Skip Navigation

European Journal of Heart Failure 2007 9(6-7):716-722; doi:10.1016/j.ejheart.2007.03.005
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Lüthje, L.
Right arrow Articles by Unterberg, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lüthje, L.
Right arrow Articles by Unterberg, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2007 European Society of Cardiology

Intrathoracic impedance monitoring to detect chronic heart failure deterioration: Relationship to changes in NT-proBNP

Lars Lüthjea,*, Dirk Vollmanna, Till Dreschera, Peter Schotta, Dieter Zenkerb, Gerd Hasenfuβa and Christina Unterberga

a Herzzentrum Göttingen, Abteilung Kardiologie und Pneumologie, Georg-August-Universität Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany
b Abteilung Thorax-Herz-Gefäβchirurgie, Georg-August-Universität, Göttingen, Germany

* Corresponding author. Tel: +49 551 39 9650; fax: +49 551 39 6293. E-mail address: larsluethje{at}med.uni-goettingen.de


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
 References
 
Background: An alert algorithm, based on intrathoracic impedance monitoring, has been incorporated into a cardiac resynchronisation device (CRT) to detect pulmonary fluid accumulation, and to audibly alert patients to decompensating chronic heart failure (CHF).

Aims: To evaluate this algorithm, alert events were correlated with changes in NT-proBNP concentration and CHF status.

Methods and results: In a prospective observational study of 62 patients (89% male, aged 67±1 year), NT-proBNP plasma concentrations, clinical CHF status, and device data were collected at enrolment, during regular follow-up and at device alerts. Over a mean follow-up of 27±2 weeks, pooled data indicated a weak, but significant inverse relationship between relative changes in intrathoracic impedance and NT-proBNP (r=0.3; p<0.001). In 52 device alerts from 35 patients, NT-proBNP increased by 66±19% from 2039±331 pg/ml (p<0.001). The increase in NT-proBNP was higher in alerts with clinical signs of CHF deterioration (n=30, 89±25%;p<0.001) than in alert events without clinical signs (n=22, 25–15%; p=n.s.).

Conclusion: Intrathoracic impedance based alert events are associated with a significant increase in NT-proBNP concentration. These data indicate that intrathoracic impedance monitoring might facilitate the outpatient management of CHF patients with implanted CRT devices.

Key Words: Cardiac resynchronisation therapy • Intrathoracic impedance monitoring • Chronic heart failure • NT-proBNP

Received September 1, 2006; Revised January 19, 2007; Accepted March 12, 2007


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
 References
 
Early detection of chronic heart failure (CHF) deterioration may reduce the morbidity, mortality and costs associated with hospitalisations for acute cardiac decompensation [1-4]. Recently, brain natriuretic peptide (BNP) and the aminoterminal portion of the high molecular weight precursor of BNP, N-terminal pro brain natriuretic peptide (NT-proBNP), have been established as new diagnostic and prognostic markers of CHF. Plasma levels of BNP and NT-proBNP reflect the severity of CHF [5] and may thereby help to detect early deterioration of CHF [6]. However, the need for blood sampling means that these markers are not particularly suited for outpatient and/or home monitoring of CHF status.

Another approach uses implantable sensors, which allow continuous monitoring of haemodynamic changes in CHF patients [7]. Recently, an intrathoracic impedance monitoring system (OptiVol– fluid index) has been incorporated into cardiac defibrillation and/or resynchronisation devices. An algorithm detects decreases in intrathoracic impedance suggestive of pulmonary fluid accumulation [8], and audibly alerts the patient of potential cardiac decompensation [9]. Recent data indicate that intrathoracic impedance monitoring might be valuable for the early detection of CHF deterioration [8,9]; however, the clinical value of the alert algorithm has not been evaluated in a prospective study. This study was therefore designed to determine the value of intrathoracic impedance monitoring by relating changes in intrathoracic impedance with changes in NT-proBNP, and by correlating device alert events with changes in NT-proBNP and clinical CHF status.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
 References
 
This prospective observational study was performed between January 2005 and February 2006 at the University of Göttingen, Germany. The study complies with the Declaration of Helsinki, and was approved by the local ethics committee. All subjects gave written informed consent to participate. Patients included in this investigation were also enrolled into the European Observational InSync Sentry– Study.

2.1. Patient selection
Patients aged >18 years were included if they had a cardiac resynchronisation triple chamber implantable cardioverter defibrillator (InSync Sentry–, Medtronic Inc., Minneapolis, MN, USA) implanted pectorally at least 4 weeks prior to inclusion. Exclusion criteria were decompensated heart failure at the time of enrolment, a life expectancy of less than 6 months, and non-compliance at inclusion or during follow-up.

2.2. Algorithm description and programming
The algorithm is described in detail elsewhere [8]. In brief, intrathoracic impedance was measured between the device "can" and the right ventricular coil (Fig. 1A). Between 12:00 and 17:00 h 64 measurements were taken and averaged for the calculation of a daily impedance value. An increase in impedance reflects an improvement of the pulmonary fluid status, whereas a decrease in impedance is associated with an increase in pulmonary fluid accumulation. To compensate for physiological fluctuations over time this daily impedance is compared to a stored reference (Fig. 1B). The reference impedance is a slow moving average of preceding daily measurements. The collection process for the reference data is started 30 days after device implantation to avoid interference from pocket oedema and local inflammation after surgery. Thereafter, an index, called OpitVol– fluid index (Fig. 1B), is calculated from the accumulated difference between the current and the reference impedance. The index progressively increases if daily impedance measurements are below the reference impedance. If the index crosses a programmable threshold (nominally set to 60), the device alerts the patient with an audible alarm tone to indicate possible fluid accumulation in the lungs.


Figure 01
View larger version (13K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 1 A: Schematic diagram illustrating the intrathoracic impedance measurement (double arrow) between the right ventricular coil (RV) and the can of the device. Atrial and left ventricular leads are not included. B: Decrease of intrathoracic impedance (right) and corresponding increase of the fluid index (left). This diagram was interrogated from the device after an alert.

 
In all subjects the fluid index was enabled and the initial threshold was set to 60 (nominal). During follow-up, optimization of the fluid index threshold was allowed according to the assessment of the investigating physician.

2.3. Data collection
Patients were evaluated at enrolment, at regular 3-month follow-up intervals, and following a device alert.

At enrolment, a detailed patient history and the prescribed CHF medication were determined. Echocardiography was performed for the evaluation of left ventricular ejection fraction, and the device interrogated to confirm the integrity of the system. CHF status and NT-proBNP concentration were evaluated as detailed below. The alarm tone of the device alert was demonstrated and patients were instructed to attend the outpatient ICD clinic as soon as possible following an alert. Patients were instructed not to reveal the cause of presentation at the hospital to the physician evaluating their CHF status.

At each follow-up visit, the same physician blinded to the cause for the patient's presentation evaluated signs and symptoms of CHF deterioration by auscultation and examination for leg oedema and jugular vein distension. NYHA class and body weight as well as exercise capacity by a six-minute walk test were determined. The six-minute walk test was always performed on the same hospital corridor. Patients were instructed to walk for 6 min at their own pace, but to cover as much distance as possible. Patients were allowed to rest whenever necessary. No encouragement was given during the test. Distance covered was measured via a roll tachometer used by an escorting physician. In case of suspected cardiac decompensation a chest X-ray was performed to detect signs of pulmonary congestion. To determine the concentration of NT-proBNP a blood sample was taken after a rest of 15 min in the supine position. Device interrogation included evaluation of the integrity of the system as well as analysis of the intrathoracic impedance data.

2.4. Data analysis
At each visit NT-proBNP samples were processed immediately after extraction and were analyzed by an electrochemoluminescence immunoassay (Elecsys pro BNP sandwich immunoassay; Roche Diagnostics, Basel, Switzerland). To compensate for individual differences, NT-proBNP concentrations were expressed as a percentage of the respective initial value. Patients were categorized into those without clinical signs of CHF deterioration and those with clinical signs of CHF deterioration. The latter included those patients who showed signs of a manifest cardiac decompensation defined as the need for hospitalisation including intravenous diuretic therapy. Patients were also classified into this category, (1) if two of the following criteria compared to the preceding visit were fulfilled: Worsening of NYHA class, reduced six-minute walk test performance (>10%), signs for pulmonary congestion on chest X-ray, or (2) if one of the aforementioned parameters and additionally two of the following parameters were fulfilled: increase in body weight, increase in leg oedema or increase in jugular vein distension. A maximum time interval of 2 weeks was allowed between alert onset and CHF status evaluation. Exceeding this limit resulted in exclusion of the respective event from the analysis.

For correlation analysis of changes in NT-proBNP and intrathoracic impedance, respective values from all patients and visits were individually normalized and pooled. Repeated measure analysis of variance (ANOVA) with Bonferroni's correction was applied for comparison of relative concentrations of NT-proBNP. A one-way ANOVA with Bonferroni post-hoc test was applied to compare temporal changes in intrathoracic impedance between groups with increasing, stable or decreasing NT-proBNP. Absolute values for NT-proBNP and six-minute walk test distance were compared between inclusion and 9-month follow-up using a paired t-test. A p value <0.05 was considered to be statistically significant. Data are given as mean±S.E.M., unless stated otherwise.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Limitations
 6. Conclusion
 References
 
3.1. Patient characteristics
A total of 62 patients were included and followed for 27.4±1.9 weeks. Patient baseline characteristics at enrolment are summarized in Table 1.


View this table:
[in this window]
[in a new window]

  		Table 1 Patient characteristics at inclusion (n=62)

 
3.2. NT-proBNP and intrathoracic impedance
Fig. 2 shows normalized, pooled data for intrathoracic impedance and NT-proBNP data for all patients for all regular and unscheduled visits (n=227). A weak but statistically significant inverse relationship was present between changes in intrathoracic impedance and NT-proBNP (r=–0.3, p<0.001).


Figure 02
View larger version (9K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 2 Pooled intrathoracic impedance and NT-proBNP data from all patients and all visits (regular and unscheduled). The respective values were normalized to the enrolment value.

 
3.3. NT-proBNP and device alerts
Overall, NT-proBNP concentrations significantly decreased during the follow-up period (Fig. 3). In line with this finding, a significant functional improvement was observed, as indicated by the increase in distance walked in the six-minute walk test.


Figure 03
View larger version (6K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 3 Absolute six-minute walk test (right) and NT-proBNP concentrations (left) at inclusion and at regular 3-month follow-up intervals. FU=follow-up.

 
The device alarm was triggered 62 times in 35 patients. A total of six alert events were excluded from analysis because the time between alert and presentation exceeded the 2 week interval. In all of these excluded events, the patients had not noticed the audible alert. In 4 other alert events, incomplete NT-proBNP data were available. Thus, 52 device alerts with complete data sets were analysed. The threshold was programmed to the nominal 60 in all but 2 alerts without clinical signs of CHF deterioration (threshold set to 30 and 40, respectively) and 3 alerts with associated clinical signs (threshold set once to 120 and twice to 40). These alerts were included in the analysis.

NT-proBNP increased significantly (by 66.1±19.1%) at the time of presentation with a device alert from 2039±331 pg/ml at the last preceding visit 9±1 weeks earlier (p<0.001). 6±1 weeks later, NT-proBNP had decreased again, close to the level at the preceding visit (p<0.01; Fig. 4A).


Figure 04
View larger version (12K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 4 Device alerts and NT-proBNP concentrations. Percentage NT-proBNP concentrations before an alert (before: 9±1 weeks), at the time of an alert (alert), and after an alert (after: 6±1 weeks). A: All alert events (n=52). B: Alerts with clinical signs of CHF deterioration (+; n=30) and alerts without clinical signs of CHF deterioration (–; n=22).

 
Clinical signs of CHF deterioration were present in 30 of the 52 alert events (58%). In the events without clinical signs of CHF deterioration, no other reason for the alert such as pleural effusion or pneumonia could be found. Treatment was not changed in these patients, and upon re-evaluation after 2 weeks (outpatient visit) no evidence for subsequent worsening of CHF was found. In Fig. 4B, changes in NT-proBNP are illustrated for alerts with and without clinical signs of CHF deterioration. As shown, there was a marked relative increase in NT-proBNP for alerts with accompanying clinical CHF signs (88.7±25.0%; p<0.001), whereas the increase for alert events without clinical CHF signs (25.0±14.9%) was not statistically significant.

Fig. 5A illustrates the frequency of alert events associated with a decreasing (<–10%), stable (0±10%) or increasing (>10%) trend in NT-proBNP. As compared to the last preceding follow-up, most alerts were associated with an increase in NT-pro-BNP >10% (Fig. 5A). In fact, in 13 of all analyzed events (25%), the increase in NT-proBNP exceeded 100%. Alerts with clinical signs of CHF deterioration showed decreasing NT-proBNP values in 13%, stable NT-proBNP values in 13% and an increasing NT-proBNP in 73%, whereas the respective values for alerts without clinical signs of CHF deterioration were 23% for decreasing, 36% for stable, and 41% for increasing NT-proBNP. The average time interval between alert onset and patient presentation was 5.2±0.6 days with no significant difference for alerts with a decreasing, stable or increasing NT-proBNP trend in this time interval. Changes in impedance within this time period were then retrospectively compared between groups with stable, increasing or decreasing NT-proBNP (Fig. 5B). This analysis was performed to reveal the potential changes in fluid status (and impedance) that may have occurred after alarm onset but before the patient presented at the outpatient clinic. As illustrated, there was an increase in impedance between alert onset and patient evaluation in patients with decreasing NT-proBNP.


Figure 05
View larger version (12K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 5 A: Diagram illustrating algorithm alerts and NT-proBNP changes in subcategories. The percentage of alerts associated with a decrease of the NT-proBNP concentration <–10% (n=8), the number of alerts with an almost stable NT-proBNP concentration (0±10%; n=12), and the number of alerts with an increase of the NT-proBNP concentration >10% (n=32) is shown. B: Diagram illustrating the intrathoracic impedance change from the alert onset to patient evaluation in the above described three subgroups with a decreasing, stable or increasing NT-proBNP concentration as compared to the preceding visit. The upper and lower margins of the box represent the upper and lower quartile, the line within the median, and the whiskers the spread of the data.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Limitations
 6. Conclusion
 References
 
This is the first study correlating OptiVol– alert events with changes in clinical CHF status and plasma levels of NT-proBNP. Our data provide evidence for the presence of an inverse relationship between changes in intrathoracic impedance and levels of NT-proBNP. Furthermore, device alert events were found to be associated with increased levels of NT-proBNP. This increase was more distinct in the presence of clinical signs and symptoms of CHF.

4.1. NT-proBNP and intrathoracic impedance
Pooled data indicate a negative correlation between changes in intrathoracic impedance and changes in NT-proBNP. Prior investigations have established BNP and its precursor NT-proBNP as markers for the diagnosis [10,11] and prognosis [12] of CHF. BNP and NT-proBNP are released in response to myocyte stretch [13], and are elevated in asymptomatic as well as symptomatic CHF [14,15]. The concentration of the peptide hormone increases with the severity of CHF, but threshold values have not yet been defined [5,16,17]. Recently, Pitzalis et al. [18] evaluated BNP as a prognostic factor in patients with CHF after CRT device implantation. Morbidity and mortality was found to be higher in those patients with high BNP values after 1 month of CRT. However, target BNP levels for the guidance of CHF therapy remain unclear [19]. Thus, it has been suggested to evaluate relative changes in BNP levels rather than absolute values for individual therapy optimization [19]. Different studies have found a significant correlation between BNP, pulmonary capillary wedge pressure and left ventricular end-diastolic pressure [22-24]. Yu et al. [8] retrospectively analysed trends in intrathoracic impedance in patients hospitalised for cardiac decompensation and revealed an inverse correlation between intrathoracic impedance and pulmonary capillary wedge pressure. Our data extend these findings by indicating the existence of a negative relationship between changes in NT-proBNP and intrathoracic impedance.

4.2. NT-proBNP and device alerts
Overall, functional parameters improved and NT-proBNP concentrations decreased during this study. This finding is in line with previous publications reporting that cardiac resynchronisation therapy improves functional as well as neurohumoral parameters [20].

In the majority of the alert events, NT-proBNP increased by >10%, and in 25% of the events, this increase exceeded 100%. With an overall increase of >50%, the algorithm therefore seems to correctly reflect a deterioration of the disease state in most cases. Apart from the retrospective analysis by Yu et al. [8], the relationship between intrathoracic impedance and changes in pulmonary fluid status have only been described in single case reports. We [9] previously described the early detection of fluid accumulation in the lung with a subsequent device alert caused by decompensating CHF. In another report, a significant increase in intrathoracic impedance was observed in a patient with a large left pneumothorax [21]. In the present study, concomitant clinical signs of CHF deterioration at a device alert were related to a marked NT-proBNP increase of approximately 90%. However, in those alerts without clinical signs there was a non-significant increase in NT-proBNP concentration of 25%. As mentioned above, high BNP levels after initiation of cardiac resynchronisation therapy have been associated with worse prognosis [18]. Thus, our results indicate that the occurrence of a device alert may also have prognostic implications, especially if clinical signs of CHF deterioration coexist.

In some of the device alert events, signs of CHF deterioration could not be confirmed upon clinical evaluation. One potential explanation for this finding could be that clinical measures are not as sensitive as intrathoracic impedance monitoring to detect early CHF deterioration. However, some of the alert events were also associated with decreasing or unchanged NT-proBNP levels. Evaluation of these alert events revealed no evidence for fluid accumulation due to other causes (e.g., local inflammation). Changes in impedance in the time period between alert onset and patient evaluation suggest another potential cause for the decrease in NT-proBNP in some alert events. In these cases, an acute increase in impedance was found for the respective time interval, indicating an improvement in pulmonary fluid status after alert onset. These changes may have resulted from an acute enhancement of patient compliance, triggered by the occurrence of the audible alert signal. It has been shown previously that many CHF patients fail to comply with their physician's instructions, e.g. by not taking prescribed medication or non-compliance with fluid intake restrictions [22,23]. Thus, enhancement of patient compliance due to the alert may have influenced our results in some events, and may play a hitherto underestimated effect in the management of CHF.


   5. Limitations
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
6. Conclusion
 References
 
The main limitation is the observational, patient unblinded design of the study. However, the physician evaluating the CHF status was blinded to the cause of presentation of the patients. Another limitation is that the correlation analysis was performed on pooled datasets. NT-proBNP concentrations at inclusion were considerably elevated, but comparable to other studies investigating CHF patients without manifest decompensation [24,25]. Finally the clinical CHF status was classified using a non-validated scheme.


   6. Conclusion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
References
 
The significant increase in NT-proBNP during device alerts in this study indicates that intrathoracic impedance monitoring is suitable to detect CHF deterioration in ambulatory patients. Use of the alert algorithm as an additional diagnostic tool might therefore facilitate the outpatient management of CHF patients with implanted CRT devices. Furthermore, our results indicate that the alert tone may enhance patient compliance, thereby possibly preventing the progress of cardiac decompensation.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
 References
 

  1. Jessup M., Brozena S. Heart failure. N Engl J Med (2003) 348(20):2007–2018.[Free Full Text]
  2. Fonarow G.C., Corday E. Overview of acutely decompensated congestive heart failure (ADHF): a report from the ADHERE registry. Heart Fail Rev (2004) 9(3):179–185.[CrossRef][Web of Science][Medline]
  3. Adams K.F. Jr., Fonarow G.C., Emerman C.L., LeJemtel T.H., Costanzo M.R., Abraham W.T., et al. Characteristics and outcomes of patients hospitalized for heart failure in the United States: rationale, design, and preliminary observations from the first 100,000 cases in the Acute Decompensated Heart Failure National Registry (ADHERE). Am Heart J (2005) 149(2):209–216.[CrossRef][Web of Science][Medline]
  4. Cleland J.G., Swedberg K., Follath F., Komajda M., Cohen-Solal A., Aguilar J.C., et al. The EuroHeart Failure survey programme — a survey on the quality of care among patients with heart failure in Europe. Part 1: patient characteristics and diagnosis. Eur Heart J (2003) 24(5):442–463.[Abstract/Free Full Text]
  5. Tsutamoto T., Wada A., Maeda K., Hisanaga T., Maeda Y., Fukai D., et al. Attenuation of compensation of endogenous cardiac natriuretic peptide system in chronic heart failure: prognostic role of plasma brain natriuretic peptide concentration in patients with chronic symptomatic left ventricular dysfunction. Circulation (1997) 96(2):509–516.[Abstract/Free Full Text]
  6. Lee S.C., Stevens T.L., Sandberg S.M., Heublein D.M., Nelson S.M., Jougasaki M., et al. The potential of brain natriuretic peptide as a biomarker for New York Heart Association class during the outpatient treatment of heart failure. J Card Fail (2002) 8(3):149–154.[CrossRef][Web of Science][Medline]
  7. Bennett T., Kjellstrom B., Taepke R., Ryden L. Development of implantable devices for continuous ambulatory monitoring of central hemodynamic values in heart failure patients. Pacing Clin Electrophysiol (2005) 28(6):573–584.[CrossRef][Medline]
  8. Yu C.M., Wang L., Chau E., Chan R.H., Kong S.L., Tang M.O., et al. Intrathoracic impedance monitoring in patients with heart failure: correlation with fluid status and feasibility of early warning preceding hospitalization. Circulation (2005) 112(6):841–848.[Abstract/Free Full Text]
  9. Luthje L., Drescher T., Zenker D., Vollmann D. Detection of heart failure decompensation using intrathoracic impedance monitoring by a triple-chamber implantable defibrillator. Heart Rhythm (2005) 2(9):997–999.[CrossRef][Web of Science][Medline]
  10. Mueller C., Scholer A., Laule-Kilian K., Martina B., Schindler C., Buser P., et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med (2004) 350(7):647–654.[Abstract/Free Full Text]
  11. Lainchbury J.G., Campbell E., Frampton C.M., Yandle T.G., Nicholls M.G., Richards A.M. Brain natriuretic peptide and N-terminal brain natriuretic peptide in the diagnosis of heart failure in patients with acute shortness of breath. J Am Coll Cardiol (2003) 42(4):728–735.[Abstract/Free Full Text]
  12. Gardner R.S., Ozalp F., Murday A.J., Robb S.D., McDonagh T.A. N-terminal pro-brain natriuretic peptide. A new gold standard in predicting mortality in patients with advanced heart failure. Eur Heart J (2003) 24(19):1735–1743.[Abstract/Free Full Text]
  13. de Lemos J.A., McGuire D.K., Drazner M.H. B-type natriuretic peptide in cardiovascular disease. Lancet (2003) 362(9380):316–322.[CrossRef][Web of Science][Medline]
  14. McDonagh T.A., Cunningham A.D., Morrison C.E., McMurray J.J., Ford I., Morton J.J., et al. Left ventricular dysfunction, natriuretic peptides, and mortality in an urban population. Heart (2001) 86(1):21–26.[Abstract/Free Full Text]
  15. Lerman A., Gibbons R.J., Rodeheffer R.J., Bailey K.R., McKinley L.J., Heublein D.M., et al. Circulating N-terminal atrial natriuretic peptide as a marker for symptomless left-ventricular dysfunction. Lancet (1993) 341(8853):1105–1109.[CrossRef][Web of Science][Medline]
  16. Braunschweig F., Fahrleitner-Pammer A., Mangiavacchi M., Ghio S., Fotuhi P., Hoppe U.C., et al. Correlation between serial measurements of N-terminal pro brain natriuretic peptide and ambulatory cardiac filling pressures in outpatients with chronic heart failure. Eur J Heart Fail (2006) 8(8):797–803.[Abstract/Free Full Text]
  17. Schou M., Gustafsson F., Kjaer A., Hildebrandt P.R. Long-term clinical variation of NT-proBNP in stable chronic heart failure patients. Eur Heart J (2007) 28(2):177–182.[Abstract/Free Full Text]
  18. Pitzalis M.V., Iacoviello M., Di Serio F., Romito R., Guida P., De Tommasi E., et al. Prognostic value of brain natriuretic peptide in the management of patients receiving cardiac resynchronization therapy. Eur J Heart Fail (2006) 8(5):509–514.[Abstract/Free Full Text]
  19. Nohria A., Givertz M.M. B-type natriuretic peptide and the stressed heart. J Am Coll Cardiol (2006) 47(4):749–751.[Free Full Text]
  20. Erol-Yilmaz A., Verberne H.J., Schrama T.A., Hrudova J., De Winter R.J., Van Eck-Smit B.L., et al. Cardiac resynchronization induces favorable neurohumoral changes. Pacing Clin Electrophysiol (2005) 28(4):304–310.[CrossRef][Medline]
  21. Timperley J., Mitchell A.R., Brown P., Betts T.R. Changes in intrathoracic impedance from a pneumothorax: insights from an implanted monitoring system. Pacing Clin Electrophysiol (2005) 28(10):1109–1111.[CrossRef][Medline]
  22. Opasich C., Rapezzi C., Lucci D., Gorini M., Pozzar F., Zanelli E., et al. Precipitating factors and decision-making processes of short-term worsening heart failure despite "optimal" treatment (from the IN-CHF Registry). Am J Cardiol (2001) 88(4):382–387.[CrossRef][Web of Science][Medline]
  23. Michalsen A., Konig G., Thimme W. Preventable causative factors leading to hospital admission with decompensated heart failure. Heart (1998) 80(5):437–441.[Abstract/Free Full Text]
  24. Hartmann F., Packer M., Coats A.J., Fowler M.B., Krum H., Mohacsi P., et al. Prognostic impact of plasma N-terminal pro-brain natriuretic peptide in severe chronic congestive heart failure: a substudy of the Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) trial. Circulation (2004) 110(13):1780–1786.[Abstract/Free Full Text]
  25. Bettencourt P., Azevedo A., Pimenta J., Frioes F., Ferreira S., Ferreira A. N-terminal-pro-brain natriuretic peptide predicts outcome after hospital discharge in heart failure patients. Circulation (2004) 110(15):2168–2174.[Abstract/Free Full Text]

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Circ Arrhythm ElectrophysiolHome page
R. Jhanjee, G. A. Templeton, S. Sattiraju, J. Nguyen, S. Sakaguchi, F. Lu, C. Ermis, S. Milstein, L. Van Heel, K. G. Lurie, et al.
Relationship of Paroxysmal Atrial Tachyarrhythmias to Volume Overload: Assessment by Implanted Transpulmonary Impedance Monitoring
Circ Arrhythm Electrophysiol, October 1, 2009; 2(5): 488 - 494.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Lüthje, L.
Right arrow Articles by Unterberg, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lüthje, L.
Right arrow Articles by Unterberg, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?