Posted on 01/16/2020 3:39:28 PM PST by ConservativeMind
A long-running dispute as to the supremacy of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) in the treatment of cardiovascular disease should be put to bed once and for all, say the authors of a new review.
Given the equal outcome efficacy but fewer adverse events with ARBs, risk-to-benefit analysis in aggregate indicates that at present there is little, if any, reason to use ACE inhibitors for the treatment of hypertension or its compelling indications, write Franz Messerli, MD (Mount Sinai Medical Center, New York, NY), and colleagues in the April 3, 2018, issue of the Journal of the American College of Cardiology.
Ever since the HOPE study, published in 2000, ACE inhibitors have become a sacred cow and nobody dared to say anything against them, Messerli told TCTMD.
The exception has been Messerli himself, along with one of the co-authors on the current review, Sripal Bangalore, MD (NYU Langone Medical Center, New York, NY). Both have for years argued in favor of ARBs because they have fewer side effects than ACE inhibitors, which are an older class of drugs. Others have consistently stood by the older agents on the grounds that they do better at preventing mortality in patients with coronary artery disease, while ARBs have been linked to a higher risk of MI. The counterargument to that has been that ACE inhibitors were tested in trials now several decades old that predated other modern secondary prevention medications, most notably statins. ARBs, by contrast, went through testing on top of these more modern medicines.
(Excerpt) Read more at tctmd.com ...
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ARBs are definitely better with regards side-effects, and the early data suggesting ACEI were better than ARBs for heart failure and ischemic heart disease/MI have not borne out on further testing. There was an interest in using ACEI and ARBs in combination for some indications - given that there are differences in their effects on bradykinin and nitric oxide, and that ARBs don’t block AT2 receptors. I haven’t seen any recent data on this though.
Thanks for linking the article!
Tissue binding differences of ACE inhibitors are major factors in how comparatively effective as anti-hypertensive they are, and more importantly, how much more effective they are in not activating in the RAA system, and in target organ damage of hypertension (post MI progressive heart failure).
An excellent center of study of tissue ACE inhibition and all of these issues, and incorporating the ARBs effects vs ACEIs, is the University of Florida’s landmark Vascular Biology Working Group. Vascular endothelium being the largest “target organ” in the body... throughout the vasculature.
All of the above, and the important data points of prevention of heart failure (an emphasis that Duke Cardiovascular Research Center shares. “counting the bodies” as it were).
What I have read says there are complications of combining an ACEI with an ARB.
It is best to pair with a Calcium Channel Blocker.
Thanks C.M!
I am not using any drugs for blood pressure, but I am using the non-drug protocols here. (and some of the supplements.)
https://www.lifeextension.com/protocols/heart-circulatory/high-blood-pressure
(Except...more at link!!)
“Medications to Help Lower Blood Pressure
If diet and lifestyle changes alone do not sufficiently lower blood pressure, blood pressure medication may be appropriate. Consult a qualified healthcare provider before beginning medical treatment for high blood pressure.
First-line recommendation
Angiotensin II receptor blockers (particularly telmisartan)
Angiotensin-converting enzyme inhibitors
Second-line recommendation
Thiazide diuretics
Third-line recommendation
Calcium channel blockers
Simultaneous use of more than one blood pressure medication, called combination therapy, may be appropriate for people in whom a single drug fails to control blood pressure.
Note: Beta-blockers are generally not recommended as first-line therapy for blood pressure reduction except in those with an indication for beta-blocker therapy such as recent heart attack or heart failure.”
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What I have read says there are complications of combining an ACEI with an ARB.
It is best to pair with a Calcium Channel Blocker.
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Yes, after a period of trial & error thats the combination that works well with me with zero discernible side effects. I use Valsartan (an ARB) paired with Amlodipine Besylate (a Calcium Channel Blocker).
ARBs truly do appear to be a better option to ACE Inhibitors...
Yes, much kinder to the kidneys.
I think that in the past MD’s, wrote for ACE’s more than ARB’s because most of the ARB’s were still under patent and much more expensive than the older generic ACE’s. Now that is no longer a consideration.
Went to suggested site but didn’t locate the study. If I interpret what you said correctly, ace inhibtor is both effective and doesn’t interact with RAA (which I looked up, too). Interesting aside, RAA is another hormone driven system. The effect of hormones on the psyche fascinates me as I’m seeing first hand the innate (testosterone/estrogen) difference between boys and girls from infancy thru toddlerhood in my grandkids.
Except if you have heart failure or coronary disease then they should be paired with a beta blocker.
Can anyone tell qhat the NNT score of these drugs are. Statins have NNT score of 125. That means 125 people have to take that drug for 5 years to prevent one heart attack. Check all this for yourself at NNT.com.
I dont take anything for my suppsedly high blood pressure. I use Naicin for my high Chlorestol since i dont trust any doctor prescibing drugs and getting a kickback from the drug companies. Yes i am going to die but so are will everyone else. I am more interested in quality of life and really dont care about how long i live.
Thats a great site!
You also need to look at whats called medical reversals. This is where they have changed common held treatment guidelines as being ineffective.
I was told to take baby asperin. Then i found out that older people(i am 61 yrs old)risk developing holes in our veins from using this treatment.
I also found that old folks need to have higher chlorestol to live longer.
I currently am embroiled in trying to get the VA to explain to me why my water reduction pill kept me puffy and bloated. I stopped the medication and now i have lost 4 inches off my waist and my foot doc is NOT a VA doc says my feet look great.
We dont have an opoid crisis in this country we have a pill problem. This is why i am refusing all my meds prescibed for me at this time. They are killing more of us than helping and i am hellbent on proveing this to be the case. Even if it kills me. Trust me i will outlive them.
How about we work together to expose this crap for what it is.
Look within the site the papers on “Tissue binding of ACE inhibitors”. The most tissue bound ACEI molecules are also those that do not activate the RAA system which is, as you’ve observed, neuro-hormonal.
The “Monday morning” raised BP levels are a result of activation of the RAA system. The RAA system is integrated into the “fight or flight” localization of blood pressure which is response to (in the caveman era) deadly threat from a predator (FIGHT, or Run like hell, the energy to do so in the musculature is “pumped” in by localized higher blood pressure to muscles, coupled with rapid conversion of stored glycogen to pure.. glucose, until exhausted).
The discovery of angiotensin converting enzyme rapid conversion of ACE I to ACEII and the related chemical action of ACE inhibitors- was made from the initial work of Brazilian scientist Sérgio Henrique Ferreira who reported a bradykinin-potentiating factor (BPF) present in the venom of Bothrops jararaca, a South American pit viper, in 1965. The venom of this deadly viper killed its victims by rapidly dropping their blood pressure to extreme low levels, and thus stopping heart and lung function, as well as they could not get away. Viper venom. Amazing.
The later definitive work of ACE inhibitor development was done by Victor Dzau, MD, PHD FACC, the former Chancellor of the Duke Medical School. See wiki on his bio. He was born in Shanghai and escaped the Chi-coms as a boy with his family.
Here is the wiki on Bothrops jaracara.
Other blood pressure drugs can aggravate the function of various target organs (especially in diabetics who have dysfunction from their poor metabolism of sugars, and the toxins— ketones which persist in the vasculature, esp. in the kidney which has reduced filtration ability, and actually “dies” in stages). Earlier drugs can reduce BP which is important of course, but in the long run, the RAA adjusts and is activated to counteract the drugs— and in so doing increases the stress on the various organs and vasculature. It is indeed a fascinating system— the emotional content/reaction can cause heart rate to accelerate, strokes to happen, and collapse. Sort of the neuro-hormonal connection referenced in the Ages of “the heart” which was/is “felt” as an emotional center, because of its reactions to the mind. Mind/Body... all that.
There are other vipers who have the peptide and are more potent— killing in the same way. Versus straight neurotoxins that instantly stop muscle function, breathing.
https://en.wikipedia.org/wiki/Bothrops_jararaca
Blood pressure study ping.
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