Who said anything about unilateral ? Of course my GP prescribed the calcium channel blocker. I did not buy it at home depot !
Not a decisive answer, as there currently is no clear guidance on ACE/ARB’s, but some thoughts on the decision:
Obviously, in some cases, traditional clinical factors would be decisive. For example, stopping an ACE inhibitor or ARB in an otherwise healthy patient with mild hypertension risks less harm than stopping the drug in a patient with compensated heart failure.
Decision-making under uncertainty is necessarily stressful, both in medicine and more generally. Some people become immobilized by true equipoise around available options. A sensible position for overworked and stressed clinicians facing a global pandemic is to recognize that, for now, the effect of ACE inhibitors and ARBs on the natural history of COVID-19 is unknown. Clinicians should attempt to make decisions that will minimize future regret for themselves and for their patients if the decision eventually is proven “wrong.”
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@JamesIgoe – I found this analysis from your cited source revealing.
Additionally, we believe that many clinicians experience bad outcomes as more emotionally burdensome after acts of commission than after acts of omission (assuming that the act of omission was consistent with standards of care). In the case of a patient who is taking an ACE inhibitor or ARB already, continuing the drug (i.e., maintaining the status quo) would be an act of omission. In contrast, stopping the drug would be the act of commission and would likely be experienced as more regretful and emotionally painful if studies eventually showed that the drug might have conferred benefit in patients with COVID-19. For a clinician in whom this distinction resonates, the analysis would favor continuing the drug; importantly, it would also remain concordant with professional society recommendations, which in turn would provide an additional layer of support for the clinician.
My decision to stop my ARB a few months ago (before Covid-19 became a consideration) was a unilateral one. When I confronted the subject during a visit to my primary care physician, I brought with me several weeks of daily blood pressure data that showed a normal average of about 105/65 mmHg. My in-office BP that day was normal and aligned with the data I presented. She still encouraged me to restart the ARB for the “protective kidney effect.” I decided to sustain the ARB removal and let Mother Nature prevail; I’m a firm believer in the axiom that the least medicine is the best medicine.
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Let me just get this out of the way. I cannot ever condone self-medicating with BP meds without a doc knowing about it. I won’t even argue about it. I will just eject myself out the conversation. Or I should. I will always say – talk to your HCP.
But otherwise, apart from that, I don’t understand how you can not realize, based on the sheer amount of time I’ve demonstrably spent here posting and reading and responding…I just don’t get why I seem not to be accorded the same benefit of the doubt that I have read and understood your (and others’) ideas and stories on multiple occasions that others are. I listen. I ask questions. I don’t JUST assume, I mean I may assume, but I don’t JUST assume. I get it. I have read your philosophy on and regimen of self-care on multiple occasions, we have dialogued a couple of times, but you seem to always come back to zero with me, that I need to be schooled or something on the uniqueness of the people on these boards. I find it tiresome. I’m not saying I know everything, I’m just tired of being patronized I guess. I get it that many people on here are likewise tired of being treated perfunctorily and formulaically by medical practitioners and that you have struggled to personalize both the relationship and treatment. How thick would I have to be not to pick up on that? From time to time, maybe not often, I’ve written comments reflecting this appreciation and further indicating I have been a “regular” patient myself far longer than I have been a nurse. I have a good idea what it’s like. In addition, I advocate on a regular basis for patients, and have said on here that I do, and have advocated ON HERE for people. But apparently that’s not getting transmitted and I remain someone who must be convinced at every turn.
I really appreciate your recent words, I really do, but what I’m trying to say is that I experience your written offerings, Terry, by turns extremely knowledge-sharing and welcoming and territorial and forbidding.
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When you don’t have any data, its helpful to go back to good old fashioned street medicine.
Take your meds. Stay at home.
That is the practical answer to everything during this time. That might be the best we can do for 18 months. Anything else is just talk. Frankly, the odds of contracting are so high that you might as well just assume 100% if your not isolating. Statistics become fairly worthless in this situation. I am advocating for more pragmatic decision making. Medical statistics are notoriously sh!t.
The fundamental thing that you all might be driving at is the impact of cardiac health. Obviously, those of us with crappy cardio are gonna be in more trouble. That is a lot of us.
We are playing cards with a deck of 51, statistically speaking.
Jeez. 105/65 would it not be dangerous to go lower ? Remember our Richard ended up with a cracked skull also not good. In so far protecting the kidneys I am not sure since low BP damages them.
Here’s a chart published in a UK source.
According to this source, numbers below 90/60 may mean your blood pressure is too low. A BP of 105/65 is considered ideal and healthy by this website. I know what low blood pressure dizziness feels like and would talk to my doctor if I felt that more than a few times or if it affected my balance.
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Just a followup/addenda to our prior discussions about ACE2. Nothing radically new, but some detail on how ACE2, normally beneficial for protecting lung tissue, is exploited by the virus…
Two more mentions of ARB/ACE in the press…
ARBs & ACE inhibitors: Angiotensin-receptor blockers (ARBs) and angiotensin-converting-enzyme (ACE) inhibitors were not associated with COVID-19 severity or mortality in a JAMA Cardiology study. Researchers looked at 360 COVID-19 patients with hypertension who were hospitalized in Wuhan from Jan. 15 to Mar. 15. Use of ARBs or ACE inhibitors did not differ significantly between those with severe and those with [non-severe] disease (33% vs. 31%) or between nonsurvivors and survivors (27% vs. 33%). The authors conclude: “These data support current guidelines and societal recommendations for treating hypertension during the COVID-19 pandemic.” (Of note, a study published last week in Circulation Research showed a reduced mortality risk in hospitalized COVID-19 patients taking these drugs.)
Link: COVID-19: ARBs & ACE Inhibitors / Cats / At-Risk Americans
Nailing the coffin shut
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The best videos I’ve seen so far on the pathophysiology of SARS Covi-2 and the damage it does within the body are by Medcram. I highly recommend them. He talks extensively about the ACE2 receptor, and he is lately breaking down in incredible detail the role of inflammation/endothelial damage. I watch them on youtube.
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I also enjoy and learn a lot from Dr. Seheult’s Medcram YouTube videos. At times it is well over my ability to absorb all the concepts but his teaching style is excellent and gives you half a chance to hang on. His graphical use of the digital blackboard gives his lectures another path to the brain.
His target audience seems to be medical professionals but his presentation gives someone like me, who did not do well in high school chemistry and biology, a shot at learning something. He seems to publish a new lecture every day and also works full time in the hospital ICU tending to Covid-19 patients.
Here’s today’s topic: Covid-19 and oxidative stress. Not for everyone but he will stretch your brain.
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Among 5,700 patients hospitalized with COVID-19 in the New York City area, the most common comorbidities were hypertension (57%), obesity (42%), and diabetes (34%). 88% had > 1 comorbidities
At triage, 30.7% were febrile, 17.3% had a respiratory rate greater than 24 breaths/min, and 27.8% received supplemental oxygen.
Mortality was 0% for male and female patients younger than 20 years. Mortality rates were higher for male compared with female patients at every 10-year age interval older than 20 years.
Of the patients who died, those with diabetes were more likely to have received invasive mechanical ventilation or care in the ICU compared with those who did not have diabetes.
Of the patients who died, those with hypertension were less likely to have received invasive mechanical ventilation or care in the ICU compared with those without hypertension. The percentage of patients who developed acute kidney injury was increased in the subgroups with diabetes compared with subgroups without those conditions.
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I avoided discussion of genetics by country and ethnicity as too akin to racism, and too broad for analysis. Granted, there could be aspects particular to some ethnicities and countries, but it seemed that rates could be explained by social welfare, urbanity, political leadership, having megacities and/or travel hubs, and not genetics. Genes play a role, but it is too crude to think at the country or state level. Right now, we see that those most affected were in cities and are older, urban, minority, overweight, and male, with preexisting conditions. Again, there might be genetic influences, particularly for preexisting conditions, but it seems more like a social and class issue.
I’ve had my DNA analyzed from a few companies, and they recently have started asking that I fill out a virus-related quiz. As part of that effort, 23AndMe provided an article on genetics, that seemed a bit better informed.
https://blog.23andme.com/23andme-research/genetics-and-covid-19-severity/3
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You had mentioned the idea of blood types, and I avoided considering this at the country level - an argument broached by someone else - and still would, because it is often used in racialized arguments, but there is a recent finding on increased negative outcomes for people with Type A blood so I wanted to revisit it, to check my assumptions.
Blood is a valid differentiator, or so it seems, but questionable at a country level. Most European countries have both high proportions of A and O blood types, the latter being protective, so it would make sense as a differentiator within populations, but possibly not between them, for the Europeans. I could do some data analysis in R/Python on blood types and infection rates to make a better back-of the-napkin claim, and there might be a correlation with the percentage of Type A across countries, but that has problems with unanalyzed variables, like country lockdown policy, healthcare, wealth distribution. density, racism, and tourism.
That said, eyeballing shows some problems. As an example, African-Americans have a high proportion of O and very low proportions of A blood types - from the Wikipedia link you provided - but are most affected. Granted obesity and other risk factors are involved, but even those are questionably ‘genetic’ considering the US’s race problem.
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Risk factors for higher mortality of patients with diabetes and COVID-19, the only new one for me is the C-reactive protein correlation, but at .05, it is questionable. Since most in this study were Type 2, my guess would be that it might indicate those with the worst control.
- Older age (P = 0.001)
- Elevated C-reactive protein (P = 0.043)
- Insulin usage (P = 0.009)
Of Note: Clinical outcomes of those who use an ACE inhibitor (ACEI) or angiotensin II type-I receptor blocker (ARB) were comparable with those of patients who do not use ACEI/ARB among COVID-19 patients with diabetes and hypertension.
I wonder if they had high CRP before, or whether it was people with otherwise normal CRP and the high number just indicated their body was fighting a worse illness? I didn’t see anything in skimming the text that said the actual levels of CRP. My CRP is always slightly high every time it’s tested, and I have good diabetes control (though not the non-diabetic level control that some have).
I use magnesium for CRP and diabetes complications in general:
Effect of magnesium supplements on serum C-reactive protein: a systematic review and meta-analysis
I also use ginger tea for CRP, inflammation, diabetes complications, and as a natural ARB as it blocks Angiotensin II Type 1 Receptor:
[6]-gingerol: a novel AT₁ antagonist for the treatment of cardiovascular disease
Both of the above are part of my Covid protocol for various reasons.
I know we went back and forth about this…
@gallagher.neal - An update to the blood type question:
New research suggests a causal link between blood group and severe COVID-19 | EurekAlert!
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