| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 1996;28:47-52.)
© 1996 American Heart Association, Inc.
Articles |
the Division of Cardiology, Department of Medicine, and the Hypertension Center, The New York Hospital-Cornell University Medical Center, New York.
| Abstract |
|---|
|
|
|---|
Key Words: aorta aortic regurgitation hypertension, arterial
| Introduction |
|---|
|
|
|---|
Although early case reports and pathological series suggest that hypertension might directly predispose to aortic regurgitation because of enlargement of the aortic root,7 8 9 10 11 12 13 14 more recent pathological6 15 and M-mode echocardiographic3 16 17 studies have not found an association between blood pressure and aortic root size when the confounding influence of aging is considered. Thus, aortic root diameter is strongly related to age,3 17 18 19 20 21 22 23 24 and senescence may result in cystic medial necrosis.4 5 6 15 In contrast, other M-mode echocardiographic studies have noted significant relations of aortic root diameter to systolic18 and diastolic19 25 pressures. Furthermore, severe aortic regurgitation due to idiopathic aortic root dilatation is associated with antecedent hypertension.3
Discrepancies in the existing literature regarding the effect of hypertension on aortic root enlargement may partially reflect methodological shortcomings in the accuracy and reproducibility of aortic and blood pressure measurements. Although M-mode echocardiography is reliable in assessing aortic root diameter,26 27 it results in systematic underestimation of aortic diameter at the sinuses of Valsalva due to cyclic cardiac translational changes17 and does not permit extensive assessment of the entire aortic root, including the supra-aortic ridge, which serves as the site of commissural insertion. Commissural support is of critical importance in the maintenance of normal geometry and hence leaflet coaptation.28 In addition, clinical estimates of blood pressure may be less accurate in reflecting vascular load and thereby target-organ damage than are ambulatory blood pressure determinations.29 30 Hence, we designed the present study to assess the effect of blood pressure on aortic size by examining comprehensive two-dimensional echocardiographic measurements of aortic root diameters in age- and sex-matched normotensive and hypertensive subjects in comparison with age, body size, and both clinic and ambulatory blood pressure measurements.
| Methods |
|---|
|
|
|---|
140/90 mm Hg]) adult volunteers studied between 1990 and 1994. The subjects were members of either a healthy, employed normotensive and hypertensive population enrolled by defined recruitment schemes into an ongoing longitudinal study or a pool of untreated hypertensive subjects referred from the Hypertension Center at The New York Hospital-Cornell Medical Center.30 31 Detailed descriptions of the subject pool have been previously reported.31 All examinations were performed at The New York Hospital-Cornell Medical Center under protocols approved by the Committee on Human Rights in Research of Cornell University Medical Center. Groups of 110 hypertensive patients (74 men and 36 women) and 110 normotensive subjects with adequate echocardiograms, in which the entire aortic root including the ascending aorta could be sufficiently visualized for reliable measurement, were matched for sex and age±2 years.
Echocardiography
All subjects underwent two-dimensional and Doppler echocardiography performed by an experienced research echocardiographer using commercially available echocardiographs equipped with 2.5- and 3.5-MHz transducers. The dimensions of the aortic root and ascending aorta were evaluated in detail by two-dimensional echocardiography. With a commercially available digitizing tablet and videocassette recorder with forward and reverse frame-by-frame review capacity, measurements at end diastole were made by the leading edge technique in the parasternal long-axis view at four locations17 : (1) aortic anulus, (2) maximal diameter of the sinuses of Valsalva, (3) supra-aortic ridge (sinotubular junction), and (4) maximal diameter of the proximal ascending aorta (Fig 1
). Measurements were taken on up to four separate cycles and averaged. Pulsed and color Doppler examinations were performed for determination of the presence and severity of aortic regurgitation.32 33
|
Blood Pressure Measurement
Supine casual brachial blood pressure was determined after the echocardiographic study by the research technician using a standard mercury sphygmomanometer. Forty-eight subject pairs additionally underwent 24-hour ambulatory blood pressure monitoring during a normal day using a SpaceLabs 90207 monitor. The monitor was placed on the nondominant arm and set to take blood pressure readings every 15 minutes during waking hours. Detailed descriptions of this procedure and its validation have been reported previously.34
Data Analysis and Statistical Methods
Data were stored and analyzed by the Crunch 4 Statistical Package (Crunch Software Corp). Mean values are presented with SD as the index of dispersion. Differences between mean values of the two groups were tested with Student's t test. The strength of the relationship of each aortic root measurement with body size and blood pressure variables was evaluated by the Pearson correlation coefficient. Independence of association was tested in multivariate analyses. Significance of differences between blood pressure quartiles was evaluated by ANOVA. Significance of differences in populations was evaluated with the
2 test. A value of P<.05 was considered statistically significant.
| Results |
|---|
|
|
|---|
Comparison of Aortic Dimensions
Table 1
shows unadjusted and adjusted aortic root dimensions in the study subjects. Aortic root diameters at the anulus and sinuses of Valsalva tended to be higher in the hypertensive group, but the differences did not achieve statistical significance. Diameters at the supra-aortic ridge and proximal ascending aorta were significantly increased in the hypertensive subjects (P<.01 for both comparisons). Similar results were obtained when the diameters were indexed by height, whereas indexing by body surface area eliminated statistical significance of the differences.
|
When the entire population was divided by sex (148 men and 72 women), diameters remained significantly larger for hypertensive than normotensive men at the supra-aortic ridge and proximal ascending aorta (P<.005 for both comparisons); diameters tended to be higher for hypertensive women at all levels but did not achieve statistical significance as a consequence of the smaller sample size.
Relation of Aortic Root Dimensions to Age, Body Size, and Hemodynamic Variables
As demonstrated in Table 2
, age did not bear a significant univariate relation to aortic diameter in this age-matched population. Aortic root diameters at all levels were significantly related to height, weight, and body surface area. Aortic diameters at all levels were also significantly related to casual systolic and diastolic pressures when the entire population was considered. Use of ambulatory blood pressures eliminated the statistical significance of relations at the anulus and sinuses of Valsalva (primarily as a consequence of smaller sample size because correlation coefficients were not substantially different), whereas ambulatory blood pressure remained strongly related to aortic diameter at the supra-aortic ridge and ascending aorta. As indicated in Table 3
, among normotensive subjects, aortic diameters were more strongly related to casual systolic pressure than to ambulatory pressure, whereas among hypertensive subjects, aortic diameters were most strongly related to ambulatory diastolic pressure, particularly in the more distal segments of the aortic root.
|
|
In multiple regression analysis (Table 4
) involving the entire study population with height (the anthropometric variable resulting in the best model), age, and casual systolic pressure entered as variables, height was the strongest predictor of aortic diameter at all levels (P<.00005 for all). Age was also an independent determinant of all aortic diameters. Systolic pressure also entered the model for each diameter except at the sinuses of Valsalva.
|
Comparison of Aortic Measurements by Severity of Pressure Load
Fig 2
shows aortic root diameters compared by quartiles of hemodynamic load. When the combined normotensive and hypertensive study population was divided into quartiles of casual systolic pressure (first quartile, <122 mm Hg; second quartile,
122 and <140; third quartile,
140 and <157; fourth quartile,
157), progressive enlargement was found only at the supra-aortic ridge (P<.005) and ascending aorta (P<.05). When the entire study population was divided into quartiles of casual diastolic pressure (first quartile, <78 mm Hg; second quartile,
78 and <84; third quartile,
84 and <92; and fourth quartile,
92), all aortic diameters were found to significantly increase with increasing blood pressure, with the most significant increases occurring in the more distal segments.
|
Aortic Regurgitation
Aortic regurgitation of any severity was found in 4.5% of the normotensive subjects and 6.4% of the hypertensive subjects. Aortic regurgitation was mild in two and moderate in three normotensive subjects, and mild in three and moderate in four hypertensive subjects.
| Discussion |
|---|
|
|
|---|
Previous studies evaluating the relation of aortic root size to blood pressure have yielded conflicting results. Recently, Vasan et al,19 using two-dimensionally guided M-mode measurement of the sinuses of Valsalva in the Framingham Heart Study, found that diastolic pressure was directly related to aortic diameter, whereas both systolic and pulse pressures were inversely related to aortic diameter after adjustment for age, height, and weight. In an earlier study3 involving 102 patients with severe aortic regurgitation, we found similar mean M-mode aortic diameters in normotensive and hypertensive groups. Age (P<.0005) and diastolic pressure (P<.05) were multivariate correlates of aortic diameter in the normotensive group, whereas only age (P<.005) predicted aortic diameter in the hypertensive group. Tell et al25 in the Cardiovascular Health Study found a relation between diastolic but not systolic pressure and M-mode echocardiographic dimensions when the entire elderly cohort was analyzed; however, when the "healthier" subgroup (no coronary heart disease or antihypertensive therapy) was examined, aortic diameter was not associated with blood pressure. Other researchers have shown either no relation of blood pressure to M-mode aortic measurements or relationships only to systolic pressure.18
In the present study, using a more thorough and accurate measurement of the entire aortic root, we found significant differences between normotensive and hypertensive subjects in aortic root diameter, primarily at the supra-aortic ridge and proximal ascending aorta. Failure to find a statistically significant difference at the sinuses of Valsalva and aortic anulus (the areas usually measured by M-mode echocardiography) may explain the relatively weak and inconsistent relations of blood pressure to aortic root diameter in previous studies and may reconcile discrepant findings in earlier pathological studies of hypertensive patients succumbing to aortic regurgitation in which higher segments of the aorta may have been examined.9 10 11
Although use of ambulatory blood pressure monitoring to eliminate individuals with white coat hypertension and to theoretically provide a more accurate measurement of blood pressure load might be predicted to strengthen any relation of blood pressure to aortic size, such an effect was noted only in the hypertensive group in the present study. Optimal measurement of pressure load might have been achieved by noninvasive estimation of central arterial pressure and vascular compliance35 or by quantitative analysis of the arterial pressure waveform.36 Despite similar mean pressures, systolic and diastolic pressures may vary considerably37 with the degree of wave amplification, being maximal in the young, normotensive individual with a compliant vasculature.38 To the extent that brachial blood pressure may overestimate central pressure in our normotensive population, the correlation between arterial pressure and aortic diameter may have been understated.
When aortic root diameter increases, aortic valve cusps are unable to expand in area, and the degree of cusp overlap is reduced, eventually leading to aortic regurgitation.12 39 40 Since the point of commissural attachment is at the supra-aortic ridge, increases in this diameter are more likely to be of greater pathophysiological significance.28 Thus, dilatation in the more distal segment of the aortic root has been shown to be associated with more-severe left ventricular structural and functional abnormalities in patients with severe aortic regurgitation due to idiopathic root dilatation in comparison with patients with severe aortic regurgitation due to valvular disease3 and to be associated with an increased likelihood of aortic complications in the Marfan syndrome.1 Therefore, the greatest hemodynamic effects of root dilatation appear to be when it occurs at the distal portions of the aortic root. Although hypertension was associated with larger measurements in the distal aortic root in the present study, there was no significant difference in the prevalence of aortic regurgitation between the normotensive and hypertensive subjects, perhaps because of their relatively young age, mild degree of hypertension, and otherwise healthy status. In fact, in a previous analysis limited to individuals with severe aortic regurgitation, antecedent hypertension was strongly associated with the presence of idiopathic aortic root dilatation as the cause of aortic regurgitation.3
Relationships of body size to aortic size have been uniformly noted in previous populations17 19 41 and were confirmed in the present study. Indexation of the aortic diameters for body surface area eliminated differences in aortic size between normotensive and hypertensive subjects, whereas indexation for height marginally amplified differences. Previous authors have suggested that the use of body surface area as a means of adjustment for differences in body size is mathematically incorrect and that indexation of aortic diameter for height is a more linear and mathematically sound way of comparing measurements.41
In conclusion, aortic root diameters at the supra-aortic ridge and proximal ascending aorta are significantly greater in hypertensive patients compared with an age- and sex-matched normotensive population. These findings may be of pathophysiological importance in the development of aortic regurgitation in hypertensive individuals.
| Acknowledgments |
|---|
| Footnotes |
|---|
Received January 15, 1996;
first decision February 29, 1996;
| References |
|---|
|
|
|---|
2. Hahn RT, Roman MJ, Mogtader AH, Devereux RB. Association of aortic dilation with regurgitant, stenotic, and functionally normal bicuspid aortic valves. J Am Coll Cardiol. 1992;19:283-288.[Abstract]
3. Roman MJ, Devereux RB, Niles NW, Hochreiter C, Kligfield P, Sato N, Spitzer MC, Borer JS. Aortic root dilatation as a cause of isolated, severe aortic regurgitation. Ann Intern Med. 1987;106:800-807.
4. Carlson RG, Lillehei CW, Edwards JE. Cystic medial necrosis of the ascending aorta in relation to age and hypertension. Am J Cardiol. 1970;25:411-415.[Medline] [Order article via Infotrieve]
5. Rottino A. Medial degeneration of the aorta. Arch Pathol. 1939;28:377-385.
6. Schlatmann TJ, Becker AE. Pathogenesis of dissecting aneurysm of the aorta: comparative histopathologic study of significance of medial changes. Am J Cardiol. 1977;39:21-26.[Medline] [Order article via Infotrieve]
7. Vasquez H. Diseases of the Heart. Philadelphia, Pa: WB Saunders Co; 1924:383-384.
8. Gager LT. The differentiation of syphilitic from functional and other forms of aortic insufficiency. Am Heart J. 1930;6:107-112.
9.
Garvin CF. Functional aortic insufficiency. Ann Intern Med. 1940;13:1799-1804.
10. Fenichel NM. Arteriosclerotic aortic insufficiency. Am Heart J. 1950;40:117-124.[Medline] [Order article via Infotrieve]
11. Gouley BA, Sickel EM. Aortic regurgitation caused by dilatation of the aortic orifice and associated with a characteristic valvular lesion. Am Heart J. 1943;26:24-38.
12. Waller BF, Zoltick JM, Rosen JH, Katz KM, Gomes MN, Fletcher RD, Wallace RB, Roberts WC. Severe aortic regurgitation from systemic hypertension (without aortic dissection) requiring aortic valve replacement: analysis of four patients. Am J Cardiol. 1982;49:473-477.[Medline] [Order article via Infotrieve]
13. Barlow J, Kincaid-Smith P. The auscultatory findings in hypertension. Br Heart J. 1960;22:505-514.
14. Puchner TC, Huston JH, Hellmuth GA. Aortic valve insufficiency in arterial hypertension. Am J Cardiol. 1960;5:758-760.[Medline] [Order article via Infotrieve]
15. Schlatmann TJ, Becker AE. Histologic changes in the normal aging aorta: implications for dissecting aortic aneurysm. Am J Cardiol. 1977;39:21-26.
16. Pearson AC, Gudipati C, Nagelhout D, Sear J, Cone JD, Labovitz AJ. Echocardiographic evaluation of cardiac structure and function in elderly subjects with isolated systolic hypertension. J Am Coll Cardiol. 1991;17:422-430.[Abstract]
17. Roman MJ, Devereux RB, Kramer-Fox R, O'Loughlin J. Two-dimensional echocardiographic aortic root dimensions in normal children and adults. Am J Cardiol. 1989;64:507-512.[Medline] [Order article via Infotrieve]
18. Reed CM, Richey PA, Pulliam DA, Somes GW, Alpert BS. Aortic dimensions in tall men and women. Am J Cardiol. 1993;71:608-610.[Medline] [Order article via Infotrieve]
19.
Vasan RS, Larson MG, Levy D. Determinants of echocardiographic aortic root size. Circulation. 1995;91:734-740.
20. Krovetz LJ. Age-related changes in size of the aortic root. Am Heart J. 1975;90:569-574.[Medline] [Order article via Infotrieve]
21.
Gerstenblith G, Frederiksen J, Yin FCP, Fortuin NJ, Lakatta EG, Weisfeldt ML. Echocardiographic assessment of a normal aging population. Circulation. 1977;56:273-278.
22.
Henry WL, Gardin JM, Ware JH. Echocardiographic measurements in normal subjects from infancy to old age. Circulation. 1980;62:1054-1061.
23. Virmani R, Avolio AP, Mergner WJ, Robinowitz M, Herderick EE, Cornhill JF, Guo S-Y, Liu T-h, Ou D-Y, O'Rourke M. Effect of aging on aortic morphology in populations with high and low prevalence of hypertension and atherosclerosis. Am J Pathol. 1991;139:1119-1129.[Abstract]
24.
Savage DD, Dryer JM, Henry WL, Mathews EC Jr, Ware JH, Gardin JM, Cohen ER, Epstein SE, Laragh JH. Echocardiographic assessment of cardiac anatomy and function in hypertensive subjects. Circulation. 1979;59:623-632.
25.
Tell GS, Rutan GH, Kronmal RA, Bild DE, Polak JF, Wong ND, Borhani NO. Correlates of blood pressure in community-dwelling older adults. Hypertension. 1994;23:59-67.
26. DePace NL, Nestico PF, Kotler MN, Mintz GS, Kimbiris D, Goel IP, Glazier-Laskey EE, Ross J. Comparison of echocardiography and angiography in determining the cause of severe aortic regurgitation. Br Heart J. 1984;51:35-45.
27.
Francis GS, Hagan AD, Oury J, O'Rourke RA. Accuracy of echocardiography for assessing aortic root diameter. Br Heart J. 1975;37:376-378.
28. Davies MJ. Pathology of Cardiac Valves. Boston, Mass: Butterworth Publishers; 1980:37-61.
29. Devereux RB, Pickering TG, Harshfield GA, Kleinert HD, Denby L, Clark L, Pregibon D, Jason M, Kleiner B, Borer JS, Laragh JH. Left ventricular hypertrophy in patients with hypertension: importance of blood pressure response to regularly recurring stress. Circulation. 1983;69:470-476.
30.
Schnall PL, Schwartz JE, Landsbergis PA, Warren K, Pickering TG. Relation between job strain, alcohol and ambulatory blood pressure. Hypertension. 1992;19:488-494.
31. Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Association of carotid atherosclerosis and left ventricular hypertrophy. J Am Coll Cardiol. 1995;25:83-90.[Abstract]
32. Ciobanu M, Abbasi AS, Allen M, Hermer A, Spellberg R. Pulsed Doppler echocardiography in the diagnosis and estimation of severity of aortic insufficiency. Am J Cardiol. 1982;49:339-343.[Medline] [Order article via Infotrieve]
33. Perry GJ, Helmcke F, Nanda NC, Byard C, Soto B. Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Coll Cardiol. 1987;9:952-959.[Abstract]
34.
Cavallini MC, Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Is white coat hypertension associated with arterial disease or left ventricular hypertrophy? Hypertension. 1995;26:413-419.
35. Roman MJ, Pini R, Pickering TG, Devereux RB. Non-invasive measurements of arterial compliance in hypertensive compared with normotensive adults. J Hypertens. 1992;10(suppl 6):S115-S118.
36. Saba PS, Roman MJ, Pini R, Ganau A, Devereux RB. Relation of carotid pressure waveform to left ventricular anatomy in normotensive subjects. J Am Coll Cardiol. 1993;22:1873-1880.[Abstract]
37. Hamilton WF, Dow P. An experimental study of standing waves in the pulse propagated through the aorta. Am J Physiol. 1939;125:48-59.
38.
O'Rourke MF, Blazek JV, Morreels CL Jr, Krovetz LJ. Pressure wave transmission along the human aorta: changes with age and in arterial degenerative disease. Circ Res. 1968;23:567-579.
39.
Guiney TE, Davies MJ, Parker DJ, Leech GJ, Leatham A. The aetiology and course of isolated severe aortic regurgitation: a clinical, pathological, and echocardiographic study. Br Heart J. 1987;58:358-368.
40. Seder JD, Burke JF, Pauletto FJ. Prevalence of aortic regurgitation by color flow Doppler in relation to aortic root size. J Am Soc Echocardiogr. 1990;3:316-319.[Medline] [Order article via Infotrieve]
41. Nidorf SM, Picard MH, Triulzi MO, Thomas JD, Newee J, King ME, Weyman AE. New perspectives in the assessment of cardiac chamber dimensions during development and adulthood. J Am Coll Cardiol. 1992;19:983-988.[Abstract]
This article has been cited by other articles:
![]() |
E. Ingelsson, M. J. Pencina, D. Levy, J. Aragam, G. F. Mitchell, E. J. Benjamin, and R. S. Vasan Aortic Root Diameter and Longitudinal Blood Pressure Tracking Hypertension, September 1, 2008; 52(3): 473 - 477. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. F. Mitchell, P. R. Conlin, M. E. Dunlap, Y. Lacourciere, J. M. O. Arnold, R. I. Ogilvie, J. Neutel, J. L. Izzo Jr, and M. A. Pfeffer Response to Wave Reflection in Systolic Hypertension: Smaller Stature, Shorter Aorta: Higher Pulse Pressure? and Questions Regarding the Aortic Measurements of Mitchell et al Hypertension, May 1, 2008; 51(5): e39 - e40. [Full Text] [PDF] |
||||
![]() |
M. J. Roman and R. B. Devereux Questions Regarding the Aortic Measurements of Mitchell et al Hypertension, May 1, 2008; 51(5): e38 - e38. [Full Text] [PDF] |
||||
![]() |
P. De Mozzi, U. G. Longo, G. Galanti, and N. Maffulli Bicuspid aortic valve: a literature review and its impact on sport activity Br. Med. Bull., March 1, 2008; 85(1): 63 - 85. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. M. Farasat, C. H. Morrell, A. Scuteri, C.-T. Ting, F. C.P. Yin, H. A. Spurgeon, C.-H. Chen, E. G. Lakatta, and S. S. Najjar Pulse Pressure Is Inversely Related to Aortic Root Diameter Implications for the Pathogenesis of Systolic Hypertension Hypertension, February 1, 2008; 51(2): 196 - 202. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. S. Vasan Pathogenesis of Elevated Peripheral Pulse Pressure: Some Reflections and Thinking Forward Hypertension, January 1, 2008; 51(1): 33 - 36. [Full Text] [PDF] |
||||
![]() |
R. M. Lang, M. Bierig, R. B. Devereux, F. A. Flachskampf, E. Foster, P. A. Pellikka, M. H. Picard, M. J. Roman, J. Seward, J. Shanewise, et al. Recommendations for chamber quantification Eur J Echocardiogr, March 1, 2006; 7(2): 79 - 108. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Bekeredjian and P. A. Grayburn Valvular Heart Disease: Aortic Regurgitation Circulation, July 5, 2005; 112(1): 125 - 134. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. F. O'Rourke and W. W. Nichols Aortic Diameter, Aortic Stiffness, and Wave Reflection Increase With Age and Isolated Systolic Hypertension Hypertension, April 1, 2005; 45(4): 652 - 658. [Full Text] [PDF] |
||||
![]() |
Y. Agmon, B. K. Khandheria, I. Meissner, G. L. Schwartz, J. D. Sicks, A. J. Fought, W. M. O'Fallon, D. O. Wiebers, and A. J. Tajik Is aortic dilatation an atherosclerosis-related process?: Clinical, laboratory, and transesophageal echocardiographiccorrelates of thoracic aortic dimensions in the populationwith implications for thoracic aortic aneurysm formation J. Am. Coll. Cardiol., September 17, 2003; 42(6): 1076 - 1083. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. N. Bella, J. W. MacCluer, M. J. Roman, L. Almasy, K. E. North, T. K. Welty, E. T. Lee, R. R. Fabsitz, B. V. Howard, and R. B. Devereux Genetic Influences on Aortic Root Size in American Indians: The Strong Heart Study Arterioscler Thromb Vasc Biol, June 1, 2002; 22(6): 1008 - 1011. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. Palmieri, J. N. Bella, D. K. Arnett, M. J. Roman, A. Oberman, D. W. Kitzman, P. N. Hopkins, M. Paranicas, D. C. Rao, and R. B. Devereux Aortic Root Dilatation at Sinuses of Valsalva and Aortic Regurgitation in Hypertensive and Normotensive Subjects : The Hypertension Genetic Epidemiology Network Study Hypertension, May 1, 2001; 37(5): 1229 - 1235. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. E. Lebowitz, J. N. Bella, M. J. Roman, J. E. Liu, D. P. Fishman, M. Paranicas, E. T. Lee, R. R. Fabsitz, T. K. Welty, B. V. Howard, et al. Prevalence and correlates of aortic regurgitation in american indians: the Strong Heart Study J. Am. Coll. Cardiol., August 1, 2000; 36(2): 461 - 467. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. Palmieri, G. de Simone, M. J. Roman, J. E. Schwartz, T. G. Pickering, and R. B. Devereux Ambulatory Blood Pressure and M;etabolic Abnormalities in Hypertensive Subjects With Inappropriately High Left Ventricular Mass Hypertension, November 1, 1999; 34(5): 1032 - 1040. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1996 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |