|Ideal sources for Wikipedia's medical content are defined in the guideline Wikipedia:Identifying reliable sources (medicine) and are typically review articles. Here are links to possibly useful sources of information about ACE inhibitor.
|WikiProject Medicine||(Rated B-class, Mid-importance)|
|WikiProject Pharmacology||(Rated C-class, Top-importance)|
|This article contains a translation of ACE-Hemmer from de.wikipedia. (418131352 et seq.)|
||This article may be expanded with text translated from the corresponding article in the German Wikipedia. (June 2014)|
- 1 Use generic names, with bracketed brand names
- 2 'Not Too technical '
- 3 Question
- 4 Update
- 5 Adding a Resource
- 6 Misunderstanding
- 7 Confused reading
- 8 SOD3 upregulation
- 9 New study
- 10 ACE-I & ARB dual therapy
- 11 empty section on clinical use of ACE inhibitors?
- 12 Blood Brain Barrier Crossing ACE Inhibitors & Dementia, Blood Pressure, RAAS
- 13 Generic Ace Inhibitors
- 14 Creatinine Levels
- 15 ACE inhibitors used for frailty
- 16 2013 BMJ study finds slowed or reversed cognitive decline in patients with dementia taking centrally-acting ACE Inhibitors
Use generic names, with bracketed brand names
Please excuse my Australian bias in citing examples of brand names =) Techelf
- This Canadian thinks that it's perfectly alright to mention the brandnames in Wikipedia, as the 'lab name' often means nothing to most users of the medication and of Wikipedia. Sometimes, for marketing purposes, the same compound may have different names in different countries, too. It will be useful to mention all the common names. -- PFHLai 22:12, 2004 Jun 28 (UTC)
- I was referring to using the Australian brand names (vs say the British), but yeah I agree with you - are the Canadian brand names different from the ones I've got here? I think we should only list the brands of the original maker of the drug though, or else the list would get unmanageable. Techelf10:20, 29 Jun 2004 (UTC)
- As a mere science student, I ain't professionally qualified to say much; but I think Canadian brandnames are usually the same as American brandnames, which are sometimes different from British brandnames. It took me awhile, when I first moved to Canada, to figure out things like, say, tylenol in my new home = panadol in my old home. ... I wouldn't worry about getting the list too long. There are only so many English-language markets on this planet, eh ! :-) -- PFHLai 16:14, 2004 Jun 29 (UTC)
- I suggest sticking with the generic names with bracketed brand names because this is the standard way doctors do it. Brand names can and will change with geography and time (especially when patents expire). As a side note, patients often tell me about their white pills or their red and white pills and I cringe because it's impossible to identify them ... Alex.tan 10:50, 1 Jul 2004 (UTC)
'Not Too technical '
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 22.214.171.124 (talk) 01:33, 15 June 2010 (UTC)
I concur. The article is definitely not too technical. The article, as written including it's graphics, is sufficient to cover the needs of a broad range of readers. It is an excellent source & review of pertinent data points that health care providers and students will find extremely helpfull. Readers that lack sufficient understanding and comprehension of the terminology, concepts, and inter-relationships presented i.e.: physiology, anatomy, and pharmacology, should refer to the more basic explanations offered at other web sites such as WebMD or the NIH web sites. As readers become better acquainted with the core concepts necessary to comprehend this excellent presentation, they will return to this site for a more comprehensive explanation. In fact, I refer patients, nurses, and Dental Hygienists to this site
How about simple one liner; Your heart is like a little pump with pipes going to your body and your body lets some water out the faucet. High blood pressure is caused by three types of problems, the pump pushing too much volume, the pipes being too small or just too much fluid in the system. Ace inhibitors stop Angiotensinogen 1 from becoming Angiotensinogen 2. By reducing Angiotensinogen 2 more fluid is allowed to leave the facet; you pee a bit more. Also the pipes become larger or dilated and both these actions lower your blood pressure. Be sure to move from laying to sitting to standing slowly when getting used to this medication. 126.96.36.199 (talk) 12:25, 16 October 2013 (UTC)Timothy Hannifin RN
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)
As far as any antihypertensive drug therapy, avoid abrupt discontinuation of drug (due to risk of tachycardia, HTN, ischemia, angina, MI, and sudden death) – consult your physician!
- Um... Do you have a reference for this? -Techelf 06:51, 18 November 2005 (UTC)
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)
Adding a Resource
I thought this document would be suitable to add as a link, but I'm not sure where to put it! ==Understanding the Biology of ACE Inhibitors== http://www.cmellc.com/geriatrictimes/images/g000617.pdf
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))
"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."
I am new to Wikipedia, but wanted to post an article from MedScape that someone else might be interested in summarizing.
From Medscape Medical News CME Centrally Active ACE Inhibitors May Help Prevent Dementia CME News Author: Janis Kelly
August 3, 2009 — New observational data from the Cardiovascular Health Study show that centrally active angiotensin-converting enzyme (ACE) inhibitors reduce cognitive decline by 65% per year of exposure, an effect that is likely due to their ability to cross the blood-brain barrier.
"If confirmed in a randomized clinical trial, our findings would add another potential therapeutic option" for prevention of cognitive decline and related diseases, lead author Kaycee M. Sink, MD, from Wake Forest University School of Medicine, in Winston-Salem, North Carolina, told Medscape Neurology.
The study is published in the July 13 issue of Archives of Internal Medicine.
Class of ACE Inhibitor Important
Dr. Sink and colleagues used data from the Cardiovascular Health Study to determine whether cumulative exposure to ACE inhibitors was associated with a lower risk for incident dementia, cognitive decline, or incident disability in instrumental activities of daily living (IADLs), compared with treatment with other antihypertensive agents in 1054 patients with treated hypertension and no congestive heart failure.
The study included 414 subjects who had taken ACE inhibitors and 640 who had taken other antihypertensive medications. The researchers found no association between exposure to all ACE inhibitors and risk for dementia, difference in cognitive-function scores, or odds of disability in IADLs.
However, analysis according to type of ACE inhibitor showed a different effect. The results showed centrally active ACE inhibitors were associated with 65% less decline in cognitive-function scores per year of exposure.
The data also reveal that non–centrally active ACE inhibitors were associated with a greater risk for incident dementia and greater odds of disability in IADLs compared with other antihypertensive medications.
Centrally active ACE inhibitors included captopril (Capoten, Bristol-Myers Squibb), fosinopril (Monopril, Bristol-Myers Squibb), lisinopril, perindopril, ramipril (Altace, King Pharmaceuticals), and trandolapril (Mavik, Abbott Laboratories). Non–centrally active ACE inhibitors included benazepril (Lotensin, Novartis Pharmaceuticals), enalapril (Vasotec, Merck), moexipril (Univasc, Schwarz Pharma), and quinapril (Accupril, Pfizer).
The study did not include enough people taking angiotensin receptor blockers to extend the analysis to those drugs, said Dr. Sink.
Reduced Incidence Likely Not Due to Antihypertensive Effect
"Our most important findings in this observational study were that centrally acting ACE inhibitors were associated with a 65% reduction in cognitive decline per year of taking the centrally active ACE inhibitors," said Dr. Sink.
"In addition, compared with participants with high blood pressure who took other types of blood-pressure–lowering medications, non–centrally active ACE inhibitors did not have this effect and might be associated with a greater risk for incremental dementia, and that cumulative (or chronic) exposure to ACE inhibitors may be needed to achieve the protective effect," Dr. Sink said.
The researchers suspect that this difference is due primarily not to the antihypertensive effects of centrally acting ACE inhibitors but to their effect on the brain's intrinsic renin-angiotensin system, which is involved in memory and cognition.
Stimulation of the renin-angiotensin system also mediates activation of inflammatory cytokines that have been implicated in degenerative dementias, explained Dr. Sink.
The researchers also suspect that the slight increase in dementia risk associated with the non–centrally acting ACE inhibitors in this comparison was probably a sign that they are "simply less helpful in the prevention of dementia and IADL disability than other antihypertension drug classes combined."
Due to the huge public-health implications of finding an intervention that could more than halve dementia risk in the elderly population, confirmation of these observational findings in a randomized clinical trial is needed.
"Randomizing older adults with hypertension to a centrally active ACE inhibitor vs a non–centrally active ACE inhibitor would test the hypothesis that centrally active ACE inhibitors have protective benefits on cognition beyond the effects of blood-pressure control," said Dr. Sink.
Should Patients Switch Medications?
Whether clinicians should switch their hypertensive patients to a centrally acting ACE inhibitor must be decided on a case-by-case basis, said Dr. Sink.
"Because there are often multiple reasons for a particular choice of antihypertensive drug in any particular patient, the decision about switching blood-pressure medications should be discussed between patient and provider.
"However, if the patient does not have a contraindication for an ACE inhibitor, then switching to a centrally active ACE inhibitor is a reasonable choice. In addition, for those already on ACE inhibitors, our study results would support the use of a centrally active ACE inhibitor over a non–centrally active one," Dr. Sink said.
Asked by Medscape Neurology to comment on the findings, Ihab Hajjar, MD, from the Institute for Aging Research and assistant professor of medicine at Harvard Medical School, in Boston, Massachusetts, said that this study adds to the support for clinical trials.
"This is the right time to study ACE inhibition on cognitive function. However, it is important to select the appropriate drug [agents that cross the blood-brain barrier] and the appropriate population [hypertensives and other high-risk groups]," Dr. Hajjar said in an interview.
However, he emphasized that lowering blood pressure is the most important goal for managing high-risk elderly patients and that the choice of drug is secondary.
"Drugs that inhibit the renin angiotensin system seem to have a preferential effect on cognition compared with other antihypertensives. As a third issue, antihypertensives that cross the blood-brain barrier may also have an even superior effect to other non–blood-brain-barrier-penetrating drugs. This is true not only for those without cognitive impairment but also for those with dementia and Alzheimer's disease," Dr. Hajjar said.
Study investigator David C. Goff Jr, MD, PhD, from Wake Forest University, has a research grant from Merck. The study was supported in part by the National Heart, Lung, and Blood Institute; the National Institute of Neurological Disorders and Stroke; and the National Institute on Aging.
Arch Intern Med. 2009;169:1195-1202. Abstract
Hypertension is an important risk factor for the development of dementia. An association has been noted between use of antihypertensive agents and a reduced risk for dementia, but mixed results have been reported on the protective effect of blood pressure reduction on cognitive decline and dementia. The brain is known to possess an intrinsic renin-angiotensin system, and centrally acting ACE inhibitors may be involved in the protective effect on dementia.
This is a prospective multicenter, population-based cohort study of cardiovascular risk factors in community-dwelling older adults to examine the association between ACE inhibitors as a class and centrally and non–centrally acting ACE inhibitors on the risk for dementia and cognitive decline in older people in the United States.
Included in analysis were 1054 participants from among 5888 participants of the Cardiovascular Health Study, selected for absence of dementia at baseline and hypertension treated with medications. Excluded were those with congestive heart failure and prevalent dementia at baseline. At baseline, all participants received magnetic resonance imaging, physical examination, cognitive and functional assessments, and laboratory tests. The predictor was ACE inhibitor use, and ACE inhibitors were further classified into centrally acting and non–centrally acting. Centrally acting ACE inhibitors were captopril, fosinopril, perindopril, ramipril, and trandolapril. Non–centrally acting ACE inhibitors were benazepril, enalapril, moexipril, and quinapril. The study start was when participants received magnetic resonance imaging, and study end was defined as date of dementia diagnosis, last evaluation, or time of loss to follow-up. Primary outcome was all-cause dementia consisting mainly of Alzheimer's disease and vascular dementia. Secondary outcomes were cognitive decline measured by the Modified Mini-Mental State Examination (3MSE) and IADLs. IADLs were assessed in 6 areas: shopping, meal preparation, money management, telephone use, and light and heavy housework. The 3MSE used an 100-point scale with higher scores indicating better cognitive performance. Average age at baseline was 75 years, 64% were women, and 76% were white. 54% reported no alcohol use, 11% to 22% had type 2 diabetes, and 18% had a history of coronary artery disease. Of 414 participants exposed to ACE inhibitors, 224 took only centrally acting and 138 only non–centrally acting, with the remaining taking both. Those using centrally acting ACE inhibitors had a higher baseline 3MSE score (93.2 vs 01.7 points). At median follow-up of 6 years, mean exposure to all ACE inhibitors was 3.24 years with mean exposure to centrally acting ACE inhibitors of 3.06 years and non–centrally acting ACE inhibitors of 2.70 years. 38% of ACE inhibitor users were continuous users with no difference in duration of use between the centrally and non–centrally acting groups. There were 158 cases of incident dementia, with 11 among those never exposed to ACE inhibitors and 47 among those exposed to all ACE inhibitors. Relative risk (RR) for dementia in ACE inhibitor users vs other antihypertensive drug users was 1.01. When analyzed by centrally vs non–centrally acting ACE inhibitors, centrally acting agents reduced the RR for dementia by 20% per year of exposure, for a hazard ratio (HR) of 1.73 for 3 years. HR for dementia for non–centrally acting ACE inhibitors vs other antihypertensives was 1.20. There was no significant difference in decline in 3MSE scores between ACE inhibitor users and non-ACE inhibitor users. When analyzed by centrally and non–centrally acting ACE inhibitors vs other antihypertensives, centrally acting agents were associated with 65% less decline per year of exposure. For IADL disability, ACE inhibitors as a class had higher risk for disability vs other antihypertensives. When non–centrally acting ACE inhibitors were examined, there was a 56% greater risk for IADL disability at 3 years vs non-ACE inhibitor drugs. HR for non–centrally acting ACE inhibitors on impaired IADL vs other antihypertensives was 1.16. Centrally acting ACE inhibitors did not show a negative impact on IADLs. The authors concluded that all outcomes favored centrally acting ACE inhibitors and that protective effects of ACE inhibitors on dementia and cognitive decline were restricted to centrally acting ACE inhibitors.
ACE inhibitors as a class vs other antihypertensive agents are not associated with protection against dementia, cognitive decline, or disability in IADLs. Centrally acting ACE inhibitors are associated with a reduced risk for dementia, cognitive decline, and disability in IADLs vs non–centrally acting ACE inhibitors and other antihypertensive agents.
http://archinte.ama-assn.org/cgi/content/full/169/13/1195 (full free text)
- "After review of the literature and pharmaceutical package inserts, captopril, fosinopril, lisinopril, perindopril, ramipril, and trandolapril were classified as crossing the blood-brain barrier (centrally active), while benazepril, enalapril, moexipril, and quinapril were classified as not (noncentrally active).20-28"
ramipril (Altace), and trandolapril (Mavik), cross the blood-brain barrier (and so are centrally active)
ACE-I & ARB dual therapy
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)
This has been summarily DISPROVEN since 2009 when this post was written. While dual therapy makes the numbers look better, it actually increases likelihood of complete renal failure leading to dialysis and dual therapy for this indication is CONTRAINDICATED. The only recommendation that still remains is an extremely cautious one in severe refractory heart failure when there is good renal function. — Preceding unsigned comment added by 188.8.131.52 (talk) 17:30, 29 December 2012 (UTC)
empty section on clinical use of ACE inhibitors?
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.184.108.40.206 (talk) 20:53, 28 December 2009 (UTC)
Blood Brain Barrier Crossing ACE Inhibitors & Dementia, Blood Pressure, RAAS
|This section requires expansion. (November 2009)|
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)
Generic Ace Inhibitors
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.
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 220.127.116.11 (talk) 18:41, 4 May 2012 (UTC)
ACE inhibitors used for frailty
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.
2013 BMJ study finds slowed or reversed cognitive decline in patients with dementia taking centrally-acting ACE Inhibitors
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
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