Optimising ACE Inhibitor Therapy of Congestive Heart Failure

1993 ◽  
Vol 24 (1) ◽  
pp. 59-70 ◽  
Author(s):  
Robert J. Cody
1998 ◽  
Vol 14 (1) ◽  
pp. 7-11 ◽  
Author(s):  
Barry E Bleske ◽  
Laura A Cornish ◽  
Steven R Erickson ◽  
John M Nicklas

Objective: Angiotensin-converting enzyme (ACE) inhibitor therapy is considered the standard of care for the treatment of congestive heart failure. Despite this, clinical experience suggests that not all patients may be receiving ACE inhibitor therapy or may be receiving low dosages. This study was performed to better understand the use of ACE inhibitor therapy in clinical practice. Design and Participants: We reviewed the medical therapy of 110 patients with a history of congestive heart failure referred to an outpatient heart failure clinic at a university teaching hospital. Outcome Measures: This observational study evaluated the use of ACE inhibitors, including dosage, as well as other drugs to treat congestive heart failure. Results: Approximately 85% (93/110) of patients were receiving an ACE inhibitor. Twenty percent (22/110) were receiving enalapril 20 mg/d or more, captopril 150 mg/d or more, lisinopril 20 mg/d or more, or quinapril 40 mg/d or more. The remaining patients (n = 71) were receiving these drugs at lower dosages. However, 21 of the remaining patients (19% of all patients) were receiving lower dosages based on patient-specific parameters; 47 of the remaining patients (43% of all patients) were eligible to have their dosage increased. Ten eligible patients were not receiving an ACE inhibitor. The majority of patients were also receiving digoxin (70%) and loop diuretic (80%) therapy. Conclusions: Approximately 85% of patients were receiving ACE inhibitor therapy, with 9% of eligible patients not receiving an ACE inhibitor. In the patients receiving ACE inhibitor therapy, approximately 50% (47/93) were receiving dosages below those suggested in the guidelines. Overall, the use of ACE inhibitor therapy is varied and intervention appears required to ensure that all patients receive appropriate therapy for the treatment of congestive heart failure.


1999 ◽  
Vol 277 (5) ◽  
pp. H1924-H1930
Author(s):  
Ingrid M. Straeter-Knowlen ◽  
Louis J. Dell'italia ◽  
Jun Dai ◽  
Gerald H. Hankes ◽  
A. Raymond Dillon ◽  
...  

Chronic mitral regurgitation (MR) in dogs results in pulmonary congestion and increased cardiac angiotensin-converting enzyme (ACE) activity and angiotensin (ANG) II levels. ACE could contribute to altered pulmonary vasomotion in heart failure, and ACE inhibitor (ACEI) therapy may normalize pulmonary vasomotion. We evaluated pulmonary artery (PA) responses to ANG II and bradykinin (BK) in control dogs, in dogs with 4 mo of MR, in MR dogs treated with the ACEI ramipril (MR + R), and in control dogs treated with ramipril (C + R). Mean PA systolic pressure increased in MR dogs (21 ± 4 mmHg) but was normal in MR + R dogs (13 ± 1 mmHg). Constriction of PA rings to ANG II was depressed in MR dogs. ACEI treatment (MR + R) restored ANG II responsiveness, but peak ANG II response (3.6 ± 0.2 g) in MR + R dogs remained lower than in C + R dogs (4.7 ± 0.2 g). Endothelium-dependent relaxation to BK was decreased (−87 ± 4% C, −65 ± 4% MR; P < 0.05). Ramipril (MR + R) restored relaxation to BK. This demonstrates that pulmonary congestion results in impaired pulmonary vasomotion to ANG II and BK, which ACEIs could normalize, supporting the use of ACEIs in clinical management of chronic congestive heart failure.


Sign in / Sign up

Export Citation Format

Share Document