Interesting! Maybe that’s why my nebivolol seemingly had no effect in protecting against the two episodes of afib I’ve had over the last several years (both happened after chugging a cold fruit smoothie).
Have you come across the topic of psychological stress-induced myocardial ischemia in your hypertension readings? It always seemed like a beta blocker would be most protective against this “fight or flight” response from a stressful event that can trigger a MI, but when last I checked (several years ago), I couldn’t find much data and what I did find never seemed to mention beta blockers.
adssx
#67
I’ve never checked this. I assume it’s hard to measure. In clinical trials and medical records, can we distinguish stress-induced MI from other myocardial ischemia? If not: we cannot know which drug works best for this.
Oh it’s definitely a thing and is measurable, and puts people prone to this at much higher risk of cardiac events. I’ll look into the literature later today to see what I can dig up.
adssx
#69
Of course, stress-induced MI is real. But can you distinguish on a dead body whether the person died of stress-induced MI or non-stress-induced MI?
A positive for telmisartan seems also to be weight/fat loss. I’m experiencing that with my regimen and think my high dose of telmisartan is helping (though I’m also taking other things like rapa and jardiance that many feel help in the weight/fat as well)
Do other bp medicines have this effect?
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adssx
#71
I didn’t believe it but a quick research confirms that telmisartan slightly decreases body weight:
It also affects fat distribution: Effects of telmisartan on fat distribution: a meta-analysis of randomized controlled trials 2015
See also: Effects of telmisartan on metabolic syndrome components: a comprehensive review 2024 (
Iranian paper
)
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I wonder if its affects on body weight/fat are in a dose dependent manner? I’m taking the 80 mg. Will be interesting to observe my body after a few months more on it as ive really just started it recently. (though I’m also taking other substances that could be decreasing the body weight/fat)
I think the idea behind PSIMI is to subject patients to a psychologically stressful stimulus and assess for signs of mild cardiac ischemia. Those who show signs of ischemia from psychological stress (vs those who don’t, while carefully controlling for other risk factors) have a much higher risk of future cardiovascular events. Thus, meds which block this effect should significantly reduce future risk in those who experience PSIMI. I’m curious if they’ve yet done studies with different classes of BP meds to assess which may be best for this use.
Edit: it’s referred to as “Mental Stress Induced Myocardial Ischemia” aka MSIMI. Here’s a recent review, but not a lot of answers yet.
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AnUser
#74
What is written in guidelines whether to start use of anti-coagulants in your case for stroke prevention because of afib?
It’s a tough call. I’ve never had episodes of afib other than those two times after chugging cold smoothies (and I know immediately when I’m in afib, unlike some who can’t tell), so is it worth being on an anticoagulent med for the rest of my life, which also carries its own risks? There aren’t any anticoag outcome studies in the subgroup of patients who only get afib from drinking cold drinks too fast. I do plan to ask my cardiologist next time I see him if it’s worth wearing a portable cardiac monitor for a month to see if I ever have any brief episodes of afib during sleep, for instance. I wore a FitBit for several months with afib detection and never got any notifications.
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AnUser
#76
I don’t know anything about this but you never know whether what the cardiologists etc are saying is medicine 2.0 or 3.0. If it’s the same case as for statins or similar drugs, that is.
If I search for studies on apixaban I found this:
Apixaban for Stroke Prevention in Subclinical Atrial Fibrillation
We included 4012 patients with a mean (±SD) age of 76.8±7.6 years and a mean CHA2DS2-VASc score of 3.9±1.1 (scores range from 0 to 9, with higher scores indicating a higher risk of stroke); 36.1% of the patients were women. After a mean follow-up of 3.5±1.8 years, stroke or systemic embolism occurred in 55 patients in the apixaban group (0.78% per patient-year) and in 86 patients in the aspirin group (1.24% per patient-year) (hazard ratio, 0.63; 95% confidence interval [CI], 0.45 to 0.88; P=0.007). In the on-treatment population, the rate of major bleeding was 1.71% per patient-year in the apixaban group and 0.94% per patient-year in the aspirin group (hazard ratio, 1.80; 95% CI, 1.26 to 2.57; P=0.001). Fatal bleeding occurred in 5 patients in the apixaban group and 8 patients in the aspirin group.

https://www.nejm.org/doi/full/10.1056/NEJMoa2310234
I know almost nothing about this or afib.
Very interesting! That’s a newer paper I hadn’t seen and wasn’t out when last I discussed this with my cardiologist. I’ll make sure to bring it up and revisit it, thanks. I already take clopidogrel (Plavix) for CVD risk reduction (since I can’t tolerate even low dose aspirin), so adding an anticoagulent to Plavix would REALLY heighten bleeding risk, and I doubt swapping the Plavix for Eliquis would be a good idea because then I wouldn’t have the antiplatelet effect for heart attack prevention.
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adssx
#78
In the studies I posted about weight gain, they used 40 mg. However, for the effects on insulin and adiponectin 80 mg be even more potent, so it could be the same for body weight?
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adssx
#79
I just noticed that "Food slightly reduces the bioavailability of telmisartan, with a reduction in the area under the plasma concentration-time curve (AUC) of about 6% with the 40 mg tablet and about 20% after a 160 mg dose" (per FDA). 6% is not a massive difference, but I was taking telmisartan 40 mg just before my meals; from now I’ll try to take it two hours after dinner to maximize absorption.
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adssx
#80
Development of Telmisartan Nanocrystal-Based Dissolving Microneedle for Brain Targeting via Trigeminal Pathway: A Potentially Promising Treatment for Alzheimer’s with an Improved Pharmacokinetic Profile 2024
Telmisartan (TMN), an angiotensin receptor blocker (ARB) drug, is being considered as an alternative therapy for Alzheimer’s disease (ALZ). However, when taken orally, its low water solubility leads to a low bioavailability and brain concentration. To overcome this problem, TMN was formulated as nanocrystals (NC), then incorporated into dissolving microneedles (DMN) to enhance drug delivery to the brain via the trigeminal route on the face.
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So We can do it internasally for the brain ?
adssx
#82
This is just a research paper. I don’t know whether intranasal telmisartan is safe or not.
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adssx
#83
Just published: Homocysteine: a futile comeback or a promising tool for the risk assessment of hypertensive patients? 2024
Nevertheless, some questions remain unsolved and require further research in our view:
- What is the contribution of Hcy in the global cardiovascular risk (fraction of attributable risk of Hcy), and is it worth to add this variable in the pre-existing CVR calculators?
- How to manage the factors influencing Hcy levels in the long term?
- Are the findings replicable in other CV diseases and other populations?
Further research seems warranted to close the current debates and precise the place of Hcy in the CVR assessment.
The above article is a comment on: Homocysteine, hyperhomocysteinemia, and H-type hypertension 2024
Generally, a plasma Hcy level higher than 10 or 15 μmol/L has been defined as hyperhomocysteinemia (HHcy). An individual with essential hypertension complicated with HHcy is considered to have H-type hypertension (HTH). Currently, HHcy is considered a novel independent risk factor for various cardiovascular diseases.
Another paper suggests that ARBs (e.g. telmisartan) are the best antihypertensive drug for people with HHcy: Homocysteine predicts vascular target organ damage in hypertension and may serve as guidance for first-line antihypertensive therapy 2021
From a clinical perspective, Hcy levels could therefore not only represent a useful marker of arterial HMOD but also potentially serve to guide the choice of the most appropriate first-line RAAS blocking antihypertensive regimen, that is, ACEi or ARB, the latter being the preferred choice in the context of elevated Hcy levels above 10 µmol/L. Clearly, future studies are needed to investigate whether indeed these theoretical considerations hold true in prospective longitudinal studies and whether Hcy levels may influence the potency of antihypertensive therapy with ACEi vs ARBs in regard to lowering BP and preventing HMOD.
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adssx
#84
I was excited about the homocysteine theory, so I bought the article. It’s garbage. (No comment on the fact that it comes from the 3rd poorest Chinese province…) It concludes that “Moreover, the curative effect may be improved if traditional Chinese medicine can be administered at the same time.” based on “Compound prescriptions such as Huanglian Wendan Decoction or Erchen Decoction, Shenxiong Glucose, Compound Danshen Dropping Pills, Breviscapine and Banxia Baizhu Tianma Decoction, Tianma Gouteng Decoction, and Qiju Dihuang Pill have certain effects on controlling BP and lowering Hcy levels.” The paper also says that “cholesterol decreasing or lipid-lowering drugs” increase Hcy levels but somehow “atorvastatin calcium tablets” decrease it. Of course, they don’t cite sources, nor do they explain the contradiction.
Worse: they mostly cite literature confirming their thesis and they don’t mention that most Mendelian randomization studies and meta-reviews of clinical trials did not find a significant causal effect of homocysteine-lowering interventions for BP:
-
Effect of vitamin B2, vitamin C, vitamin D, vitamin E and folic acid in adults with essential hypertension: a systematic review and network meta-analysis 2024: “Among the five vitamins, only vitamin E was significantly more effective at reducing SBP (mean difference: −14.14 mm Hg, 95% credible intervals: −27.62 to –0.88) than placebo. In addition, no evidence was found that any of the five vitamins influenced DBP, 24 hours SBP, 24 hours DBP, or HR.”
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Phenome-wide association study of genetically predicted B vitamins and homocysteine biomarkers with multiple health and disease outcomes: analysis of the UK Biobank 2023: they didn’t find a causal link between high Hcy and hypertension
- 1 mmHg of reduction… wow…
Folic acid supplementation and blood pressure: a GRADE-assessed systematic review and dose-response meta-analysis of 41,633 participants 2021: “The pooled results of 22 studies, including 41,633 participants, showed that folic acid supplementation significantly decreased systolic BP (SBP) (WMD: −1.10 mmHg; 95% CI: −1.93 to −0.28; p = 0.008).
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Blood Pressure Variability in CKD: Treatable or Hypertension’s Homocysteine? 2019: “The once promising ability to reduce elevated serum homocysteine levels did not prove, for example, to lessen the risk of cardiovascular outcomes aside from stroke.”
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Is there a causal role for homocysteine concentration in blood pressure? A Mendelian randomization study 2016: “Overall, the present findings do not corroborate the hypothesis that homocysteine has a causal role in blood pressure, especially in SBP.”
- Here as well, tiny effect: High-dose folic acid supplementation effects on endothelial function and blood pressure in hypertensive patients: a meta-analysis of randomized controlled clinical trials 2009: “The pooled estimate of effect of folic acid supplementation on systolic and diastolic blood pressure was −2.03 mm Hg (95% confidence interval [CI], −3.63 to −0.43; P = .04) and 0.01 mm Hg (95% CI, −1.12 to 1.13; not significant), respectively.”
Even this paper does not conclude this but: “As such, the debate as to the causal link between hyperhomocysteinemia and hypertension continues.”
So does it mean the Hcy hypothesis for hypertension should go to the trash? Probably, until we have more data.
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I think the combination of telmisartan with an SGLT2 Inhibitor is no-brainer for anyone that wants maximum benefits from this wonderful molecules
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