TY - JOUR
T1 - Gene variant of the bradykinin B2 receptor influences pulmonary arterial pressures in heart failure patients
AU - Olson, Thomas P.
AU - Frantz, Robert P.
AU - Turner, Stephen T.
AU - Bailey, Kent R.
AU - Wood, Christina M.
AU - Johnson, Bruce D.
PY - 2009
Y1 - 2009
N2 - Background: Pulmonary arterial pressure (PAP) varies considerably in heart failure (HF) despite similar degrees of left ventricular (LV) dysfunction. Bradykinin alters vascular tone and common variations in the kinin B2 receptor (BDKRB2) gene exists. We hypothesized that genetic variation in this receptor would influence PAP in HF. Methods: 131 HF patients (> lyr history systolic HF), without COPD, not currently smoking, BMI < 40, without atrial fibrillation completed the study which included a blood draw for genotyping and neurohormones, (ACE, A-II, Bradykinin, ANP, BNP, and catecholamines), an echocardiogram for cardiac function and systolic PAP (PAPsys). Results: Mean LVEF was 29%±12%,NYHAclass 22+1, age 56±12 yr, BMI 28±5 kg/m2. Forty-six patients(35%) were homozygous for the +9 allele, 58 (44%) were heterozygous (+9/-9) and 27 (21 %)were homozygous for the -9 allele of the BDKRB2. PAPsysaveraged 42±13, 38±12, and 35±11 mmHg for +9/+9,+9/-9 and -9/ -9, respectively (p = 0.03). There was a trend towards gene effect for plasma ACE with the highest values in +9/+9 and lowest in -9/-9 patients (9.5±10.7, 7.1±8.7, and 5.4±6.4 U/L, respectively, p=0.06). There were no differences in plasma bradykinin or A-II, LVEF, or NYHA across genotypes. Conclusion: These data suggest the +9/+9 polymorphism of the BDKRB2 receptor influences pulmonary vascular tone instable HF.
AB - Background: Pulmonary arterial pressure (PAP) varies considerably in heart failure (HF) despite similar degrees of left ventricular (LV) dysfunction. Bradykinin alters vascular tone and common variations in the kinin B2 receptor (BDKRB2) gene exists. We hypothesized that genetic variation in this receptor would influence PAP in HF. Methods: 131 HF patients (> lyr history systolic HF), without COPD, not currently smoking, BMI < 40, without atrial fibrillation completed the study which included a blood draw for genotyping and neurohormones, (ACE, A-II, Bradykinin, ANP, BNP, and catecholamines), an echocardiogram for cardiac function and systolic PAP (PAPsys). Results: Mean LVEF was 29%±12%,NYHAclass 22+1, age 56±12 yr, BMI 28±5 kg/m2. Forty-six patients(35%) were homozygous for the +9 allele, 58 (44%) were heterozygous (+9/-9) and 27 (21 %)were homozygous for the -9 allele of the BDKRB2. PAPsysaveraged 42±13, 38±12, and 35±11 mmHg for +9/+9,+9/-9 and -9/ -9, respectively (p = 0.03). There was a trend towards gene effect for plasma ACE with the highest values in +9/+9 and lowest in -9/-9 patients (9.5±10.7, 7.1±8.7, and 5.4±6.4 U/L, respectively, p=0.06). There were no differences in plasma bradykinin or A-II, LVEF, or NYHA across genotypes. Conclusion: These data suggest the +9/+9 polymorphism of the BDKRB2 receptor influences pulmonary vascular tone instable HF.
KW - Genetics
KW - Heart failure
KW - Hemodynamics
KW - Pulmonary hypertension
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U2 - 10.4137/ccrpm.s2147
DO - 10.4137/ccrpm.s2147
M3 - Article
AN - SCOPUS:62849090490
SN - 1179-5484
VL - 2009
SP - 9
EP - 17
JO - Clinical Medicine: Circulatory, Respiratory and Pulmonary Medicine
JF - Clinical Medicine: Circulatory, Respiratory and Pulmonary Medicine
IS - 3
ER -