Neurohormonal mechanisms and the role of angiotensin-converting enzyme (ACE) inhibitors in heart failure

1994 ◽  
Vol 8 (5) ◽  
pp. 685-692 ◽  
Author(s):  
Andrew J. S. Coats ◽  
S. Adamopoulos
1990 ◽  
Vol 3 (5) ◽  
pp. 318-331
Author(s):  
Mark A. Munger ◽  
Stephanie F. Gardner ◽  
Robert C. Jarvis

The angiotensin-converting enzyme (ACE) inhibitors represent the gold standard of vasodilator therapy for congestive heart failure through blunting of the endocrinologic manifestations of heart failure. The future role of these agents may be in the asymptomatic and mild stages of heart failure. ACE inhibitors have been shown to decrease morbidity and mortality with the natural history of this disease being altered. The future will bring many new ACE inhibitors to market, with the challenge for physicians and pharmacists to understand the important distinctions of each specific agent. © 1990 by W.B. Saunders Company.


1998 ◽  
Vol 8 (1) ◽  
pp. 89-92
Author(s):  
L Woosnam ◽  
M Hasan

The clinical syndrome of heart failure affects more than 1% of the population, and its prevalence increases steeply with advancing age, especially after 75, where it reaches approximately 10%. It is one of the commonest reasons for the admission of elderly people to hospital.Despite recent advances in treatment of heart failure with angiotensin-converting enzyme (ACE) inhibitors, which were proven to provide survival benefit, the rates of morbidity and mortality from heart failure remain high, and new therapeutic strategie s are needed.


2020 ◽  
Vol 41 (19) ◽  
pp. 1810-1817 ◽  
Author(s):  
Iziah E Sama ◽  
Alice Ravera ◽  
Bernadet T Santema ◽  
Harry van Goor ◽  
Jozine M ter Maaten ◽  
...  

Abstract Aims The current pandemic coronavirus SARS-CoV-2 infects a wide age group but predominantly elderly individuals, especially men and those with cardiovascular disease. Recent reports suggest an association with use of renin–angiotensin–aldosterone system (RAAS) inhibitors. Angiotensin-converting enzyme 2 (ACE2) is a functional receptor for coronaviruses. Higher ACE2 concentrations might lead to increased vulnerability to SARS-CoV-2 in patients on RAAS inhibitors. Methods and results We measured ACE2 concentrations in 1485 men and 537 women with heart failure (index cohort). Results were validated in 1123 men and 575 women (validation cohort). The median age was 69 years for men and 75 years for women. The strongest predictor of elevated concentrations of ACE2 in both cohorts was male sex (estimate = 0.26, P < 0.001; and 0.19, P < 0.001, respectively). In the index cohort, use of ACE inhibitors, angiotensin receptor blockers (ARBs), or mineralocorticoid receptor antagonists (MRAs) was not an independent predictor of plasma ACE2. In the validation cohort, ACE inhibitor (estimate = –0.17, P = 0.002) and ARB use (estimate = –0.15, P = 0.03) were independent predictors of lower plasma ACE2, while use of an MRA (estimate = 0.11, P = 0.04) was an independent predictor of higher plasma ACE2 concentrations. Conclusion In two independent cohorts of patients with heart failure, plasma concentrations of ACE2 were higher in men than in women, but use of neither an ACE inhibitor nor an ARB was associated with higher plasma ACE2 concentrations. These data might explain the higher incidence and fatality rate of COVID-19 in men, but do not support previous reports suggesting that ACE inhibitors or ARBs increase the vulnerability for COVID-19 through increased plasma ACE2 concentrations.


2002 ◽  
Vol 36 (3) ◽  
pp. 471-478 ◽  
Author(s):  
James S Kalus ◽  
Jean M Nappi

OBJECTIVE: To review the literature assessing the differences in response to angiotensin-converting enzyme (ACE) inhibitors and β-blockers in black patients compared with the response in non-black patients in the management of systolic heart failure. DATA SOURCES: A MEDLINE search (January 1966–May 2001) was performed using heart failure, blacks, Negroid race, adrenergic β-antagonists, and angiotensin-converting enzyme inhibitors as key words. English-language articles were identified. Additional pertinent articles were identified from review of the references of these articles. STUDY SELECTION AND DATA EXTRACTION: All identified references were reviewed. All articles deemed relevant to the subject of this article were included. DATA SYNTHESIS: It has been suggested that the antihypertensive effect of ACE inhibitors and β-blockers may be less in black patients than in other racial groups. Retrospective reanalyses of major heart failure trials have suggested that black patients may not realize a significant benefit in morbidity or mortality when heart failure is managed with ACE inhibitors or β-blockers. It has also been suggested that black patients may respond more favorably than non-black patients to the combination of hydralazine and isosorbide dinitrate. CONCLUSIONS: Published reanalyses of ACE inhibitor and β-blocker trials in heart failure provide weak data to support a lack of benefit in black patients. The published literature on this topic is limited by its retrospective nature. Firm conclusions regarding the influence of race on effectiveness of ACE inhibitors and β-blockers cannot be made until prospective trials, with planned analysis of the effect of race, have been performed.


Circulation ◽  
2000 ◽  
Vol 101 (8) ◽  
pp. 844-846 ◽  
Author(s):  
Ulrich P. Jorde ◽  
Pierre V. Ennezat ◽  
Jay Lisker ◽  
Vanarani Suryadevara ◽  
Jason Infeld ◽  
...  

2013 ◽  
Vol 305 (3) ◽  
pp. R205-R215 ◽  
Author(s):  
Derick Okwan-Duodu ◽  
Jerome Landry ◽  
Xiao Z. Shen ◽  
Roberto Diaz

The renin angiotensin system (RAS) is a network of enzymes and peptides that coalesce primarily on the angiotensin II type 1 receptor (AT1R) to induce cell proliferation, angiogenesis, fibrosis, and blood pressure control. Angiotensin-converting enzyme (ACE), the key peptidase of the RAS, is promiscuous in that it cleaves other substrates such as substance P and bradykinin. Accumulating evidence implicates ACE in the pathophysiology of carcinogenesis. While the role of ACE and its peptide network in modulating angiogenesis via the AT1R is well documented, its involvement in shaping other aspects of the tumor microenvironment remains largely unknown. Here, we review the role of ACE in modulating the immune compartment of the tumor microenvironment, which encompasses the immunosuppressive, cancer-promoting myeloid-derived suppressor cells, alternatively activated tumor-associated macrophages, and T regulatory cells. We also discuss the potential roles of peptides that accumulate in the setting of chronic ACE inhibitor use, such as bradykinin, substance P, and N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), and how they may undercut the gains of anti-angiogenesis from ACE inhibition. These emerging mechanisms may harmonize the often-conflicting results on the role of ACE inhibitors and ACE polymorphisms in various cancers and call for further investigations into the potential benefit of ACE inhibitors in some neoplasms.


Sign in / Sign up

Export Citation Format

Share Document