LETTER TO THE EDITOR
Utility of a BNP as a marker for RV dysfunction in acute pulmonary embolism
Igor I. Tulevski, MD
Department of Cardiology, Rm. B2-239, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
Barbara J. M. Mulder, MD, PhD and
Dirk J. van Veldhuisen, MD, PhD, FACC
i.i.tulevski{at}amc.uva.nl
We read with interest the study by Morrison et al. (1), in which it was shown that rapid measurement of brain natriuretic peptide (BNP) concentrations in blood is a sensitive and specific test for differentiating patients with heart failure from those with primary pulmonary causes of dyspnea in acute-care settings. The investigators stated that correct, accurate and early diagnosis of left ventricular (LV) dysfunction is imperative for improved survival. However, recent data indicate that this statement also applies to right ventricular (RV) dysfunction (2,3). The clinical diagnosis of RV dysfunction, however, is usually more complex than that of LV dysfunction. The RV function plays an important role in conditions of increased pulmonary vascular resistance (such as pulmonary embolism), resulting in increased workload of the RV and eventually in RV dysfunction and failure. Right ventricular function may deteriorate with increase in RV afterload accompanied by an increase in neurohormonal activation, but the increase of RV systolic pressure will be limited (2,3). A suddenly increased pressure load on the RV, is poorly tolerated because of the inability of the normally thin-walled RV to develop and sustain high wall tension and stress (3).
In two recent studies (2,3) we showed there was no correlation between RV systolic pressure and BNP levels. In our opinion (unpublished results involving 114 patients with acute pulmonary embolism), patients with relatively low RV systolic pressure and high BNP (above 180 pg/ml) are at imminent risk for RV failure.
Concerning prognosis and management of patients with acute pulmonary embolism, BNP concentrations between 80 and 300 pg/ml are of particular interest (3). Indeed, low BNP levels have excellent negative predictive value, and most patients with high BNP levels probably have clinically manifest heart failure, leaving patients with intermediate BNP levels in a "difficult to interpret" zone. Serial BNP measurements in combination with echocardiography should help to solve this important clinical problem.
We found significantly higher plasma BNP levels in patients with RV dysfunction due to pulmonary embolism compared to patients with pulmonary embolism and normal RV function (3).
Therefore, BNP is of clinical importance as a supplementary tool for assessment of RV function and discrimination among patients with normal RV function, RV dysfunction, and RV failure under circumstances of acute RV pressure overload. This might add to the purpose of the Morrison et al. (1) study and differentiate heart failure from dyspnea of pulmonary etiologies even more accurately.
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References
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1. Morrison LK, Harrison A, Krishnaswamy P, et al. Utility of a rapid B-natriuretic peptide assay in differentiating congestive heart failure from lung disease in patients presenting with dyspnea. J Am Coll Cardiol. 2002;39:202–209[Abstract/Free Full Text]
2. Tulevski II, Groenink M, van der Wall EE, et al. Increased brain and atrial natriuretic peptides in patients with chronic right ventricular pressure overload: correlation between plasma neurohormones and right ventricular dysfunction. Heart. 2001;86:27–30[Abstract/Free Full Text]
3. Tulevski II, Hirsch A, Sanson BJ, et al. Increased brain natriuretic peptide as a marker for right ventricular dysfunction in acute pulmonary embolism. Thromb Haemost. 2001;86:1193–1196[Medline]
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