| Angiotensin-converting enzyme genotype modulates pulmonary function and exercise capacity in treated patients with congestive stable heart failure. | |
| | |
MedLine Citation:
|
PMID: 12356632 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
BACKGROUND: The gene encoding ACE exhibits an insertion/deletion polymorphism resulting in 3 genotypes (DD, ID, and II), which affects serum and tissue ACE activity as well as other vasoactive substances. Pulmonary function is frequently abnormal in patients with congestive heart failure (CHF), the mechanism of which has not been completely characterized. ACE inhibition has been shown to improve diffusion across the alveolar-capillary membrane and to improve exercise capacity and gas exchange in CHF. The aim of the current study was to determine if ACE genotype is associated with altered pulmonary function and exercise intolerance in patients with treated CHF. METHODS AND RESULTS: Fifty-seven patients (stratified according to ACE genotype as 17 DD, 28 ID, 12 II) with ischemic and dilated cardiomyopathy, left ventricular ejection fraction (LVEF) <35%, and <10 pack-years of smoking history were studied. All patients were receiving standard therapy for left ventricular systolic dysfunction. Pulmonary function, LVEF, serum ACE, plasma angiotensin II, atrial natriuretic peptide, and brain natriuretic peptide were measured at baseline. Peak VO2 and gas exchange measurements were assessed with graded exercise. Resting LVEF was similar among the genotype groups (25% to 28%), and no differences were observed in diastolic function or pulmonary artery pressures (P>0.05). Mean peak VO2 and forced vital capacity (% Pred) were significantly reduced (P<0.05), whereas mean serum ACE activity and plasma angiotensin II concentration were highest in DD homozygotes. Subjects homozygous for the D-allele also demonstrated higher mean ventilatory equivalents for carbon dioxide (VE/VCO2) during exercise (P<0.05). CONCLUSIONS: ACE DD genotype is associated with decreased exercise tolerance in CHF, possibly mediated by altered pulmonary function. Pharmacological strategies effecting more complete inhibition of serum and tissue ACE and/or potentiation of bradykinin may improve exercise capacity in patients with CHF and ACE DD genotype. |
| | |
Authors:
|
M Roselle Abraham; Lyle J Olson; Michael J Joyner; Stephen T Turner; Ken C Beck; Bruce D Johnson |
Publication Detail:
|
Type: Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
|
Title: Circulation Volume: 106 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 2002 Oct |
Date Detail:
|
Created Date: 2002-10-01 Completed Date: 2002-10-24 Revised Date: 2007-11-15 |
Medline Journal Info:
|
Nlm Unique ID: 0147763 Medline TA: Circulation Country: United States |
Other Details:
|
Languages: eng Pagination: 1794-9 Citation Subset: AIM; IM |
Affiliation:
|
Division of Cardiovascular, Mayo Clinic and Foundation, Rochester, Minn 55905, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Angiotensin II
/
blood Atrial Natriuretic Factor / blood Echocardiography Exercise Test Exercise Tolerance / genetics* Female Genotype Heart Failure / blood, physiopathology*, therapy Humans Lung / physiopathology* Male Middle Aged Natriuretic Peptide, Brain / blood Peptidyl-Dipeptidase A / blood, genetics* Pulmonary Gas Exchange Regression Analysis Respiratory Function Tests Stroke Volume |
| Grant Support | |
ID/Acronym/Agency:
|
HL71478/HL/NHLBI NIH HHS; M01-RR00585/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
|
11128-99-7/Angiotensin II; 114471-18-0/Natriuretic Peptide, Brain; 85637-73-6/Atrial Natriuretic Factor; EC 3.4.15.1/Peptidyl-Dipeptidase A |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: 7-hexanoyltaxol-eluting stent for prevention of neointimal growth: an intravascular ultrasound analy...
Next Document: Emotional and physical precipitants of ventricular arrhythmia.