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The American Journal of Emergency... May 2021Tranexamic acid (TXA) is an antifibrinolytic agent which inhibits conversion of plasminogen to plasmin, a key step in kallikrein activation and bradykinin formation....
Tranexamic acid (TXA) is an antifibrinolytic agent which inhibits conversion of plasminogen to plasmin, a key step in kallikrein activation and bradykinin formation. Tranexamic acid is used in prophylactic management of hereditary angioedema; however, evidence for TXA in angiotensin converting enzyme (ACE) inhibitor-induced angioedema (ACEI-AE) is limited. We describe a patient who presented to the emergency department with ACEI-AE who was successfully treated with TXA. This case suggests that TXA may be a beneficial treatment modality in the management of ACEI-AE and warrants further investigation.
Topics: Angioedema; Angiotensin-Converting Enzyme Inhibitors; Antifibrinolytic Agents; Female; Humans; Lisinopril; Middle Aged; Tranexamic Acid
PubMed: 33164754
DOI: 10.1016/j.ajem.2020.10.029 -
DICP : the Annals of Pharmacotherapy Nov 1990
Review
Topics: Angiotensin-Converting Enzyme Inhibitors; Cough; Humans
PubMed: 2275228
DOI: 10.1177/106002809002401107 -
Drug Safety Sep 1996ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This antihypertensive efficacy... (Review)
Review
ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This antihypertensive efficacy probably accounts for an important part of their long term renoprotective effects in patients with diabetic and non-diabetic renal disease. The renal mechanisms underlying the renal adverse effects of ACE inhibitors--intrarenal efferent vasodilation with a consequent fall in filtration pressure--are held to be involved in their renoprotective effects as well. The fall in filtration pressure presumably contributes to the antiproteinuric effect as well as to long term renoprotection. The former is suggested by the positive correlation between the fall in filtration fraction and the reduction in proteinuria found during ACE inhibition. The latter is suggested by the correlation between the (slight) reduction in glomerular filtration rate at onset of therapy and a more favourable course of renal function in the long term. Such a fall in filtration rate at the onset of ACE inhibitor treatment is reversible after withdrawal, and can be considered the trade-off for long term renal protection in patients with diabetic and nondiabetic chronic renal disease. In conditions in which glomerular filtration is critically dependent on angiotensin II-mediated efferent vascular tone (such as a post-stenotic kidney, or patients with heart failure and severe depletion of circulating volume), ACE inhibition can induce acute renal failure, which is reversible after withdrawal of the drug. Systemic and renal haemodynamic effects of ACE inhibition, both beneficial and adverse, are potentiated by sodium depletion. Consequently, sodium repletion contributes to the restoration of renal function in patients with ACE inhibitor-induced acute renal failure. Our the other hand, co-treatment with diuretics and sodium restriction can improve therapeutic efficacy in patients in whom the therapeutic response of blood pressure or proteinuria is insufficient. Patients at the greatest risk for renal adverse effects (those with heart failure, diabetes mellitus and/or chronic renal failure) also can expect the greatest benefit. Therefore, ACE inhibitors should not be withheld in these patients, but dosages should be carefully titrated, with monitoring of renal function and serum potassium levels.
Topics: Angiotensin-Converting Enzyme Inhibitors; Drug Interactions; Humans; Hypertension; Kidney; Kidney Diseases; Renal Insufficiency; Risk Assessment
PubMed: 8879974
DOI: 10.2165/00002018-199615030-00005 -
Medizinische Monatsschrift Fur... Jan 2017A patient with cardiac insufficiency takes the ACE-Inhibitor Enalapril as well as Spironolactone regularly. In the interaction monographs of the German ABDA-database... (Review)
Review
A patient with cardiac insufficiency takes the ACE-Inhibitor Enalapril as well as Spironolactone regularly. In the interaction monographs of the German ABDA-database there is a note that combined use of these substances should be avoided due to an increased risk of hyperkalemia – is there a medication related problem? There is evidence from clinical studies, that combined use of ACE-inhibitors and potassium-sparing agents indeed increases the risk of severe hyperkalemia. The risk seems to be related to the dose of the potassium-sparing agent. However, in patients with cardiac insufficiency NYHA-class II-IV and an ejection fraction of ≤ 35%, the addition of spironolactone to an ACE-inhibitor and betablocking agent reduces mortality and hospitalization for cardiovascular problems. Therefore the combination is indicated in these patients. To minimize the risk for severe adverse events close monitoring of serum potassium and renal function is mandatory. Moreover, additional risk factors for hyperkalemia such as intake of potassium supplements or NSAID should be avoided.
Topics: Angiotensin-Converting Enzyme Inhibitors; Diuretics; Drug Therapy, Combination; Heart Failure; Humans; Hyperkalemia; Spironolactone
PubMed: 29952529
DOI: No ID Found -
Drug and Therapeutics Bulletin Apr 1989
Review
Topics: Angiotensin-Converting Enzyme Inhibitors; Enalapril; Heart Failure; Humans; Hypertension; Lisinopril
PubMed: 2562398
DOI: No ID Found -
American Journal of Health-system... Oct 2000The pharmacology of angiotensin-converting-enzyme (ACE) inhibitors and their role in the renin-angiotensin system (RAS) are described, and pharmacokinetic properties and... (Review)
Review
The pharmacology of angiotensin-converting-enzyme (ACE) inhibitors and their role in the renin-angiotensin system (RAS) are described, and pharmacokinetic properties and common adverse events are presented. ACE inhibitors play a vital role in the RAS by regulating the potent vasoconstrictor angiotensin II. All ACE inhibitors share the same basic structure; however, they can be separated on the basis of their functional (binding) group: carboxyl, sulfhydryl, or phosphinyl. These functional groups are, in part, responsible for differences in the pharmacokinetic and safety profiles of these agents. Captopril and lisinopril are the only ACE inhibitors that are not prodrugs requiring activation through hepatic biotransformation. Differences among the ACE inhibitors in lipophilicity are described; fosinopril has the greatest lipophilicity and lisinopril the least. ACE is found in numerous tissues, and there is increasing evidence of differences among ACE inhibitors in their ability to inhibit tissue ACE. Most ACE inhibitors are eliminated mainly by the kidneys and to a lesser extent through the liver. Lisinopril is the only ACE inhibitor that does not require hepatic metabolism. In the selection of an ACE inhibitor for once-daily use to treat hypertension, differences in trough-peak ratios are clinically relevant. Fosinopril, ramipril, and trandolapril have minimum trough-peak ratios of 50% or greater. ACE inhibitors are generally well tolerated, with hypotension, cough, and hyperkalemia being the most frequently reported adverse effects for the entire class. Drug interactions across the ACE inhibitor class as well as agent-specific interactions are described. Factors to be considered in the selection of an ACE inhibitor include differences in potency, affinity for ACE, pharmacokinetics, and toxicity that are related to structural properties of the drug; whether the trough-peak ratio enables use of a once-daily dose; and potential adverse effects related to a drug's functional (binding) group.
Topics: Angiotensin-Converting Enzyme Inhibitors; Drug Interactions; Heart Failure; Humans; Hypertension; Myocardial Infarction; Renin-Angiotensin System
PubMed: 11030016
DOI: 10.1093/ajhp/57.suppl_1.S3 -
The Annals of Pharmacotherapy Jun 2002Angiotensin-converting enzyme (ACE) inhibitors are often associated with an increased incidence of cough and bronchial responsiveness that may cause further... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Angiotensin-converting enzyme (ACE) inhibitors are often associated with an increased incidence of cough and bronchial responsiveness that may cause further deterioration of patients with impaired pulmonary function.
OBJECTIVE
To review the available literature on the incidence of cough and bronchial responsiveness associated with ACE-inhibitor therapy in patients with asthma, chronic obstructive pulmonary disease (COPD), and congestive heart failure (CHF).
DATA SOURCES
Literature was accessed through MEDLINE (1985-September 2001). Key search terms included cough, bronchospasm, asthma, congestive heart failure, chronic obstructive pulmonary disease, ACE inhibitors, and angiotensin II receptor blockers.
DATA SYNTHESIS
The literature reports several cases of increased bronchial responsiveness associated with ACE inhibitors. Larger, controlled studies evaluating the increased risk in patients with pulmonary dysfunction are limited. Data from these trials are summarized in this article.
CONCLUSIONS
The literature shows that patients with primary airway disease such as asthma and COPD are not at an increased risk of developing cough or bronchoconstriction as a result of ACE-inhibitor therapy. Despite the ability of ACE inhibitors to improve exercise tolerance, perfusion, and gas transfer, patients with CHF may be at higher risk of developing cough than the general population. Whether this cough is attributed to ACE inhibition or increased left-ventricular dysfunction remains uncertain. If increased bronchial responsiveness does occur, angiotensin II receptor antagonists are another reasonable option.
Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Asthma; Bronchial Diseases; Clinical Trials as Topic; Heart Failure; Humans; Pulmonary Disease, Chronic Obstructive; Receptors, Angiotensin; Renin-Angiotensin System
PubMed: 12022909
DOI: 10.1345/aph.1A332 -
Postgraduate Medicine Jul 2013Angiotensin-converting enzyme (ACE) inhibitors are a heterogeneous class, varying in pharmacologic properties, which have different therapeutic impacts on patient... (Comparative Study)
Comparative Study Review
Angiotensin-converting enzyme (ACE) inhibitors are a heterogeneous class, varying in pharmacologic properties, which have different therapeutic impacts on patient profiles, including lipophilicity, tissue-ACE binding, duration of action, half-life, and increased bradykinin availability. Among the ACE inhibitor class, the agent perindopril, in particular, has pleiotropic effects that are not equally shared by other ACE inhibitors, including bradykinin site selectivity and subsequent enhancement of nitric oxide and inhibition of endothelial cell apoptosis. Moreover, there is a large amount of evidence to suggest that perindopril therapy may reduce cardiovascular event rates in patients, yet perindopril is rarely prescribed in the United States. Ramipril is another ACE inhibitor with both a favorable clinical profile and impressive outcomes data. Our review compares the pharmacologic and trial data among perindopril, ramipril, and other ACE inhibitors. In patients with or at high risk for coronary heart disease who do not have heart failure, or in patients with heart failure with preserved ejection fraction, perindopril should be among the preferred treatment agents in the ACE inhibitor class. Ramipril has an impressive track record of improving cardiovascular outcomes, too, and should be considered a preferred agent among the ACE inhibitor class.
Topics: Angiotensin-Converting Enzyme Inhibitors; Cardiovascular Diseases; Cardiovascular System; Coronary Disease; Heart Failure; Humans; Hypertension; Myocardial Infarction; Perindopril; Ramipril
PubMed: 23933903
DOI: 10.3810/pgm.2013.07.2687 -
Emergency Medicine Clinics of North... Feb 2022Angioedema is a well-recognized and potentially lethal complication of angiotensin-converting enzyme inhibitor (ACEi) therapy. In ACEi-induced angioedema, bradykinin... (Review)
Review
Angioedema is a well-recognized and potentially lethal complication of angiotensin-converting enzyme inhibitor (ACEi) therapy. In ACEi-induced angioedema, bradykinin accumulates due to a decrease in its metabolism by ACE, the enzyme that is primarily responsible for this function. The action of bradykinin at bradykinin type 2 receptors leads to increased vascular permeability and the accumulation of fluid in the subcutaneous and submucosal space. Patients with ACEi-induced angioedema are at risk for airway compromise because of the tendency for the face, lips, tongue, and airway structures to be affected. The emergency physician should focus on airway evaluation and management when treating patients with ACEi-induced angioedema.
Topics: Angioedema; Angiotensin-Converting Enzyme Inhibitors; Humans
PubMed: 34782093
DOI: 10.1016/j.emc.2021.09.004 -
Expert Opinion on Drug Safety Oct 2014ACE inhibitors are first-line therapy in patients with chronic kidney disease (CKD). The main adverse effects of ACE inhibitors are hypotension, renal function... (Review)
Review
INTRODUCTION
ACE inhibitors are first-line therapy in patients with chronic kidney disease (CKD). The main adverse effects of ACE inhibitors are hypotension, renal function impairment and hyperkalemia.
AREAS COVERED
This paper reviews evidence from clinical studies regarding adverse effects of ACE inhibitors in patients with CKD. The safety aspects of ACE inhibitors are discussed in relation to their pharmacological action, drug-drug interactions, drug-diet interaction, precautions needed in certain clinical conditions and other adverse effects.
EXPERT OPINION
The main adverse effects of ACE inhibitors follow from their interaction with renin-angiotensin-aldosterone system (RAAS)-activity and volume depletion. This interaction can be turned into clinical benefit and increase efficacy of ACE inhibitors by reduction in dietary sodium or adding diuretics. Dual RAAS-blockade is no longer advocated in patients with CKD because of the safety issues, and combination of ACE inhibitors with moderate reduction in dietary sodium intake is a better alternative. The intensified treatment regimens based on ACE inhibitors can potentially improve renoprotection, but increase the risk of adverse effects. Better strategies to address safety concerns are needed. INTRODUCTION of clinical rules and safety indicators may help clinicians to identify hazardous co-prescriptions and adverse dietary habits and can decrease the frequency of adverse effects.
Topics: Angiotensin-Converting Enzyme Inhibitors; Drug Interactions; Food-Drug Interactions; Humans; Hyperkalemia; Hypotension; Kidney Function Tests; Renal Insufficiency; Renal Insufficiency, Chronic; Renin-Angiotensin System
PubMed: 25148900
DOI: 10.1517/14740338.2014.951328