Why is your resting heart rate so high? It’s worth monitoring to make sure telmisartan doesn’t increase it further—it raised mine. I also didn’t notice any effect on blood sugar with a 40mg dose or during a couple of weeks of trying 80mg.

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I have always had a high resting heart rate. Not sure what I can do about that. Suggestions?

How to lower your resting heart rate

By doing these four things you can start to lower your resting heart rate and also help maintain a healthy heart:

  1. Exercise more . When you take a brisk walk, swim, or bicycle, your heart beats faster during the activity and for a short time afterward. But exercising every day gradually slows the resting heart rate.
  2. Reduce stress . Performing the relaxation response, meditation, tai chi, and other stress-busting techniques lowers the resting heart rate over time.
  3. Avoid tobacco products. Smokers have higher resting heart rates. Quitting brings it back down.
  4. Lose weight if necessary. The larger the body, the more the heart must work to supply it with blood. Losing weight can help slow an elevated resting heart rate.
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Cardio exercise, particularly Zone 2, combined with a moderate amount of HIIT.

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Ivabradine could help. It won’t further lower your BP. Another option would be to switch from telmisartan to a BP lowering medication that also reduces heart rate. Beta blockers, Non-Dihydropyridine Calcium Channel Blockers

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I’m going to try low dose Ivabradine to see if it can mitigate the resting heart rate increase from Retatrutide and my thyroid medication. The fact that it doesn’t reduce blood pressure is a major plus for me, since mine is already really good and don’t want my diastolic number to lower even further.

5mg Nebivolol might get it down around 10bpm and (not that you need to) further reduce your BP a little

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5mg x 2/day works for me to normalize my resting heart rate from both tirzepatide and stimulants (to the same level as without both).

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That’s great information. Around how much did your RHR go down on it? Any side effects such as fatigue, less endurance, etc?

I ordered some yesterday so hopefully I can get started in a couple of weeks when it arrives.

~2-3bpm. Not a lot. Oura reports min overnight as RHR: 53bpm. Whoop reports average overnight: 60bpm. Whoop overall average heart rate is 70bpm (I think this includes exercise). All went up 2-3 beats with the tirzepatide/stimulants, and now back down with ivabradine. No side effects. Tinnitus is better, which I didn’t know beforehand is one potential benefit. I just happened to notice my tinnitus was much better and sometimes totally gone and attribute it to the Ivabradine based on the clinical/anecdotal evidence that it can help with that.

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Playing with a thread summary delivered through an AI created podcast from NotebookLM. Give a listen, very interesting as a way to catch up on a thread.

https://notebooklm.google.com/notebook/3cec1e5b-faaa-4e58-aa41-f13a55ee6056/audio

Seems like the tool sure spends a lot of time on giving warnings etc, seemed to wrap up the conversation 3 times.

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So a pretty small effect of Ivabradine then. Maybe because your RHR wasn’t much higher to begin with.

Holy cow. The audio here is AI generated from this thread? I’m blown away

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That would make sense. I primarily took it to see if it could reduce some of the dysautonomia/POTS symptoms I started experiencing that are likely a result of a minor bout of long covid (exacerbated by stimulants and possibly GLP-1s). It does seem to work well for that.

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Suloxide, a mix of purified glycosaminoglycans?

Sulodexide, traded as Aterina, is a highly purified mixture of glycosaminoglycans composed of heparan sulfate (80%) and dermatan sulfate (20%). - (Sulodexide - Wikipedia)

Meta-analysis on BP lowering:

Considering the effects of glycosaminoglycans on endothelial function and sodium homeostasis, we hypothesized that sulodexide may lower blood pressure (BP). In this meta‐analysis, we therefore investigated the antihypertensive effects of sulodexide treatment.

Methods

We selected randomized controlled trials that investigated sulodexide treatment of at least 4 weeks and measured BP at baseline and after treatment. Two reviewers independently extracted data on study design, risk of bias, population characteristics and outcome measures. In addition, we contacted authors and pharmaceutical companies to provide missing data.

Results

Eight studies, totalling 3019 subjects (mean follow‐up 4.4 months) were included. Mean age was 61 years and mean baseline BP was 135/75 mmHg. Compared with control treatment, sulodexide resulted in a significant systolic (2.2 mmHg [95% CI 0.3, 4.1], P = 0.02) and diastolic BP reduction (1.7 mmHg [95% CI 0.6, 2.9], P = 0.004). Hypertensive patients displayed the largest systolic BP and diastolic BP reductions (10.2/5.4 mmHg, P < 0.001). Higher baseline systolic and diastolic BP were significantly associated with larger systolic (r 2=0.83, P < 0.001) and diastolic BP (r 2=0.41, P = 0.02) reductions after sulodexide treatment. In addition, systolic (r 2=0.41, P = 0.03) and diastolic BP reductions (r 2=0.60, P = 0.005) were significantly associated with albuminuria reduction.

Conclusion

Our data suggest that sulodexide treatment results in a significant BP reduction, especially in hypertensive subjects. This indicates that endothelial glycosaminoglycans might be an independent therapy target in cardiovascular disease. Future studies should further address the BP lowering potential of sulodexide.

Sulodexide is a highly purified mixture of glycosaminoglycans (GAGs) that is currently marketed in a number of countries in Europe, South America and Asia for various cardiovascular conditions. GAGs are large, negatively charged, linear polymers that are present on the surface of all endothelial cells and in the extracellular matrix. Here, GAGs interact with a wide range of processes that are involved in the development of cardiovascular disease, including shear mediated nitric oxide (NO) production and non‐osmotic sodium storage 6. Sulodexide has been shown to improve endothelial function and lipid profiles, exert anti‐inflammatory, anti‐thrombotic and fibrinolytic activity, inhibit leucocyte adhesion and diminish platelet aggregation 7. Because of these vasoprotective effects, sulodexide has been studied in numerous clinical trials. For instance, sulodexide has been shown to decrease claudication symptoms in peripheral artery disease patients and to prevent atherothrombotic events after acute myocardial infarction 8, 9. In addition, a series of small studies demonstrated that sulodexide decreased albuminuria 10. However, two recently performed large randomized controlled trials could not reproduce these findings 11, 12. Noticeably, no clinical trials have thus far investigated the antihypertensive potency of sulodexide.

The BP lowering effects of sulodexide may relate to both increased NO production and non‐osmotic sodium storage

Non‐osmotic sodium storage may also contribute to the antihypertensive potency of sulodexide 6. Sulodexide consists of negatively charged GAGs, which have been shown to be able to bind and osmotically inactivate sodium ions in the skin interstitium 36, 37, 38. In addition, GAGs in the ESL have been shown to be able to bind sodium under flow conditions 39. Considering the large systemic volume of the ESL, non‐osmotic sodium storage in the ESL may have significant implications for BP and extracellular volume regulation 40. Sulodexide may therefore increase the capacity for non‐osmotic sodium storage and prevent sodium from deteriorating endothelial cell function or expanding extracellular volume and causing BP to rise

A cardiovascular outcome trial in 3986 myocardial infarction patients demonstrated that sulodexide was able to reduce mortality and reinfarction rate compared with standard therapy, excluding antiplatelet and anticoagulant therapy

Is it safe, is this a good source?

Toxicity

Sulodexide seems to be well tolerated. Most adverse effects reported are related to the GI system and seem to be transient in nature. Among others adverse reactions are diarrhea, epigastralgia, dyspepsia, heartburn and dizziness. Allergic reactions, such as skin rash, have also been reported but are very rare. (https://go.drugbank.com/drugs/DB06271)

What do people think? Has anyone heard of this before?

BP and Sodium is more complicated (tissue sodium accumulation e.g in skin might play a role).

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Blood pressure and the brain: the conundrum of hypertension and dementia 2025

Many studies have begun to examine the cumulative burden of hypertension in late life through examination of younger to middle-aged adults. In the Coronary Artery Risk Development in Young Adults (CARDIA) study, every 5 mmHg increment in time-weighted average (TWA) of SBP in young adults is associated with approximately 1-year greater brain age. Likewise, participants with TWA BP over the recommended guidelines (SBP <120 mmHg, DBP <80 mmHg) had on average 3-year greater brain age compared to age peers with healthy BP.24 Additionally, individuals with moderate to increasing BP trajectories were more likely to have higher abnormal WM volume and/or lower grey matter CBF.25
In more recent years, the findings from the SPRINT-MIND trial have received considerable attention showing that intensive BP control (<120 mmHg) did not significantly reduce the risk of probable dementia as compared to standard BP control (<140 mmHg) in individuals with hypertension, but did find that intensive BP treatment reduced the risk of mild cognitive impairment (MCI) and the combined rate of MCI or probable dementia.
More comprehensive evidence came from a recent meta-analysis of 14 clinical trials (96 158 participants), including SPRINT-MIND,45 which found that BP lowering with anti-hypertensive medication compared to control was associated with a lower risk of dementia or cognitive impairment, although with a very small absolute risk reduction (0.39%).
Beyond the broad potential effects of anti-hypertensive medications, it is important to further explore whether certain class-specific anti-hypertensive drugs show a more beneficial effect in reducing dementia risk and if different effects of different drugs might explain the inconsistent trial results (SPRINT-MIND, for instance, allowed all anti-hypertensive drugs). […] A recent meta-analysis also concluded that angiotensin II receptor blockers, along with calcium channel blockers, could significantly reduce dementia risk.51 A drug’s ability to cross (vs. not cross) the blood–brain barrier (BBB) is also likely to impact its role in reducing cognitive decline: BBB-penetrant renin–angiotensin drugs appear to reduce cognitive decline in older adults with normal cognition more than do drugs that are not BBB penetrant.
Hypertension makes the BBB leaky
One of the outstanding questions in the field is whether hypertension-induced BBB leakage is involved in the initiation of dementia or is a consequence of the complex neurovascular pathology.150 The answer remains unclear, but many studies have used young hypertensive animals to study this mechanism. Findings have shown a higher BBB leakage in cardiovascular regulatory regions in young hypertensive rats compared to normotensive controls.

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Nebivolol gives me crazy nightmares if i take it after 6:00pm so I’m thinking about taking it in the morning then carvedilol afternoon to see how it works out :thinking:

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Beta blockers can mess up with melatonin and trigger RBD ( https://academic.oup.com/sleep/article/45/Supplement_1/A346/6592654 ). Why are you using a beta blocker? They’re not the first line treatment for blood pressure and they come with many issues (glycemic dysregulation being another one).

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I went to my yearly checkup yesterday and blood pressure was 108/68 !! The nurse checked several times and also several times during my stress test. Afterward the doc wanted to know if I was on something to increase my NO. I said just celery and he shook his head. Also I was still conversational after 15 minutes of BRUCE protocol and my heart rate was 140. It took me till I got home to think what the difference might be. I’m pretty sure it was the chelation, which has been shown to lower blood pressure.

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Are you taking minoxidil? Other medicine?