Gene Variant of the Bradykinin B2 Receptor Influences Pulmonary Arterial Pressures in Heart Failure Patients

2009 ◽  
Vol 3 ◽  
pp. CCRPM.S2147
Author(s):  
Thomas P. Olson ◽  
Robert P. Frantz ◽  
Stephen T. Turner ◽  
Kent R. Bailey ◽  
Christina M. Wood ◽  
...  

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 (>1yr 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%, NYHA class 2 ∓ 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. PAPsys averaged 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 in stable HF.

EP Europace ◽  
2003 ◽  
Vol 4 (Supplement_2) ◽  
pp. B105-B105
Author(s):  
M. Heinke ◽  
H. Kuhnert ◽  
R. Surber ◽  
G. Dannberg ◽  
H.R. Figulla ◽  
...  

2016 ◽  
Vol 10 ◽  
pp. CMC.S38447
Author(s):  
Valentine N. Amadi ◽  
Olufemi E. Ajayi ◽  
Anthony O. Akintomide ◽  
Olugbenga O. Abiodun ◽  
Olaniyi J. Bamikole ◽  
...  

Background Pulmonary hypertension (PH) is common in heart failure patients. Literature on PH in heart failure is sparse in Nigeria. This study was carried out to determine the prevalence of PH in heart failure patients and ascertain the relationship between left ventricular systolic and diastolic function and the degree of PH. Methods A total of 125 heart failure patients had echocardiography done. PH was diagnosed using tricuspid regurgitation jet and pulmonary ejection jet profile. Results PH was present in 70.4% of heart failure patients. Estimated mean pulmonary arterial pressure increased with increasing severity of systolic and diastolic dysfunction and had significantly negative correlation with ejection fraction, fractional shortening, and early mitral annular tissue diastolic velocity ( E′), but positive correlation with left ventricular end-systolic volume, right ventricular dimension, transmitral E to A ratio, and E/E′ ratio. Conclusion PH is very common in heart failure and has significant relationship with left ventricular function.


2017 ◽  
Vol 11 ◽  
pp. 117954681774663
Author(s):  
Tuoyo Omasan Mene-Afejuku ◽  
Michael Olabode Balogun ◽  
Anthony Olubunmi Akintomide ◽  
Rasaaq Ayodele Adebayo ◽  
Olufemi Eyitayo Ajayi ◽  
...  

Background: Hypertensive heart failure (HHF) is the commonest form of heart failure in Nigeria. There is paucity of data in Nigeria on 24-hour Holter electrocardiography (24-HHECG) and important predictors of arrhythmias among HHF patients. Objectives: To determine the 24-HHECG characteristics among HHF patients. To determine the clinical and echocardiographic predictors of arrhythmias detected using 24-HHECG among HHF patients. Methods: A total of 100 HHF patients as well as 50 age-matched and sex-matched apparently healthy controls were prospectively recruited over a period of 1 year. They all had baseline laboratory tests, echocardiography, and 24-HHECG. Results: Hypertensive heart failure patients had significantly higher counts of premature ventricular contractions (PVCs) than the controls ( P ≤ .001). Ventricular tachycardia (VT) was recorded in 29% of HHF patients as compared with controls who had no VT on 24-HHECG. The standard deviation of all normal to normal sinus RR intervals over 24 hours (SDNN) was abnormally reduced among HHF patients when compared with controls ( P = .046). There was positive correlation between atrial fibrillation (AF) and the following parameters: PVCs ( r = .229, P = .015), New York Heart Association (NYHA) ( r = .196, P = .033), and VT ( r = .223, P = .018). Following multiple linear regression, left ventricular ejection fraction (LVEF) ( P ≤ .001) and serum urea ( P = .037) were predictors of PVCs among HHF patients. Serum creatinine ( P ≤ .001), elevated systolic blood pressure (SBP) ( P = .005), and PVCs ( P ≤ .001) were important predictors of VT among HHF patients. Conclusions: Renal dysfunction and reduced LVEF were important predictors of ventricular arrhythmias. High counts of PVCs and elevated SBP were predictive of the occurrence of VT among HHF patients. The NYHA class and ventricular arrhythmias have a significant positive correlation with AF. The SDNN is reduced in HHF patients.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 5039-5039 ◽  
Author(s):  
Xhylsime Kqiku ◽  
Gabor Kovacs ◽  
Sonja Reitter ◽  
Heinz Sill ◽  
Horst Olschewski

Abstract Abstract 5039 Background: Pulmonary hypertension (PH) is characterized by elevated pulmonary arterial pressure and increased pulmonary vascular resistance, leading to right-sided heart failure and death. PH is defined as an increase in mean pulmonary arterial pressure (mPAP) ≥25 mmHg at rest. PAP values can be non-invasively estimated by Doppler echocardiography while right heart catheterization is needed for definite diagnosis. Hematologic disorders are associated with PH but it is unknown if myelodysplastic syndromes (MDS) bear an increased risk for PH. The objective of this study was to investigate the prevalence of PH in patients with MDS. Patients and Methods: From March 2009 to July 2011 consecutive MDS patients were recruited from the Hematology Division of the Medical University of Graz and enrolled in this PH screening program. All patients underwent Doppler echocardiography. PH was suspected if resting systolic pulmonary arterial pressure (SPAP) exceeded 40 mmHg. Additionally six minute walk distance (6MWD), pulmonary function test (PFT), laboratory tests including N-terminal pro brain natriuretic peptide (NT-proBNP), IPSS Score and WHO functional class were determined. Results: Fourty four MDS patients (female:male=18:26, age 70±12 years, disease onset 5±8 years, NYHA functional class I:II:III:IV=21:16:7:0, IPSS low/intermediate-I/intermediate- II/high/unknown=16:14:8:3:3; hemoglobin: 11±2 g/dl, white blood cell count 4±3 g/l; platelet count 159±125 g/l; regular transfusions n=19; WHO Classification: RCUD/RARS/RCMD/MDS del(5q)/RAEBI/RAEB II/MDSU=2:3:21:2:6:6:4 ) were included. Six patients had elevated SPAP (PH group, SPAP: 56±9mmHg) vs. 38 patients with normal values (SPAP 29±5mmHg). PH group were slightly older (79±9 vs. 69±11 years, p=0.53), had a decreased right ventricular function (TAPSE: 18±5mm vs. 22±4mm, p=0.05), a larger left atrium (46±5mm vs. 36±9mm measured in the parasternal long axis, p=0.005), a slightly decreased left ventricular systolic function (fractional shortening: 30±11% vs. 38±9 %, p=0.1) a significantly lower 6MWD (275±117m vs. 438±105m, p=0.01) and higher NT proBNP (4515±4732 pg/ml vs. 313±252 pg/ml, p=0.001) than patients with normal SPAP. In 4/6 PH group patients a relevant diastolic dysfunction of the left ventricle was suggested by echocardiography. Conclusion: According to our data, PH is present in about 15% of MDS patients and is associated with decreased physical capacity and heart failure. This suggests that PH may be considered as a relevant comorbidity in this cohort of patients. The reason of PAP increase may be multifactorial, postcapillary factors probably playing a relevant role. Disclosures: No relevant conflicts of interest to declare.


Circulation ◽  
2001 ◽  
Vol 104 (suppl_1) ◽  
Author(s):  
Wolfgang F. Konertz ◽  
J. Edward Shapland ◽  
Holger Hotz ◽  
Simon Dushe ◽  
Jan Peter Braun ◽  
...  

Background Progressive remodeling and dilation of cardiac chambers is responsible in part for myocardial dysfunction in chronic heart failure. Preclinical studies with suitable animal models indicate that a passive cardiac constraint device can promote reverse remodeling, with improvement in cardiac function. We hypothesize that such a device could provide benefit for stable heart failure patients in New York Heart Association (NYHA) class II and III . Methods and Results From April 1999 to March 2000, 27 patients received Acorn’s Cardiac Support Device (CSD) during an initial safety/feasibility study. In 11 patients, the only surgical measure was CSD placement. Most patients suffered from idiopathic cardiomyopathy; 4 were in NYHA class II, one was in class II/III, and 6 were in class III. All were stable on intensive medical treatment. The CSD, a textile polyester device, was fitted snugly around the heart during surgery. All patients survived surgery and recovered smoothly. Three months after surgery, 56% of patients were in NYHA class I, 33% were in class II, and 11% were in class II/III. Echocardiography showed an improvement in left ventricular ejection fraction from an average of 22% to 28% and 33% at 3 and 6 months, respectively. Simultaneously, the left ventricular end-diastolic dimension decreased from 74 mm to 68 mm and 65 mm, respectively. Mitral valve regurgitation (on a scale of 0 to 4+) decreased from 1.3 to 0.7 by 3 months. Quality-of-life indices correlated with the apparent reversal of ventricular remodeling. Preoperative cardiac medications remained virtually unchanged after implant. Conclusions In the short- and intermediate-term, CSD implantation seems to ameliorate symptoms and improve cardiac and functional performance in heart failure patients. Worldwide randomized trials are currently underway.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Lucas S Zier ◽  
Christopher Barnett ◽  
Elyse Foster

A thirty year-old man with an unknown surgery for congenital heart disease presented with intermittent chest pain and progressive decline in his exercise tolerance. Cardiovascular examination revealed a soft S1, loud S2 without splitting, right ventricular heave, a sustained and laterally displaced apical impulse and clubbing of his fingers. An echocardiogram showed d-transposition of the great arteries (d-TGA), a dilated, sub-pulmonic left ventricle (LV) with reduced function, smaller than expected sub-aortic right ventricle with reduced function, and elevated sub-pulmonic left ventricular systolic pressure without LV outflow tract obstruction. Cardiac MRI revealed d-TGA status post Senning repair, biventricular dysfunction without baffle obstruction, no evidence of repaired atrial or ventricular septal defect or delayed gadolinium enhancement. Cardiac catheterization showed a suprasystemic pulmonary artery pressure, a pulmonary vascular resistance of 18.4 Wood units and a small right to left shunt due to a baffle leak. No coronary disease was found on angiography. The patient was diagnosed with severe pulmonary arterial hypertension and biventricular dysfunction. This pattern of heart failure was discordant from the expected sequelae of palliated congenital heart defects as pulmonary arterial hypertension and LV dysfunction are both uncommon long-term complications after atrial switch. Systematic evaluation for a unifying cause of the patient’s pattern of heart failure was unrevealing until the patient presented with decompensated heart failure and evidence of stimulant withdrawal. Urine toxicology was positive for methamphetamine and the patient was diagnosed with methamphetamine induced pulmonary arterial hypertension and subpulmonic LV dysfunction. This case demonstrates the importance of understanding the common, long-term patterns of heart failure in repaired congenital heart disease and the need to search for alternative etiologies when the pattern is inconsistent. This case further shows the toxic effects of methamphetamine on the pulmonary vasculature and myocardium, which in our patient resulted in a highly unique pattern of sub-pulmonic LV dysfunction and pulmonary arterial hypertension.


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