(Hypertension. 1996;28:22-30.)
© 1996 American Heart Association, Inc.
Articles |
Relationship Between Left Ventricular Geometry and Natriuretic Peptide Levels in Essential Hypertension
the Division of Hypertension and Nephrology (T.N., F.Y., A.M., K.I., T.I., T.O., H. Matsuoka) and Research Institute (Y.S., K.K., H. Matsuo), National Cardiovascular Center, Osaka, Japan.
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Abstract |
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Previous studies have shown that plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are increased in essential hypertension. However, whether left ventricular geometry affects plasma ANP and BNP levels remains unknown. To investigate the effect of left ventricular geometry on plasma ANP and BNP levels in essential hypertension, we measured plasma ANP and BNP levels in 90 patients with essential hypertension. All patients were hospitalized, and fasting blood samples were obtained in the early morning after 30 minutes of bed rest. Plasma ANP and BNP levels were measured by immunoradiometric assay. Hypertensive patients were classified into four groups according to echocardiographic findings that showed normal geometry, concentric remodeling, eccentric hypertrophy, or concentric hypertrophy. Mean plasma ANP and BNP levels in all essential hypertensive patients were higher than those in age-matched normotensive control subjects. Plasma ANP levels in hypertensive patients with concentric remodeling, eccentric hypertrophy, and concentric hypertrophy were higher than in normotensive control subjects, although there were no differences between normotensive subjects and hypertensive patients with normal geometry. Plasma BNP levels tended to be higher in hypertensive patients with normal geometry, concentric remodeling, and eccentric hypertrophy than in normotensive control subjects; however, the differences were not significant. Plasma BNP levels and BNP/ANP ratio were specifically higher in concentric hypertrophy. There were significant correlations between ANP and left ventricular mass index, relative wall thickness, interventricular septal thickness, posterior wall thickness, and mean arterial pressure. Plasma BNP levels significantly correlated with relative wall thickness, interventricular septal thickness, posterior wall thickness, and left ventricular mass index but not with mean arterial pressure. In addition, plasma BNP levels were well correlated with ANP levels, and the slope for the linear regression model was steeper in concentric hypertrophy than in the other four groups. These results show that plasma ANP and BNP levels are increased in essential hypertensive patients with left ventricular hypertrophy. Furthermore, BNP secretion is augmented to a greater extent in concentric hypertrophy. Thus, measurement of plasma ANP and BNP levels may be useful for the detection of concentric left ventricular hypertrophy in patients with essential hypertension.
Key Words: hypertrophy • hypertension, essential • natriuretic peptides
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Introduction |
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One of the complications of hypertension, LVH, is known to be an independent risk factor for all of the cardiovascular complications of hypertension.1 Therefore, its early detection is very important in the management of the hypertensive patient. LVH in essential hypertension presents in one of two patterns: concentric hypertrophy and eccentric hypertrophy.2 It has been reported that the prevalence of death or cardiovascular complications associated with hypertension was higher in hypertensive patients with concentric hypertrophy than in other groups, including patients with eccentric hypertrophy.3 Shigematsu et al4 recently reported that hypertensive patients with concentric LVH had the most advanced extracardiac target-organ damage compared with other groups. These findings suggest that early diagnosis of concentric hypertrophy in essential hypertension and intensive antihypertensive treatment for these patients are very important.
Electrocardiography, the standard method of recognizing LVH, is recommended for the assessment of every hypertensive patient. However, electrocardiography detects LVH in only a minority of the cases in which it is identified by echocardiography. Furthermore, only 3% to 8% of patients with uncomplicated hypertension of mild to moderate severity are identified at autopsy or on echocardiography as having LVH.5 6 Although echocardiography provides information about the structure and function of the left ventricle and is more sensitive than electrocardiography for the diagnosis of LVH, the results may not be adequate in all patients, especially in those with obesity or pulmonary disease.
ANP is a cardiac hormone that has diuretic, natriuretic, and vasodilator actions.7 The pathophysiological significance of increased plasma ANP levels has been reported in various diseases, such as heart failure and renal failure.8 Previous reports have shown that mean plasma ANP levels in hypertensive patients are higher than in normotensive subjects, although values overlapped between the two groups.9 10 11 BNP, which was first isolated from the porcine brain, has a striking similarity to ANP with regard to both its amino acid sequence and pharmacological spectrum.12 BNP is also produced by the heart and is secreted mainly from the ventricle in humans.13 It has been reported that plasma BNP levels are increased in heart failure,13 myocardial infarction,14 15 and hypertrophic cardiomyopathy.16 Several reports have shown that plasma BNP levels are also higher in patients with essential hypertension compared with normotensive subjects despite significant overlap between the two groups.17 18 19 20 However, there have been few reports regarding the relationships between LVH and ANP and BNP in hypertension. It has been reported that plasma ANP levels are increased in hypertensive patients with LVH determined by electrocardiography.21 It has also been shown that plasma BNP levels are increased in patients with greater LV mass determined by echocardiography.18 However, the effects of LV geometry on plasma ANP and BNP levels in hypertension remain unknown. In the present study, we investigated the effects of LV geometry on plasma ANP and BNP levels by measuring these levels in hypertensive patients with or without LVH.
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Methods |
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Patients
Ninety patients with essential hypertension were studied after informed consent was obtained (56±12 years of age; 46 men, 44 women). Blood pressure was measured at least three times at outpatient clinics; hypertension was defined as systolic pressure greater than or equal to 160 mm Hg, diastolic pressure greater than or equal to 95 mm Hg, or both. A diagnosis of essential hypertension was established by medical history; physical examination; hormone measurements, including PRA and aldosterone, catecholamine, and cortisol levels; and other screening tests. All patients were hospitalized and administered a 7-g sodium diet. Patients enrolled in the study either had never been treated for hypertension, or if treated, discontinued antihypertensive therapy at least 1 week before study. Before blood sampling, heart rate and blood pressure were measured in the morning (8 to 9 AM) after patients had fasted overnight and rested supine for 30 minutes. Blood was then withdrawn via the antecubital vein. All patients had normal cardiac sinus rhythm.
Blood was immediately transferred into two chilled glass tubes, one containing disodium EDTA (1 mg/mL) and aprotinin (500 U/mL) for measurement of plasma ANP and BNP and the other containing disodium EDTA (1 mg/mL) for measurement of PRA and plasma aldosterone levels. Blood was centrifuged immediately at 4°C, and the plasma was frozen and stored at -80°C until assayed. Age- and sex-matched normotensive subjects (50±10 years of age; 28 men, 22 women) who had no history of hypertension and no evidence of cardiac disease served as controls.
Assays for ANP, BNP, PRA, and Aldosterone
Plasma ANP levels were measured with a specific immunoradiometric assay (Shiono RIA ANP assay kit, Shionogi Co, Ltd) as previously reported.22 This assay system uses two monoclonal antibodies against 
-human ANP, one recognizing a carboxy-terminal sequence and the other the ring structure of ANP, and measures -human ANP by sandwiching it between the two antibodies without extraction of plasma. The minimal detectable quantity of -human ANP is 5 pg/mL. The correlation between the plasma level of -human ANP measured by this method and that by the extraction method was highly significant, in the range of 20 to 1500 pg/mL (r=.97, P<.001). The cross-reactivity with human BNP was less than 0.001% on a molar basis. Plasma levels of BNP were measured with a highly sensitive immunoradiometric assay (Shiono RIA BNP assay kit, Shionogi Co) as previously reported.23 24 25 This assay system uses two monoclonal antibodies against human BNP, one recognizing a carboxy-terminal sequence and the other the ring structure of human BNP, and measures human BNP by sandwiching it between the two antibodies without extraction of plasma. The minimal detectable quantity of human BNP is 2 pg/mL. The correlation between the plasma level of human BNP measured by this method and that by the extraction method was highly significant, in the range of 0 to 1500 pg/mL (r=.98, P<.001). Cross-reactivity for -human ANP was less than 0.001% on a molar basis. The plasma samples frozen at -80°C were stable for the assays for more than 20 days after sampling, and all samples were measured within 4 weeks after sampling. PRA was measured by radioimmunoassay (Renin RIA Beads, Dinabot Co, Ltd); plasma aldosterone levels were measured by radioimmunoassay with an aldosterone assay kit (Shionogi Co).
Echocardiographic Examination
M-mode echocardiography was obtained by two-dimensional monitoring with a phased-array ultrasonic sector scanner (77020A, Hewlett-Packard) and a 2.5-MHz transducer or Toshiba Sonolayer SSH-160A echocardiograph and transducers with an oscillator frequency of 2.5 or 3.75 MHz. The strip-chart records were taken at a paper speed of 50 mm/s. The patients were examined in the partial left lateral decubitus position. LV chamber recording was obtained at the tip of the mitral valve. IVST and PWT were measured at end diastole, and left atrial diameter was measured at end systole. LV internal dimensions were made at end diastole (LVIDd) and end systole (LVIDs), in accordance with the recommendations of the American Society of Echocardiography.26
LV mass was calculated with the regression equation described by Devereux and Reichek27 : LV Mass=1.04[(IVST+LVIDd+PWT)3-(LVIDd)3]-13.6. LVMI, percent fractional shortening, and RWT were calculated by standard formulas. Upper normal limits for LVMI at our institution are 114 and 106 g/m2 for males and females, respectively. Patients with increased LVMI were considered to have concentric hypertrophy if their RWT was 0.44 or greater. If this ratio was less than 0.44, the hypertrophy was considered to be eccentric. Patients with normal LVMI and increased RWT greater than 0.44 were considered to have concentric remodeling, and patients with normal LVMI and RWT less than 0.44 were considered to have normal geometry.
Pulsed Doppler examination of transmitral flow was recorded from the apical four-chamber view as previously reported.28 The sample volume was placed in the LV inflow tract between the mitral annulus and the tips of the mitral leaflets. This position was adjusted to maintain the sample volume at an angle that was as parallel as possible to the transmitral flow by using the audible signal and spectral display. When the maximum peak velocity in early diastole was detected, the velocity profile was recorded at a paper speed of 50 mm/s. The peak velocities in early diastole (E) and late diastole (A) were then measured from three to five consecutive cardiac systoles displaying the highest measurable profiles. The average of each respective peak velocity was calculated, and the ratio of peak velocities, A/E, was determined.
Statistics
Data are expressed as mean±SD. Comparisons between groups were performed by one-way ANOVA. The significance of differences between the mean values in the control group and each hypertension group were tested with Duncan's multiple comparison test. Correlation coefficients were calculated by linear regression analysis. Comparisons between normotensive subjects and all hypertensive patients were done by unpaired t test. ANCOVA was used for comparison of the slopes of regression lines. Multiple regression analysis was applied for analysis of the dependency between variables. A value of P<.05 was considered statistically significant.
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Table 1
shows the clinical characteristics, blood pressure, heart rate, serum creatinine, PRA, and plasma aldosterone, plasma sodium, and plasma potassium levels for normotensive control subjects and the four hypertensive groups. There were no differences in age, proportion of female subjects, heart rate, serum creatinine, PRA, plasma aldosterone, plasma sodium, and plasma potassium between the five groups. Hypertensive patients had significantly higher blood pressures than normotensive subjects. Patients in the LVH groups appeared to have higher blood pressures than those in the non-LVH group, but the differences were not significant.
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Table 2 shows echocardiographic data. LV internal diameters at end diastole and end systole were greater in the eccentric hypertrophy group than the other three groups, whereas they were smaller in the concentric remodeling group than the normal geometry group. IVST, PWT, and RWT were greater in the concentric hypertrophy group than the other three groups. LVMI was greater in the eccentric and concentric hypertrophy groups than in the normal geometry and concentric remodeling groups. Percent fractional shortening and left atrial dimension were similar among the four groups. A/E ratio was greater in the eccentric and concentric hypertrophy groups than in the normal geometry group. A and E did not differ among the four groups.
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Fig 1 shows plasma ANP and BNP levels in normotensive subjects and all hypertensive patients. Plasma ANP and BNP levels were higher in all hypertensive patients compared with normotensive subjects. Fig 2 shows plasma ANP (left) and BNP (middle) levels in the normotensive subjects and four hypertensive patient groups. Plasma ANP levels in hypertensive patients with concentric remodeling were higher than in normotensive subjects. Plasma ANP levels in the groups with eccentric hypertrophy and concentric hypertrophy were higher than in normotensive subjects and hypertensive patients with normal geometry. Plasma BNP levels in hypertensive patients with normal geometry, concentric remodeling, and eccentric hypertrophy tended to be higher than in the normotensive control group; however, the differences were not significant. In particular, plasma BNP levels in the concentric hypertrophy group were markedly increased compared with the other four groups. Fig 2 also shows the BNP/ANP ratio (right) for the five groups. This ratio was similar between the normotensive subjects and hypertensive patients with normal geometry, concentric remodeling, and eccentric hypertrophy. However, this ratio markedly increased in the concentric hypertrophy group.
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P<.05,
Fig 3 shows the relationships between plasma ANP levels and LVMI, RWT, IVST, and PWT, which were significant in all cases (LVMI, r=.49; RWT, r=.46; IVST, r=.40; PWT, r=.43; all P<.001). Fig 4 shows the relationships between plasma BNP levels and LVMI, RWT, IVST, and PWT, which were significant in all cases (LVMI, r=.50; RWT, r=.66; IVST, r=.59; PWT, r=.61; all P<.001). There was a weak correlation between plasma ANP and mean arterial pressure (r=.25, P<.05), but plasma BNP levels did not correlate with mean arterial pressure. Fig 5 shows the relationships between BNP/ANP ratio and LVMI, RWT, IVST, and PWT. There was a weak but statistically significant correlation between BNP/ANP ratio and LVMI compared with the correlation between BNP/ANP ratio and RWT, IVST, and PWT (LVMI, r=.45; RWT, r=.63; IVST, r=.56; PWT, r=.57; all P<.001). There were no significant relationships between plasma ANP levels and the diastolic function indexes A/E, A, or E (A/E, r=.02; A, r=.17; E, r=.12; all P=NS). There also were no significant relationships between plasma BNP levels and these diastolic function indexes (A/E, r=.11; A, r=.08; E, r=-.11; all P=NS).
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Fig 6 shows the relationship between plasma BNP and ANP levels in normotensive subjects and each group of hypertensive patients. There was a good correlation between plasma BNP and ANP levels in all patients (r=.75, P<.001). Correlations were weak between plasma BNP and ANP levels in the group of normotensive control subjects and hypertensive patients with normal geometry. In patients with concentric remodeling, eccentric hypertrophy, and concentric hypertrophy, there were good correlations between plasma BNP and ANP levels. The slope for the linear regression model for the group with concentric hypertrophy was steeper than that for the other three groups (P<.05).
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Fig 7 shows the distribution of plasma ANP and BNP levels in normotensive control subjects and hypertensive patients with normal geometry, concentric remodeling, eccentric hypertrophy, and concentric hypertrophy. Ninety-four percent of normotensive subjects showed plasma ANP and BNP levels in the normal range (mean±2 SD). Eighty-nine percent of hypertensive patients with normal geometry had normal plasma ANP levels; 83% of patients with normal geometry had normal plasma BNP levels; and 11% and 17% of those patients had plasma ANP and BNP levels, respectively, above the upper limit of normal. Sixty-six percent of patients with concentric remodeling had normal plasma ANP and BNP levels. Plasma ANP and BNP levels in patients with eccentric hypertrophy were in the normal range in 64% of the patients. In contrast, 44% and 28% of patients with concentric hypertrophy had plasma ANP and BNP levels, respectively, in the normal range. Plasma ANP ranged widely, with 41% of the values between the upper normal limit and two times the upper normal limit, 9% between two and three times the upper normal limit, and 6% greater than three times the upper normal limit. Plasma BNP also ranged widely, with 28% between the upper normal limit and two times the upper limit, 9% between two and three times the upper normal limit, and 35% greater than three times the upper normal limit. Thus, about 44% of patients with concentric hypertrophy had plasma BNP levels that were greater than two times the upper normal limit.
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Tables 3 and 4 present the results of multiple regression analyses assessing the association of LVMI, RWT, systolic pressure, and A with plasma ANP and BNP levels. LVMI independently correlated with plasma ANP levels, whereas RWT and LVMI independently correlated with plasma BNP levels.
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The sensitivity of an ANP value 
25 pg/mL for predicting LVH in all hypertensive patients was 44%, with a specificity of 88%. The sensitivity of a BNP value 18 pg/mL for predicting LVH in all hypertensive patients was 60%, with a specificity of 82%. The sensitivity of an ANP value 25 pg/mL for predicting concentric hypertrophy in all hypertensive patients was 69%, with a specificity of 76%. The sensitivity of a BNP value 18 pg/mL for predicting concentric hypertrophy in all hypertensive patients was 75%, with a specificity of 74%. The sensitivity of an ANP value 25 pg/mL for predicting eccentric hypertrophy in all hypertensive patients was 40%, with a specificity of 60%. The sensitivity of a BNP value 18 pg/mL for predicting eccentric hypertrophy in all hypertensive patients was 40%, with a specificity of 54%.
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Discussion |
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In the present study, we showed that plasma ANP and BNP levels are increased in essential hypertensive patients with LVH and that plasma BNP levels and the BNP/ANP ratio are specifically higher in concentric hypertrophy than eccentric hypertrophy despite comparable blood pressures and LVMI values. These results suggest that there is a relationship between LV geometry and ANP and BNP secretion in hypertension. Measurement of plasma ANP and BNP levels may therefore be useful for the detection of LVH in hypertensive patients. Furthermore, plasma BNP levels that are more than twofold higher than the upper limit of normal and higher BNP/ANP ratios may be indications of concentric LVH in patients with essential hypertension. Thus, measurement of plasma ANP and BNP levels may be useful in determining which patients will need intensive antihypertensive treatment.
ANP is released by the atria and has diuretic, natriuretic, and vasodilator actions.7 It has been reported that plasma ANP levels are higher in essential hypertensive than in normotensive individuals, although the values overlap.9 10 11 A considerable overlap in the distribution of ANP among the groups also was observed in the present study. The increased ANP levels in hypertension were considered to act as a feedback mechanism to increase sodium excretion and decrease elevated blood pressure. With the development of LVH in hypertension, LV compliance decreases, leading to increased atrial work.29 Atrial stretch due to increased atrial work is a major stimulus for ANP release, and hypertensive patients with LVH therefore have higher ANP levels. In this study, there were weak but statistically significant correlations between plasma ANP levels and LVMI, IVST, PWT, and RWT. Multiple regression analysis revealed that LVMI correlated independently with plasma ANP levels. These relatively weak correlations, as well as the overlap in the distributions in ANP values among the groups, may be partly explained by the fact that the effects of LVH on plasma ANP levels are indirect because other factors such as blood pressure, body fluid volume, sodium intake, renal function, and age also are involved in stimulating ANP secretion.21 30 31 32
BNP was first isolated in porcine brain,12 but the main site of BNP secretion is thought to be the left ventricle in humans.13 It has been reported that plasma BNP levels are considerably elevated in heart failure13 and plasma BNP levels are inversely correlated with LV ejection fraction and positively correlated with LV end-systolic and end-diastolic volumes in patients with heart failure.33 Another study has shown that plasma BNP levels are markedly elevated in patients with hypertrophic cardiomyopathy.16 These findings suggest that LV dysfunction or LVH may be associated with greater BNP secretion. With respect to hypertension, a few reports have shown that plasma BNP levels are increased in patients with essential hypertension compared with normotensive subjects.17 18 19 20 Kohno et al18 have reported that plasma BNP levels are increased in hypertension with increased LV mass and that plasma BNP levels are closely correlated with LVMI, with a correlation coefficient of .91. These findings are partly consistent with the results of the present report. We extended our investigation by demonstrating that plasma BNP levels and BNP/ANP ratio are greater in concentric hypertrophy than eccentric hypertrophy, despite the fact that LVMI and blood pressures were comparable between the two LVH groups. In addition, multiple regression analysis revealed that LVMI and RWT were significantly correlated with plasma BNP levels and the relation was closer in RWT than in LVMI. These results suggest that the degree of hypertrophied wall thickness, rather than the total ventricular mass, may be associated with increased plasma BNP levels in essential hypertension. Thus, BNP may reflect the pathophysiological process occurring in the left ventricle more exactly than ANP, if ventricular hypertrophy or alterations of LV hemodynamics directly stimulate BNP secretion from the left ventricle.
In this study, the diagnostic sensitivity and specificity of ANP and BNP for LVH in hypertension were similar. However, increments in BNP levels in patients with LVH were greater than increments in ANP levels. It should be noted that plasma ANP levels are easily influenced by blood pressure, age, sodium intake, renal function, postural change, and exercise.19 21 30 31 32 34 35 Because the increment in plasma ANP levels by LVH is relatively small, these influences cannot be ignored if blood samples are obtained in nonstandardized settings. Therefore, this study was carried out with all patients hospitalized and their sodium intake controlled. In addition, fasting blood samples were taken with the patients in a supine position 30 minutes after bed rest. Furthermore, the groups were similar in age, serum creatinine and plasma aldosterone levels, and PRA. In contrast to ANP, it is difficult to change BNP with postural change or exercise (unpublished data, 1995). Thus, plasma BNP levels may be a better marker for LVH than ANP in screening for hypertensive patients.
Left atrial enlargement is often accompanied by hypertension. Roman et al36 previously reported the importance of left atrial size for ANP secretion in valvular heart disease. They showed that left atrial size is a strong independent determinant for plasma ANP levels in patients with regurgitant valvular heart disease and control subjects. However, in the present study, left atrial size did not differ significantly between hypertensive patients with and without LVH. Therefore, left atrial size does not seem to contribute to the increased plasma ANP and BNP levels in hypertensive patients. It is known that hypertensive patients often have LV diastolic impairment. Lang et al37 reported that plasma BNP and ANP levels correlated inversely with the degree of diastolic dysfunction determined by Doppler echocardiography in patients with ischemic heart disease without systolic dysfunction. Our hypertensive patients also had higher A/E ratios with LVH; however, A/E ratio and plasma ANP and BNP levels were not significantly related. Thus, the contribution of LV diastolic dysfunction to plasma ANP and BNP levels in essential hypertensive patients needs further study. In addition, augmented synthesis and secretion were observed in a model of nonhemodynamic cardiac hypertrophy with cultured neonatal rat ventricular cardiocytes.38 In cardiac hypertrophy induced by endothelin and phenylephrine, levels of ANP and BNP gene expression were significantly higher. Thus, not only hemodynamic overload but also cardiac hypertrophy itself may be related to the increased plasma BNP and ANP levels in essential hypertensive patients with LVH.
LVH confers a considerable risk for increased morbidity and mortality that is independent of the risk imparted by the severity of hypertension, age, or other factors.1 The magnitude of that risk is apparently reflected by the degree of LVH.1 In addition, the incidence of adverse cardiovascular events, including sudden death, in patients with essential hypertension was highest in those with concentric hypertrophy, lowest in patients without LVH, and intermediate in patients with eccentric hypertrophy.3 Therefore, reversal or reduction of LVH seems to be a logical goal for antihypertensive therapy. Indeed, reversibility of LVH with antihypertensive therapy has been demonstrated in both clinical39 and experimental40 studies. Furthermore, the therapeutic reversal of LVH has been shown to reduce cardiovascular mortality.41 These findings suggest that early diagnosis of concentric hypertrophy in hypertensive patients and institution of antihypertensive therapy may be very important in improving prognosis. Because electrocardiographic criteria for LVH are insensitive for the detection of increased LV mass5 6 and echocardiographic results are labor- and time-intensive and may not be adequate in all patients, especially in those with obesity or pulmonary disease, measurements of plasma ANP and BNP levels may be useful for the detection of concentric LVH in essential hypertensive patients.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported in part by Special Coordination Funds for Promoting Science and Technology (Encouragement System of COE) from the Science and Technology Agency of Japan, the Ministry of Health and Welfare, the Human Science Foundation of Japan, and Ueda Memorial Heart Foundation. The technical assistance of Yoko Saito is gratefully acknowledged.
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Footnotes |
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Reprint requests Toshio Nishikimi, MD, Division of Hypertension and Nephrology, National Cardiovascular Center, 5-7-1, Fujishirodai, Suita, Osaka 565, Japan.
Received August 14, 1995;
first decision February 27, 1996;
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