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Ann Thorac Surg 2003;76:287-290
© 2003 The Society of Thoracic Surgeons


Case report

Decreased plasma neurohormones and improved cardiac performance after surgical treatment of chronic pulmonary embolism

Igor I. Tulevski, MDa*, Paul Bresser, PhDb, Alexander Hirsch, BSa, Maarten Groenink, PhDa, Richard N. Channick, MDc, Stuart W. Jamieson, MDd, Barbara J. M. Mulder, PhDa

a Department of Cardiology, Amsterdam The Netherlands
b Department of Pulmonology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
c Divisions of Pulmonary and Critical Care Medicine, San Diego, California, USA
d Division of Cardiothoracic Surgery, University of California San Diego, San Diego, California, USA

Accepted for publication January 8, 2003.

* Address reprint requests to Dr Tulevski, Department of Cardiology, B2-239, Academic Medical Center (AMC), Meibergdreef 9, 1100 DD Amsterdam, The Netherlands
e-mail: i.i.tulevski{at}amc.uva.nl


    Abstract
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 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
The findings of this case report suggest that quantitative assessment of plasma neurohormones and magnetic resonance imaging functional parameters in patients with right ventricular pressure overload due to chronic pulmonary embolism might be used as indicators for right ventricular function before and after intervention. Monitoring of changes in these parameters may provide quantitative follow-up of right ventricular function in these patients.


    Introduction
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 Abstract
 Introduction
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 Acknowledgments
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Diagnosis of right ventricular (RV) dysfunction is difficult, but of great clinical importance, in patients with (chronic) RV pressure overload due to pulmonary embolism (PE) [1]. A more accurate estimation of RV function in these patients might be useful in the determination of the optimal moment for medical or surgical intervention in order to prevent or delay irreversible RV failure.

Recently, neurohumoral activation of the RV in state of overload has gained increased attention. Brain natriuretic peptide (BNP) is a marker for ventricular dysfunction and is secreted in both atria and ventricles, especially in failing ventricles [2]. We have recently demonstrated [3] that levels of plasma neurohormones, BNP, and atrial natriuretic peptide (ANP) were inversely correlated with RV ejection fraction (EF) in patients with chronic RV pressure overload due to congenital heart disease. However, the role of plasma neurohormones and their applicability in detection of RV dysfunction in patients with chronic pulmonary embolism are as yet unclear.

In August 1999, a 56-year-old man with known chronic pulmonary embolism since 1995 was referred because of gradually progressive dyspnea and a decline in his functional capabilities (NYHA class III–IV/IV). Ventilation-perfusion scintigraphy in 1995 exhibited multiple mismatched segmental defects with repeated studies in 1998 and 1999 being essentially unchanged. On admission, echocardiography demonstrated severe right atrial (RA) and RV enlargement; the tricuspid regurgitant envelope was 5.7 m/sec, suggesting a peak pulmonary artery systolic pressure (PAP) of approximately 140 mmHg. Cardiac magnetic resonance imaging (MRI) demonstrated severe RA and RV dilatation, RV hypertrophy, and the interventricular septum bulging towards the LV (Fig 1A) . Right ventricular EF was 44%, stroke volume 62 mL/beat, and LVEF was 74%. Plasma neurohumoral status of the patient revealed markedly increased concentrations of BNP, ANP, and N-terminal-ANP; in addition, levels of other plasma neurohormones were increased (Table 1).



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Fig 1. End-diastolic midventricular magnetic resonance image (A) before and (B) after pulmonary thromboendarterectomy. (LV = left ventricle; RV = right ventricle.)

 

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Table 1. Quantitative Variables of Right Ventricular Function

 
At heart catheterization, hemodynamic studies revealed a RA pressure of 7 mm Hg, a RV pressure of 126/17 mm Hg, a pulmonary arterial pressure of 126/34 with a mean pressure of 68 mm Hg, a pulmonary capillary wedge pressure of 9 mm Hg, and a cardiac output of 2.7 L/min. Pulmonary vascular resistance was 1748 dynes/sec per cm-5. Pulmonary angiography revealed evidence of bilateral, surgically-accessible, chronic thromboembolic disease. Given his significant pulmonary hypertension in the setting of progressive functional disability, and with the chronic thrombemboli surgically accessible, a pulmonary thromboendarterectomy (PTE) was performed. The surgery resulted in significant hemodynamic improvement. Two months postoperatively the functional status of the patient was estimated to be NYHA classification I/IV, and plasma neurohumoral status (Table 1) and cardiac MRI were repeated (Figure 1).

Plasma neurohormone levels after PTE decreased significantly (Table 1). The RV stroke volume had increased from 62 mL to 76 mL/beat, RVEF from 44% to 59%, the interventricular septum regained its normal shape, and the LV end-diastolic volume rose from 87 mL prior to PTE to 110 mL after PTE. Echocardiography has confirmed improved biventricular function; systolic PAP was estimated to be 65 mm Hg.


    Comment
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 Abstract
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 Acknowledgments
 References
 
The most widely used tool in clinical practice for the diagnosis and follow-up of RV dysfunction is echocardiography. As demonstrated before both by catheterization [4] and echocardiography [5], PTE results in a significant and rapid decline in RV afterload associated with a marked improvement in the functional status of the patients. For long-term postoperative follow-up of RV function in these patients, however, repeated catheterization is not a useful tool. Also, the value of echocardiography seems limited in this respect due to its technical limitation (acoustic window), and the absence of a reliable mathematical assumption due to complex geometry of RV. Regarding these limitations, quantitative diagnostic measurements like plasma neurohormones and MRI, might be helpful in elucidating the RV function in patients with chronic PE, both before and after PTE surgery.

The potential prognostic value of BNP has been underscored in previous studies regarding RV as well as LV pathology [2, 3]. In chronic RV pressure overload, plasma BNP levels are considered to reflect RV dysfunction rather than RV pressure. In patients with chronic thromboembolic pulmonary hypertension, plasma BNP levels were demonstrated by Nagaya and coworkers [1] to increase in proportion to the extent of RV dysfunction. These observations are consistent with our recently reported studies [3, 6].

In conclusion, this case report suggests that the increased secretion of plasma neurohormones, and BNP and ANP in particular, corresponds to RV function in patients with chronic PE. If our results can be confirmed with larger numbers of patients, plasma levels of neurohormones may be of clinical importance as a supplementary tool for the quantitative assessment of RV function under circumstances of chronic RV pressure overload. This may be of considerable importance in the diagnostic process, timing of treatment and possibly also postoperative prognosis of patients with RV overload due to chronic PE.


    Acknowledgments
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
Doctor Tulevski is supported by the Netherlands Heart Foundations (NHS) and Interuniversity Cardiology Institute of the Netherlands (ICIN = KNAW).


    References
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 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 

  1. Nagaya N., Ando M., Oya H., et al. Plasma brain natriuretic peptide as a noninvasive marker for efficacy of pulmonary thromboendarterectomy. Ann Thorac Surg 2002;74:180-184.[Abstract/Free Full Text]
  2. Tulevski I.I., Hirsch A., Sanson B.J., et al. Increased brain natriuretic peptide as a marker for right ventricular dysfunction in acute pulmonary embolism. Thromb Haemost 2001;86:1193-1196.[Medline]
  3. Tulevski I.I., Groenink M., Van der Wall E.E., et al. Increased brain and atrial natriuretic peptides in patients with chronic right ventricular pressure overload: correlation between plasma neurohomones and right ventricular dysfunction. Heart 2001;86:27-30.[Abstract/Free Full Text]
  4. Archibald C.J., Auger W.R., Fedullo P.F. Outcome after pulmonary thromboendarterectomy. Sem Thorac Cardiovasc Surg 1999;11:164-171.[Medline]
  5. Menzel T., Wagner S., Kramm T., et al. Pathophysiology of impaired right and left ventricular function in chronic embolic pulmonary hypertension: changes after pulmonary thromboendarterectomy. Chest 2000;118:897-903.[Abstract/Free Full Text]
  6. Tulevski I.I., Mulder B.J.M., Van Veldhuisen D.J. Utility of a BNP as a marker for RV dysfunction in acute pulmonary embolism. J Am Coll Cardiol 2002;39:2080.[Free Full Text]




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