Submitted on February 3, 2005
Accepted on September 13, 2005
Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP in hypertrophic cardiomyopathy
Shinsuke Kido1, Naoyuki Hasebe1*, Yoshinao Ishii2, and Kenjiro Kikuchi1
1 First Department of Internal Medicine, Asahikawa Medical College, Asahikawa, Hokkaido, Japan
2 Department of Cardiology, Asahikawa City Hospital, Asahikawa, Hokkaido, Japan
* To whom correspondence should be addressed. E-mail: haselove{at}asahikawa-med.ac.jp.
Aims: To investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP) in patients with hypertrophic cardiomyopathy (HCM). Methods: 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 using blood samples from coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal control (n=8). Results: HCM patients were divided into obstructive (HOCM) and non-obstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384±101 to 1268±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, 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. Conclusions: Tachycardia potentiates the cardiac secretion of ANP, not BNP in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction.
