(Hypertension. 1996;27:319-323.)
© 1996 American Heart Association, Inc.
Articles |
Comparison of Changes in Cardiac Structure After Treatment in Secondary Hypertension
From the Division of Hypertension and Kidney Disease, National Cardiovascular Center, Osaka, Japan.
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Abstract |
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Abstract To investigate the role of aldosterone and the renin-angiotensin system in cardiac structure, we performed echocardiography in patients with secondary hypertension. The relation between blood pressure or hormonal influences and left ventricular hypertrophy has not been well established in secondary hypertension. Sixteen patients with primary aldosteronism and 11 with unilateral renovascular hypertension who had completely normalized blood pressure after operation or percutaneous transluminal angioplasty were evaluated by echocardiography before and after surgery or other interventional treatment. Blood pressure was not statistically different between the groups before treatment and was normalized after treatment in both groups. Left ventricular hypertrophy was mild in both groups before treatment, and its degree was not statistically different between the groups. At the end of the follow-up period, all parameters of primary aldosteronism and left ventricular mass index in patients with unilateral renovascular hypertension were significantly reduced. In patients with primary aldosteronism, changes in end-diastolic left ventricular internal dimension correlated positively with changes in left ventricular mass index (r=.58, P<.01). In patients with unilateral renovascular hypertension, changes in mean blood pressure and left ventricular mass index were significantly correlated (r=.77, P<.01). The expanded plasma volume induced by an excess of aldosterone and high blood pressure may play an important role in the increase of left ventricular mass in primary aldosteronism. In unilateral renovascular hypertension, high blood pressure mainly contributes significantly to increased left ventricular mass. Therefore, different factors may modulate the development of left ventricular hypertrophy in patients with secondary hypertension.
Key Words: primary aldosteronism • hypertension, renovascular • echocardiography • renin • hypertrophy • aldosterone
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Introduction |
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In patients with chronic systemic arterial hypertension, LVH is common,1 but it remains unclear whether it is only the result of long-term elevations in arterial BP or is a manifestation of nonhemodynamic factors acting on the myocardium.2 Hypertensive patients frequently exhibit discrepancies between arterial pressure levels and the degree of LVH.3 Numerous quantitative and qualitative findings suggest that factors other than BP levels can modulate LVH development, especially neurohumoral influences. Khairallah and Kanabus4 documented a significant increase in ventricular weight after 6 days of infusing a mildly pressor dose of angiotensin II. A significant relationship between renin and LVH independent of BP has been found in spontaneously hypertensive rats.5 Morphometric and morphological findings in vitro and in vivo have linked arterial hypertension accompanied by elevated circulating aldosterone levels with an excessive accumulation of collagen, producing myocardial fibrosis.6 Some hypertensive patients may also have a degree of physiological or pathological volume overload that is imposed on the left ventricle by various factors.7 8
The relationship between BP or hormonal influences and LVH has not been well established in secondary hypertension. PA, which is characterized by volume dependency, low PRA, and suppressed angiotensin, differs from unilateral RVH in the pathogenesis of hypertension. In the present study, we assessed the effects of the renin-angiotensin system, aldosterone, and BP on LVH in hypertensive patients and compared the echocardiographic findings of the left ventricle in patients who had PA with the findings of those who had unilateral RVH, before treatment and at the end of the follow-up period. We excluded patients who had taken any antihypertensive drugs during the follow-up period because of the likelihood of complications with essential hypertension. We thus assessed the pure effect of renin angiotensin system and aldosterone on LVH in hypertensive patients.
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Methods |
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Patients
Our study was based on 44 patients with PA and 60 with RVH who were admitted to the National Cardiovascular Center in Japan. We excluded 28 patients with PA and 49 with RVH for the following reasons: suboptimal echocardiographic studies were obtained (5 patients with PA, 8 with RVH); the patient's clinical records revealed angina pectoris, prior myocardial infarction, valvular heart disease, or previous congestive heart failure (8 with PA, 12 with RVH); they had been treated with antihypertensive drugs after surgery or other interventional treatment (7 with PA, 22 with RVH); or they had moved out of the study area (8 with PA, 7 with RVH). The study population consisted of 16 patients with PA (5 men, 11 women) who had undergone adrenalectomy and 11 patients with unilateral RVH (4 men, 7 women) who had undergone balloon angioplasty or surgical revascularization.
Sixteen of the 27 patients had never taken antihypertensive drugs before treatment. Six patients with PA and 5 with unilateral RVH were taking antihypertensive drugs at the time of the initial evaluation. Three patients with PA were taking calcium antagonists (nifedipine) and 3 were taking spironolactone. Three patients with unilateral RVH were taking calcium antagonists (nifedipine) and 2 were taking ß-blockers (metoprolol, propranolol). BP and echocardiography were measured at least 2 weeks after discontinuation of any antihypertensive drugs during admission. After surgery or interventional treatment, BP was normalized and none of the patients received any antihypertensive drugs.
BP was determined by standard sphygmomanometric methods. Before treatment, BP was calculated by determining the mean of eight BP readings for 2 days measured with patients in the supine position on a regular salt diet (7 g NaCl daily). At the end of the follow-up period, a physician monitored BP and heart rate after patients had rested supine for at least 10 minutes on two visits in an outpatient clinic, and the two values were averaged.
The diagnosis of PA was based on hypokalemia, elevated plasma aldosterone concentration with no response to a saline suppression test, and low PRA levels.
Adenoma was documented by computed tomographic scanning of the adrenal gland and adrenal scintillation scanning and finally confirmed by surgical resection and pathological examination.9 The diagnosis of unilateral RVH was based on high levels of PRA, stimulation of PRA by captopril, and high renal vein PRA levels in the stenotic site. Stenosis of the renal artery (usually >75%) was documented by digital subtraction angiography or arteriography of the renal artery.9
Standard 12-lead electrocardiograms were recorded at 25 mm/s and 0.1 mV/mm standardization before treatment and at the end of follow-up. The standard criteria used for the electrocardiographic diagnosis of LVH were as follows: (1) the Sokolow and Lyon10 precordial voltage criteria (the sum of the S wave in V1 and R wave in V5 or V6 greater than 35 mm), or (2) four or more points based on the scoring system of Romhilt and Estes.11 The cardiothoracic ratio was calculated from the chest roentgenogram. This study was done after informed consent had been obtained from all patients.
Echocardiographic Examination
Before and after treatment,
M-mode
echocardiography was obtained by
two-dimensional monitoring with a phased-array ultrasonic
sector scanner (Hewlett-Packard 77020A) and a 2.5-MHz transducer or an
echocardiograph (Toshiba Sonolayer SSH-160A) and
transducers with an oscillator frequency of 2.5 or 3.75 MHz.
Strip-chart records were taken at a paper speed of 50 mm/s.
Patients were examined in a partial left lateral decubitus
position. LV chamber recording was obtained at the tip of the
mitral valve. Measurements of interventricular septal
thickness (IVST), posterior wall thickness (PWT), and LV internal
dimension measurements were made at end diastole (LVIDd)
and end systole (LVIDs), in accordance with the recommendations of the
American Society of
Echocardiography.12
LVM was calculated with the regression equation described by Devereux and Reichek,13 LVM=1.04x[(IVST+LVIDd+PWT)3-(LVIDd)3]-13.6. LVM/height2.7 was calculated with the allometric approach described by De Simone and colleagues.14 The percent change in LV internal dimension from end diastole to end systole was calculated (LV fractional shortening) to provide an index of myocardial performance. Two blinded observers made measurements for at least 3 consecutive cardiac cycles and the results were averaged.15 Intraobserver and interobserver reproducibilities were good, with correlations between LVM measurements of .96 and .91 (P<.001), respectively. When the between-observer difference was less than 2 mm for IVST or PWT and less than 3 mm for LVIDd or LVIDs, the measurements were accepted directly and averaged.
Assay
PRA and aldosterone concentration were determined
during admission before treatment under the condition of no
antihypertensive medications for at least 2 weeks. Blood samples for
PRA and aldosterone concentration were taken at 7
AM with the patient supine and on the last day of a 7-day
low sodium diet (7 g NaCl daily). PRA and aldosterone
concentration were measured by radioimmunoassays as previously
reported.16 17 Each hormone was measured twice before
treatment and after intervention and at the end of the follow-up
period, and the two values were averaged. Serum potassium and sodium
concentrations were also measured.
Statistics
Data are expressed as mean±SD. Statistical
analysis was
performed by Student's t test for paired and unpaired data
where appropriate. Linear regression analysis was used to
determine whether any correlation existed between the variables.
Differences were considered statistically significant at a value of
P<.05.
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Results |
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Patient Characteristics and Follow-up Data
Table 1
lists the clinical characteristics of
the PA and unilateral RVH groups. Age, sex, body surface area, and body
mass index distribution were similar in the two groups. Body surface
area and body mass index did not differ before and after treatment. The
mean duration of follow-up was similar in the two groups (6.9±4.3
years in the PA group and 5.8±2.8 years in the unilateral RVH
group).
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Significant reductions in systolic and diastolic
BPs occurred in the two groups after treatment (165±15/101±10 to
122±9/79±5 mm Hg for PA patients; 159±12/99±6 to
125±11/80±5
mm Hg for RVH patients); the difference between the groups was not
significant (Table 2).
Electrocardiography revealed no differences in
voltage or changes in ST segment and T wave before treatment between
the two groups. After treatment, significant reductions in
electrocardiographic voltages were seen in both groups. Cardiothoracic
ratio on chest roentgenogram before treatment was significantly greater
in patients with PA than in those with unilateral RVH, and the former
exhibited a significant reduction of the cardiothoracic ratio at the
end of the follow-up period.
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Echocardiographic Findings
The echocardiographic findings of
the two groups
are shown in Table 3.
Echocardiography before treatment revealed no
significant differences between the groups in parameters
such as interventricular septal thickness, posterior
wall thickness, left atrial and ventricular dimensions, LV
end-diastolic dimension index, LV
end-systolic dimension index, and LVMI. Both groups showed
mild LVH.
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At the end of the follow-up period, interventricular septal thickness, posterior wall thickness, left atrial and ventricular dimensions, and LVMI decreased significantly in patients with PA, whereas only LVMI decreased significantly after treatment in patients with unilateral RVH. Fractional shortening increased after treatment in PA patients. There was a significant difference between the two groups in the changes in LV end-diastolic dimension (-9.6±3.7% versus -2.1±3.9%, P<.01) and in LV end-diastolic index (-11.7±4.1% versus -3.0±3.9%, P<.01). Changes in LVMI in PA patients were greater than in those with unilateral RVH (-39±14% versus -18±17%, respectively; P<.01). Devereux et al18 reported that one criterion of LVH was an LVMI greater than 134 g/m2 in men and greater than 110 g/m2 in women. One patient with PA and two with unilateral RVH still had abnormal LVMI values after treatment.
In PA patients,
changes in end-diastolic LV internal
dimension correlated with changes in LVMI (r=.58,
P<.01) (Figure, a). Changes in mean BP were
not correlated with changes in LVMI (r=.17,
P=NS)
(Table 4). Plasma aldosterone concentration
before treatment was significantly correlated with changes in LVMI
(r=.63, P<.01) (Table 4). In
unilateral RVH
patients, changes in mean BP and changes in LVMI were significantly
correlated (r=.77, P<.01) (Figure,
b). We did
not observe any relationship between PRA and changes in LVMI
(r=.23, P=NS) (Table 4).
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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We compared cardiac structure in two different types of secondary hypertension, PA and unilateral RVH, using the noninvasive technique of echocardiography. PA, characterized by volume dependency, low PRA, and suppressed angiotensin, differs considerably from unilateral RVH, which is characterized by high renin activity and angiotensin. We evaluated the possible correlations between BP, presumed expanded plasma volume, aldosterone and PRA, and changes in LVH or ventricular anatomy. Our study indicates that the presumed expanded plasma volume induced by aldosterone excess in PA may play an important role in LVH as well as in BP. In unilateral RVH, however, only BP may mainly contribute to LVH.
A direct relationship between body fluid volumes and arterial pressure was indicated by a study of nephrectomized dogs.19 Ikäheimo et al20 reported that renal transplantation apparently reduced LV and left atrial volumes toward normal ranges and diminished LVH. In a natural volume-overload state (pregnancy), LV dimensions and LVMI increased during gestation and decreased postpartum.21 Some hypertensive patients may also have a component of volume overload imposed on the left ventricle by various factors.8 9 However, the relationship between volume overload and LVH in PA has not been established. According to LaPlace's law, LV dilatation increases ventricular wall stress. The left ventricle adapts by increasing muscle mass, causing the myocardial wall to thicken. LVH in PA may be reduced by decreasing volume overload. Denolle et al22 reported that patients with PA showed significant reductions in LVMI but no difference in LV end-diastolic dimension after resection of an adenoma. In patients with unilateral RVH and normal plasma volume and bilateral renal artery stenosis with vascular volume expansion, LV end-diastolic dimension was larger in those with bilateral compared with unilateral renal artery stenosis.23 Our PA patients showed significant decreases in LV end-diastolic dimension and a significantly higher cardiothoracic ratio on chest roentgenogram than unilateral RVH patients. Cardiothoracic ratio decreased after treatment only in PA patients. The reductions of LV end-diastolic dimension and LVMI were greater in PA than unilateral RVH patients. Thus, volume overload induced by aldosterone excess may play an important role in LVH in PA. Mirsky et al24 reported that at a low given afterload, fractional shortening increased at a low preload level in the dog, suggesting that fractional shortening is influenced by preload and afterload. Because both preload and afterload decreased in PA, fractional shortening might increase after treatment.
In in vivo studies, the degree of LVH was associated with the interacting effects of the hemodynamic component superimposed on the primary hemodynamic pattern in the high-resistance two-kidney, one clip rat. The interaction between pressure and volume increased LV wall thickness.25 26 A close correlation between the degree of LVH and BP levels was also found in rats with RVH.6 Early studies of selected patients suggested that postmortem LVM was closely related to systolic BP.27 Rowlands et al28 reported that systolic BP appears to be important in the pathogenesis of LVH and that echocardiographically assessed changes in LVM in hypertensive patients correlate with changes in BP. In several groups of patients with uncomplicated essential hypertension, systolic BP was only weakly related to echocardiographic LVM, with correlation coefficients of .24 to .45.29 30 However, some studies have compared the relationships between echocardiographically determined LVM and 24-hour BP measurement.28 31 BP may be important in the pathogenesis of LVH in unilateral RVH.
We previously reported that BP seemed to play an important role in LVH in PA and unilateral RVH,32 but we were unable to assess this relationship separately in these two conditions. Although we observed both groups only before treatment, we could not assess the importance of the renin-angiotensin system and aldosterone in LVH. In the present study, after the same patients had been observed before and after treatment, it became evident that BP seemed to contribute significantly to LVH in unilateral RVH. Furthermore, our results indicated that the decreases in LV end-diastolic dimension or plasma aldosterone concentration correlated more closely with the decrease in LVMI than with the decrease in BP in PA. Volume load rather than pressure load may play an important role in LVH in PA.
Neurohumoral influences, namely, the renin-angiotensin and adrenergic systems, seem to be particularly important in LVH. A connection between the renin-angiotensin system and cardiac hypertrophy was established by studies that demonstrated a close correlation between BP and cardiac weight in both untreated and treated rats with RVH.33 34 However, Buttrick et al35 found that PRA in the absence of pressure elevation did not play a primary role in increasing heart weight and defining the hypertrophic cardiac phenotype in rats. Pressure overload stimulated by the renin-angiotensin system increased heart weight and caused myosin isozyme shifts. In humans, a close relation between the renin-angiotensin system and cardiac hypertrophy is not necessarily clear, since Devereux et al36 reached a different conclusion after finding that in patients with similar levels of mild to moderate hypertension, the severity of LVH was equivalent in high-, normal-, and low-renin patients. These results suggest that the renin-angiotensin system does not play a major independent role in LVH in humans. We found no correlation between PRA and BP or LVMI in patients with unilateral RVH. Therefore, pressure overload stimulated by the renin-angiotensin system rather than the renin-angiotensin system itself may play a role in LVH in unilateral RVH.
In an experimental model, the aldosterone receptor antagonist spironolactone at a dose insufficient to reduce BP prevented perivascular/interstitial fibrosis and scarring. A larger spironolactone dose, which did reduce BP, prevented LVH.37 On the basis of clinical observations, Duprez et al38 reported a significant correlation between LVMI and plasma aldosterone concentration in essential hypertension. Nonmyocyte cells of the cardiac interstitium may play a major role in pathological LVH. Taken together, these results suggest that an excess of aldosterone may play an independent role in LVH. Attenuation of the effects of elevated circulating aldosterone levels by antialdosterone therapy may cause a regression of LVH in humans.
Potential limitations of the present study need to be considered. There were no significant differences between the patients with PA and those with unilateral RVH in LV end-diastolic dimension and index before treatment. In a previous report, LV end-diastolic dimension was not different in both groups, but LV end-diastolic dimension index was increased in the PA patients. This discrepancy may be partly explained by the small sample size compared with our previous report.32 After the same patients had been observed before and after treatment, however, significant differences were seen between the two groups in the changes in LV end-diastolic dimension, LV end-diastolic index, and LVMI. Aldosterone mediating expanded plasma volume and hypertension may play an important role in the increase of LVM in PA.
In conclusion, the present study has shown that in patients with PA, the expanded plasma volume induced by aldosterone excess seemed to contribute to LVH as well as BP. Further studies are needed to establish the exact mechanism by which aldosterone is directly involved in the development of LVH and whether aldosterone antagonists reduce LVH in PA. In unilateral RVH, however, BP plays an important role in the pathogenesis of LVH. Different factors may modulate the development of LVH in patients with secondary hypertension.
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Selected Abbreviations and Acronyms |
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Footnotes |
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Reprint requests to Toshio Nishikimi, MD, Division of Hypertension and Kidney Disease, National Cardiovascular Center, 5-7-1, Fujishirodai, Suita, Osaka 565, Japan.
Received April 3, 1995; first decision May 10, 1995; accepted November 7, 1995.
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References |
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