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So i was at a presentation recently and i had the same experience that i often have when i ask people about the blood pressure medicine their own mm quite often people will tell me their own losartan or one of the arbs that stands for angiotensin receptor blocker again these are fairly informed patients for the most part and i asked him if they tried ramipril
Lisinopril one of the ace inhibitors i with a lot of those folks they just give me the deer-in-the-headlights look and that’s because they were the ace inhibitors were never discussed with them by their doc and others say well you know what i didn’t want to trial because i don’t like i get the coffee when i take x inhibitors and they think i’m a nut when and
Maybe i am but i will still continue to push this issue sometimes i have my own coughing spells even when i’m giving a presentation it’s usually only if there’s it’s during allergy season but they say you know see you got this coffee why why do you continue to take case inhibitors just take let’s our tent i used to take losartan i started on that and then i read
Up on them and there’s a very strong reason why you should be on ace inhibitors not arps what we’ll get into that in just a minute first a brief introduction my name is ford brewer f ord brewer br eak wer with previa we we help focus on prevention so you you don’t have to have that heart attack that stroke that dementia heart failure prevention is takes discipline
And it seems like the hard route but as many of us know you we all know sometimes the easy route is not the easy the easy route in the in the beginning is not the easiest in the long term so i’m just going to go through the basics of it one of the review articles on aces versus orbs and i’ll give you the the information below this is differences in the clinical
Effects of angiotensin converting enzyme inhibitors and angiotensin receptor blockers a c e so ace inhibitors and arb angiotensin receptor blockers a critical review of the evidence now why don’t we start by talking about what is angiotensin what’s angiotensin receptor blockers what are these things to do angiotensin brady kind and they’re well angiotensin is a
Is a type of hormone a prostaglandin type thing that is chemical that’s made by our precursors made by the lungs angiotensinogen that’s converted by angiotensin to angiotensin one then angiotensin 2 these hormones or prostaglandins actually cause an increase and again pardon my visuals here they could cause an increase in the water the fluid that you retain and
An increase in the tone they’ve asked the muscle tone of the media the vascular tone so those two things increase the blood pressure the kidneys have a couple of different roles in this area and obviously cortisol the adrenal glands they have significant roles as well as well as obviously the liver and lungs so that angiotensin reen and system increases our blood
Pressure so they found out that by making a type of chemical called an angiotensin converting enzyme inhibitor they slowed that down so the iranian rena and angiotensin system plays a major role in the in the pathophysiology in the mechanism of high blood pressure ace inhibitors have were the first drugs out there and sure enough they worked great they did a lot
Of good things they have some more side effects and it’s probably like nice and maybe like some of the other things where the thing that causes the side effect very well maybe the thing that because of the improved health outcomes the ace aces and arbs are equally important in the treatment of high blood pressure but think about it is it the high blood pressure
Itself that’s causing the problems or the outcome of the high blood pressure there are the whu-oh says that hypertension is the leading risk factor for mortality the diseases associated with blood pressure or caused thirteen percent of deaths in the world or 7.5 million deaths per year so hypertension again the high blood pressure itself is not what’s killing you
It’s causing other problems like heart attacks stroke that do kill you so what we want to look for is the long term effect of the medication not the immediate short-term decrease in blood pressure and the arbs will decrease blood pressure just as effectively as ace inhibitors it’s just that they don’t have as good an impact on the the outcomes we mentioned now this
Started happening in the late 90s early 2000s based on some observation about um again the first class to come out was the ace inhibitors they found that you had a cough that was again up to 20% of us get some coffee with ace inhibitors it’s again probably associated with some prostaglandin release so they said they developed a new type of of pill with a different
Mechanism instead of inhibiting a sin hit the ace angiotensin converting enzyme it blocked specific receptors and so they called them angiotensin receptor blockers arbs so they they expected to get the same positive impact on things like nephropathy diabetes heart failure and they didn’t they started to notice this in the late 90s then there was the i can give you
A couple of these citations if you want to look them up you can pull them right out of this article and i’ll give you that citation the valsartan hypertensive long-term use evaluation strossen hall in 26 2006 did a meta-analysis involving more than 55,000 patients in that one they found actually an increase in myocardial infarction that was the weird signal that
Surprised everybody they’ve done a lot of research since then on this specific issue and it does not appear that arbs actually increased heart attacks they don’t decrease them though another analysis by turnbull demonstrated aysen and arbs did not different regarding their effect on stroke risk they did affect heart attack risk very differently so as you can imagine
What happened with all this information coming out well there was a huge amount of criticism debate statements that all these studies are flawed bottom line at the end of the day there’s recognition that aids are our ace inhibitors are not arms arbs are not ace inhibitors they don’t do the same thing and they don’t have the same long-term impact in 2011 there was
Another analysis this was a meta-analysis looking at 30 seven clinical trials concluding this was done by bangalore and associates the conclusion was although arbs do not increase the risks of mi and total mortality they do not decrease the risks event of mi and mortality significantly even when compared with the placebo so nevertheless herbs did significantly
Reduce the risk of heart failure stroke and new onset diabetes so let’s take a look what did arbs actually impact here’s another way of looking at it total mortality know that n s means non significant so not a significant impact on total mortality cardiovascular mortality again was non significant heart heart failure and stroke were significantly decreased by
Arbs myocardial infarction was decreased somewhat but again not significantly now why is this let’s go take a look at what’s going on here well first of all they do two different things as i mentioned before the here’s some another way of looking at remember we looked at that angiotensin system angiotensinogen is made by i think the liver and then converted to
Rainin by rainin to angiotensin one then angiotensin 2 ace inhibitors stop this process so therefore you get an increased amount of breda kine and brady kine and is no longer being blocked or broken down that has a big impact we’ll talk about that in just a minute the arbs however only impact the angiotensin ii receptor blockers actually the 81 and 82 blockers
They block the the receptors so what’s the big difference here with both of them you get not so much angiotensin impact but only with the ace inhibitors do you get a big increase in bradykinin well why does that matter brady condon is a big deal evidently so again inhibition ace inhibition causes a couple of things number one angiotensin one is not broken down
To angiotensin 2 so we get all of the positive things that you would get and this is also shared with arbs herbs do this as well they decrease vasoconstriction they decrease monocyte adhesion they decrease smooth muscle cell proliferation oxidant release and endothelial some endothelial dysfunction bradykinin however has a significant boost to these activities
What does increase bradykinin do and again we’re not breaking better kind and down anymore with the ace inhibitors you get increased vaso dal dilatation increased inhibition of monocytes ii that’s endothelial nitric oxide is improved tissue plasminogen levels fibrinolysis increased anti remodeling effect increased antioxidant effects and therefore improved in the
Thelia function so there you have it now if your doc just didn’t tell you about any of this stuff don’t be surprised most doc’s don’t it’s a lot easier and quicker to just write a script for an arb again this has gone on thirteen minutes thank you very much for your attention
Transcribed from video
Do Losartan and other ARBS prevent heart attack ? (no) – FORD BREWER MD MPH By Ford Brewer MD MPH
