md_a
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- Aug 31, 2015
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Ro Dann on FB:
There is an extremely important connection between ACE-inhibitor medication for hypertension and the virus.
SUMMARY:
Pre-SARS-CoV-2, if someone went to an emergency dept. with a dry cough and trouble breathing, and was taking the blood pressure medication ACE-inhibitors, they would likely diagnose it as a side effect of the medication and take the person off of their ACE-I, and switch it to Losartan. This would be especially true if the person was African-American or a smoker, who are most susceptible to this side effect, and also have more hypertension than other ethnicities. In prescribing instructions, people who are taking ACE-I’s should be immediately taken off when these side effects present. Now, they don’t take them off their ACE-I and, instead, test for the virus, which has the same symptoms. The patient then remains on their ACE-I, and is treated with epinephrine and corticosteroids, as well as with a respirator, but many die. According to the American Heart Association, they keep patients on their ACE-I to protect their heart from “cardiac injury”, which is the cause of death in many cases of SARS-CoV-2. The test for cardiac injury is an increased level of troponin. However, ACE-I’s themselves not only cause the same symptoms as the virus-they also might “potentiate” (increase) an increase in troponin from the virus (as a study showed it did with alcohol). So, cardiac injury might be avoided if patients were taken off their ACE-I, like they would have been pre-virus, in which case they probably wouldn’t have cardiac injury and die. Furthermore, the Wuhan study of 89 fatalities, published on April 3, found that respiratory failure was the cause of death for 94%, so cardiac injury may play a small part in increased fatalities. Also noted in this study was that, unusually, hypertension alone was a common comorbidity with fatalities, with a total of 68% having co-morbidities that would have included blood pressure medication such as ACE-inhibitors. The researchers commented on this occurrence, noting that “the increased prevalence of hypertension in China may play a role in COVID-19 related deaths.” So, if the patient remains on ACE-I, then bradykinin, creatinine and troponin would likely increase, raising the risk of death, either from respiratory failure (bradykinin-induced angioedema) or cardiac injury (troponin) or other organ failure, which can be the result of prolonged ventilation. So, a conservative approach would be to treat a patient, who is taking an ACE-I, as they would if they were having the serious side effect of their medication, and immediately take them off of it so as not to increase the side effect, whether or not they test positive for the virus. Also, we could go back to the pre-2018 definition of hypertension, which would, from the many indications and studies included here, take many millions of Americans out of danger from the virus. Finally, as many people as possible could be switched to Losartan.
WHAT DOCTORS ARE SAYING:
Comments on an April 1 article by the American College of Cardiologists and the American Heart Association stating to not stop giving COVID-19 patients ACE-inhibitors.
Dr. William DeMedio-This article says don’t stop ACEI Or ARB meds in people with CoV19, but the science is not settled. I want to see if SARS outcomes are improved or impaired by these meds; or no net change. There is more than one way to lower BP for the short term in these people. How about a study switching some to a different class of antihypertensive, eg CCB or even a PDE 5 inhibitor? We could compare rate of SARS and death. ACE inhibitors increase pulmonary inflammation. That is why some people cough on them. Some studies suggest they may be associated with lung cancer. I do not think they are fully exonerated yet. This needs more work for an answer.
Dr. Wayne Greaves
@Dr. William DeMedio I am concerned that recommendations are being made on so little data and such limited concern. As a HCW myself I am unsure what to do. The data from Italy is very troubling with pre-hospital use of 36%ACEIs and 16% ARBs among Covid-19 persons that died. I sure hope someone is looking carefully at the emerging US data as the cases increase so we can have an answer based on more robust data. On another note, some have suggested at least for those on ACEIs which tend to increase bradykinin and thereby pro-inflammatory response that Vitamin D levels should be checked proactively and those with low levels be given Vit D to decrease inflammation in those who are at risk of pneumonia/ARDS.
Dr. STEPHEN ALGEO-Now with reports that in the US African American patients are recording worse outcomes with Covid-19 you have to wonder whether racial differences in ACE metabolism/physiology are a factor. As a cardiologist I am aware that African-Americans do not respond as well to ACE-inhibitors when used for both hypertension and CHF as other groups.
Dr. Francine Moring-ACE inhibitors block zinc. Zinc is needed in T cells. It helps decrease viral replication. Hydroxychloroquine acts like an ionophore, allowing zinc to get into cells.
https://www.medscape.com/viewarticle/927952
Furthermore, Dr. Fauci, from a March 18 interview, focuses just on ACE-inhibitors:
HB: Another clinical issue that really come up the last few days is this issue about ACE and ARBs in individuals who are either on them or develop disease. Now the Heart Failure Society of America, ACC, and AHA just came out with a statement yesterday. I don't know how familiar you are with the question, Tony, but I'll let you comment.
AF: Well, I am quite familiar with the question. So, here's the issue -- and this is something that I take a little bit more seriously about we really need to get data and we need to get data fast, Howard, and here's the reason why. If you look at the mechanistic rationale for concern, it's there and it's -- and it's firm, and that is, that when you give an ACE inhibitor or an ACE inhibitor can result -- I say can -- can result in an increased expression of the receptor for ACE. So, what is possible is that people who are on ACE inhibitors, a very commonly used drug for hypertension, that they may be, without knowing it, increasing the expression of receptors for the virus, itself.
That's an extrapolation, that's not based on known data, but it is a possibility that we need to address. I was struck by something that I read just early this morning, Howard, there was an article -- I think Bloomberg published it from a medical summary that in -- I believe it was Italy or in Europe, but I think it was in Italy, that 99% of the people who died had an underlying condition, that's not surprising. However, when they broke down the underlying conditions, 75% of it was hypertension, which was, to me, a bit of a red flag, because Italy is a very developed country. And I would imagine, if you knew the patient had hypertension, then the patient, almost certainly, had a physician.
And that physician almost certainly treated the person for their hypertension. So, if you could imagine -- and again, this is just my putting some dots together, Howard. This is no data, I'm just -- you know, giving you right off the top of my head. If 75% of those so-called underlying conditions was hypertension, and the hypertension was well-controlled, why should someone who has hypertension that's well controlled have a much greater chance of dying than somebody else with any other kind of underlying condition? I mean I look upon someone who has well-controlled hypertension and nothing else wrong with them as a reasonably healthy person, yet it was skewed towards people with hypertension, which tells me I don't know what the answer is, but somebody better look really carefully and that's what we're hopefully going to get that data from the Italian scientists. https://edhub.ama-assn.org/jn-learning/audio-player/18324686
The following is a series of studies and articles describing:
1. The action of ACE-inhibitors and its side effects: dry cough and angioedema (swollen airways) mainly due to increased bradykinin
2. Symptoms of SARS-CoV-2 are the same as side effects of ACE-inhibitors, again from bradykinin, so people taking ACE-inhibitors would have a magnified effect of symptoms if they become infected. Also, the unusually high number of people with only hypertension that have died connects the virus with ACE-I’s.
3. Unlike with other viruses, people often become “re-infected”, which doesn’t make sense normally, but this does make sense if they are still on their ACE-inhibitor, which has so much to do with the excessive symptoms.
4. How prescription guidelines recently changed, and how countries differ re: ACE-inhibitor prescriptions.
5. Official position of Medical Community: no one should stop taking ACE-inhibitors, even if infected with SARS-CoV-2.
6. What to do about the problem.
REFERENCES
1.The action of ACE-inhibitors and its side effects: dry cough and angioedema (swollen airways) mainly due to increased bradykinin
https://edhub.ama-assn.org/jn-learning/audio-player/18324686
http://www.scielo.br/scielo.php…
https://www.ncbi.nlm.nih.gov/pubmed/11827930
https://cvpharmacology.com/vasodilator/ACE
https://www.ncbi.nlm.nih.gov/pubmed/10893650 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3638407/… https://www.nationaljewish.org/conditions/angioedema
https://www.merckmanuals.com/…/allergic,-autoimm…/angioedema
2.Symptoms of SARS-CoV-2 are the same as side effects of ACE-inhibitors, again from bradykinin, so people taking ACE-inhibitors would have a magnified effect of symptoms if they become infected. Also, the unusually high number of people with only hypertension that have died connects the virus with ACE-I’s.
https://www.usatoday.com/…/what-coronavirus-doe…/5009057002/ https://www.preprints.org/manuscript/202004.0023/v1 https://aliveandwellaustin.com/…/what-we-want-you-to-know-…/
www.jacionline.org › article › pdf
" Ibuprofen augments bradykinin-induced ... - JACI
www.jacionline.org › article › pdf
https://www.ncbi.nlm.nih.gov/pubmed/28935640 https://www.scientificamerican.com/…/snakes-could-be-the-o…/ https://www.pharmaceutical-journal.com/…/…/10884359.article…
3.Unlike with other viruses, people often become “re-infected”, which doesn’t make sense normally, but this does make sense if they are still on their ACE-inhibitor, which has so much to do with the excessive symptoms.
https://www.france24.com/…/20200328-can-the-coronavirus-inf…
4.How prescription guidelines recently changed, and how countries differ re: ACE-inhibitor prescriptions. US used new guidelines for prescribing ACE-inhibitors in late 2017, greatly increasing people on these meds, especially younger people and newly prescribed. Side effects of cough and angioedema can occur up to a year after new prescription. That flu season was especially bad with far more illnesses, hospitalizations and deaths. The exact same problem of greater deaths from angioedema occurred in 2003, with the SARS virus, because there was another increase in ACE-inhibitor prescriptions due to the 2003 change in the threshold defining “hypertension”. So, both in 2003 and in 2018, when there was a large spike in “pneumonia and flu deaths”, there were suddenly far more people being prescribed ACE-inhibitors, the first-line med for hypertension.
https://newsroom.heart.org/…/high-blood-pressure-redefined-…
https://www.tctmd.com/…/new-european-hypertension-guideline…
5.Official position of Medical Community: no one should stop taking ACE-inhibitors, even if infected with SARS-CoV-2, even though Dr. Fauci wants this connection to be looked at “very carefully”.
https://www.ahajournals.org/doi/10.1161/JAHA.120.016219
https://newsroom.heart.org/…/patients-taking-ace-i-and-arbs…
https://jamanetwork.com/journals/jama/fullarticle/2763803
http://www.scielo.br/scielo.php…
https://edhub.ama-assn.org/jn-learning/audio-player/18324686
6.How to lower hospitalizations and deaths: 1.by lowering the number of people on ACEI’s by changing definition of hypertension back to 2017 guidelines, 2.by mandatory self-quarantine for those staying on ACEI’s, and 3.by treating hospital cases, for those on ACEI’s, first for the ACEI side effect, and immediately take them off ACI’s, which is only following the prescription instructions! Then, possibly use Icatibant, which breaks down bradykinin, may be effective. Possibly in the future, block bradykinin B1 receptor, which ACEI actually induces instead, with SSR240612. This also lowers blood pressure!Those who have blood pressure that is not considered to be high according to the original definition of hypertension should stop taking ACE-inhibitors, as is the case in Germany, Netherlands, and South Korea. ACE normally breaks down bradykinin, but it is low with zinc-deficiency (ACE is a zinc enzyme). ACE-inhibitors lower zinc, as does smoking and oral contraceptives, and all of these increase risk for angioedema. Plaquinil, on the other hand, increases zinc in the cells, so it can be used to treat angioedema. Also, bradykinin is high in lupus, which is effectively treated with plaquinil. So, plaquinil has been shown to work on virus-induced angioedema, which is apparently ACE-inhibitor and bradykinin-induced as well.
https://www.google.com/search… https://www.preprints.org/manuscript/202004.0023/v1 https://www.ncbi.nlm.nih.gov/pubmed/11827930
R. Sehgal 1, R. Khan 2, https://doi.org/…/ajrccm-conference.2019.199.1_MeetingAbstr…
https://link.springer.com/article/10.1186/s13075-018-1774-x
https://www.ncbi.nlm.nih.gov/pubmed/3003288
Compiled by Joan Tendler, M.Arch., West Allis, [email protected] 414-828-3637
There is an extremely important connection between ACE-inhibitor medication for hypertension and the virus.
SUMMARY:
Pre-SARS-CoV-2, if someone went to an emergency dept. with a dry cough and trouble breathing, and was taking the blood pressure medication ACE-inhibitors, they would likely diagnose it as a side effect of the medication and take the person off of their ACE-I, and switch it to Losartan. This would be especially true if the person was African-American or a smoker, who are most susceptible to this side effect, and also have more hypertension than other ethnicities. In prescribing instructions, people who are taking ACE-I’s should be immediately taken off when these side effects present. Now, they don’t take them off their ACE-I and, instead, test for the virus, which has the same symptoms. The patient then remains on their ACE-I, and is treated with epinephrine and corticosteroids, as well as with a respirator, but many die. According to the American Heart Association, they keep patients on their ACE-I to protect their heart from “cardiac injury”, which is the cause of death in many cases of SARS-CoV-2. The test for cardiac injury is an increased level of troponin. However, ACE-I’s themselves not only cause the same symptoms as the virus-they also might “potentiate” (increase) an increase in troponin from the virus (as a study showed it did with alcohol). So, cardiac injury might be avoided if patients were taken off their ACE-I, like they would have been pre-virus, in which case they probably wouldn’t have cardiac injury and die. Furthermore, the Wuhan study of 89 fatalities, published on April 3, found that respiratory failure was the cause of death for 94%, so cardiac injury may play a small part in increased fatalities. Also noted in this study was that, unusually, hypertension alone was a common comorbidity with fatalities, with a total of 68% having co-morbidities that would have included blood pressure medication such as ACE-inhibitors. The researchers commented on this occurrence, noting that “the increased prevalence of hypertension in China may play a role in COVID-19 related deaths.” So, if the patient remains on ACE-I, then bradykinin, creatinine and troponin would likely increase, raising the risk of death, either from respiratory failure (bradykinin-induced angioedema) or cardiac injury (troponin) or other organ failure, which can be the result of prolonged ventilation. So, a conservative approach would be to treat a patient, who is taking an ACE-I, as they would if they were having the serious side effect of their medication, and immediately take them off of it so as not to increase the side effect, whether or not they test positive for the virus. Also, we could go back to the pre-2018 definition of hypertension, which would, from the many indications and studies included here, take many millions of Americans out of danger from the virus. Finally, as many people as possible could be switched to Losartan.
WHAT DOCTORS ARE SAYING:
Comments on an April 1 article by the American College of Cardiologists and the American Heart Association stating to not stop giving COVID-19 patients ACE-inhibitors.
Dr. William DeMedio-This article says don’t stop ACEI Or ARB meds in people with CoV19, but the science is not settled. I want to see if SARS outcomes are improved or impaired by these meds; or no net change. There is more than one way to lower BP for the short term in these people. How about a study switching some to a different class of antihypertensive, eg CCB or even a PDE 5 inhibitor? We could compare rate of SARS and death. ACE inhibitors increase pulmonary inflammation. That is why some people cough on them. Some studies suggest they may be associated with lung cancer. I do not think they are fully exonerated yet. This needs more work for an answer.
Dr. Wayne Greaves
@Dr. William DeMedio I am concerned that recommendations are being made on so little data and such limited concern. As a HCW myself I am unsure what to do. The data from Italy is very troubling with pre-hospital use of 36%ACEIs and 16% ARBs among Covid-19 persons that died. I sure hope someone is looking carefully at the emerging US data as the cases increase so we can have an answer based on more robust data. On another note, some have suggested at least for those on ACEIs which tend to increase bradykinin and thereby pro-inflammatory response that Vitamin D levels should be checked proactively and those with low levels be given Vit D to decrease inflammation in those who are at risk of pneumonia/ARDS.
Dr. STEPHEN ALGEO-Now with reports that in the US African American patients are recording worse outcomes with Covid-19 you have to wonder whether racial differences in ACE metabolism/physiology are a factor. As a cardiologist I am aware that African-Americans do not respond as well to ACE-inhibitors when used for both hypertension and CHF as other groups.
Dr. Francine Moring-ACE inhibitors block zinc. Zinc is needed in T cells. It helps decrease viral replication. Hydroxychloroquine acts like an ionophore, allowing zinc to get into cells.
https://www.medscape.com/viewarticle/927952
Furthermore, Dr. Fauci, from a March 18 interview, focuses just on ACE-inhibitors:
HB: Another clinical issue that really come up the last few days is this issue about ACE and ARBs in individuals who are either on them or develop disease. Now the Heart Failure Society of America, ACC, and AHA just came out with a statement yesterday. I don't know how familiar you are with the question, Tony, but I'll let you comment.
AF: Well, I am quite familiar with the question. So, here's the issue -- and this is something that I take a little bit more seriously about we really need to get data and we need to get data fast, Howard, and here's the reason why. If you look at the mechanistic rationale for concern, it's there and it's -- and it's firm, and that is, that when you give an ACE inhibitor or an ACE inhibitor can result -- I say can -- can result in an increased expression of the receptor for ACE. So, what is possible is that people who are on ACE inhibitors, a very commonly used drug for hypertension, that they may be, without knowing it, increasing the expression of receptors for the virus, itself.
That's an extrapolation, that's not based on known data, but it is a possibility that we need to address. I was struck by something that I read just early this morning, Howard, there was an article -- I think Bloomberg published it from a medical summary that in -- I believe it was Italy or in Europe, but I think it was in Italy, that 99% of the people who died had an underlying condition, that's not surprising. However, when they broke down the underlying conditions, 75% of it was hypertension, which was, to me, a bit of a red flag, because Italy is a very developed country. And I would imagine, if you knew the patient had hypertension, then the patient, almost certainly, had a physician.
And that physician almost certainly treated the person for their hypertension. So, if you could imagine -- and again, this is just my putting some dots together, Howard. This is no data, I'm just -- you know, giving you right off the top of my head. If 75% of those so-called underlying conditions was hypertension, and the hypertension was well-controlled, why should someone who has hypertension that's well controlled have a much greater chance of dying than somebody else with any other kind of underlying condition? I mean I look upon someone who has well-controlled hypertension and nothing else wrong with them as a reasonably healthy person, yet it was skewed towards people with hypertension, which tells me I don't know what the answer is, but somebody better look really carefully and that's what we're hopefully going to get that data from the Italian scientists. https://edhub.ama-assn.org/jn-learning/audio-player/18324686
The following is a series of studies and articles describing:
1. The action of ACE-inhibitors and its side effects: dry cough and angioedema (swollen airways) mainly due to increased bradykinin
2. Symptoms of SARS-CoV-2 are the same as side effects of ACE-inhibitors, again from bradykinin, so people taking ACE-inhibitors would have a magnified effect of symptoms if they become infected. Also, the unusually high number of people with only hypertension that have died connects the virus with ACE-I’s.
3. Unlike with other viruses, people often become “re-infected”, which doesn’t make sense normally, but this does make sense if they are still on their ACE-inhibitor, which has so much to do with the excessive symptoms.
4. How prescription guidelines recently changed, and how countries differ re: ACE-inhibitor prescriptions.
5. Official position of Medical Community: no one should stop taking ACE-inhibitors, even if infected with SARS-CoV-2.
6. What to do about the problem.
REFERENCES
1.The action of ACE-inhibitors and its side effects: dry cough and angioedema (swollen airways) mainly due to increased bradykinin
https://edhub.ama-assn.org/jn-learning/audio-player/18324686
http://www.scielo.br/scielo.php…
https://www.ncbi.nlm.nih.gov/pubmed/11827930
https://cvpharmacology.com/vasodilator/ACE
https://www.ncbi.nlm.nih.gov/pubmed/10893650 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3638407/… https://www.nationaljewish.org/conditions/angioedema
https://www.merckmanuals.com/…/allergic,-autoimm…/angioedema
2.Symptoms of SARS-CoV-2 are the same as side effects of ACE-inhibitors, again from bradykinin, so people taking ACE-inhibitors would have a magnified effect of symptoms if they become infected. Also, the unusually high number of people with only hypertension that have died connects the virus with ACE-I’s.
https://www.usatoday.com/…/what-coronavirus-doe…/5009057002/ https://www.preprints.org/manuscript/202004.0023/v1 https://aliveandwellaustin.com/…/what-we-want-you-to-know-…/
www.jacionline.org › article › pdf
" Ibuprofen augments bradykinin-induced ... - JACI
www.jacionline.org › article › pdf
https://www.ncbi.nlm.nih.gov/pubmed/28935640 https://www.scientificamerican.com/…/snakes-could-be-the-o…/ https://www.pharmaceutical-journal.com/…/…/10884359.article…
3.Unlike with other viruses, people often become “re-infected”, which doesn’t make sense normally, but this does make sense if they are still on their ACE-inhibitor, which has so much to do with the excessive symptoms.
https://www.france24.com/…/20200328-can-the-coronavirus-inf…
4.How prescription guidelines recently changed, and how countries differ re: ACE-inhibitor prescriptions. US used new guidelines for prescribing ACE-inhibitors in late 2017, greatly increasing people on these meds, especially younger people and newly prescribed. Side effects of cough and angioedema can occur up to a year after new prescription. That flu season was especially bad with far more illnesses, hospitalizations and deaths. The exact same problem of greater deaths from angioedema occurred in 2003, with the SARS virus, because there was another increase in ACE-inhibitor prescriptions due to the 2003 change in the threshold defining “hypertension”. So, both in 2003 and in 2018, when there was a large spike in “pneumonia and flu deaths”, there were suddenly far more people being prescribed ACE-inhibitors, the first-line med for hypertension.
https://newsroom.heart.org/…/high-blood-pressure-redefined-…
https://www.tctmd.com/…/new-european-hypertension-guideline…
5.Official position of Medical Community: no one should stop taking ACE-inhibitors, even if infected with SARS-CoV-2, even though Dr. Fauci wants this connection to be looked at “very carefully”.
https://www.ahajournals.org/doi/10.1161/JAHA.120.016219
https://newsroom.heart.org/…/patients-taking-ace-i-and-arbs…
https://jamanetwork.com/journals/jama/fullarticle/2763803
http://www.scielo.br/scielo.php…
https://edhub.ama-assn.org/jn-learning/audio-player/18324686
6.How to lower hospitalizations and deaths: 1.by lowering the number of people on ACEI’s by changing definition of hypertension back to 2017 guidelines, 2.by mandatory self-quarantine for those staying on ACEI’s, and 3.by treating hospital cases, for those on ACEI’s, first for the ACEI side effect, and immediately take them off ACI’s, which is only following the prescription instructions! Then, possibly use Icatibant, which breaks down bradykinin, may be effective. Possibly in the future, block bradykinin B1 receptor, which ACEI actually induces instead, with SSR240612. This also lowers blood pressure!Those who have blood pressure that is not considered to be high according to the original definition of hypertension should stop taking ACE-inhibitors, as is the case in Germany, Netherlands, and South Korea. ACE normally breaks down bradykinin, but it is low with zinc-deficiency (ACE is a zinc enzyme). ACE-inhibitors lower zinc, as does smoking and oral contraceptives, and all of these increase risk for angioedema. Plaquinil, on the other hand, increases zinc in the cells, so it can be used to treat angioedema. Also, bradykinin is high in lupus, which is effectively treated with plaquinil. So, plaquinil has been shown to work on virus-induced angioedema, which is apparently ACE-inhibitor and bradykinin-induced as well.
https://www.google.com/search… https://www.preprints.org/manuscript/202004.0023/v1 https://www.ncbi.nlm.nih.gov/pubmed/11827930
R. Sehgal 1, R. Khan 2, https://doi.org/…/ajrccm-conference.2019.199.1_MeetingAbstr…
https://link.springer.com/article/10.1186/s13075-018-1774-x
https://www.ncbi.nlm.nih.gov/pubmed/3003288
Compiled by Joan Tendler, M.Arch., West Allis, [email protected] 414-828-3637