| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 1997;29:723-727.)
© 1997 American Heart Association, Inc.
Articles |
Left Ventricular Hypertrophy Precedes Other Target-Organ Damage in Primary Aldosteronism
The Second Department of Internal Medicine, Ehime (Japan) University School of Medicine.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
To elucidate whether there is a difference in the progression of target-organ damage between primary aldosteronism and essential hypertension, we compared left ventricular hypertrophy and extracardiac target-organ damage in 23 patients with primary aldosteronism and 116 patients with essential hypertension. The severity of hypertensive retinopathy and the renal involvement in primary aldosteronism were subclinical and similar to those in essential hypertension without left ventricular hypertrophy but significantly milder than those in essential hypertension with left ventricular hypertrophy. There was a strongly significant correlation between the degree of left ventricular mass index and the severity of hypertensive retinopathy and renal involvement independent of office blood pressure in essential hypertension. In contrast, left ventricular hypertrophy markedly progressed despite the mild extracardiac target-organ damage in primary aldosteronism. Left ventricular end-diastolic dimension index in primary aldosteronism (3.16±0.50 cm/m2) was significantly larger than in essential hypertension without (2.87±0.23) and with (2.88±0.22) left ventricular hypertrophy. On the other hand, there was no difference in extracardiac target-organ damage between 13 primary aldosteronism patients with eccentric left ventricular hypertrophy and the 26 essential hypertensive patients with eccentric left ventricular hypertrophy. The results suggest that predominantly volume load, be it due to aldosteronism or other mechanisms, resulting in eccentric left ventricular hypertrophy is less likely to cause extracardiac target-organ damage than hemodynamic or nonhemodynamic mechanisms resulting in concentric left ventricular hypertrophy.
Key Words: hyperaldosteronism • hypertension, essential • hypertrophy, left ventricular • hemodynamics
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The mineralocorticoid hormone aldosterone plays a key role in blood pressure homeostasis, the regulation of circulating volume, and the maintenance of sodium-potassium balance.1 Besides the action of aldosterone in the kidney, where it regulates electrolyte transport in renal tubules, several studies argue the direct action of aldosterone on the heart.2 3 4 It is still controversial whether cardiac structural changes in the clinical setting are due to long-term elevations in blood pressure or are a manifestation of nonhemodynamic factors acting on the myocardium.5 6
In animal models, both cardiac load and high circulating aldosterone levels regulate cardiac fibroblasts and result in excessive fibrous tissue accumulation in the myocardium that leads to pathological LVH.7 The fibrous tissue response, however, does not appear to be specific to the heart. A reactive fibrosis of the systemic vasculature has been reported with chronic aldosterone administration.8 Thus, aldosterone excess may play an important role in fibrosis of both the heart and systemic organs in experimental studies.
In EH, Duprez et al9 concluded that aldosterone seemed to play an important role in LVH independent of its relationship with arterial pressure. Moreover, we have shown that LVH and structural remodeling of the heart in EH progress in parallel with hypertensive retinopathy and renal involvement.10
Human aldosterone-producing adenoma, or PA, is relatively uncommon, and there is a paucity of information about the simultaneous effects of prolonged aldosterone excess on three major target organs—the heart, brain, and kidneys.
The purpose of the present study was severalfold: (1) to assess the effects of prolonged aldosterone stimulation on the heart, brain, and kidneys; (2) to evaluate the progression of major target-organ damage in patients with PA; and (3) to compare the target-organ damage associated with PA with that in EH patients.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Patients
The study population comprised 23 patients with PA and 116 (65 men and 51 women) with uncomplicated EH. The patients who had preexisting cardiac disease; preexisting medical illnesses, such as diabetes mellitus; or M-mode echocardiograms that were not sufficiently good for detection of clear internal lines of the interventricular septum and left ventricular (LV) posterior wall, were excluded from the analysis. Each patient gave informed consent to the protocol.
The diagnosis of PA was made by computed tomographic scanning of the adrenal gland, sampling of adrenal vein aldosterone, adrenal scintillation scanning, and the response of plasma renin activity to various stimuli. All PA patients were operated on, and the diagnosis was confirmed by histology. In all EH patients, a complete medical history and physical examination and appropriate laboratory evaluation failed to reveal a secondary cause for the hypertension.10 To match the LVH between PA patients and EH patients with LVH, we chose no subject whose LV mass index was greater than 140 g/m2. All participants either had never received antihypertensive therapy or had discontinued their medications at least 4 weeks previously.
Blood pressure was measured in triplicate by a single physician who was expert in the evaluation of hypertension using an appropriately sized arm cuff and mercury sphygmomanometer after patients had rested 5 minutes in the sitting position. The arithmetic mean of the last two measurements was calculated. Korotkoff phase V was taken for diastolic pressure. Hypertension was defined as systolic pressure greater than or equal to 140 mm Hg and/or diastolic pressure greater than or equal to 90 mm Hg.11
Hypertensive Retinopathy and Renal Involvement
Hypertensive retinopathy was assessed directly from funduscopy by a single ophthalmologist who was blinded to blood pressure levels and echocardiographic data. The funduscopic grades were classified according to the grading of Keith et al.12 Creatinine was analyzed by Jaffe's method (normal range of serum creatinine for our laboratory, 44.2 to 106.1 mmol/L). Serum uric acid was analyzed by the uricase-peroxidase method (normal range for our laboratory, 160.6 to 475.8 mmol/L). Electrolytes, serum creatinine, urinary creatinine, and serum uric acid were measured with an automatic analyzer (model TBA-60S, Toshiba Inc).
Neurohumoral Factors
A blood sample was taken at 7 AM on the day of echocardiographic examination from the brachial vein with patients in the supine position for 30 minutes after overnight fasting. Plasma renin activity and plasma aldosterone concentration were measured by radioimmunoassay kits (RIABEADS and RIAKIT II, respectively, Dinabot Co Ltd) as described previously.13 On the same day, 24-hour urine was collected for measurement of urinary epinephrine and norepinephrine by high-performance liquid chromatography with electrochemical detection.14
Echocardiographic Measurement
Echocardiographic studies were conducted by standard methods, as previously outlined,10 15 with an SSD-870 echocardiograph with a 3.5-MHz transducer (Aloka Inc) according to the recommendations of the American Society of Echocardiography.16 LV mass was estimated from the following formula of Devereux and Reichek17 (Penn convention): LV Mass (grams)=1.04x[(LVDd+IVST+PWT)3-(LVDd)3]-13.6, where LVDd is LV end-diastolic dimension, IVST is interventricular septal thickness, and PWT is posterior wall thickness. The LV end-diastolic dimension index and LV mass index were calculated for each patient by dividing LV end-diastolic dimension and LV mass by body surface area, respectively. Relative wall thickness was measured at end diastole as 2x(PWT/LVDd).18
Patterns of LV Geometry
LVH was defined as an LV mass index 2 SD or more above the mean value of normotensive control subjects. The cutoff values for LVH were 108 g/m2 in men and 104 g/m2 in women.10 The partition values of 0.44 for relative wall thickness, representing approximately the 99th percentile in normotensive control subjects, was used for both men and women.10 EH patients were grouped by LV mass index; 82 patients had LVH and 34 did not have LVH. LV mass indexes in EH patients with LVH were matched with those in PA patients. Patients with increased LV mass index and increased relative wall thickness were considered to have concentric LVH, and those with increased LV mass index and normal relative wall thickness were considered to have eccentric LVH.19
Statistical Analysis
All values are expressed as mean±SD. Statistical evaluation was performed by one-way ANOVA with subsequent Scheffe's multiple range tests. In addition, serum creatinine concentration and retinal funduscopic grade (treated as a continuous variable) were assessed by ANCOVA with age and duration of hypertension as covariates. Categorical variables were compared with Fisher's exact and 
2 tests. We performed a multivariate regression analysis to select appropriate independent variables producing the highest partial correlation with hypertensive retinopathy or renal involvement. Results were considered significant at a value of P<.05.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Clinical Profiles and Echocardiographic Characteristics
Clinical profiles, body mass index, and office systolic and diastolic pressures did not differ significantly among the three groups (Table 1
). PA patients were younger than patients in both EH groups. Duration of hypertension was also shorter in PA patients than in patients in both EH groups. Although relative wall thickness did not differ significantly among the three groups, LV end-diastolic dimension index in PA patients was larger than in both EH groups. Moreover, as shown in the Figure, the prevalence of eccentric LVH in PA patients (13 of 23, 57%) was significantly higher than in EH patients (26 of 116, 22%) (2=11.1, P<.01). On the other hand, the prevalence of concentric LVH in PA patients (2 of 23, 9%) was similar to that in EH patients (8 of 116, 7%) (2=0.93, P=NS).
|
|
Neurohumoral Factors and Electrolytes
Neurohumoral factors in 23 PA patients and 116 EH patients are shown in Table 2. There were no significant differences in 24-hour urinary epinephrine and norepinephrine excretions among the three groups. Plasma renin activity and serum potassium concentrations were lower in PA patients than in both EH groups, whereas sodium excretion in each group was similar. Plasma aldosterone concentrations in PA patients were higher than in both EH groups.
|
Hypertensive Retinopathy and Renal Involvement
Table 3 shows the hypertensive retinopathy in each group, which was found to be most strongly concentrated in EH patients with LVH. However, hypertensive retinopathy was minimal in PA patients and EH patients without LVH. As shown in Table 2
, serum creatinine concentration was highest in EH patients with LVH. There were no significant differences in serum creatinine concentration between PA patients and EH patients without LVH. Similarly, serum uric acid concentration was highest in male EH patients with LVH (422.3±83.3 mmol/L, P<.05). Serum uric acid concentrations did not differ significantly between male PA patients (339.0±53.5 mmol/L) and male EH patients without LVH (374.7±71.4 mmol/L). This difference was not found in women. Creatinine clearance in EH patients with LVH (76.3±26.9 mL/min, P<.05) was significantly lower than in PA patients (91.6±23.9 mL/min) and EH patients without LVH (81.3±26.0 mL/min). Moreover, as shown in Table 4, serum creatinine concentration and retinal funduscopic grade did not differ significantly among 13 PA patients with eccentric LVH and 26 EH patients with eccentric LVH.
|
|
Correlations Among Clinical Variables in Both Groups
Serum uric acid concentration and LV mass index correlated significantly in male EH patients (r=.34, P<.05). The results from a multivariate analysis are shown in Table 5. LV mass index and age were found to be significantly associated with serum creatinine concentration and retinal funduscopic grade in EH patients. However, in PA patients, age, LV mass index, relative wall thickness, office systolic and diastolic pressures, and body mass index were not associated with serum creatinine concentration and retinal funduscopic grade.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Our results indicate that the progression of damage in three major target organs is disparate among PA and EH patients. In PA patients, LVH preceded hypertensive retinopathy and hypertensive renal involvement.
There is a paucity of information in human subjects relating the effects of prolonged hypersecretion of aldosterone on target organs. Campbell et al20 reported that in five patients with adrenal adenoma proved by autopsy, reactive and/or reparative fibrosis was found in the heart, pancreas, adrenal glands, and lung but not in the kidneys or liver. This necropsy study supports our results that the influence of aldosterone on the heart preceded the influence on the kidneys and brain in PA patients.
It is well established that aldosterone plays an important role in the pathogenesis of cardiovascular fibrosis.7 21 22 23 24 Immunohistochemical studies of intact tissue have demonstrated the presence of mineralocorticoid receptors in the cardiovascular system, supporting the possibility of direct aldosterone actions in the heart and blood vessels.2 3 4 On the other hand, the main consequence of a prolonged hypersecretion of aldosterone is a potassium loss. In the animal model, hypokalemia induced by a potassium-free diet is associated with cardiac myocytolysis and subsequent reparative fibrosis.25 Furthermore, harmful effects of aldosterone also have been suggested indirectly by the results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS),26 which established that elevated plasma aldosterone was associated with the pathogenesis and progression of heart failure. Taken together, these observations indicate that direct and indirect aldosterone actions play an important role in the myocardial structural changes that lead to pathological hypertrophy.
The kidneys are one of the major target organs affected by hypertension. However, in the early stages of hypertension, patients usually are asymptomatic, and changes in serum creatinine concentration are within normal limits. Renal hemodynamic changes with a rising serum uric acid concentration are the most prominent early signs.27 Kobrin et al28 studied the correlation between serum uric acid concentration and echocardiographically determined LV mass index and indicated that the hemodynamic effect of EH in the heart preceded effects in the kidneys. In the present study, there was a strongly significant correlation between LV mass index and serum creatinine concentration in EH patients. There was also a weak but significant positive correlation between LV mass index and serum uric acid concentration in male EH patients. However, serum creatinine and serum uric acid concentrations in PA patients were significantly lower than those in EH patients with LVH, whereas LV mass indexes in both groups were similar. Thus, these observations clearly indicate that LVH precedes renal involvement in PA patients.
Because the retina is the only tissue in which the arteries and arterioles can be examined directly, ophthalmoscopic examination provides the opportunity for observing the progress of the vascular effects of sustained hypertension. Several studies have shown that retinal changes vary in parallel with the degree of LVH in EH.10 29 30 31 LVH is a potent sign of generalized preclinical disease.32 In contrast, the severity of hypertensive retinopathy in PA patients is low, and there is also no significant relation between the severity of hypertensive retinopathy and degree of LV mass index. This finding contrasts with findings in EH, in which higher grades of hypertensive retinopathy have been associated with higher LV mass index.
Eccentric LVH is uncommon in individuals younger than 50 years of age, but it occurs in 10% to 20% of hypertensive individuals older than 60 years.33 In the present study, there was a significant difference in the prevalence of eccentric LVH between PA patients (57%) and EH patients (24%). This might reflect the difference in plasma volume between the groups. In PA patients, aldosterone excess induces sodium-mediated volume expansion, reflected by the inhibition of renin release; and in parallel with these presumed alterations in plasma volume, LV structural changes progress.34 35 Recently, the concomitant level of hemodynamic volume load on the heart has been recognized as an important factor that regulates LV mass in hypertension independently of the effect of blood pressure.36 37 In the present study, office blood pressure also did not differ significantly between PA and EH patients. Given these observations, hemodynamic volume load on the heart may be a stronger determinant of LVH than blood pressure in PA. Furthermore, one possible mechanism that explains the precedence of LVH in PA appears to be in part the elevated hemodynamic volume load on the heart.
Hypertensive patients with concentric LVH are subject to frequent cardiovascular events associated with hypertension, as reported by Koren et al.38 Patients with concentric LVH have been found to have more advanced funduscopic abnormalities and greater involvement than other hypertensive patients.10 These findings agree with the result that concentric LVH associated with hypertension was related to increased total peripheral resistance.19 39 In the present study, the prevalence of eccentric LVH was high and that of concentric LVH was relatively low in PA. Therefore, these LV geometric characteristics seem likely to be associated with mild peripheral vascular damage in PA.
In conclusion, the present results suggest that predominantly volume load, be it due to aldosteronism or other mechanisms, resulting in eccentric LVH is less likely to cause extracardiac target-organ damage than hemodynamic or nonhemodynamic mechanisms resulting in concentric LVH.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Footnotes |
|---|
Reprint requests to Yuji Shigematsu, MD, The Second Department of Internal Medicine, Ehime University School of Medicine, Shigenobu-cho, Onsen-gun, Ehime 791-02, Japan.
Received March 18, 1996;
first decision April 18, 1996;
first decision September 4, 1996;
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Orth DN, Kovacs WJ, DeBold CR. The adrenal cortex. In: Wilson JD, Foster DW, eds. Williams Textbook of Endocrinology. Philadelphia, Pa: WB Saunders Co; 1992;8:489-619.
2. Pearce P, Funder JW. High affinity aldosterone binding sites (type I receptors) in rat heart. Clin Exp Pharmacol Physiol. 1987;14:859-866.[Medline] [Order article via Infotrieve]
3. Barnett CA, Pritchett EL. Detection of corticosteroid type I binding sites in heart. Mol Cell Endocrinol. 1988;56:191-198.[Medline] [Order article via Infotrieve]
4.
Lombes M, Oblin M-E, Gasc J-M, Baulieu EE, Farman N, Bonvalet J-P. Immunohistochemical and biochemical evidence for a cardiovascular mineralocorticoid receptor. Circ Res. 1992;71:503-510.
5. Frohlich ED, Tarazi RC. Is arterial pressure the sole factor responsible for hypertensive cardiac hypertrophy? Am J Cardiol. 1979;44:959-963.[Medline] [Order article via Infotrieve]
6. Frohlich ED. Left ventricular hypertrophy, cardiac diseases and hypertension: recent experiences. J Am Coll Cardiol. 1989;14:1587-1594.[Medline] [Order article via Infotrieve]
7.
Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium: fibrosis and renin-angiotensin-aldosterone system. Circulation. 1991;83:1849-1865.
8. Hall CE, Hall O. Hypertension and hypersalimentation, I: aldosterone hypertension. Lab Invest. 1965;14:285-294.[Medline] [Order article via Infotrieve]
9. Duprez DA, Bauwens FR, De Buyzere ML, De Backer TL, Kaufman JM, Hoecke JV, Vermeulen A, Clement DL. Influence of arterial blood pressure and aldosterone on left ventricular hypertrophy in moderate essential hypertension. Am J Cardiol. 1993;71:17A-20A.[Medline] [Order article via Infotrieve]
10. Shigematsu Y, Hamada M, Mukai M, Matsuoka H, Sumimoto T, Hiwada K. Clinical evidence for an association between left ventricular geometric adaptation and extracardiac target organ damage in essential hypertension. J Hypertens. 1995;13:155-160.[Medline] [Order article via Infotrieve]
11.
The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The fifth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V). Arch Intern Med. 1993;153:154-183.
12. Keith NM, Wagener HP, Barker MW. Some different types of essential hypertension: their course and prognosis. Am J Med Sci. 1939;197:332-343.
13. Dazai Y, Iwata T, Hiwada K. Augmentation of the renal tubular dopaminergic activity by oral calcium supplementation in patients with essential hypertension. Am J Hypertens. 1993;6:933-937.[Medline] [Order article via Infotrieve]
14.
Wu AHB, Gornet TG. Preparation of urine samples for lipid-chromatographic determination of catecholamines: bonded-phase phenylboronic acid, cation-exchange resin, and alumina adsorbents compared. Clin Chem. 1985;31:298-302.
15. Shigematsu Y, Hamada M, Mukai M, Matsuoka H, Sumimoto T, Hiwada K. Mechanism of atrial fibrillation and increased incidence of thromboembolism in patients with hypertrophic cardiomyopathy. Jpn Circ J. 1995;59:329-336.[Medline] [Order article via Infotrieve]
16.
Sahn DJ, DeMaria A, Kisslo J, Weyman A, The Committee on M-Mode Standardization of the American Society of Echocardiography. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation. 1978;58:1072-1083.
17.
Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method. Circulation. 1977;55:613-618.
18. Reichek N, Devereux RB. Reliable estimation of peak left ventricular systolic pressure by M-mode echocardiographic-determined end-diastolic relative wall thickness: identification of severe valvular aortic stenosis in adult patients. Am Heart J. 1982;103:202-209.[Medline] [Order article via Infotrieve]
19. Ganau A, Devereux RB, Roman MJ, De Simone G, Pickering TG, Sabe PS, Vargiu P, Simongini I, Laragh JH. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol. 1992;19:1550-1558.[Abstract]
20. Campbell SE, Diaz-Arias AA, Weber KT. Fibrosis of the human heart and systemic organs in adrenal adenoma. Blood Pressure. 1992;1:149-156.[Medline] [Order article via Infotrieve]
21.
Brilla CG, Pick R, Tan LB, Janicki JS, Weber KT. Remodeling of the rat right and left ventricles in experimental hypertension. Circ Res. 1990;67:1355-1364.
22. Young M, Fullerton M, Dilley R, Funder J. Mineralocorticoids, hypertension, and cardiac fibrosis. J Clin Invest. 1994;93:2578-2583.
23.
Robert V, Van Thiem N, Cheav SL, Mouas C, Swynghedauw B, Delcayre C. Increased cardiac types I and III collagen mRNAs in aldosterone-salt hypertension. Hypertension. 1994;24:30-36.
24. Robert V, Silvestre J-S, Charlemagne D, Sabri A, Trouve P, Wassef M, Swynghedauw B, Delcayre C. Biological determinants of aldosterone-induced cardiac fibrosis in rats. Hypertension. 1995;26(part 1):971-978.
25. Darrow D, Miller HC. The production of cardiac lesions by repeated injections of desoxycorticosterone acetate. J Clin Invest. 1942;21:601-611.
26.
Swedberg K, Eneroth P, Kjekshus J, Wilhelmsen L. Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. Circulation. 1990;82:1730-1736.
27. Messerli FH, Frohlich ED, Dreslinski GR, Suarez DH, Aristimuno GG. Serum uric acid in essential hypertension: an indicator of renal vascular involvement. Ann Intern Med. 1980;93:817-821.
28.
Kobrin I, Frohlich ED, Ventura HO, Messerli FH. Renal involvement follows cardiac enlargement in essential hypertension. Arch Intern Med. 1986;146:272-276.
29. Dimmitt SB, West JNW, Eames SM, Gibson JM, Gosling P, Littler WA. Usefulness of ophthalmoscopy in mild to moderate hypertension. Lancet. 1989;1:1103-1105.[Medline] [Order article via Infotrieve]
30. Dahlof B, Stenkula S, Hansson L. Hypertensive retinal vascular changes: relationship to left ventricular hypertrophy and arteriolar changes before and after treatment. Blood Pressure. 1992;1:35-44.[Medline] [Order article via Infotrieve]
31. De Leonardis V, Becucci A, De Scalzi M, Cinelli P. Low incidence of cardiac hypertrophy in essential hypertensives with no retinal changes. Int J Cardiol. 1992;35:95-99.[Medline] [Order article via Infotrieve]
32. Devereux RB, Alderman MH. Role of preclinical cardiovascular disease in the evolution from risk factor exposure to development of morbid events. Circulation. 1993;88(part 1):1444-1455.
33. Savage DD, Garrison RJ, Kannel WB, Levy D, Anderson SJ, Stokes J III, Feinleib M, Castelli WP. The spectrum of left ventricular hypertrophy in a general population sample: the Framingham Study. Circulation. 1987;75(suppl I):I-26-I-33.
34. Tarazi RC, Ibrahim MM, Bravo EL, Dustan HP. Hemodynamic characteristics of primary aldosteronism. N Engl J Med. 1973;289:1330-1335.
35. Suzuki T, Abe H, Nagata S, Saitoh F, Iwata S, Ashizawa A, Kuramochi M, Omae T. Left ventricular structural characteristics in unilateral renovascular hypertension and primary aldosteronism. Am J Cardiol. 1988;62:1224-1227.[Medline] [Order article via Infotrieve]
36.
Ganau A, Devereux RB, Pickering TG, Roman MJ, Schnall PL, Santucci S, Spitzer MC, Laragh JH. Relation of left ventricular hemodynamic load and contractile performance to left ventricular mass in hypertension. Circulation. 1990;81:25-36.
37. Leenen FHH, Tsoporis J. Cardiac volume load as a determinant of the response of cardiac mass to antihypertensive therapy. Eur Heart J. 1990;11(suppl G):100-106.
38. Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med. 1991;114:345-352.
39. Dunn FG, Chandraratna P, de Carvalho JG, Basta LL, Frohlich ED. Pathophysiologic assessment of hypertensive heart disease with echocardiography. Am J Cardiol. 1977;39:789-795.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  E. Born-Frontsberg, M. Reincke, L. C. Rump, S. Hahner, S. Diederich, R. Lorenz, B. Allolio, J. Seufert, C. Schirpenbach, F. Beuschlein, et al. Cardiovascular and Cerebrovascular Comorbidities of Hypokalemic and Normokalemic Primary Aldosteronism: Results of the German Conn's Registry J. Clin. Endocrinol. Metab., April 1, 2009; 94(4): 1125 - 1130. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Reincke, L. C. Rump, M. Quinkler, S. Hahner, S. Diederich, R. Lorenz, J. Seufert, C. Schirpenbach, F. Beuschlein, M. Bidlingmaier, et al. Risk Factors Associated with a Low Glomerular Filtration Rate in Primary Aldosteronism J. Clin. Endocrinol. Metab., March 1, 2009; 94(3): 869 - 875. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. L. Muiesan, M. Salvetti, A. Paini, C. Agabiti-Rosei, C. Monteduro, G. Galbassini, E. Belotti, C. Aggiusti, D. Rizzoni, M. Castellano, et al. Inappropriate Left Ventricular Mass in Patients With Primary Aldosteronism Hypertension, September 1, 2008; 52(3): 529 - 534. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Catena, G. Colussi, R. Lapenna, E. Nadalini, A. Chiuch, P. Gianfagna, and L. A. Sechi Long-Term Cardiac Effects of Adrenalectomy or Mineralocorticoid Antagonists in Patients With Primary Aldosteronism Hypertension, November 1, 2007; 50(5): 911 - 918. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Fallo, F. Veglio, C. Bertello, N. Sonino, P. Della Mea, M. Ermani, F. Rabbia, G. Federspil, and P. Mulatero Prevalence and Characteristics of the Metabolic Syndrome in Primary Aldosteronism J. Clin. Endocrinol. Metab., February 1, 2006; 91(2): 454 - 459. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. S. Vasan, J. C. Evans, E. J. Benjamin, D. Levy, M. G. Larson, J. Sundstrom, J. M. Murabito, F. Sam, W. S. Colucci, and P. W. F. Wilson Relations of Serum Aldosterone to Cardiac Structure: Gender-Related Differences in the Framingham Heart Study Hypertension, May 1, 2004; 43(5): 957 - 962. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. F. Young Jr. Minireview: Primary Aldosteronism--Changing Concepts in Diagnosis and Treatment Endocrinology, June 1, 2003; 144(6): 2208 - 2213. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. Rossi, V. Di Bello, C. Ganzaroli, A. Sacchetto, M. Cesari, A. Bertini, D. Giorgi, R. Scognamiglio, M. Mariani, and A. C. Pessina Excess ldosterone Is Associated With Alterations of Myocardial Texture in Primary Aldosteronism Hypertension, July 1, 2002; 40(1): 23 - 27. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. H. El-Gharbawy, V. S. Nadig, J. M. Kotchen, C. E. Grim, K. B. Sagar, M. Kaldunski, P. Hamet, Z. Pausova, D. Gaudet, F. Gossard, et al. Arterial Pressure, Left Ventricular Mass, and Aldosterone in Essential Hypertension Hypertension, March 1, 2001; 37(3): 845 - 850. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Kodama, Y. Shigematsu, M. Hamada, K. Hiwada, Y. Kazatani, K. Matsuzaki, and E. Murakami The Effect of Coronary Vasospasm on the Direction of ST-Segment Deviation in Patients With Both Hypertrophic Cardiomyopathy and Vasospastic Angina Chest, May 1, 2000; 117(5): 1300 - 1308. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Rizzoni, M. L. Muiesan, E. Porteri, M. Salvetti, M. Castellano, G. Bettoni, G. Tiberio, S. M. Giulini, C. Monteduro, G. Garavelli, et al. Relations between cardiac and vascular structure in patients with primary and secondary hypertension J. Am. Coll. Cardiol., October 1, 1998; 32(4): 985 - 992. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||