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Am J Physiol Heart Circ Physiol 290: H1064-H1070, 2006. First published September 19, 2005; doi:10.1152/ajpheart.00110.2005
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Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy

Shinsuke Kido,1 Naoyuki Hasebe,1 Yoshinao Ishii,2 and Kenjiro Kikuchi1

1First Department of Internal Medicine, Asahikawa Medical College, 2Department of Cardiology, Asahikawa City Hospital, Asahikawa, Hokkaido, Japan

Submitted 3 February 2005 ; accepted in final form 13 September 2005

The aim of this study was to investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP, respectively) in patients with hypertrophic cardiomyopathy (HCM). HCM patients with normal left ventricular (LV) systolic function and intact coronary artery (n = 22) underwent rapid atrial pacing test. The cardiac secretion of ANP and BNP and the lactate extraction ratio (LER) were evaluated by using blood samples from the coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and the time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal controls (n = 8). HCM patients were divided into obstructive (HOCM) and nonobstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384 ± 101 to 1,268 ± 334 pg/ml (P < 0.05); however, it was not significant in control and HNCM groups. In contrast, the cardiac secretion of BNP was fairly constant and rather significantly decreased in HCM (P < 0.01). The cardiac ANP secretion was significantly correlated with changes in LER (r = –0.57, P < 0.01) and tau (r = 0.73, P < 0.001) in HCM patients. Tachycardia potentiates the cardiac secretion of ANP, not BNP, in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction.

left ventricular outflow tract obstruction; lactate extraction ratio; left ventricular diastolic function; cardiac event; atrial and brain natriuretic peptides



Address for reprint requests and other correspondence: N. Hasebe, First Dept. of Internal Medicine, Asahikawa Medical College, 2-1-1-1 Midorigaoka Higashi, Asahikawa, Hokkaido 078-8510, Japan (email: haselove{at}asahikawa-med.ac.jp)







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