Talk:ACE inhibitor

message: There was a sign saying the article was too technical. Anyone who wants to know how an Ace Inhibitor works will need to obviously understand its cellular function. The article is infact not too technical for anyone who understands the RAAS system, which is not too difficult to understand. No doubt some doughnut will put the sign back on. This person needs to pick up a cell biology text book first and they will see that it is in fact not too difficult to understand  —Preceding unsigned comment added by 139.184.30.134 (talk) 01:33, 15 June 2010 (UTC)
thread_title: 'Not Too technical '

message: I've read that it's not advisable to stop taking ACE inhibitors once you've started taking them, due to their effect on the body's feedback systems.  I would like to see information on how to get off them successfully.
:Please direct these questions to the Village Pump.
:The body's feedback system quite rapidly gets used to the absence of ACE inhibition. It is not generally considered dangerous. There is, however, a possibility that the disease for which you were prescribed an ACEi will recur, e.g. arterial hypertension.
:You don't say why you want to stop using an ACEi. Is it the dry cough? There are alternatives. Discuss it with your physician, instead of asking a bunch of strangers on Wikipedia :-). JFW | T@lk 19:58, 8 Jan 2005 (UTC)
replies: text: Um... Do you have a reference for this? -Techelf 06:51, 18 November 2005 (UTC)
thread_title: Question

message: Sorry, I'm not very wiki savvy and I'm not sure I should update the page. The following can be expounded on a bit:
"A persistent dry cough is a relatively common adverse effect believed to be associated with the increases in bradykinin levels produced by ACE inhibitors"
The increase in bradykinin levels actually causes a cascade including an increase in arachidonic acid metabolites and nitric oxide which can cause inflamation of the lungs. The bradykinin levels themselves don't directly cause the problem. 
There are also several effective treatments for the ACE inhibitor induced cough. The most effective are Picotamide and Ozagrel which are thromboxane antagonists and decrease thromboxane production. These drugs are not available in the U.S., however. Sulindac (available in the U.S.), an NSAID (non-steroid anti-inflammatory drug) inhibits prostraglandin synthesis and reduces bradykinins, however it can raise the risk of myocardial infarction.  Finally, there's Theophylline which is used for treatment of asthma. Because it has a very narrow therapeutic index (the difference between an effective dose and dangerous dose is slim), it's not usually a good choice.
:The other problem with theophylline is that it often raises serum lipids, not such a good thing in the type of patients who need antihypertensives. ----Dan 17:28, 13 October 2006 (UTC)
thread_title: Update

message: when an ACE inhibitor alone proves insufficient; and in chronic heart failure (usually furosemide) for improved symptomatic control.
*this line gives the idea that furosemide itself is an ACEi. it is not!
Furosemide is a loop diuretic and it is of good use in edemas and in the management of very high potassium levels.
please, let's rephrease this sentence so no mistake is commited.
(HelenoBR 03:31, 25 October 2007 (UTC)
thread_title: Misunderstanding

message: "Recent studies in Canada have shown that a combination of ACE and Aniostensin II receptor antagonists have caused heart and kidney failure in some patients. Individually, these drugs are excellent but they should not be used in combination. Combination with other BP drugs such as beta blocker or calcium channel blocker is not a problem. Anyone taking both ACE and Aniotensin II receptor antagonist should consult their doctor as soon as possible.
While counterintuitive at first glance, the combination therapy of angiotensin II receptor antagonists with ACE inhibitors may be superior to either agent alone."
Firstly, this paragraph needs citing and verification. It also seems to contradict the last quoted sentence. 91.104.122.46 (talk) 19:33, 7 February 2009 (UTC)
thread_title: Confused reading

message: Struck upon a curious study (); could be possibly mentioned in the \effects\ section. Best regards, --CopperKettle 14:48, 1 June 2009 (UTC)
thread_title: [[SOD3]] upregulation

message: The wiki entry says that there is "compelling evidence" showing the renoprotective effects of dual drug therapy. However, the cited article specifically states in its abstract that "long-term clinical trials are needed and encouraged to further establish the significant role of dual blockade in renal protection particularly in diabetic nephropathy." (http://www.ncbi.nlm.nih.gov/pubmed/15853685). 
Quartertone (talk) 21:35, 20 August 2009 (UTC)
thread_title:  ACE-I & ARB dual therapy 

message: the section on the clinical use of ACE inhibitors is empty,and as i placed and expand template there.i did not delete the section,as this is essential information.please,if you edit this page,add information into the section.169.244.148.235 (talk) 20:53, 28 December 2009 (UTC)
thread_title:  empty section on clinical use of ACE inhibitors?  

message: At best this just looks rubbish, at worst this is an attempt to introduce a new theory/marketing authorisation and is not an important therapeutic category (?yet)Arfgab (talk) 22:09, 10 April 2010 (UTC)
thread_title: Blood Brain Barrier Crossing ACE Inhibitors & Dementia, Blood Pressure, RAAS  

message: As of 2003, captopril, enalapril, and lisinopril were already available as generics, at sharply reduced prices.  Benazepril, ramipril now also generic.  Others?  Should be mentioned in article.
See: ACE Inhibitors: Summary of Recommendations - Consumer Reports Best Buy Drugs - free public education project
99.190.133.143 (talk) 20:40, 21 March 2012 (UTC)
replies: text: Klbrain (talk) 23:07, 8 October 2017 (UTC)
thread_title:  Generic Ace Inhibitors 

message: I remember reading somewhere that creatinine levels needed to be monitored? That they are expected to rise but anything over 30% indicates that treatment should be stopped? Maybe someone with more expertise?  — Preceding unsigned comment added by 137.43.182.241 (talk) 18:41, 4 May 2012 (UTC)
replies: text: This seems to have been resolved; currently discussed in the 2nd paragraph of the "Adverse effects" section. Klbrain (talk) 23:05, 8 October 2017 (UTC)
thread_title:  Creatinine Levels 

message: In the section "Mechanism of action" there is a subsection "Effects". It contains the phrase:
ACE inhibitors are now used to reverse frailty and muscle wasting in elderly patients without heart failure.
This statement is not correct. The reference cited makes only passing reference to use of ACEi for sarcopenia without providing any context. When I follow the citation provided in THAT article it references some observational studies which MAY suggest a benefit but still only refers to it as a potential treatment in the future.
As a doctor who prescribes these medications on a daily basis, I can assure the community that this is not even close to being ready for prime time. But don't take my word for it - follow the evidence. If this statement can be supported by a guideline, a product monograph, or at LEAST a well-designed randomized controlled trial showing benefit, then it may be retained with the qualifier that this is a new treatment which has the potential to show promise but is not yet strongly supported by available evidence. 
If all we have is a citation of a citation of a citation which shows some retrospectively noted correlations, then it should be removed completely.
Thanks,
Chris Krause  — Preceding unsigned comment added by 207.195.1.6 (talk) 17:28, 29 December 2012 (UTC)
thread_title:  ACE inhibitors used for frailty 

message: Where before treatments for cognitive decline in patients with dementia yielded at best only slowed decline in mental function, this 2013 British Medical Journal study on Centrally acting ACE inhibitors (CACE-Is) found both slowed decline and actual improvement in mental function in some patients with Alzheimer's, vascular, and mixed dementia:  
:Conclusions Cognitive scores may improve in the first 6 months after CACE-I treatment and use of CACE-Is is associated with a reduced rate of cognitive decline in patients with dementia.  
Non-centrally-active ACE inhibitors provided no benefit.  
FREE FULL TEXT:  http://www.bmjopen.bmj.com/content/3/7/e002881.full  
BMJ Open 2013;3:e002881 doi:10.1136/bmjopen-2013-002881 
Published 22 July 2013
The centrally acting ACE inhibitors in the study were  
perindopril, 
ramipril, 
trandolapril, 
captopril, 
fosinopril, 
lisinopril, 
prinivil and 
monopril.
Here's a thoughtful summary in a pharmacist resource, Drug Topics:  
Title:  Centrally acting ACE inhibitors reduce rate of cognitive decline in dementia patients
AUG 15, 2013  http://drugtopics.modernmedicine.com/drug-topics/news/centrally-acting-ace-inhibitors-reduce-rate-cognitive-decline-dementia-patients
:: Non-centrally acting ACE inhibitors gave no protection from Alzheimer's.  Given the different effects, the article should at least note the distinction between centrally-acting and non-centrally-acting ACE inhibitors.  
::::Ocdnctx (talk) 20:54, 27 October 2013 (UTC)
thread_title:  2013 BMJ study finds slowed or reversed cognitive decline in patients with dementia taking centrally-acting ACE Inhibitors 

message: Review to replace primary source doi:10.1016/j.amjmed.2014.07.011 JFW | T@lk 21:37, 25 January 2015 (UTC)
replies: text: , although added rather than replaced. Klbrain (talk) 23:03, 8 October 2017 (UTC)
thread_title:  Angiooedema 

message: Medical uses says "A typical treatment plan often includes an ACE inhibitor, a beta blocker, a long-acting nitrate, ..." sadly without a source. Can anyone confirm if it should be nitrate or nitrite (which seems more plausible). - Rod57 (talk) 20:01, 21 January 2016 (UTC)
replies: text: Long-acting nitrate in that context is correct, short-hand for something like isosorbide mononitrate; see nitrovasodilator for a description of the class. Klbrain (talk) 22:55, 8 October 2017 (UTC)
replies: text:   Thanks, I've piped the Nitrate wikilink to Nitrate (pharmacology) - Rod57 (talk) 15:42, 11 October 2017 (UTC)
thread_title:  Nitrate or nitrite 

message: The mechanism and effects are different, in a way that makes a difference. — Preceding unsigned comment added by Ocdcntx (talk • contribs) 15:40, 13 January 2019 (UTC)
replies: text: Agree that this would be helpful; feel free to add. Klbrain (talk) 16:50, 14 January 2019 (UTC)
thread_title:  Needs discussion of centrally-acting vs. other ACE inhibitors 

message: Just a letter to the BMJ, but worth keeping an eye on: https://www.bmj.com/content/368/bmj.m325/rr
The active site of ACE2 appears to bind both angiotensin II and the SARS coronavirus spike glycoprotein through an FQ-containing motif shared by quinapril. The active site of ACE2 thus resembles the N terminal active site of ACE. In patients lacking the systemic blood pressure for an ACE inhibitor like quinapril, an ARB such as losartan could be substituted as a first approximation, since we found it useful for West Nile virus encephalitis. Shtove 22:29, 13 March 2020 (UTC)
thread_title:  Coronavirus