Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label glaucoma. Show all posts
Showing posts with label glaucoma. Show all posts

Friday, May 8, 2026

Erectile Dysfunction Drugs Linked to Lower Glaucoma Risk in Men

 Didn't your competent? doctor already prescribe this for stroke recovery and dementia risk reduction?

Erectile Dysfunction Drugs Linked to Lower Glaucoma Risk in Men

Also from ARVO: HDL and AMD risk in women, statin use and glaucoma risk

DENVER -- Men using phosphodiesterase type 5 (PDE-5) inhibitors for erectile dysfunction (ED) had a modestly lower risk of glaucoma, according to a study reported here.

During 3 years of follow-up, men taking PDE-5 inhibitors had a reduced likelihood for glaucoma suspect (risk factors) and open-angle glaucoma (OAG). The absolute difference ranged from 1-3% for glaucoma suspect and about 1% for OAG. The relative risk differential achieved statistical significance each year for both conditions (P=0.04 to P<0.01).

"The association is likely vascular in origin, as PDE-5 inhibitors enhance [nitric oxide-cyclic guanosine monophosphate] signaling, improving ocular blood flow and optic nerve perfusion," concluded Abdelrahman M. Elhusseiny, MD, of the University of Miami, and colleagues in a poster presentation at the Association for Research in Vision and Ophthalmology (ARVO) meeting. "PDE-5 inhibitors do not produce sustained intraocular pressure reduction, suggesting the effect is not mediated by aqueous humor dynamics. Further prospective studies are needed to clarify mechanisms, evaluate long-term effects, and determine clinical implications."

PDE-5 inhibitors (such as sildenafil [Viagra], tadalafil [Cialis], and vardenafil [Levitra]) are prescribed primarily for ED and pulmonary hypertension, but the drugs' vascular and cryoprotective effects may have broader therapeutic implications, the investigators noted. To examine the issue, they queried the TriNetX clinical network for the years 2005-2025 to identify men at least 40 years old with diagnosed ED, and then grouped them according to history of PDE-5 inhibitor use.

The primary analysis included two propensity-matched groups of 23,603 men each (PDE-5 users and non-users). Mean follow-up in each group was almost 1,000 days. The primary endpoints were glaucoma suspect and OAG.

After a year of follow-up, rates of glaucoma suspect and OAG were 6.49% and 2.13% versus 9.73% and 3.22% for PDE-5 inhibitor users and non-users, respectively (P<0.01 for both comparisons). Rates of both conditions increased in both groups and between-group differences shrank during the next 2 years. At the end of follow-up, rates of glaucoma suspect and OAG were 11.17% and 3.88% among PDE-5 inhibitor users versus 12.06% (P=0.01) and 4.28% (P=0.04) among non-users.

Higher HDL Linked to Lower AMD Risk in Women

Higher levels of high-density lipoprotein (HDL) in women were associated with a small but statistically significant lower risk of developing neovascular age-related macular degeneration (nAMD), according to a study reported at ARVO.

Women with HDL levels ≥60 mg/dL had a 1% absolute difference in nAMD (10.2% vs 11.2%) with women who had low HDL (<50 mg/dL). The difference translated into a 9% reduction in relative risk (95% CI 0.83-0.99, P=0.03). However, the difference no longer remained significant in a time-to-event analysis (HR 0.93, 95% CI 0.85-1.02, P=0.11). A comparison of low versus normal HDL (50-59 mg/dL) showed no difference, and neither high nor low HDL levels altered nAMD risk in men.

"These findings suggest there may be sex-specific, lipid-related mechanisms involved in AMD progression, and highlight the need for further research into the role of HDL and retinal disease biology," said Adriana Kaganovski, of SUNY Downstate Health Sciences University in New York City, in a recorded summary of the study.

Lipid metabolism has been implicated in AMD pathogenesis but the influence of HDL on AMD risk remains unclear, said Kaganovski. To examine whether sex-specific HDL categories are associated with AMD risk, investigators searched the TriNetX network to identify adults with diagnosed nAMD and HDL measurements within 6 months of diagnosis. Men and women were stratified by sex-specific HDL levels for comparisons of high versus low and low versus normal levels.

Data analysis involved matched cohorts (4,347 to 8,911 participants each) to compare nAMD prevalence by HDL levels in men and women. For men, nAMD prevalence was 9-10% regardless of HDL level. Among women, nAMD prevalence was about 10-11%, and only the comparison of high versus low HDL produced a statistically significant difference.

Statin Use and Glaucoma Risk

Previously documented neuroprotective effects of statins may extend to glaucoma, according to a retrospective analysis involving more than 500,000 patients.

Statin use was modestly associated with the 5-year incidence of OAG (5.0% vs 5.3%, P<0.001). In a separate analysis of glaucoma-associated surgery, reflecting progressive disease, statin users had significantly lower hazards for incisional surgery, minimally invasive glaucoma surgery (MIGS), and selective laser trabeculoplasty (SLT).

"Our results are consistent with our hypothesis that statin use is associated with lower risk of glaucoma onset and progression," concluded Forest Lin, of the University of South Florida in Tampa, and colleagues in a poster presentation. "Prospective trials are needed to further elucidate the relationship between statin usage and glaucoma."

Statins' neuroprotective potential in glaucoma remains poorly understood, as previous studies have yielded inconsistent results, the investigators noted. To inform the issue, they tested the hypothesis that statin use would be associated with a decreased risk of OAG and progressive disease, as reflected in surgery and other interventions.

A search of the TriNetX database produced matched cohorts of 218,677 patients each for the analysis of glaucoma incidence and matched cohorts of 51,551 patients each for the analysis of progressive disease.

Over a 5-year period, 10,223 statin users and 10,801 non-users had new diagnoses of OAG, a difference that translated into a 9% reduction in the hazard ratio (95% CI 0.89-0.94). Statin use was associated with larger reductions in HRs for incisional surgery (HR 0.83, 95% CI 0.78-0.88), MIGS (HR 0.82, 95% CI 0.78-0.87), and SLT (HR 0.88, 95% CI 0.84-0.92). Statin users were more likely to be treated with ocular hypotensive agents (HR 1.39, 95% CI 1.37-1.41).

Monday, February 10, 2025

Higher Levels of 'Good' Cholesterol Linked to Increased Glaucoma Risk


 You'll have to ask your competent? doctor to PRECISELY SOLVE THIS CONUMDRUM FOR YOU!

CVD risk or glaucoma? Neither is good, your doctor better figure out an answer!

Higher Levels of 'Good' Cholesterol Linked to Increased Glaucoma Risk

Meanwhile, higher levels of LDL-C were associated with reduced risk

A computer rendered cutaway of a cholesterol molecule.

Key Takeaways

  • Higher levels of high-density lipoprotein cholesterol were associated with an increased risk of glaucoma.
  • High levels of low-density lipoprotein cholesterol, total cholesterol, and triglycerides were associated with a reduced risk of glaucoma.
  • "Good" and "bad" cholesterol labels might need to be reassessed outside of cardiovascular disease.

Higher levels of high-density lipoprotein cholesterol (HDL-C) were associated with an increased risk of glaucoma, while high levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol, and triglycerides were associated with a reduced risk, a prospective study showed.

Among over 400,000 older U.K. Biobank participants, higher levels of HDL-C were associated with an increased risk of glaucoma (HR for 1-SD increase 1.05, 95% CI 1.02-1.08, P=0.001), while high levels of the other commonly used serum lipid measures were all linked to a reduced risk:

  • LDL-C: HR 0.96, 95% CI 0.94-0.99, P=0.005
  • Total cholesterol: HR 0.97, 95% CI 0.94-1.00, P=0.037
  • Triglycerides: HR 0.96, 95% CI 0.94-0.99, P=0.008

"The causal relationship between blood lipids and glaucoma deserves further exploration, and it is recommended that age- and sex-specific effects be taken into account when assessing the relationship between lipids and glaucoma," wrote Zhenzhen Liu, MD, PhD, of Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science in China, and colleagues in the British Journal of Ophthalmologyopens in a new tab or window.

After adjusting for confounders, a 1-SD increment in HDL-C genetic risk was associated with a 5% greater hazard of glaucoma (HR 1.05, 95% CI 1.00-1.11, P=0.031). However, the polygenic risk score for LDL-C, total cholesterol, and triglycerides did not show a significant association with glaucoma.

Jeremy Sivak, PhD, of Krembil Research Institute at Toronto Western Hospital, told MedPage Today that "the results are surprising because the team found that so-called 'good' cholesterol is associated with greater risk of developing glaucoma, and 'bad' cholesterol is associated with lower risk. This result challenges some earlier studies that have reported the opposite association."

Sivak said that the concepts of "good" and "bad" cholesterol come from cardiovascular disease. "The role of these types of blood lipids in glaucoma is likely to be very different, and might be related to the regulation of fluid flow and pressure in the eye. One important take-away from this study is that these 'good' and 'bad' labels might need to be reassessed in the context of other diseases."

As for the findings about risk, the "differences are highly statistically significant, but the absolute differences in lipid levels are relatively small, revealed only by the large numbers of participants," Sivak noted. The data suggest that "there are variables in play that are still not accounted for and, as noted by the authors, correlations do not necessarily mean causation."

Sivak said one strength of the study is that it's prospective and follows the same population over time, while other research compared different patients at one point in time. "There seems to be good justification for further research in this area given the prospective study design and high statistical significance of the analyses," he added.

Victoria L. Tseng, MD, PhD, of the University of California Los Angeles Stein Eye Institute, noted that it is currently suspected that "vascular disease resulting from high cholesterol could compromise blood flow to the optic nerve and potentially be a risk factor to develop glaucoma or for it to get worse."

Is there a message for clinicians from this research? "I don't think we have sufficient evidence to recommend medication changes based on these findings," Tseng said. "Patients would benefit from continued chronic disease monitoring and management with their primary care providers to maximize systemic health in conjunction with their ocular conditions."

For this study, the researchers included 400,229 U.K. Biobank participants. Mean age was 56.4, 54% were women, and 94.9% were white. Of these patients, 26.8% had hypertension, 3.5% had diabetes, 3.3% had heart disease, and most (84.7%) had not used statins.

Over a mean 14.44 years of follow-up, 1.72% of patients were diagnosed with glaucoma. They were more likely to be older, non-white, and have a higher waist-to-hip ratio. They also had higher rates of diabetes (5.4%), hypertension (33.4%), and heart disease (4.8%).

The authors noted limitations to their study, including the almost entirely white patient population and the possibility that glaucoma cases were missed due to reliance on hospital records and self-assessments.

  • author['full_name']

    Randy Dotinga is a freelance medical and science journalist based in San Diego.

Disclosures

This study was supported by the Guangzhou Basic Research Program, City & University (Institute) Joint Funding Project, the National Natural Science Foundation of China of Guangdong Province, and the National Natural Science Foundation of China.

The study authors had no disclosures.

Sivak had no disclosures.

Tseng had no disclosures.

Primary Source

British Journal of Ophthalmology

Source Reference: opens in a new tab or windowMa Y, et al "Associations between serum lipids and glaucoma: a cohort study of 400 229 UK Biobank participants" Br J Ophthalmol 2025; DOI: 10.1136/bjo-2024-326062.

Wednesday, June 14, 2023

New Evidence Links Calcium Channel Blockers to Increased Risk of Glaucoma

I'll have to talk to my doctor since I'm doing Nifedipine ER  and Losartan

Calcium channel blockers include:
  • Amlodipine (Norvasc®)
  • Diltiazem (Cardiazem®, Tiazac®, Tiazac® XC )
  • Felodipine (Plendil®)
  • Nifedipine XL (Adalat XL®)
  • Verapamil (Isoptin®, Isoptin® SR, Verelan®)

New Evidence Links Calcium Channel Blockers to Increased Risk of Glaucoma

Meta-analysis shows highest glaucoma risk with CCB monotherapy, reduced IOP with beta-blockers

A photo of a man’s eye bulging from glaucoma.

Use of calcium channel blockers (CCBs), particularly cardioselective agents, had a modest but statistically significant association with glaucoma, a large meta-analysis showed.

Overall, patients with a history of CCB treatment had a 23% higher likelihood of developing glaucoma as compared with individuals who never used the antihypertensives. The likelihood almost doubled among patients who received single-agent cardioselective CCBs. In contrast, beta-blocker therapy was associated with modestly reduced intraocular pressure (IOP), which is associated with a reduced risk of glaucoma.

A number of other commonly used medications had no clear associations with glaucoma or IOP, including lipid-lowering drugs, antidepressants, and diabetes medications, reported Anthony Khawaja, MD, PhD, of University College London, and colleagues in the European Eye Epidemiology (E3) Consortiumopens in a new tab or window.

"While our novel findings require further studies to determine whether the associations are causal, these findings will be of interest to physicians caring for glaucoma patients with systemic comorbidities," the authors stated in Ophthalmologyopens in a new tab or window.

"A potentially harmful association of CCBs for glaucoma is particularly noteworthy, as this is a commonly prescribed class of medication," they added. "If further studies confirm a casual nature for this association, this may inform alternative treatment strategies for hypertensive patients with, or at risk of, glaucoma."

Adds to Existing Evidence

The findings add to evidence from previous studies showing that systemic beta-blockers lower IOP, and at least one prior study has shown an association between CCBs and glaucoma, said Roma Patel, MD, MBA, of Baylor College of Medicine and Ben Taub Hospital in Houston, and a clinical spokesperson for the American Academy of Ophthalmology.

"The study's contribution is one of power," Patel told MedPage Today via email. "The dataset used for this analysis represented over 143,000 individuals with glaucoma. Because of the size of population studied, this study was able to find that an even stronger association between CCBs with direct cardiac effects and glaucoma versus analysis of all CCBs and glaucoma. Perhaps this will help researchers figure out if there is a causal link. We know that glaucoma is ultimately related to dysfunction and death of the retinal ganglion cells. We don't concretely know the effects of calcium blockade at that level so it poses a good research question."

With respect to implications for clinical practice, Patel added, "I believe it's fair to tell patients there is a known association for calcium channel blockers and glaucoma but we don't fully understand why and there is no evidence of a causal relationship. If the patient chooses to discuss with their PCP [primary care physician] or cardiologist about a different treatment regimen for their cardiac issue, that is up to the patient. But I am not encouraging that conversation with my patients."

"I do encourage my patients to talk to their PCP or cardiologist about avoiding evening anti-hypertensive medications because we do know that low blood pressure overnight can lead to glaucoma progression," she said. "It's important to remember that the eye lives within the human body and all of our systems are connected. But if the cardiologist feels that a certain medicine is warranted, I recommend we follow that recommendation because we all know that the eye can't live without the heart."

Glaucoma is the leading cause of irreversible vision impairment worldwide, and IOP currently is the only modifiable risk factor for glaucoma onset and progression, Khawaja and co-authors noted. Several types of medication are known or suspected of modulating glaucomaopens in a new tab or window risk by affecting optic nerve head perfusion, retinal ganglion cell survival, and aqueous humor outflow facility.

A study based on U.S. health claimsopens in a new tab or window suggested that selective serotonin reuptake inhibitors were associated with a reduced risk of primary open-angle glaucoma and CCBs with an increased risk. Other medications that may influence glaucoma riskopens in a new tab or window include beta-blockers, metformin, statins, and bupropion. Additionally, some medications have been associated with higher IOPopens in a new tab or window, including angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), statins, and sulfonylureas.

"For many of the cited associations, there have been inconsistent findings between studies, and few studies have accounted for polypharmacy or important confounders," Khawaja and colleagues noted.

Clarifying Study

To continue the line of research, investigators in the E3 Consortium performed a meta-analysis of 11 European cohort studies involving a total of 143,240 participants, all of whom were included in analyses of glaucoma associations. Analyses of IOP included 47,177 participants. Medication use encompassed multiple types of antihypertensives, lipid-lower medications, antidepressants, and antidiabetic medications (limited only to participants with diagnosed diabetes). For antihypertensives, the investigators distinguished monotherapy from combination therapy.

Multivariable analyses showed that any CCB use was associated with a glaucoma OR of 1.23 (95% CI 1.08-1.39) versus no use. Patients who received CCB monotherapy had a glaucoma OR of 1.96 (95% CI 1.23-3.12). No other medications were clearly associated with glaucoma, the authors reported. Systemic beta-blockers were associated with marginally lower IOP (-0.33 mmHg, 95% CI -0.57 to -0.08). Monotherapy with selective beta-blockers was associated with a 0.45 mmHg reduction in IOP (95% CI -0.74 to -0.16) and non-selective agents with a 0.54 mmHg reduction in IOP (95% CI -0.94 to -0.15).

High-ceiling diuretics (such as furosemide and torasemide/torsemideopens in a new tab or window) had a "suggestive" association with lower IOP (-0.30 mmHg, 95% CI -0.47 to -0.14), but not when used as monotherapy.

None of the other medications included in the analysis had associations with IOP.

  • author['full_name']

    Charles Bankhead is senior editor for oncology and also covers urology, dermatology, and ophthalmology. He joined MedPage Today in 2007. Follow

Disclosures

The study was supported by multiple governmental, nonprofit, and philanthropic organizations.

Khawaja disclosed relationships with AbbVie, Aerie, Google Health, Novartis, Reichert, Santen, and Thea.

Patel disclosed no relevant relationships with industry.

Primary Source

Ophthalmology

Source Reference: opens in a new tab or windowVergroesen JE, et al "Association of systemic medication use with glaucoma and intraocular pressure: The E3 Consortium" Ophthalmol 2023; DOI: 10.1016/j.ophtha.2023.05.00

Tuesday, May 26, 2020

Severe Neovascular Glaucoma Exacerbation as a Complication of Carotid Artery Stenting: A Case Report

I can see almost zero use for stenting a carotid artery if the Circle of Willis is complete, you would have three arteries still feeding the brain.  If fact I would have the artery closed in that case to prevent the chance of plaque breaking loose and causing  a stroke. 

Don't listen to what I have to say, I'm not medically trained.

I guess this is why gluing is not done for brain work:
FDA issues warning about Covidien brain device that has killed nine - Onyx glue

Talk to your doctor about the dangers of stroke due to the endarterectomy procedure and why you would want to put inflexible metal stents in flexible arteries. Don't listen to me, but ask your doctor plenty of questions.   Ask for a guarantee of no stroke due to any procedure.  

Instead of doing a carotid endarterectomy with its attendant risks, why not glue it up or close it some other way?

  1. Verify that the Circle of Willis is complete. Mine obviously is since one carotid artery is completely blocked and I am having no cognitive issues(arrogance is not one of my issues).

  2. Glue the offending artery shut, No risky surgery.

You need to know where the blockage is, above or below the split to the face.

Illustration of human head and neck with enlarged pull-out view of carotid artery disease.

The latest here:

Severe Neovascular Glaucoma Exacerbation as a Complication of Carotid Artery Stenting: A Case Report

First Published May 22, 2020 Case Report






Neovascular glaucoma (NVG) has been rarely reported as an acute complication of carotid endarterectomy, but there is scant literature available regarding this potential condition following carotid artery stenting (CAS). We present a case of severe worsening of NVG occurring after bilateral CAS with progressive deterioration of vision ultimately leading to blindness.

A 66-year-old male with multiple stroke risk factors, bilateral cataract extraction, proliferative diabetic retinopathy of left eye, and nonproliferative diabetic retinopathy of right eye, and prior left eye pars plana vitrectomy presented with episodes of transient right eye vision loss in context of bilateral high-grade internal carotid artery stenoses. He underwent right CAS with subsequent elevation of bilateral intraocular pressures (IOPs) concerning for acute NVG. Over time, the patient had some interval improvement in IOPs and underwent planned left CAS. After the procedure, he again developed elevated IOPs, concerning for acute NVG which eventually led to right eye pars plana vitrectomy for vitreous hemorrhage and refractory IOP elevation. At 6-month follow-up from initial stenting, the patient was blind in both eyes.

We present a case of recurrent IOP elevations following CAS eventually resulting in bilateral eye blindness. This case is important not only as an illustration of an underrecognized postprocedural CAS complication but also as a demonstration of likely elevated risk of NVG following CAS for patients with other predisposing risk factors for ocular hypertension such as glaucoma, proliferative diabetic retinopathy, prior cataract extraction, and prior pars plana vitrectomy.