International Journal of Cardiology 123 (2008) e43 – e44 www.elsevier.com/locate/ijcard
Letter to the Editor
Bradycardia can induce increased serum natriuretic peptide-level Tímea Kováts, András Wettstein, Erzsébet Nagy, János Tomcsányi ⁎ St. John of God Hospital, Budapest, Hungary Received 27 September 2006; accepted 18 November 2006 Available online 27 February 2007
Abstract Here we report a case of an elderly woman whose antihypertensive beta-blocker therapy induced sinus arrest with a 40 bpm junctional escape rhythm. Although there was no sign of heart failure during bradycardia, a highly elevated amino-terminal pro-brain natriuretic peptide (NT-proBNP) serum level was detected. Cessation of the beta-blocker agent resulted in normal sinus rhythm and a rapid fall in the NTproBNP serum level. As a rare phenomenon, bradycardia-related cardiomyopathy is discussed. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Bradycardia; Brain natriuretic peptide (BNP); Beta-blocker
A 94 year-old woman was admitted to our department after 4 days of worsening weakness and dyspnea. She had no symptoms of angina. Her medical history included recurrent basal cell carcinoma, vertebrobasilar insufficiency, and hypertension. Beta-blocker (5 mg bisoprolol per day) and thiazide diuretics were administered as an antihypertensive therapy. At admission, her blood pressure was 120/ 80 mm Hg, pulse rate was 44 bpm. There was no sign of overt heart failure. The 12-lead electrocardiogram showed sinus arrest with narrow-QRS complex junctional escape rhythm (Fig. 1). Routine laboratory tests (including TSH and troponin-T) displayed normal values. However, aminoterminal pro-brain natriuretic peptide (NT-proBNP) serum level was highly increased (22420 pg/ml; normal reference value is below 270 pg/ml). Echocardiographic findings displayed normal systolic ventricular function and mild degenerative mitral and aortic insufficiency. Beta-blocker therapy was discontinued for assumed therapy-induced bradyarrhythmia. Due to the stabile hemodynamic parameters, temporary pacemaker was not implanted.
⁎ Corresponding author. BIK Hospital, Cardiology Department, Árpád fejedelem ú. 7, Budapest 1027 Hungary. E-mail address:
[email protected] (J. Tomcsányi). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.11.144
The patient's bradyarrhythmia resolved in 48 h and sinus rhythm with 90 bpm frequency returned (Fig. 2). Control NT-proBNP serum level was markedly lower (2117 pg/ml). Free from her actual symptoms the patient was discharged from the hospital. While tachycardia-related cardiomyopathy is a wellknown and frequent cause of arrhythmia-induced elevated natriuretic peptide level [1–3], bradycardia-related cardiomyopathy is a rare phenomenon. In our case report, the betablocker therapy-triggered bradyarrhythmia (sinus arrest with junctional escape rhythm) was followed by a parallel marked increase in the serum NT-proBNP level, which promptly decreased after the cessation of the arrhythmia. In patients with decreased left ventricular function, betablockers' negative inotropic effect can explain the initial NT-proBNP elevation [4]. However, highly increased serum NT-proBNP level due to maintained beta-blocker therapy, to our knowledge, is not known, and the negative inotropic effect of the beta-blockers alone does not provide a sufficient explanation for the extremely elevated NTproBNP level. The main trigger for regulated BNP secretion is the myocardial wall stretch [5]. In the present case, increased myocardial wall stretch was induced by bradyarrhytmia. However, the bradyarrhytmic episode was not long enough to cause left ventricular systolic dysfunction or dilation.
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Fig. 1. At admittance, electrocardiogram showed sinus arrest with junctional escape rhythm (HR: 44 bpm).
Fig. 2. After cessation of the beta-blocker therapy, electrocardiogram showed restored sinus rhythm (HR: 90 bpm).
Our aim with this study is to point out that not only tachycardia, but also bradycardia can cause cardiomyopathy, and elevated NT-proBNP level caused by increased myocardial wall stretch might indicate even the subclinical cardiomyopathy [6]. References [1] Crozier IG, Ikram H, Nicholls MG, Espiner EA, Yandle TG. Atrial natriuretic peptide in spontaneous tachycardias. Br Heart J 1987;58(2): 96–100. [2] Jourdain P, Bellorini M, Funck F, et al. Short-term effects of sinus rhythm restoration in patients with lone atrial fibrillation: a hormonal study. Eur J Heart Fail 2002;4(3):263–7.
[3] Kido S, Hasebe N, Ishii Y, Kikuchi K. Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy. Am J Physiol Heart Circ Physiol 2006;290(3):H1064–70. [4] Hartmann F, Packer M, Coats AJS, et al. NT-proBNP in severe chronic heart failure: rationale, design and preliminary results of the COPERNICUS NT-proBNP substudy. Eur J Heart Fail 2004;6(3): 343–50. [5] Schmitt M, Cockcroft JR, Frenneaux MP. Modulation of the natriuretic peptide system in heart failure: from bench to bedside? Clin Sci (Lond) 2003;105(2):141–60. [6] Wang TJ, Larson MG, Levy D, et al. Plasma natriuretic peptide levels and the risk of cardiovascular events and death. N Engl J Med 2004;350(7): 655–63.
