CLINICAL RESEARCH: HEART FAILURE
B-Type Natriuretic Peptide Strongly Reflects Diastolic Wall Stress in Patients With Chronic Heart Failure
Comparison Between Systolic and Diastolic Heart Failure
Yoshitaka Iwanaga, MD*,*,1,
Isao Nishi, MD*,
Shinichi Furuichi, MD*,
Teruo Noguchi, MD*,
Kazuhiro Sase, MD*,
Yasuki Kihara, MD, FACC ,
Yoichi Goto, MD* and
Hiroshi Nonogi, MD*
* Division of Cardiology, National Cardiovascular Center, Suita, Japan
Department of Cardiovascular Medicine, Kobe City General Hospital, Kobe, Japan
Manuscript received January 25, 2005;
revised manuscript received July 13, 2005,
accepted August 22, 2005.
* Reprint requests and correspondence: Dr. Yoshitaka Iwanaga, Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, 54 Shogoinn-kawaharacho, Kyoto 606-8507, Japan. (Email: yiwanaga{at}kuhp.kyoto-u.ac.jp).
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Abstract
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OBJECTIVES: We explored the stimulus for B-type natriuretic peptide (BNP) secretion in the clinical setting of heart failure (HF).
BACKGROUND: Increasingly, plasma BNP levels are being incorporated into the clinical assessment and management of systolic heart failure (SHF) as well as diastolic heart failure (DHF). However, heterogeneity in BNP levels among individuals with HF can cause some confusion in interpreting results.
METHODS: In 160 consecutive patients presenting with HF, we measured plasma BNP levels and performed echocardiography and cardiac catheterization. Systolic and diastolic meridional wall stress was calculated from echocardiographic and hemodynamic data.
RESULTS: Although plasma BNP had a significant correlation (r2 = 0.296 [p < 0.001]) with left ventricular end-diastolic pressure (EDP) as previously reported, the correlation between plasma BNP and end-diastolic wall stress (EDWS) (r2 = 0.887 [p < 0.001]) was more robust. In a subanalysis of 62 patients with DHF, a similar result was obtained (r2 = 0.143 for EDP and r2 = 0.704 for EDWS). In a comparison between SHF and DHF, the BNP level was significantly higher in SHF (p < 0.001). Although EDP did not show any difference, EDWS was significantly higher in SHF than in DHF (p < 0.001).
CONCLUSIONS: The present study shows that plasma BNP levels reflect left ventricular EDWS more than any other parameter previously reported, not only in patients with SHF, but also in patients with DHF. The relationship of left ventricular EDWS to plasma BNP may provide a better fundamental understanding of the interindividual heterogeneity in BNP levels and their clinical utility in the diagnosis and management of HF.
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Abbreviations and Acronyms
| | AS = aortic stenosis | | BNP = B-type natriuretic peptide | | CHF = congestive heart failure | | DHF = diastolic heart failure | | EDP = end-diastolic pressure | | EDWS = end-diastolic wall stress | | EF = ejection fraction | | HF = heart failure | | LV = left ventricle/ventricular | | LVEDVI = left ventricular end-diastolic volume index | | LVMI = left ventricular mass index | | SHF = systolic heart failure | | SWS = systolic wall stress |
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Plasma B-type natriuretic peptide (BNP) levels are reported not only to be a strong marker of left ventricular (LV) dysfunction, but also a marker to predict morbidity and mortality accurately in patients with chronic heart failure (HF) (1,2). Recently, BNP-guided therapy for chronic HF has been suggested. Troughton et al. (3) demonstrated that pharmacotherapy guided by BNP levels reduces cardiovascular events and delays time to first cardiovascular event compared with intensive clinically guided therapy. Recent reports also demonstrated the contribution of LV diastolic function to plasma BNP levels and the usefulness of BNP in the diagnosis of diastolic HF (4).
However, heterogeneity in BNP levels among individuals with HF has been recognized, and it has caused some confusion in interpreting results (5). Previous human studies have suggested correlations between BNP levels and cardiac functional or dimensional indexes such as end-diastolic pressure (EDP), ejection fraction (EF), pulmonary capillary wedge pressure, and LV volume, none of which sufficiently explain the heterogeneity (6–9). Therefore, it is essential to determine the stimulus for BNP secretion in the clinical setting of HF. In vitro studies have clarified the mechanism of secretion and regulation of BNP precisely (10). Stretch of cardiomyocytes is reported to be the most important stimulus of BNP regulation (11). It is also believed that BNP in humans may be released from the heart in response to increased wall stress. However, there have been few human studies exploring a direct relationship between wall stress and BNP regulation (12). Vanderheyden et al. (13) have very recently demonstrated, for the first time, in 40 patients with aortic stenosis (AS), a significant correlation of BNP with LV end-diastolic wall stress (EDWS). In their study, however, subjects were limited to patients with AS. Hence, there now is a need for the same assessment in patients with HF of various etiologies. Accordingly, in the present study, we evaluated plasma BNP levels in 160 consecutive patients presenting with HF of various etiologies including diastolic HF.
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Methods
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Patients.
Among the patients referred to our National Cardiovascular Center Hospital between October 2003 and December 2004, we included in this study those admitted with congestive heart failure (CHF) consecutively. Patients who did not undergo LV catheterization or had renal dysfunction (serum creatinine >2.0 mg/dl) were excluded. A sample of 160 patients was obtained. For all participants, cardiac catheterization and echocardiograms were performed at a compensated CHF stage (before discharge), and plasma BNP was measured on the day before cardiac catheterization. The clinical characteristics of these patients are listed in Table 1.
BNP assay.
Blood was collected into tubes containing EDTA, and plasma BNP was measured using a validated and commercially available immunoassay kit (Tosoh Co. Ltd., Japan).
Cardiac catheterization.
Left ventricular pressure was recorded with a 5-F pigtail catheter connected to a fluid-filled transducer. Left ventricular volume and EF were determined with left ventriculography with contrast medium using Kennedy’s formula.
Echocardiography.
Echocardiographic examinations were performed with a Sonos 5500 machine equipped with a 2.5-MHz probe. M-mode images were obtained to measure left atrial and ventricular dimensions (14). The left ventricular mass index (LVMI) was estimated from the formula of Devereux et al. (15). The severity of mitral regurgitation was quantified on a semicontinuous scale from none (0) to moderately severe (3+). In patients with sinus rhythm, the pulsed Doppler transmitral flow velocity was recorded to measure a ratio of peak mitral E-wave velocity to peak mitral A-wave velocity (E/A ratio) and the deceleration time of the mitral E-wave velocity.
On the basis of hemodynamic and echocardiographic data, end-diastolic and systolic meridional wall stresses (WS) were calculated. These were obtained by using the formula: WS = 0.334 x P(LVID)/WT(1 + WT/LVID), where P = LV pressure (i.e., peak systolic pressure or EDP, which was obtained during cardiac catheterization), LVID = left ventricular internal dimension, and WT = wall thickness (16). In the present study, the posterior wall thickness was used to assess WT regardless of regional wall motion abnormalities. In the analysis of the interobserver reproducibility of the posterior wall thickness measurement in 48 patients with CHF, a high degree of the reproducibility was found with an intraclass correlation coefficient value 0.830 (95% confidence interval 0.609 to 0.925), and absolute difference was small (mean ± SD; 0.01 ± 1.16 mm). Also, adequate M-mode images were not available in three patients, and they were excluded in the present study.
Statistical analysis.
Comparisons between groups were made using chi-square analysis for proportions and unpaired Student t tests for continuous variables. Linearity of a relationship between two variables was assessed by linear regression analysis; p < 0.05 was considered significant. Results were expressed as mean ± SEM.
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Results
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Patient characteristics.
Clinical characteristics of the group of 160 patients are summarized in Table 1. Mean age was 66.8 ± 1.0 years (range 20 to 87 years), and 31% of the patients were women. In all, 98 patients had HF symptoms with an LV EF of  50%. These comprised the systolic heart failure group (SHF). The diastolic heart failure group (DHF) was comprised of 62 patients with preserved systolic function (LV EF >50%). Mean age and body mass index did not differ significantly between SHF and DHF groups, while there was a trend of more female patients in DHF. A history of hypertension and etiologies of dilated cardiomyopathy and ischemic cardiomyopathy/old myocardial infarction were more prevalent in SHF. Patients with SHF were more likely to be taking angiotensin-converting enzyme inhibitors or angiotensin receptor blockers and diuretics.
Geometric and functional parameters obtained by echocardiography or cardiac catheterization are shown in Table 2. In total patients, mean EF was 41.5 ± 1.1% (range 13% to 66%), and mean LVMI and LV end-diastolic volume index (LVEDVI) were 166 ± 4 g/m2 and 106 ± 4 ml/m2, respectively.
Correlations of plasma BNP to echocardiographic and hemodynamic parameters.
Scatter plots of plasma BNP levels (dependent variable) against some echocardiographic and hemodynamic parameters (independent) are shown in Figure 1. There were strong correlations between LV EF, LVEDVI or LV end-systolic volume index, or LV EDP and plasma BNP (coefficient of correlation; r2 = 0.325, 0.343, 0.421, and 0.328, respectively). There were weak correlations with parameters of transmitral Doppler flow r2 = 0.201 and 0.101 for E/A and deceleration time, respectively. In contrast, LVMI and left atrial diameter did not show significant correlations with BNP levels. Although LV systolic wall stress (SWS) calculated by echocardiographic and hemodynamic parameters showed a modest correlation (r2 = 0.277), a correlation of BNP with LV EDWS was much more robust (r2 = 0.887).
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Figure 1 Correlation between B-type natriuretic peptide (BNP) and left ventricular functional parameters in all 160 patients. (A) Left ventricular ejection fraction (EF) (%). (B) End-diastolic pressure (EDP) (mm Hg). (C) End-systolic wall stress (SWS) (kdynes/cm2). (D) End-diastolic wall stress (EDWS) (kdynes/cm2).
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Although age, gender, and atrial fibrillation were not significantly associated, body mass index (BMI) and New York Heart Association functional class  II were associated with BNP levels (p < 0.001 in both).
Comparison between SHF and DHF.
Plasma BNP levels were significantly higher in SHF than in DHF (median [interquartile range]; 267 [136 to 583] and 105 [64 to 146] pg/ml, respectively, p < 0.001); however, EDP levels did not show any differences as shown in Figure 2 and Table 2. Other parameters such as SWS, EDWS, LV end-diastolic dimension, LVMI, LVEDVI, and LV peak systolic pressure were significantly higher in SHF than in DHF (p < 0.001). Scatter plots in patients with SHF and DHF are demonstrated in Figures 3A and 3B and Figures 3C and 3D, respectively. End-diastolic wall stress showed a better correlation with BNP (r2 = 0.704) than EDP (r2 = 0.143) in DHF as well as in SHF.
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Figure 2 Differences of B-type natriuretic peptide (BNP) and left ventricular functional parameters between systolic heart failure (SHF) (n = 98) and diastolic heart failure (DHF) (n = 62). The box defines the interquartile range with the median indicated by the crossbar. The error bars indicate the 10th and 90th percentiles. EDP = end-diastolic pressure (mm Hg); EDVI = end-diastolic volume index (ml/m2); EDWS = end-diastolic wall stress (kdynes/cm2); SWS = end-systolic wall stress (kdynes/cm2).
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Figure 3 Correlation between B-type natriuretic peptide (BNP) and left ventricular functional parameters in 98 patients with systolic heart failure (SHF) (A and B) and in 62 patients with diastolic heart failure (DHF) (C and D); (A and C) end-diastolic pressure (EDP) (mm Hg) and (B and D) end-diastolic wall stress (EDWS) (kdynes/cm2).
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Subanalysis in patients without local wall motion abnormality.
It is conceivable that this estimation of wall stress did not accurately reflect the entire non-uniform LV wall stress in patients with regional asynergy in LV wall motion or with variation in segmental LV wall thickness. In the present study, 83% of patients with ischemic cardiomyopathy or old myocardial infarction and 28% with dilated cardiomyopathy had regional wall motion abnormalities. Therefore, a subanalysis was performed for patients without local wall motion abnormality (n = 105). As a result, an even stronger correlation was obtained as shown (r2 = 0.919). A correlation in patients with regional wall motion abnormality (n = 55) was still strong (r2 = 0.820).
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Discussion
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Heterogeneity of BNP levels among individuals with HF can cause some confusion in interpreting results. It has been unclear why some patients with LV EF <35% have BNP levels in the normal range whereas others exhibit extremely elevated levels, and why some patients with isolated diastolic dysfunction (i.e., with normal EF) show a similar increase of plasma BNP as do the patients with severe systolic dysfunction. One of the answers to the question has been the change of EDP levels in the LV (6). Another recent report has demonstrated that heterogeneity of BNP levels in patients with systolic HF reflects the severity of diastolic abnormality, right ventricular function, and mitral regurgitation in addition to LV EF, age, and renal function (7). The present study demonstrates the significance of LV EDWS in the regulation of BNP in patients with HF in general. This was true not only in patients with SHF but also with DHF. Although correlation analysis suggested a relationship between other parameters of LV geometry and function including EDP and plasma BNP levels, the correlation between LV EDWS and BNP was the most robust (r2 = 0.887). Many studies including ours have shown that BNP levels correlate well with changes in filling pressures during tailored therapy (6,17), while O’Neill et al. (18) recently reported that plasma BNP might not correlate closely with changes in intracardiac filling pressures. In any case, plasma BNP levels are not uniform across different patients with the same LVEDP (i.e., interindividual heterogeneity), and this may be because BNP is determined more by EDWS than by filling pressure. Left ventricular EDWS might account for the wide variations that they observed in patients with HF.
The present result suggests that LV EDWS may regulate BNP secretion in humans. Indeed, experiments using cultured neonatal rat ventricular cells showed that cardiac myocytes are able to respond to mechanical stretch by increasing BNP secretion and gene expression (11). Wiese et al. (19), using isolated human myocardium, have also demonstrated that, while the isometric contraction mode did not have any influence on BNP expression, diastolic overstretch increased BNP gene expression in a time-dependent manner. This implies that diastolic stretch (i.e., preload rather than afterload) seems to be the mechanical factor responsible for the induction of BNP expression and may be the reason that in the present study LV EDWS shows a better correlation with the plasma BNP levels than does LV SWS. Furthermore, in vitro studies have implicated the contributions of local paracrine and autocrine factors in the stretch-induced BNP activation (11). Local angiotensin II was shown to play a critical role in the development of stretch-induced cardiac hypertrophy and to at least partly regulate mechanical load-induced BNP expression. Recently, in addition to stimuli such as myocyte stretching and neurohumoral activation, acute myocardial hypoxia has been reported to increase cardiac BNP gene transcription and raise the plasma proBNP concentration in an animal study (20). This mechanism may explain the increase in plasma BNP in patients with acute coronary syndromes and myocardial infarction (21). In the present study, because such patients with acute ischemia were not included, the correlation between LV EDWS and plasma BNP might actually be stronger.
Myocardial wall stress is one of the primary determinants of myocardial oxygen consumption (22). Cardiac decompensation is thought to result when the feedback loop that normalizes wall stress to abnormal loading of the heart dysfunctions. The increased wall stress may act directly or indirectly via cellular mediators such as angiotensin, endothelin, inflammatory cytokines, reactive oxygen species, and matrix metalloproteinase to orchestrate a variety of molecular and cellular remodeling events determining the structural and functional properties of the myocardium and, ultimately, the rate of disease progression (23–27). Therefore, usefulness of plasma BNP levels in predicting morbidity and mortality accurately in patients with chronic HF may be explained by the relationship between the LV EDWS and BNP. Many other factors, such as age, gender, body mass, genetics, etc., are also known to affect plasma BNP levels. However, the demonstration of the link between the hemodynamics (LV EDWS) and neurohormonal factor (BNP) may support the usefulness of BNP-guided treatment of HF. Although more randomized studies are needed, pharmacotherapy guided by BNP levels is intriguing and promising (3).
There are several methods to estimate the wall stress, and we used a formula based on M-mode echocardiographic variables (16). This method may have several limitations. For example, when there is regional asynergy in LV wall motion and variation in local LV wall thickness, the estimate may not reflect the entire non-uniform LV wall stress correctly. To test this possibility, we analyzed the data of the patients without LV asynergy demonstrated by echocardiogram and LV ventriculography. We obtained an even better correlation. Interestingly, a correlation in patients with a local wall motion abnormality was still strong (r2 = 0.820). There are several other limitations to our study. Echocardiography and blood sampling were typically performed the day before cardiac catheterization. This time lag could have influenced the results. A further limitation is that the study population was composed of the patients who were in stable condition and could tolerate LV cardiac catheterization; thus, patients who could not bear cardiac catheterization (e.g., patients with New York Heart Association functional class IV HF) were excluded.
In the present study, we demonstrated that plasma BNP levels strongly reflect EDWS in the LV more than any other parameter previously reported. In addition, EDWS accurately accounts for the increase in plasma BNP levels even in patients with diastolic HF. The relationship of LV EDWS to plasma BNP may give a better understanding to the interindividual heterogeneity of plasma BNP levels and its clinical utility in the diagnosis and management of HF.
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Footnotes
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This study was supported by a research grant from Osaka Heart Club (Japan) and a grant for Clinical Vascular Function from Kimura-Kinenn Foundation (Japan).
1 Dr. Iwanaga is presently affiliated with the Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. 
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Abstract
Methods