the height of blood pressure, and the odds ratio of calcium deposit between extensive and minor peripheral atherosclerosis was 4.67 (95% CI, 1.41 to 15.45) for any score and 8.63 (95% CI, 2.10 to 35.5) or 8.13 (95% CI, 1.64 to 40.3) for scores above 50 or 100. Thus, high blood pressure and in particular its duration rather than its value promotes the presence and overall extent of coronary calcium, a potential predictor of sudden coronary death, in parallel with the extent of peripheral atherosclerosis. The mechanisms of the interaction of hypertension and coronary calcification may be multifactorial and not specific to hypertension.
Key Words: tomography • atherosclerosis • risk factors • coronary arteriosclerosis
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Introduction |
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The early detection of preclinical cardiovascular alterations such as left ventricular hypertrophy,1 arterial wall thickening2 and stiffening,3 and atherosclerotic plaque in extracoronary vessels4 is particularly useful in hypertension to better delineate cardiovascular risk and evaluate the effects of antihypertensive drugs.1 Surprisingly, coronary atherosclerosis has not received attention in the investigation of hypertensive patients in the absence of clinical coronary heart disease. A likely reason has been the lack of available noninvasive techniques of measurement of coronary atherosclerosis. However, the detection of preclinical coronary atherosclerosis would have great importance because the initiation of coronary atherosclerosis is the primary determinant of clinical coronary heart disease,5 a major complication of hypertension.6 Therefore, the purpose of the present study was to evaluate noninvasively the presence and extent of coronary calcium deposit, an invariable marker of coronary intimal atheroma, in asymptomatic hypertensive men by using an ultrafast computed tomographic (CT) technique.7
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Methods |
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Seventy-three control normotensive men (35 to 65 years of age) with a supine diastolic pressure less than 90 mm Hg (Korotkoff phase V) and no current or previous antihypertensive treatment and 73 age-matched hypertensive men with a supine diastolic pressure of 90 mm Hg or higher on an average of three outpatient visits and/or receiving current antihypertensive treatment were entered into the study. Control subjects and patients were sampled from an ongoing risk factor screening program conducted at work sites for employees of several companies within the Paris area by a group of occupational health physicians8 (Prévention Cardiovasculaire en Médecine du Travail [PCV METRA]). All patients had essential hypertension documented by appropriate laboratory tests. The duration of hypertension was determined by questioning the subject. Hypertension duration was coded as 0 year in 54 patients with newly diagnosed hypertension (<6 months) and was estimated as the time since the first prescription of drugs in 19 patients with hypertension known for 1 year or more. Among hypertensive patients, 50 were never treated, 19 were currently treated, and 4 had been previously treated. The type of antihypertensive drugs used in currently treated patients was distributed as follows: diuretics in 1 subject, ß-blockers in 4 subjects, angiotensin-converting enzyme inhibitors in 7 subjects, calcium channel blockers in 2 subjects, and a combination of two or three of these drugs in 5 subjects. Hypertension was uncomplicated in all patients, and none had neurological, cardiac, or renal involvement or arteriopathy of the lower limbs. All study subjects underwent an evaluation of traditional cardiovascular risk factors.8 Body mass index (weight per height squared) was used to measure excess weight. Blood lipids, including total cholesterol, high-density lipoprotein (HDL) cholesterol (after the precipitation of low-density lipoprotein [LDL] and very-low-density lipoprotein by phosphotungstic acid magnesium chloride), and triglycerides, were measured by enzymatic methods after an overnight fast.8 LDL cholesterol level was calculated from total cholesterol, HDL cholesterol, and triglyceride values according to the classic Friedewald formula. Blood glucose level was measured after an overnight fast. Fifty-eight percent of control subjects and patients had hypercholesterolemia, defined as total cholesterol of 6.5 mmol/L or higher,9 but no subject in either group had diabetes mellitus, defined as fasting blood glucose of 7.7 mmol/L or higher.10 Subjects on current lipid-lowering drugs or undergoing antidiabetic treatment were excluded to avoid the possible influence of these treatments on vascular status. Smoking habits were carefully assessed by questioning the subject.8 A current smoker was defined as someone who had regularly smoked each day for the previous 3 months regardless of the amount smoked. Lifelong dose of smoking was estimated by multiplying the mean number of cigarettes smoked daily by the number of years of smoking and was expressed in pack-years. Control subjects and patients were carefully adjusted to similar levels of total cholesterol and smoking habits to avoid the possible confounding effects of these factors on the comparison of coronary status. After giving informed consent, subjects and patients were submitted to noninvasive arterial investigations.11
Arterial Investigations
An ultrafast CT scanner (IMATRON) was used for detection of
calcium deposits in epicardial coronary arteries according to a
previously described procedure.8 Briefly, 20 contiguous
slices (60 mm) were acquired caudally to the bifurcation of the main
pulmonary artery, triggered at 80% of the RR interval, and
analyzed automatically for determination of the presence and
amount of calcium in the left trunk main artery, left anterior
descending coronary artery, left circumflex artery, and right
coronary artery. The threshold for a calcific lesion was set at
a CT peak density of 130 Hounsfield units with an area larger than or
equal to 1 mm2. The maximal density of each lesion was
transformed into four classes as follows: 1, 130 to 199 Hounsfield
units; 2, 200 to 299; 3, 300 to 399; and 4, 400 or
greater.12 A lesion score was then calculated by
multiplying the density number by the area of the lesion in square
millimeters.12 A total coronary calcium score was
defined as the sum of lesion scores of all 20 slices. Concomitantly,
the extent of atherosclerosis in
extracoronary vessels was evaluated echographically in
accordance with the recent guidelines for management of
hypertension.4 Three peripheral sites were
examined: the extracranial carotid arteries on both sides, the whole
abdominal aorta, and the femoral arteries on both sides. Examinations
were performed with high-resolution B-mode echography (Ultramark 4,
Advanced Technologies Laboratories) according to a careful and
standardized procedure reported in detail elsewhere.8 The
presence of atherosclerotic plaque, defined as an echogenic structure
encroaching into the vessel lumen with a distinct focal area, was
searched for in each of the three sites investigated. The presence of
plaque was considered positive in one site when one or more plaques
were found regardless of the precise location and amount of plaque.
Finally, the number of peripheral sites with plaque was
defined in each subject as follows: 0 site with plaque, no presence of
plaque at any site; 1 site with plaque, presence of plaque at a single
site that may be carotid, aortic, or femoral; 2 sites with plaque,
presence of plaque at two sites that may be carotid and aortic, carotid
and femoral, or aortic and femoral; and 3 sites with plaque, presence
of plaque at the carotid, aortic, and femoral sites.
Statistical Analysis
Quantitative variables are expressed as mean±SD and
compared by ANOVA, except for variables with non-normal
distribution, which were compared by the nonparametric
Mann-Whitney test.13 The 
2 test was
used for comparison of qualitative variables. Odds ratios (with
95% confidence intervals [CI]) for coronary calcium scores
higher than 0, 50, or 100 were calculated between control subjects and
patients by the logit method. Univariate Spearman rank
correlations were performed between coronary calcium score and
the study parameters. Multiple linear regression
analysis was performed between the logarithm (calcium score +1)
and the study parameters. Logistic regression
analysis was performed between coronary calcium scores
higher than 0, 50, or 100 (presence/absence), and the study
parameters were characterized in a dichotomous way into two
classes, according to the median value. The odds ratios for
coronary calcium scores higher than 0, 50, or 100 were
calculated between the two classes of each study parameter
from the ß coefficient of the logistic regression. Statistical
significance was considered to be a value of P<.05.
Statistical analysis was carried out on a computer (Apple
Macintosh) with the use of Excel (Microsoft) and JMP (SAS Institute)
software.
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Results |
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Comparison of study parameters (exclusive of coronary calcium) between patients and control subjects did not show any difference in age, blood lipids, frequency of hypercholesterolemia, smoking status, and number of peripheral sites with plaque but did show higher values for body mass index (P<.05), blood pressure (P<.001), and blood glucose (P<.01) in patients than in control subjects (Table 1
).
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Compared with control subjects, hypertensive patients had higher
coronary calcium scores (P<.05) and a higher
frequency of calcium score higher than 0 (P<.05), 50
(P<.05), and 100 (P<.01) (Table 2). Fig 1 shows that the distribution of
the log-transformed calcium score was shifted to the right, with a
small peak of high calcium scores in patients compared with control
subjects. The odds ratios for coronary calcium score between
patients and control subjects were 1.95 (P=.05) for scores
higher than 0; 2.38 (P<.05) for those higher than 50; and
4.84 (P<.01) for those higher than 100 (Table 3).
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Table 4 shows univariate correlations
between coronary calcium score and the study
parameters. In control subjects, no correlation was
significant, whereas in patients, significant correlations existed with
age (P<.05), hypertension duration (P<.01), and
the number of peripheral sites with plaque
(P<.001).
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Table 5 shows the multiple regression analysis
between the explanatory variables and coronary calcium
score. When the number of peripheral sites with plaque was
not included as an explanatory variable, multiple regression
analysis showed age and hypertension duration to be
significantly associated with coronary calcium score
(P<.05). The addition of the number of
peripheral sites with plaque to the group of explanatory
variables in the multiple regression removed the statistical
significance of age and hypertension duration, whereas the number of
peripheral sites with plaque was strongly associated with
calcium score (P<.001). In contrast, in the control group,
the multiple regression analysis was not significant.
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Fig 2 shows the odds ratios for coronary calcium
scores higher than 0, 50, or 100 between the two classes of each risk
factor in the hypertensive group. The odds ratio for calcium scores
higher than 0 was significant only between patients with 2 or 3
peripheral sites with plaque and patients with 0 or 1
peripheral site with plaque (4.67; 95% CI, 1.41 to 15.45;
P<.05). The odds ratio for calcium scores higher than 50
was significant (1) between patients with 2 or 3 peripheral
sites with plaque and patients with 0 or 1 peripheral site
with plaque (8.63; 95% CI, 2.10 to 35.5; P<.001), (2)
between patients with hypertension duration of 1 year or more and
patients with hypertension duration of 0 year (4.41; 95% CI, 1.08 to
18; P<.05), and (3) between patients with total
cholesterol of 6.60 mmol/L or higher and patients with
cholesterol lower than 6.60 mmol/L (4.88; 95% CI, 1.22 to
19.5; P<.05). The odds ratio for calcium scores higher than
100 was significant (1) between patients with 2 or 3
peripheral sites with plaque and patients with 0 or 1
peripheral site with plaque (8.13; 95% CI, 1.64 to 40.3;
P<.001) and (2) between patients with hypertension duration
of 1 year or more and patients with hypertension duration of 0 year
(8.35; 95% CI, 1.95 to 35.9; P<.001). The odds ratio for
calcium scores higher than 100 was almost significant between patients
with higher cholesterol and those with lower
cholesterol (3.03; 95% CI, 0.71 to 12.9;
P<.13). The multiple logistic regression of
coronary calcium score on the study parameters was
not significant in the control group.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Coronary artery disease is a major complication of hypertension6 and usually remains silent until a catastrophic clinical event occurs.14 As its primary determinant is coronary atherosclerosis,5 a marker that can indicate which hypertensive individuals have the greatest potential for developing coronary atherosclerosis is particularly useful. Coronary calcification is well recognized as a marker of atherosclerosis15 but not as a reliable indicator of coronary stenosis because calcification may occur before the atheroma narrows the lumen of coronary vessels.15 To date, ultrafast CT is the noninvasive technique that allows the most accurate determination of the presence and amount of coronary calcium deposit.16 Nevertheless, the interscan reliability of coronary calcium quantification with ultrafast CT seems relatively poor. In a study of 142 asymptomatic hypercholesterolemic subjects (recruited in our center of preventive cardiovascular medicine), the variability of total calcium score was 16% between two examinations within the same day, but when a log-transformed score was used (in the present work), the variability dropped to 7%.17 Another study of 91 patients who underwent two scans within 24 hours showed that the variability of total calcium score was inversely related to the absolute value of the calcium score.18 In the present work the expression of total calcium score according to three classes (score higher than 0, 50, or 100) may attenuate this score-dependent variability, especially for higher score classes. Furthermore, the differences observed in repeated coronary calcium score measurement have less importance in transversal studies such as the present work than in prospective studies evaluating the significance of serial calcium score.
We have therefore used ultrafast CT to investigate the coronary status of symptom-free hypertensive men younger than 65 years compared with age-matched normotensive control men. We found a higher prevalence of coronary calcification and a larger amount of coronary calcium deposit in the presence of hypertension. Moreover, the risk of coronary calcium deposit regardless of score was doubled, and overall the risk for extensive calcium deposit (characterized by a calcium score higher than 100) was quintupled in hypertensive patients compared with control subjects. This latter observation suggests that hypertension predisposes in particular to the extensive deposit of calcium in coronary arteries. Our findings are reinforced by two previous reports19 20 showing that a history of hypertension was independently associated with the probability of detectable coronary calcium evaluated by ultrafast CT in asymptomatic at-risk subjects. However, unlike our present work, the subjects in these previous reports were not selected specifically for hypertension; they included men and women with a wide range of ages, from 20 to 85 years; and the diagnosis of hypertension was self-reported without actual blood pressure data. Another report has also shown that increased systolic pressure measured during childhood and young adult life was strongly related to the presence of coronary calcification assessed by ultrafast CT.21 However, all of these findings conflict with a study in asymptomatic high-risk adult subjects in which no association was found between coronary calcium assessed by digital subtraction fluoroscopy and blood pressure.22 This lack of association may be due to the methodology used, which assessed coronary calcification in a dichotomous way by presence or absence and did not provide an estimation of coronary calcium deposit.22
The observation that hypertension promotes coronary calcium deposit, an anatomic marker of coronary atherosclerosis, supports the concept that hypertension is an important pathogenic factor in the development of coronary disease.23 The precise mechanisms of the interrelationships between coronary atherosclerosis, calcification, and hypertension are complex. Hypertension may participate in the atherogenic process through the arterial wall trauma induced by the rise in arterial pressure and/or particular coexistent shearing conditions.23 Furthermore, calcification of the atheroma is an active process in which osteopontin,24 a protein involved in mineralization, may play an important role,25 and high expression of the gene for osteopontin may be induced by stimuli related to the arterial wall trauma.26 Unfortunately, the present clinical study cannot help elucidate these basic mechanisms.
Nevertheless, we have obtained several findings that may provide new insights into the analysis of the interaction of hypertension and coronary calcification. First, we found that the duration of hypertension strongly influenced coronary calcification, whereas the height of blood pressure did not. The lack of relationship between the height of blood pressure and coronary calcification in hypertensive patients confirms similar data reported in autopsy studies.23 It suggests that the raised blood pressure itself may not be the direct cause of coronary disease. On the contrary, the duration of hypertension had a strong influence on coronary calcification; this influence was independent of age, as shown in the multivariate analysis. This observation is important because age was also related to coronary calcification in hypertensive patients as previously reported in various at-risk populations.8 12 16 19 27 28 Moreover, the influence of hypertension duration was strengthened when extensive coronary calcium deposit (calcium score higher than 100) was considered, since the odds ratio for coronary calcium score higher than 100 exceeded 8 between known and newly diagnosed hypertension. The mechanisms by which the duration of hypertension influences coronary calcification may be multifactorial and not specific for hypertension. Hypertension duration represents the time of exposure to high blood pressure but also to coexistent cardiovascular risk factors that may interact with the coronary calcification process. Among these risk factors, we have analyzed in particular the influence of lipid metabolism. Total cholesterol was not associated with coronary calcium score regardless of value, but it seemed to influence higher calcium scores (higher than 50 or 100) because the odds ratios for scores higher than 50 and 100 were nearly 5 and 3, respectively, between hypertensive patients with higher cholesterol and those with lower cholesterol. This suggests that elevated blood cholesterol levels may participate in the mechanisms of coronary calcification, especially for extensive calcium deposit, in the presence of hypertension, as demonstrated for atheroma in experimental studies.23 In contrast, the other lipid parameters, HDL and LDL cholesterols and triglycerides, were not associated with coronary calcification; neither were nonlipidic risk factors such as body mass index, blood glucose, and smoking. Finally, the present work did not investigate other potential risk factors, such as a lack of physical exercise, heredity, and newer risk factors such as lipoprotein(a). All these potential risk factors merit further investigation, especially the role of genes because a recent study in inbred mice provided the first evidence that coronary calcification is determined in part by genetic factors.29
Another interesting observation of the present study was the strong, independent association between coronary calcium score and the number of peripheral artery sites with plaque assessed by echography. Between patients with extensive peripheral atherosclerosis (2 and 3 peripheral sites with plaque) and those with no or minor peripheral atherosclerosis (0 or 1 peripheral site with plaque), the odds ratio for coronary calcium deposit regardless of score exceeded 4 and the odds ratio for extensive coronary calcium deposit (score higher than 50 or 100) exceeded 8. In contrast, no association existed between the extent of peripheral atherosclerosis and coronary calcium score in the control group. These results indicate that hypertension promotes the parallel development of extensive atherosclerosis in extracoronary and coronary vessels, as previously reported in other at-risk populations.8 30 The clinical relevance of the increased risk of coronary calcium deposit in hypertensive patients must be questioned. Coronary calcifications are likely important for predicting subsequent cardiac events or death in individuals. Some studies have shown an increased incidence of coronary events in asymptomatic subjects with coronary calcium.28 31 Autopsy studies have also shown that extensive coronary atherosclerosis might be related to sudden coronary heart disease deaths.5 32 33 34 Additional longitudinal studies are needed to determine more definitely whether coronary calcium deposit can better determine subsequent risk of coronary event and death in asymptomatic middle-aged hypertensive patients.15
In conclusion, the present study indicates that hypertension and particularly its duration promotes the presence and overall extent of calcium deposit in coronary arteries in parallel with the extent of atherosclerosis in extracoronary vessels. However, these findings were obtained in men and therefore cannot be extrapolated to women.
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Acknowledgments |
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We thank the Banque Nationale de Paris, l'Oréal SA, Matra Sa, Procter & Gamble France, and the Automobiles Peugeot for sponsoring the Groupe de Prévention Cardiovasculaire en Médecine du Travail (PCV METRA). We thank the PCV METRA group (P. Segond, Chairman). We thank Anne-Marie de La Provôté for her excellent secretarial assistance and Isabelle d'Argentré for her invaluable assistance in ultrafast CT data entry.
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Footnotes |
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Reprint requests to Prof Alain Simon, Centre de Médecine Préventive Cardiovasculaire, Hôpital Broussais, 96 rue Didot, 75674 Paris, France.
Received December 29, 1995; first decision January 10, 1996; accepted January 10, 1996.
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