Angioedema secondary to angiotensin-converting enzyme inhibitors

1994 ◽  
Vol 108 (8) ◽  
pp. 696-698 ◽  
Author(s):  
J. P. M. Pracy ◽  
J. A. McGlashan ◽  
R. M. Walsh ◽  
M. J. Gleeson

AbstractAngioedema secondary to angiotensin-converting enzyme (ACE) inhibitors is rare, but it is a side effect which is likely to be seen more frequently because of the increased use of these drugs to treat cardiac failure and hypertension. Presentation is variable and the diagnosis may go unrecognized for many months or years. The cases reported illustrate problems both in the diagnosis and management of this life-threatening condition.

2010 ◽  
Vol 1 (1) ◽  
pp. 62-64
Author(s):  
A. S Galyavich

The paper analyzes the use of angiotensin-converting enzyme (ACE) inhibitors in patients after prior myocardial infarction. It presents the data of controlled studies, which indicate that it is warranted to use ACE inhibitors to improve prognosis in patients. It is concluded that it is unreasonable for a physician not to prescribe ACE inhibitors to post-myocardial infarction patients with obvious or asymptomatic left ventricular dysfunction and to diabetic patients (if no contraindications).


2016 ◽  
Vol 84 (12) ◽  
Author(s):  
Erik Rupnik ◽  
Stojan Kariž ◽  
Črtomir Iglič ◽  
Mihaela Zidarn

Background. Angioedema is a rare but potentially very serious complication of treatment with angiotensin converting enzyme inhibitors (ACEI). Angioedema is due to the accumulation of bradykinin, because angiotensin converting enzyme is the key enzyme for its degradation.Case reports. We present two patients with life-threatening angioedema while taking ACEI. Both patients had already had episodes of angioedema. Angioedema didn't respond to adrenaline. In both patients intubation was difficult.Conclusion. In the acute phase of angioedema due to ACEI it is necessary to protect the airways. Bradykinin receptor inhibitors shorten the duration of episodes of angioedema. In the long term it is essential to permanently avoid ACEI.


Author(s):  
Suleiman Aminu ◽  
Mohammed Auwal Ibrahim ◽  
Abdullahi Balarabe Sallau

Abstract Background Recent COVID-19 outbreak has prompted the search of novel therapeutic agents to treat the disease. The initial step of the infection involves the binding of the virus through the viral spike protein with the host angiotensin converting enzyme 2 (ACE2). In this study, the interaction of some ACE or ACE2 inhibitors and their analogues as well as selected compounds with the viral spike protein as a strategy to hinder viral-ACE2 interaction were investigated. SARS-CoV-2 spike protein as well as the ligands were retrieved from protein databank and ChEBI database respectively. The molecules were prepared before initiating the virtual screening using PyRx software. Discovery studio was used to further visualize the binding interactions between the compounds and the protein. Results The ACE inhibitors and their analogues fosinopril (1-), fosinopril and moexipril have the best binding affinity to the protein with binding energies < − 7.0 kcal/mol while non-flavonoid stilben-4-ol binds with free binding energy of − 7.1 kcal/mol. Others compounds which belong to either the flavonoids, terpenes and alkaloid classes also have binding energies  < − 7.0 kcal/mol. Such high binding energies were enhanced via hydrogen bond (h-bond) interactions in addition to other interactions observed between the compounds and the amino acid residues of the protein. Conclusions The ACE inhibitors and their analogues as well as the selected compounds could serve as inhibitors of the spike protein as well as lead in drug discovery processes to target the SARS-CoV-2 virus.


1990 ◽  
Vol 18 (6) ◽  
pp. 1184-1185 ◽  
Author(s):  
MRIDULA CHOPRA ◽  
JOHN McMURRAY ◽  
JENNIFER STEWART ◽  
HENRY J. DARGIE ◽  
W. EWEN SMITH

Summary Free radical (FR) scavenging may be a therapeutically useful adjunctive property of angiotensin converting enzyme (ACE) inhibitors. In this study we have shown that SH-containing ACE inhibitors (captopril, epicaptopril, zofenopril) are potent FR scavengers at a concentration of 4 × 10-5m whereas non-SH ACE inhibitors (enalaprilat, quinaprilat and perindoprilat) have no FR-scavenging activity at this concentration. Furthermore, the SH-containing agents preferentially scavenged general radicals rather than superoxide radicals, i.e. suggesting that these drugs would be effective in quenching the culprit FR in ischaemia/reperfusion injury.


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