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(Hypertension. 1995;26:369-373.)
© 1995 American Heart Association, Inc.

Articles

Prevalence and Determinants of Cardiac and Vascular Hypertrophy in Hypertension

Mary J. Roman; Thomas G. Pickering; Riccardo Pini; Joseph E. Schwartz; Richard B. Devereux

From the Division of Cardiology, Department of Medicine, The New York Hospital–Cornell Medical Center, NY.

	Abstract

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Abstract Hypertrophy of the capacitance arteries has recently been documented in hypertensive patients by noninvasive ultrasound techniques. To better define the prevalence and determinants of vascular hypertrophy and its potential association with ventricular hypertrophy in hypertension, we compared carotid and cardiac ultrasound findings in 172 normotensive and 172 unmedicated hypertensive subjects matched for age and sex. Despite similar body size, hypertension was associated with increased left ventricular wall thicknesses, mass, and mass index (89 versus 80 g/m², P<.0001 for all comparisons) and increased carotid wall thickness (0.82 versus 0.77 mm) and cross-sectional area (17.1 versus 15.3 mm², P<.005 for both comparisons). Among the 172 normotensive subjects, left ventricular hypertrophy was noted in 9 (5.2%) and arterial hypertrophy was found in 9 (5.2%), whereas ventricular hypertrophy was found in 21 (12.2%) and arterial hypertrophy in 19 (11%) hypertensive subjects. Arterial hypertrophy was found in 9% of hypertensive subjects with normal ventricular mass and in 24% with left ventricular hypertrophy (P<.05). Among hypertensive subjects carotid wall thickness and cross-sectional area were most strongly related to age and systolic pressure (P<.0001 for all comparisons), with little contribution from body size. Carotid relative wall thickness was only related to increasing age (P<.01). In contrast, left ventricular wall thickness and mass were strongly related to body size and systolic pressure (P<.0001 for all comparisons) but not to age (P=NS). Thus, among otherwise healthy, asymptomatic hypertensive subjects, left ventricular and arterial hypertrophy are similarly prevalent (when the latter is defined by methods that take into account the influence of aging) and are associated with each other. Although both arterial and left ventricular size are strongly related to blood pressure, aging is the most important determinant of arterial size, even in hypertension, whereas body size is the most important determinant of left ventricular mass.

Key Words: carotid arteries • hypertension, arterial • hypertrophy • atherosclerosis • ultrasonography

	Introduction

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The presence of hypertrophy of large capacitance arteries and medium-sized muscular arteries in human hypertension has recently been documented with noninvasive, high-resolution, in vivo ultrasound imaging.^{1 2 3 4 5 6 7} Intimal-medial thickening of the common carotid,^{1 2 3 4 5 6} femoral,² and radial arteries⁷ and to a lesser extent arterial lumen enlargement¹ occur in hypertensive patients compared with matched normotensive subjects. Furthermore, these changes in capacitance arteries parallel those in the left ventricle, presumably because of the sustained pressure load and additional nonhemodynamic and genetic factors.^{1 3 6}

Preliminary data suggest that vascular hypertrophy might occur earlier and/or be more prevalent than cardiac hypertrophy in hypertension. In a previous study we detected left ventricular (LV) hypertrophy in 14% of otherwise healthy hypertensive subjects, whereas vascular hypertrophy (defined as a common carotid artery intimal-medial thickness of >0.96 mm [above the 95th percentile of a matched control population]) was present in 28%.¹ In addition, an increased augmentation index, reflecting at least in part increased arterial stiffness, is associated with higher LV mass in healthy subjects, independent of age, sex, and blood pressure, suggesting that vascular stiffness might precede and contribute to the development of LV hypertrophy.⁸ The major effect of aging on vessel wall thickness^{1 3 7 9} suggests that a single cut point to define normality might underestimate the prevalence of arterial hypertrophy in younger individuals and overstate its occurrence in older individuals. Therefore, we designed the present study to examine the determinants of common carotid artery size in normotensive adults to more accurately define normal relations and thereby the presence of hypertrophy in hypertension.

	Methods

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Study Population
The study population consisted of 172 otherwise healthy, asymptomatic hypertensive individuals who were matched for age and sex with 172 healthy normotensive subjects evaluated in the context of worksite-based studies of hypertension or referred from the Hypertension Center of The New York Hospital–Cornell Medical Center for noninvasive cardiovascular evaluation.¹⁰ One hundred twenty-seven subjects (74%) had essential hypertension (blood pressure 140/90 mm Hg), 36 (21%) had borderline or white coat hypertension,¹¹ and 9 (5%) had isolated systolic hypertension (systolic pressure 160 mm Hg and diastolic pressure <90 mm Hg). Thirty-nine percent of hypertensive subjects had never received pharmacological therapy; the remaining subjects were studied after medications had been discontinued for from 3 weeks to 5 years. We analyzed an expanded population of 305 (including the 172 study subjects) healthy normotensive subjects (mean age, 48±12 years; range, 24 to 88 years) to establish normal limits for common carotid arterial size taking into account effects of age and body size. Subjects were studied under protocols approved by the Committee on Human Rights in Research of Cornell University Medical College.

Ultrasound Studies
All subjects underwent standard M-mode and two-dimensional echocardiographic examination performed by a highly skilled research technician using commercially available equipment. Two-dimensionally guided M-mode tracings were coded and read blindly by a single observer; measurements were made on up to six cycles with the use of a digitizing tablet and were averaged. Wall thicknesses and chamber dimensions were taken according to the American Society of Echocardiography recommendations^{12 13} ; LV mass was calculated with the use of the Penn convention¹⁴ and adjusted for body surface area. LV hypertrophy was considered present if LV mass index was greater than or equal to 125 g/m² in men or greater than or equal to 110 g/m² in women.^{15 16}

Carotid ultrasonography was performed as previously described.¹ In brief, using a 7.5-MHz duplex transducer, we scanned the extracranial carotid arteries from multiple approaches to detect the presence of discrete atherosclerosis.¹⁷ Two-dimensionally guided M-mode tracings of the distal common carotid artery approximately 1 cm proximal to the bulb were recorded on videotape and subsequently acquired and digitized in real time with a frame-grabber. The intimal-medial thickness of the far wall (IMT_d) and internal diameter (D_d) of the artery at end diastole (minimum diameter) were measured with electronic calipers on several cycles and averaged. Arterial size was further characterized by calculating cross-sectional area according to the formula [IMT_d+(D_d/2)]²-[(D_d/2)]². Arterial relative wall thickness was calculated as IMT_d/(D_d/2). The accuracy and reproducibility of ultrasound measurement of the carotid artery have been previously demonstrated.^{1 2 7 18}

Data Analysis
Data were stored on a personal computer and analyzed with the CRUNCH4 statistical package (Crunch Software Corp). Mean values were compared with Student's t test and are presented with the SD as the index of dispersion. Relations between continuous variables were evaluated by linear regression. Independence of association was assessed by multiple stepwise regression. Differences in prevalences between two groups were compared by ² analysis.

	Results

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Comparison of LV and Carotid Artery Structure
The 172 normotensive and 172 hypertensive subjects were composed of 126 women and 218 men with a mean age of 53±12 years (range, 24 to 88 years). Mean body surface area (1.86±0.21 and 1.90±0.22 m², respectively) and body mass index (25.9±4.0 and 26.7±4.1 kg/m²), a measure of obesity, were similar in the two groups. By definition, blood pressures were substantially higher in the hypertensive subjects (153±20/93±11 versus 123±13/74±9 mm Hg).

LV absolute and relative wall thicknesses, end-diastolic diameter, mass, and mass index were significantly increased in hypertensive subjects compared with normotensive control subjects (Table 1). Common carotid artery wall thickness, end-diastolic diameter, and cross-sectional area were likewise increased on average in the hypertensive group. Although the average increases in vessel diameter and wall thickness were similar, the variability of relative wall thickness was higher and did not differ between the two groups.

View this table: [in this window] [in a new window]   Table 1. Comparison of Left Ventricular and Carotid Structure in Matched Normotensive and Hypertensive Subjects

Ventricular and Vascular Hypertrophy
In the expanded population of 305 healthy normotensive subjects, common carotid artery intimal-medial thickness and cross-sectional area were related to age (r=.40 and .38, respectively; P<.0001 for both comparisons), systolic pressure (r=.38 and .41, respectively; P<.0001 for both), and body surface area (r=.15, P<.01 and r=.26, P<.0001, respectively). The multiple regression equation predicting intimal-medial thickness was IMT_d=0.00586 Age+0.015267 Body Surface Area+0.16569 and that for diastolic cross-sectional area was CSA_d=0.15669 Age+6.56617 Body Surface Area-5.4103. Blood pressure was not included in the equations because the goal of the study was to determine the effect of hypertension on vascular size. The ratios of observed to predicted IMT_d and CSA_d were calculated for each subject. Arterial hypertrophy was identified in the age- and sex-matched population if the ratio of observed/predicted dimension exceeded 2 SD above the mean ratio in the large control population.

Prevalences of both LV and arterial hypertrophy were 5.2% among the normotensive subjects and similarly increased in the hypertensive group (LV hypertrophy in 12.2% and arterial hypertrophy in 11%) (Fig 1). Among the hypertensive subjects with LV hypertrophy, arterial hypertrophy was present in 24%, whereas arterial hypertrophy was present in only 9% of hypertensive subjects without LV hypertrophy (P<.05) (Fig 2). Discrete carotid atherosclerosis (plaque) was present in 24% of subjects and was associated with an increased LV mass (170 versus 156 g, P<.01) and mass index (88.7 versus 82.7 g/m², P<.01) after adjustment for differences in age and blood pressure.

View larger version (70K): [in this window] [in a new window]   Figure 1. Bar graph shows prevalences of left ventricular hypertrophy (hatched bars) and common carotid artery hypertrophy (stippled bars) in 172 healthy normotensive and 172 asymptomatic, unmedicated hypertensive subjects.

View larger version (49K): [in this window] [in a new window]   Figure 2. Bar graph shows comparison of prevalences of hypertrophy of the common carotid artery in hypertensive subjects in whom left ventricular hypertrophy (LVH) is either absent or present.

Determinants of LV and Carotid Artery Structure in Hypertension
Among hypertensive subjects common carotid intimal-medial thickness and cross-sectional area were most strongly related to age and blood pressure (Table 2). The relation of these measures to body size was stronger in multivariate than in univariate analyses. In contrast, both LV wall thickness and mass were most strongly related to body surface area and systolic pressure, with little or no relationship to age. Common carotid artery relative wall thickness was related only to increasing age (r=.20, P<.01), and LV relative wall thickness tended to increase with age (r=.15, P=.06). Carotid cross-sectional area was also related to LV mass (r=.33, P<.00005). Carotid artery wall thickness (0.79±0.17 versus 0.84±0.20 mm), cross-sectional area (16.4±5.2 versus 17.6±5.4 mm²), and LV mass (166±37 versus 171±52 g) did not significantly differ between never-treated and previously treated hypertensive subjects.

View this table: [in this window] [in a new window]   Table 2. Relations of Left Ventricular and Common Carotid Artery Structure to Age, Body Size, and Blood Pressure in Hypertensive Subjects

	Discussion

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The present study confirms the presence of hypertrophy of the capacitance vessels in hypertension in a large population of otherwise healthy asymptomatic hypertensive men and women who were matched for age, sex, and body size with normotensive men and women. It also confirms our previous reports of the association of LV hypertrophy with carotid hypertrophy and atherosclerosis.^{1 10} However, in contrast to earlier findings in a smaller population in which a single cut point for the definition of vascular hypertrophy was used,¹ the prevalences of LV and vascular hypertrophy were found to be similar when the effects on vascular size of age and to a lesser extent body surface area were considered.

Although previous studies comparing common carotid artery structure in matched hypertensive and normotensive groups have uniformly detected a substantial (7% to 27%) increase in vessel wall thickness attributable to hypertension,^{1 2 3 4 5 6} findings with regard to diastolic luminal diameter have been variable, with some studies reporting no difference in diameter.^{2 3 6} We used cross-sectional area rather than diastolic diameter as a primary measure of vascular size because it incorporates changes in both vessel wall thickness and diameter and is conceptually comparable to LV mass as a measure of vascular size. In the current study the proportional increases in wall thickness and diastolic diameter in hypertensive subjects were similar (6%), whereas the increase in cross-sectional area was higher (11%). The smaller but significant increase in intimal-medial thickness noted in this study compared with earlier studies likely represents the substantially larger current study population. The lower prevalence of vascular hypertrophy in hypertension noted in the current study compared with our previous report¹ likely reflects the different definition of vascular hypertrophy. However, the major effect of age on common carotid intimal-medial thickness and cross-sectional area in both hypertensive and normotensive subjects noted in this and previous studies^{3 9} strongly suggests that this variable should be considered in defining normality in a manner similar to body size being considered for interindividual differences in LV mass.

There have been few previous attempts to establish definitions of vascular hypertrophy, particularly with the use of methods that take into account differences in age, body size, sex, or race. Furthermore, the extent to which intimal-medial thickening represents hypertrophy as opposed to "early atherosclerosis" is uncertain and may vary depending on individual and population characteristics.^{17 19} Intimal-medial thicknesses greater than 1.0 mm in the common carotid artery or greater than 1.2 mm in the carotid bulb have been proposed as measures of "intimal-medial thickening" that is considered more likely to represent diffuse atherosclerosis than hypertrophy based on an association of these values with increased serum low-density lipoprotein cholesterol levels but not with hypertension.²⁰ We previously used 0.96 mm as the upper normal limit for common carotid intimal-medial thickness (95th percentile of a control population) and found carotid hypertrophy in 28% of 43 otherwise healthy hypertensive subjects.¹ Bonithon-Kopp et al²¹ defined common carotid arterial hypertrophy as the presence of intimal-medial thickness greater than 0.80 mm, which represents 1 SD above the mean of 717 men and women between the ages of 60 and 69 years, 19% of whom were taking lipid-lowering drugs. A more comprehensive attempt to quantify carotid artery hypertrophy has been made by the Atherosclerosis Risk in Communities (ARIC) study by developing nomograms based on race and sex relating thicknesses of various carotid artery segments to age.⁹ The present study, albeit smaller than the two cited above,^{9 21} has the advantage of using well-characterized, asymptomatic, unmedicated normotensive individuals in the control population. Girerd et al⁷ defined hypertrophy of the radial artery as a wall thickness greater than 0.244 mm, a value representing the 95th percentile in 40 normotensive subjects, and found hypertrophy to be present in 91% of 33 never-treated hypertensive subjects but in only 22% of 27 treated hypertensive subjects.

The extent to which previous pharmacological therapy in a substantial percentage of the hypertensive subjects influences our results is uncertain. Although most classes of antihypertensive agents²² and sodium restriction²³ may reduce LV mass, the duration of this potential effect after cessation of therapy is unknown. Although a recent study has demonstrated thinner walls of the muscular radial artery in treated compared with untreated hypertensive patients⁷ and isradipine treatment has reduced carotid artery wall thickness in hypertensive and normotensive rats,²⁴ we are not aware of comparable data in humans. Were such a reduction to occur and persist after cessation of therapy, one might predict that our study has underestimated the absolute prevalences of ventricular and vascular hypertrophy in hypertension, although the relative prevalences might remain similar. However, the finding that neither ventricular nor vascular size varied significantly between never-treated and previously treated hypertensive subjects suggests that previous pharmacological therapy had a negligible effect on the study results. An additional methodological consideration, ie, the healthy and asymptomatic status of our hypertensive subjects, is likely the most important factor governing the prevalences of hypertrophy in the present study.

In conclusion, significant differences in common carotid artery intimal-medial thickness, diastolic diameter, and cross-sectional area exist in hypertension. In both normotensive and hypertensive subjects vascular structure is most strongly related to the aging process, whereas LV structure is most strongly related to body size. When these relations are considered in defining hypertrophy, LV and vascular hypertrophy are similarly prevalent. Although increasing carotid intimal-medial thickness has been shown to independently predict subsequent myocardial infarction in Finnish men,²⁵ the prognostic significance of vascular hypertrophy per se, either additive to or independent of LV hypertrophy, remains to be defined.

	Acknowledgments

 
This work was supported in part by grants HL-18323 and HL-47540 from the National Heart, Lung, and Blood Institute, Bethesda, Md.

	Footnotes

 
Reprint requests to Mary J. Roman, MD, Division of Cardiology, Department of Medicine, The New York Hospital–Cornell Medical Center, 525 E 68th St, New York, NY 10021.

	References

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