Second Propedeutic Department of Internal Medicine, Hippokration General Hospital, Aristotle University of Thessaloniki, 63 Solonos Street, 54248 Thessaloniki, Greece
Received May 7, 2004; accepted May 26, 2004 * Corresponding author. Tel.: +30 2310892058; fax: +30 2310992834 (E-mail: ktziomalos{at}yahoo.com).
Dear Editor,
We read with great interest the paper by Cowie et al., on clinical applications of B-type natriuretic peptide (BNP) testing.1 Atrial (ANP) and B-type natriuretic peptide are peptide hormones released in response to myocyte stretch. Novel biomarkers have been evaluated for four clinical purposes: prognostic screening in asymptomatic individuals, risk stratification in patients with clinical disease, diagnosis of clinical disease in patients with symptoms of uncertain cause and guidance in the selection or titration of drugs in patients with known disease. A dramatic rise in the number of studies exploring the potential clinical use of measurement of the natriuretic peptides for all the above purposes has been observed after the development of commercially available assays for both B-type natriuretic peptide and its inactive N-terminal fragment.
Left ventricular hypertrophy (LVH) is a strong risk factor for future cardiovascular events independent of blood pressure levels in patients with essential hypertension. Electrocardiographic criteria for LVH have proven to be insensitive. The most widely used method for estimating LVH is echocardiography, but it seems to be uneconomical. Therefore, a simple screening test might be highly useful for early identification of patients who might benefit from intensive therapy. In the literature, there are conflicting reports about the use of BNP as a marker for LVH in hypertensives.24 We have shown that in patients with essential hypertension, plasma BNP levels were positively correlated with left ventricular mass index, while plasma ANP levels did not have a similar correlation. Plasma concentrations of BNP and ANP were slightly higher in hypertensive patients in comparison to normotensive controls, but there was no statistically significant difference between the two groups. Plasma BNP and ANP levels were not correlated with systolic, diastolic and pulse pressure.5
The above results could be explained from the secretion of BNP primarily by ventricular myocytes. Elevated plasma BNP levels are considered to reflect ventricular structural and functional alterations. Increased cardiac chamber wall stretch is the major stimuli for the release of natriuretic peptides. ANP secretion is immediately released in response to atrial stretch, while BNP secretion usually requires a long-term stimulus. However, it is well-known that plasma BNP levels are affected by age, gender renal failure and drugs, such as β-blockers and diuretics.1 It has also been reported that plasma BNP levels may be elevated before the establishment of left ventricular hypertrophy in hypertensive patients.6 In conclusion, although it seems that plasma B-type natriuretic peptide is related to left ventricular mass in patients with essential hypertension, the above mentioned multi-factorial aetiology of elevated plasma BNP levels shows that they must not be used as a replacement for echocardiography in the clinical assessment of left ventricular hypertrophy.
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