Bradyarrhythmia Can Increase the Plasma Level of N-Terminal Pro-Brain Natriuretic Peptide

Abstract

Background and Objectives Myocardial wall stretch is the main trigger for pro-brain natriuretic peptide (pro-BNP) secretion. The reduced heart rate associated with bradyarrhythmia increases stroke volume, resulting in increased wall tension. Therefore, we propose that bradyarrhythmia could increase plasma N-terminal pro-BNP (NT-pro-BNP) levels. Subjects and Methods We enrolled 125 patients who received a temporary pacemaker because they had sinus node dysfunction (SND) or atrioventricular blocks (AVBs). Patients with renal dysfunction, hyperkalemia, reduced left ventricular systolic function (left ventricular ejection fraction [LVEF], <40%), and atrial fibrillation were excluded. Heart failure (HF) was defined as an NT-pro-BNP level of >300 pg/mL. We evaluated history of hypertension, diabetes mellitus, and ischemic heart disease, plasma NT-pro-BNP levels, body mass index (BMI), LVEF, left atrial diameter (LAD), and escape rhythm rate. Results The log plasma NT-pro-BNP level of the patients with AVBs was significantly increased compared to that of the patients with SND (3.17±0.55 vs. 2.93±0.64 pg/mL, respectively; p=0.03). The incidence of HF was 72.5% (106 patients; 44 male patients). Further, the incidence of HF was significantly higher among patients with AVBs than among patients with SND. The type of bradyarrhythmia was found to be the only predictor of HF after adjusting for age, history of hypertension, LAD, and LVEF. The LVEF, LAD, and ventricular rate were similar between the 2 groups. Conclusion As in the case of patients with tachyarrhythmia, bradyarrhythmia may increase plasma NT-pro-BNP levels, leading to HF. Therefore, the possibility of HF should be considered in patients with bradyarrhythmia. Key words: Arrhythmias, Cardiac; Pro-Brain Natriuretic Peptide; Heart Failure