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3 New Findings on AFib and What They Mean

3 New Findings on AFib and What They Mean

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If you’re among the 1 in 5 U.S. adults who have an abnormal heart rhythm problem called atrial fibrillation, there’s been a flurry of new research about the condition that offers some guidance on your everyday choices and how those impact your risk of recurrence.

“The major risk is stroke, and preventing stroke is the name of the game with AFib.
Three new studies shed light on some common questions: whether your morning coffee matters, whether a diabetes drug might help lower recurrence risk, and what new data reveals about AFib’s link to dementia.

Here’s what the latest research suggests:
Coffee doesn’t increase the risk of recurrent atrial fibrillation. A small but well-designed new study showed that people who drank a cup of coffee daily were not more likely than non-coffee drinkers to have a repeat atrial fibrillation episode after successful treatment with electrical cardioversion – a quick procedure where a doctor delivers a brief, controlled shock to the heart to put it back into a normal rhythm. People in the study agreed ahead of time to be randomly assigned to one of two groups: those who continued drinking coffee as they did before the study, and those who abstained for six months.

Why it matters: Many people and even some doctors still assume coffee triggers AFib, a long-held bit of “common wisdom” that isn’t backed by strong evidence, Prystowsky said. It’s a top concern for newly diagnosed patients, but experts say coffee is rarely a problem except in people with palpitations. The design of this latest study, randomizing people before asking them to keep drinking or abstain, makes the results particularly trustworthy, he said.

What you can do: If you’re going to change one beverage you consume to manage atrial fibrillation risk, go ahead and keep drinking coffee and instead focus on reducing or cutting out alcohol.

Metformin helped reduce AFib recurrence in a small study of people with overweight and obesity. In a study of 99 people with overweight or obesity who had an ablation procedure, where doctors burn or freeze tiny areas of heart tissue to stop the abnormal signals that cause AFib, those who took the type 2 diabetes drug metformin after ablation were less likely to have recurrent AFib. None of the people in the study had diabetes, although 40% of them met prediabetic blood sugar criteria. The study was presented at an American Heart Association conference this month and hasn’t been published in a peer-reviewed journal.

Why it matters: Doctors are talking about this study because it’s another step toward understanding the connection between weight and AFib risk. An important previous study showed that people who lost 10% of their body weight were six times more likely to survive four years without recurrence. “It wasn’t just weight loss, though,” Prystowsky said, noting that those who lost weight had improved glucose and blood pressure levels.
Interestingly, in this latest metformin study, people saw AFib benefits without significant weight loss. That suggests the drug may be affecting the body in other ways, possibly through metabolism, inflammation, or fat around the heart, though researchers don’t yet know the exact mechanism, Prystowsky said.

What you can do: “The most important takeaway from this small study is reinforcing the idea that the management of obesity makes a huge difference in outcomes for atrial fibrillation,” Philbin said. He and Prystowsky agreed the study was too small for a doctor to recommend that a patient take metformin to reduce AFib risk, though. The study was “hypothesis-forming rather than game-changing, but it reinforces some ideas we know about atrial fibrillation that we know will work: you should exercise. You should lose weight. You should not drink alcohol,” Philbin said. He and his colleagues plan to explore whether AFib patients benefit from six weeks of supervised exercise and dietitian guidance the way heart attack survivors do.

Another study just linked AFib with dementia risk. Published this month in JACC: Advances, the analysis looked at 670,745 Medicare patients 65 and older and found that those who developed AFib after non-cardiac surgery were more likely to later be diagnosed with dementia. In cardiac surgery patients, dementia rates were similar regardless of AFib (about 4%). But after non-cardiac surgery, dementia was diagnosed in nearly 13% of people with AFib, versus 9% without – a 20% increased risk. Non-cardiac procedures ranged widely, with orthopedic (including joint replacements), gastrointestinal, and circulatory surgeries most common.

Why it matters: The study authors wrote it was “notable” that cardiac surgery patients who developed AFib weren’t more likely to get dementia, suggesting their AFib may have been triggered by the surgery itself. They couldn’t explain why non-cardiac surgery patients had a higher dementia risk and found no clear contributing factors like high blood pressure, diabetes, or prior stroke or heart failure. They hypothesized that undetected mild strokes or heart attacks, which can damage the brain and blood vessels, might play a role. The link between AFib and dementia is established, and while silent strokes and heart attacks are suspected contributors, the data shows a link rather than a cause. Prystowsky tells patients who get AFib after non-cardiac surgery that they have a higher risk of recurrence and need to be aware of it.

What you can do: If you’re heading into surgery, worrying about AFib shouldn’t be at the top of your list, Prystowsky said. But if you like to be prepared, both Philbin and Prystowsky advised that wearing a device like a smartwatch that can check your pulse and rhythm can help you spot any issues early. And if you’ve already had AFib after a non-cardiac surgery, regular monitoring is especially important – and you should call your doctor if your device flags an abnormal pulse or rhythm.

Reference:
https://www.webmd.com/heart-disease/atrial-fibrillation/news/20251118/3-new-findings-on-afib-and-what-they-mean
https://my.clevelandclinic.org/health/diseases/16765-atrial-fibrillation-afib
https://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/syc-20350624

Medications that have been suggested by doctors worldwide are available on the link below:
https://mygenericpharmacy.com/category/products/disease/heart-disease

Metformin may weaken cardiovascular, insulin benefits of exercise…

Metformin may weaken cardiovascular, insulin benefits of exercise…

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This is a fascinating and nuanced topic that sits at the intersection of two foundational treatments for type 2 diabetes. The headline is based on real research, but it requires important context to be fully understood. Here’s a breakdown of what the science says, what it means, and who should be concerned.

The Core Finding: The “Metformin-Exercise Interaction”

The claim originates primarily from a series of studies, most notably a 2013 randomized controlled trial published in The Journal of Clinical Endocrinology & Metabolism and other follow-up research.

The studies found that in older, overweight, or pre-diabetic adults, taking metformin seemed to blunt some of the key physiological benefits of exercise compared to a placebo group that did the same exercise regimen.

The blunted benefits were specifically in two areas:

  1. Insulin Sensitivity: Exercise is one of the most powerful ways to improve insulin sensitivity. The studies found that the group taking metformin saw a significantly smaller improvement in insulin sensitivity from their exercise training than the placebo group.
  2. Mitochondrial Function: Exercise trains your muscles’ mitochondria (the cellular power plants) to become more efficient and numerous. The metformin group showed a reduced improvement in markers of mitochondrial health.

The proposed mechanism is that metformin and exercise act on the same pathway, but in somewhat opposing ways.

  • Exercise signals through AMPK (AMP-activated protein kinase), a cellular energy sensor. When you exercise, you deplete energy, activating AMPK. This tells the cell to ramp up energy production (improve mitochondria) and increase glucose uptake (improve insulin sensitivity).
  • Metformin also works primarily by activating AMPK.

The theory is that by chronically activating AMPK pharmacologically, metformin might “pre-empt” or dull the cell’s robust response to the natural AMPK signal from exercise. It’s as if the cell is already being “shouted at” by the drug, so it doesn’t “hear” the shout from exercise as clearly.

Crucial Context and Limitations

This is where the “may” in the headline becomes critically important. This interaction is not a universal rule and has several important caveats:

  • Population Specific: The effect has been most consistently observed in at-risk, non-diabetic individuals (e.g., those with pre-diabetes or insulin resistance) and older, overweight populations. The evidence is much less clear for people with established type 2 diabetes.
  • Benefit Blunting vs. Benefit Elimination: The studies show a reduction in the improvement, not a complete elimination. The metformin+exercise group still saw benefits—just not as much as the exercise-only group.
  • Cardiovascular Benefits Are Broader: The term “cardiovascular benefits” can be misleading. While mitochondrial and insulin-sensitivity improvements are crucial for metabolic cardiovascular health, exercise provides a host of other cardiovascular benefits that are likely NOT blunted by metformin, such as:
    • Lowering blood pressure
    • Improving cholesterol levels
    • Strengthening the heart muscle
    • Improving endothelial function (blood vessel health)
    • aiding in weight management

What This Means For You: Practical Takeaways

  1. For People with Type 2 Diabetes: Do NOT stop taking metformin. For you, the proven, powerful benefits of metformin in controlling blood glucose and reducing the risk of diabetes complications far outweigh the potential slight blunting of exercise’s effect on insulin sensitivity. The combination of metformin and exercise is still a cornerstone of effective diabetes management.
  2. For People with Pre-Diabetes: This is the group where the conversation is most relevant. If you are using exercise as your primary tool to prevent the onset of type 2 diabetes, it’s worth having a discussion with your doctor. They might consider whether lifestyle intervention alone is sufficient before adding metformin. However, for many, the combination is still recommended as the most effective strategy.
  3. For Healthy Individuals or Athletes: This research is likely not relevant to you. Metformin is not prescribed for this population, and the studies did not involve them.
  4. The Overarching Principle: Exercise is Non-Negotiable. Regardless of whether you take metformin, exercise remains one of the most powerful health interventions available. Its benefits extend far beyond the specific metrics that might be slightly blunted. The worst decision you could make based on this research is to stop exercising.

Conclusion

The statement “Metformin may weaken cardiovascular, insulin benefits of exercise” is scientifically accurate but easily misinterpreted.

  • The Science: It appears that metformin can attenuate some of the specific cellular and metabolic adaptations to exercise, particularly improvements in insulin sensitivity and mitochondrial biogenesis, likely through competing actions on the AMPK pathway.
  • The Reality: For the vast majority of people taking metformin (especially those with type 2 diabetes), this potential interaction is a minor consideration. The powerful, combined benefits of both the medication and physical activity make them a winning combination for long-term health.

Always consult your doctor before making any changes to your medication or exercise regimen. They can provide personalized advice based on your specific health status and goals.

https://www.pharmacytimes.com/view/metformin-may-diminish-the-cardiometabolic-benefits-of-exercise

https://www.medicalnewstoday.com/articles/metformin-diabetes-lower-exercise-benefits

https://scitechdaily.com/popular-diabetes-drug-metformin-may-cancel-out-exercise-benefits-study-warns

https://mygenericpharmacy.com/category/disease/heart-disease

Blood vessels in eyes may help predict heart disease and biological aging risk.

Blood vessels in eyes may help predict heart disease and biological aging risk.

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That’s a fascinating and accurate insight. This field of research is growing rapidly and holds significant promise for non-invasive health diagnostics.
Here’s a detailed breakdown of how the blood vessels in your eyes (the retina) can serve as a window to your heart health and biological age.

Why the Retina is a Unique “Window”
The retina is the only place in the body where you can directly and non-invasively view microvascular blood vessels (arterioles and venules). These tiny vessels are sensitive to the same pressures and damage that affect the entire circulatory system, including the heart and brain. Changes in their structure and function often mirror what’s happening in vessels you can’t see.

  1. Predicting Heart Disease Risk
    The condition of the retinal vessels, known as Retinal Vascular Caliber, is a key indicator.

What Doctors Look For:
Narrowing of Arterioles: This is a classic sign of hypertension (high blood pressure). The constant high pressure causes the vessel walls to thicken, making the central light reflex (the visible column of blood) appear narrower.

Arteriovenous (AV) Nicking: This occurs when a hardened retinal artery compresses a vein where they cross, causing the vein to appear “nicked” or pinched. It’s a sign of chronic hypertension and advanced vascular damage.

Microaneurysms, Hemorrhages, and Cotton-Wool Spots: These are signs of more severe damage, often seen in diabetic retinopathy and hypertensive retinopathy. Since diabetes is a major risk factor for heart disease, these findings are a red flag for systemic cardiovascular issues.

The Link to Heart Disease:
The same processes that damage retinal vessels—inflammation, oxidative stress, and endothelial dysfunction also damage the coronary arteries supplying the heart.

Studies have shown that people with narrower retinal arterioles and wider venules have a higher risk of developing hypertension, coronary heart disease, heart failure, and stroke, even after accounting for traditional risk factors like smoking and cholesterol.

  1. Predicting Biological Aging Risk
    This is an even more cutting-edge application. The concept is that the “age” of your retinal vessels may be a better indicator of your overall health and mortality risk than your chronological age.

Retinal Age Gap: Researchers are using advanced AI to analyze retinal images and predict a person’s “biological age” based on the health of their retinal vasculature. How it works: A deep learning model is trained on thousands of retinal images from healthy people to learn what a “normal” retina looks like at different chronological ages.

The Key Finding: People whose retinas look “older” than their actual age (a positive “retinal age gap”) have a significantly higher risk of death from all causes, and specifically from cardiovascular disease. A large study found that every 1-year increase in the retinal age gap was associated with a 2-3% increase in all-cause and cause-specific mortality risk.

Why it Reflects Biological Aging:
The retina is part of the central nervous system (it’s an extension of the brain). Its health is closely linked to brain health. The microvasculature in the retina is sensitive to cumulative lifelong damage from factors like high blood pressure, high blood sugar, and oxidative stress—all key drivers of biological aging.

Therefore, an “aged” retina suggests accelerated aging and cumulative damage throughout the entire body’s vascular and neurological systems. The Future: AI and Routine Screening
The traditional method of a doctor manually examining the retina is being supercharged by Artificial Intelligence.

Automated Analysis: AI algorithms can now quickly and accurately measure retinal vessel caliber, detect lesions, and even calculate a “retinal age” from a simple, non-invasive photograph.

Potential for Widespread Use: Because retinal imaging is quick, cheap, and non-invasive, it has the potential to become a powerful tool for mass screening. A routine eye exam could one day provide a risk assessment for heart disease, stroke, and overall health, prompting earlier intervention.

The blood vessels in your eyes are far more than just tools for vision. They are a unique and accessible mirror of your body’s circulatory and neurological health. By examining them, doctors and AI can get an early, direct look at the silent damage caused by conditions like hypertension and diabetes, potentially predicting your risk for major heart events and even your rate of biological aging.

Disclaimer: This information is for educational purposes only. While retinal health is an exciting area of predictive medicine, it is not a standalone diagnostic tool. Always consult with your primary care physician and a cardiologist for a comprehensive assessment of your heart disease risk.

This is a fascinating and rapidly advancing area of research. The claim that blood vessels in the eyes can help predict heart disease and biological aging risk is strongly supported by scientific evidence.

Here’s a detailed breakdown of how it works, the science behind it, and what it means for the future.

The Window to Your Health: The Retina

The back of your eye, called the retina, is the only place in the body where doctors can directly and non-invasively view a network of tiny blood vessels (microvasculature) and nerves.

The health of these small vessels is a mirror of the health of similar-sized vessels throughout your body, including in your brain, heart, and kidneys. Damage to these microvessels is often a very early sign of systemic (whole-body) diseases.

1. Predicting Heart Disease (Cardiovascular Risk)

The link between the retina and heart disease primarily revolves around a condition known as Retinopathy.

How it Works:

  • Shared Physiology: The small vessels in your retina are similar in size, structure, and function to the small vessels that supply the heart muscle itself. Factors that damage one are likely to damage the other.
  • The Damage Process: Conditions like high blood pressure (hypertension) and atherosclerosis (clogging of the arteries) don’t just affect large arteries. They also cause:
    • Narrowing (Arteriolosclerosis): The retinal arteries become thicker and narrower.
    • AV Nicking: Where arteries cross over veins, they can compress them, a sign of chronic high blood pressure.
    • Hemorrhages & Microaneurysms: Weakened vessel walls can leak blood or form tiny bulges.
  • What Doctors Look For: An eye doctor (ophthalmologist) or even an AI algorithm analyzing a retinal image can identify these changes. Their presence is classified as Hypertensive Retinopathy or, if related to diabetes, Diabetic Retinopathy.

The Evidence:
Multiple large-scale studies have shown that people with these retinal changes have a significantly higher risk of:

  • Coronary heart disease
  • Heart failure
  • Stroke
  • Death from cardiovascular causes

Essentially, the retina acts as an “early warning system,” showing damage from high blood pressure and vascular disease long before a major cardiac event like a heart attack occurs.

2. Predicting Biological Aging Risk

This is an even more cutting-edge application. The concept is that the condition of your retinal vessels can reveal your “biological age” as opposed to your “chronological age.”

How it Works: Researchers use a metric called the “Retinal Age Gap.”

  1. Training an AI: Scientists train a sophisticated deep-learning algorithm on hundreds of thousands of retinal images from healthy people.
  2. Learning the Pattern: The AI learns what a “healthy” retina looks like at different chronological ages (e.g., age 40, 50, 60). It becomes an expert at predicting someone’s age just from their retinal scan.
  3. Calculating the Gap: The AI then analyzes a new person’s retina and gives a “retinal age” prediction. The difference between this predicted biological age and the person’s actual chronological age is the “Retinal Age Gap.”
    • Example: If the AI says your retina looks like that of a 50-year-old, but you are only 45, you have a +5-year Retinal Age Gap.

What the Research Shows:
A large study published in the British Journal of Ophthalmology found that:

  • A large Retinal Age Gap (e.g., your retina is “older” than you are) is significantly associated with a higher risk of death, particularly from cardiovascular disease.
  • This link remained strong even after accounting for traditional risk factors like age, smoking, and BMI.

Why is this a powerful indicator?
The retina is part of the central nervous system (it’s an extension of the brain). Its health is intimately tied to the overall health of your circulatory system and cellular aging processes. An “older” retina suggests accelerated aging and cumulative damage throughout the body’s vascular and neurological systems.

The Future: AI and Retinal Scans

This research is moving quickly from the lab to the clinic, powered by Artificial Intelligence (AI).

  • Automated Screening: AI can analyze a routine retinal photo in seconds, providing a quantitative and objective assessment of cardiovascular risk and biological age.
  • Accessibility: A quick, non-invasive retinal scan could become a standard part of a general health check-up, not just an eye exam, making advanced risk prediction more accessible.
  • Personalized Medicine: It could help doctors identify high-risk individuals earlier, allowing for more aggressive and personalized preventative strategies (like lifestyle changes and medications).

Limitations and Important Caveats

  1. It’s a Predictor, Not a Crystal Ball: A retinal scan is a powerful risk indicator, but it’s not a definitive diagnosis. It adds to the overall picture alongside blood tests, blood pressure readings, and family history.
  2. Still in Development: While the science is robust, the use of “retinal age” as a clinical tool is still being refined and validated.
  3. Cannot Replace Specific Tests: It won’t tell you your exact cholesterol levels or if a specific artery is blocked. It assesses the health of your microvasculature, which is a proxy for systemic health.

Conclusion

The idea that the blood vessels in your eyes can predict heart disease and biological aging is not science fiction; it’s solid science. Your retina provides a unique, real-time window into the health of your entire circulatory system and the pace of your body’s aging. With the help of AI, this “window” is poised to become a revolutionary tool in preventative medicine, helping people take control of their health long before serious problems arise.

https://www.medicalnewstoday.com/articles/blood-vessels-eyes-predict-heart-disease-biological-aging-risk

https://health.medicaldialogues.in/health-topics/eye-health/eye-scans-may-predict-heart-disease-and-biological-ageing-say-researchers-157448

https://healthsci.mcmaster.ca/aging-in-plain-sight-what-new-research-says-the-eyes-reveal-about-aging-and-cardiovascular-risk

Beta Blockers, the Standard Treatment After a Heart Attack, May Offer No Benefit for Heart Attack Patients and Women Can Have Worse Outcomes

Beta Blockers, the Standard Treatment After a Heart Attack, May Offer No Benefit for Heart Attack Patients and Women Can Have Worse Outcomes

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You’ve hit on a very important and nuanced point in cardiology. The statement “Beta-blockers may be harmful for women with some heart conditions” is an oversimplification of a complex issue, but it points to a real and critical area of research: sex-based differences in cardiovascular disease and treatment.

Let’s break down what this means, separating fact from fiction.

The Core of the Issue: Not “Harmful” but “Potentially Less Effective or Different Risk-Benefit”

For the vast majority of heart conditions (like coronary artery disease, heart attack, heart failure), beta-blockers are lifesaving for both men and women. The benefits are well-proven.

However, research over the past two decades has revealed that the degree of benefit and the side effect profile can differ significantly between women and men. The idea of “harm” primarily comes from two areas:

  1. Increased Side Effects: Women consistently report a higher incidence and severity of side effects from beta-blockers.
  2. Lack of Efficacy in Certain Female-Predominant Conditions: For some conditions that primarily affect women, beta-blockers may not work as intended and could potentially exacerbate symptoms.

1. Increased Side Effects in Women

Women are more likely to experience side effects from beta-blockers, often at the same doses prescribed to men. This is due to well-documented pharmacokinetic and pharmacodynamic differences:

  • Body Size and Composition: Women generally have lower body weight, less muscle mass, and a higher percentage of body fat, which can affect drug distribution.
  • Metabolism: Enzymes in the liver (like CYP450) that metabolize drugs can work differently in women.
  • Absorption and Elimination: Gastrointestinal motility and kidney function can vary.

Common side effects that are more frequent or severe in women include:

  • Bradycardia (excessively slow heart rate)
  • Hypotension (low blood pressure)
  • Fatigue and Depression
  • Cold hands and feet (due to peripheral vasoconstriction)

The “Harm” Here: If side effects are severe enough, they can lead to poor quality of life and, crucially, non-adherence to medication. A patient who stops taking a lifesaving drug because of intolerable side effects is certainly being harmed by the therapy in an indirect way.

2. Specific Heart Conditions Where Beta-Blockers Are Questioned for Women

This is where the “harm” concept becomes more direct.

A. Coronary Microvascular Dysfunction (CMD)

  • What it is: A condition where the tiny blood vessels (microvasculature) in the heart don’t function properly, causing chest pain (angina). It is much more common in women, especially after menopause.
  • The Problem with Beta-Blockers: Traditional beta-blockers work mainly on larger coronary arteries. In CMD, the problem is in the microvessels. Some beta-blockers that are non-selective (like propranolol) can cause unopposed alpha-receptor stimulation, leading to constriction of these very microvessels, potentially worsening blood flow and chest pain.
  • Current Thinking: Cardiologists are now more cautious. While certain beta-blockers can still be helpful for controlling heart rate, they are not a one-size-fits-all solution for CMD. Other medications like calcium channel blockers (e.g., verapamil) or ranolazine are often preferred or used in combination.

B. Takotsubo Cardiomyopathy (“Broken Heart Syndrome”)

  • What it is: A temporary weakening of the heart muscle, often triggered by extreme stress. It overwhelmingly affects postmenopausal women.
  • The Problem with Beta-Blockers: The long-term use of beta-blockers for Takotsubo patients is controversial. Since the condition is often triggered by a massive catecholamine (adrenaline) surge, the intuitive thought was to block these receptors. However, large registry studies have not shown a clear benefit for beta-blockers in preventing recurrence. There is a theoretical concern that in the acute phase, certain beta-blockers could worsen the condition by leading to unopposed alpha-effects and increased blood pressure.

C. Heart Failure with Preserved Ejection Fraction (HFpEF)

  • What it is: A type of heart failure where the heart pumps normally but is too stiff to fill properly with blood. It is more common in older women, especially those with hypertension, obesity, and diabetes.
  • The Problem with Beta-Blockers: Unlike Heart Failure with Reduced Ejection Fraction (HFrEF), where beta-blockers are a cornerstone of therapy, no medication has conclusively been proven to reduce mortality in HFpEF. Beta-blockers are often prescribed to control heart rate or atrial fibrillation, but they can sometimes worsen the problem by limiting the heart rate needed to fill a stiff ventricle, leading to low cardiac output and fatigue.

The Bigger Picture: The Historical Lack of Women in Clinical Trials

A major reason these differences are only now being understood is that for decades, cardiovascular clinical trials predominantly enrolled middle-aged men. The results were then applied to women, assuming the biology and response were the same. We now know this is not the case.

Conclusion and Key Takeaway

It is inaccurate and dangerous to say that women with heart conditions should avoid beta-blockers. For conditions like heart attack and heart failure with reduced ejection fraction, they are essential.

However, the correct, modern interpretation is:

Cardiovascular treatment must be personalized, and biological sex is a critical factor in that personalization. For women, especially with conditions like coronary microvascular dysfunction, Takotsubo cardiomyopathy, or HFpEF, the use of beta-blockers requires careful consideration. The choice of specific beta-blocker, the dose, and the balance of benefits versus a higher risk of side effects must be thoughtfully evaluated by a healthcare provider.

If you are a woman prescribed a beta-blocker, the most important thing is to:

  • Take it as prescribed unless your doctor tells you otherwise.
  • Report any side effects to your doctor promptly. Do not just stop taking the medication.
  • Have an open conversation with your cardiologist about the specific reason for the prescription and whether it’s the best option for your particular heart condition.

Disclaimer: This information is for educational purposes only and is not a substitute for professional medical advice. Always consult your healthcare provider for diagnosis and treatment decisions tailored to your individual health needs.

Reference:

https://www.mountsinai.org/about/newsroom/2025/beta-blockers-the-standard-treatment-after-a-heart-attack-may-offer-no-benefit-for-heart-attack-patients-and-women-can-have-worse-outcomes

https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaf673/8243876

https://www.medicalnewstoday.com/articles/common-heart-attack-pill-beta-blockers-may-be-harmful-women-some-heart-conditions

Medications that have been suggested by doctors worldwide are available on below link

https://mygenericpharmacy.com/category/disease/heart-disease

Extreme heat linked to increased cardiovascular disease

Extreme heat linked to increased cardiovascular disease

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According to research released today (Monday) in the European Heart Journal, Australians lose an average of nearly 50,000 years of healthy life to cardiovascular disease each year as a result of hot weather. This amounts to approximately 7.3 percent of the overall burden resulting from cardiovascular disease-related illnesses and deaths. According to the study, if greenhouse gas emissions continue on their current trajectory, this number may double or even triple by the middle of the century.

The study’s authors point out that their findings also apply to people worldwide because the risk of cardiovascular disease rises with temperature. Our hearts have to work harder to keep us cool in hot weather. Particularly for those who already have cardiovascular disease, this increased pressure can be harmful. Many of us have witnessed firsthand how a warming climate can worsen our health, especially during extended hot spells. The precise number of people who are suffering from severe heart disease or passing away too soon as a result of rising temperatures is still unknown, though, and we must comprehend how this burden will grow in the future.

Disability-adjusted life years (DALYs), a metric that counts the number of years of healthy life lost due to illness or death, were employed by the researchers. The researchers used data from the Australian Burden of Disease Database on cardiovascular disease-related illness or death from 2003 to 2018 to determine the current impact of high temperatures.

The amount of cardiovascular disease or mortality that can be linked to hot weather in various Australian regions and the nation at large was then determined using a statistical model. According to this, cardiovascular disease brought on by hot weather results in the loss of 49,483 years of healthy life on average every year. Rather than illness, the majority of these years were lost to death.

The researchers then examined the likely future effects of climate change caused by greenhouse gas emissions using their model. They made use of two of the Intergovernmental Panel on Climate Change’s climate change scenarios: one in which emissions stabilize (also known as Representative Concentration Pathway 4.5 or RCP4.5), and another in which emissions continue to rise (RCP8.5).

The effects of population growth and potential adaptations to higher temperatures were also examined. According to the model, under the RCP4.5 scenario, the number of DALYs lost as a result of cardiovascular disease brought on by hot weather will rise by 83.5 percent by 2030, to 90,779.7 DALYs. It is anticipated that this figure will increase even more by 2050, reaching 139,828.9 DALYs, or 182.6 percent more. The DALYs are expected to rise by 92.7 percent to 95,343.0 DALYs in 2030 and by 225.6 percent to 161,095.1 in 2050 under the more severe RCP8.5 scenario.

According to Professor Bi, this study provides a comprehensive picture of the disease burden throughout Australia by integrating some important factors, including population changes, climate change, and adaptation strategies. Because of this, our study is among the first of its kind in the world. There is always some degree of uncertainty in forecasting future disease burden, and our models are predicated on assumptions that might not account for all relevant real-world information. Nevertheless, despite these uncertainties, the thoroughness of our methodology makes the study particularly useful for organizing future mitigation and adaptation plans for climate change.

The basic connection between elevated temperatures and heightened cardiovascular risk has been established worldwide, although our study is centered on Australia. The general pattern that higher temperatures increase the burden of cardiovascular disease is probably true in many regions of the world, even though the precise risks may differ based on regional climates, population composition, and degrees of adaptation. The model also indicates that by implementing strategies that assist individuals in adapting to hotter weather, the impact of high temperatures on cardiovascular disease could be significantly reduced.

Professor Bi continues, Our research indicates that the risks associated with higher temperatures are likely to increase, particularly for vulnerable groups, as climate change brings more frequent and intense heat. It emphasizes how crucial it is to take preventative measures in hot weather, like drinking plenty of water, finding cool places, and getting medical attention when necessary. Additionally, our findings urge immediate funding for adaptation and mitigation measures, such as public health campaigns, urban cooling plans, and enhanced emergency response during hot weather.

Aspirin may prevent cancer metastasis by boosting the immune response

Aspirin may prevent cancer metastasis by boosting the immune response

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Approximately 50% of individuals will receive a cancer diagnosis at some point in their lives, usually in their later years. Although cancer cells can separate and spread to other parts of the body, it is easiest to treat cancer that is contained in its original location. By strengthening the body’s immune response, aspirin may help prevent metastases, or secondary tumors, according to researchers looking into how cancer spreads. Aspirin assisted immune cells in eliminating cancer cells that were spreading in their mouse study. People are being studied to see if aspirin or medications that target the same pathway can help prevent or postpone the recurrence of cancers.

Based on data from 2010-2011, Cancer Research UK reports that half of all people in Wales and England who receive a cancer diagnosis will live for at least ten years following their diagnosis. For some of the more common cancers, the percentage is significantly higher. According to data from 2013 to 2017, over 75% of people in England who have been diagnosed with either prostate or breast cancer will still be alive ten years later. Early detection, before the cancer has a chance to spread from its original site, is essential to a successful outcome. Over 90% of cancer-related deaths occur after the disease has spread to another area of the body.

Researchers from the University of Cambridge in the United Kingdom have now found that aspirin, a widely accessible and inexpensive pain reliever, may be able to stop the spread of some cancers. Aspirin affected platelets, which are tiny cells that cause blood to clot, in mice by reducing their production of thromboxane A2 (TXA2), a clotting factor that inhibits immune T cells, according to a study published in Nature. These T cells can then eliminate any cancer cells that are spreading because TXA2 isn’t suppressing them as much.

The study generates a valid hypothesis on how to prevent cancer recurrence and spread using a very simple intervention for patients, according to Nilesh Vora, MD, a board-certified hematologist and medical oncologist who serves as the medical director of the MemorialCare Todd Cancer Institute at Long Beach Medical Center in Long Beach, CA. This article’s main point is that aspirin stops cancers from spreading by lowering TXA2 and releasing suppressed T cells. Although treatment for early-stage cancers has advanced significantly, if cancer cells have spread from the original tumor site, there is still a chance that the cancer will recur elsewhere in the body.

The immune system is weakened inside the original tumor’s microenvironment, making it less effective at eliminating cancer cells. However, the immune system may target these lone cancer cells once they migrate. There is a special window of opportunity for treatment when cancer first spreads because cancer cells are more susceptible to immune attack. Patients with early cancer who are at risk of recurrence should benefit greatly from therapies that target this window of vulnerability.

Surprising new use for old drug
In mice, the researchers had previously discovered 15 genes that affected the spread of cancer. They discovered that some primary cancers in the liver and lungs metastasized less frequently in mice deficient in a gene that produces the protein ARHGEF1. They deduced from this that ARHGEF1 inhibits T cells that eliminate metastatic cells. They then found that when cells are exposed to the clotting factor TXA2, this gene is activated. Although recent evidence now contradicts the data on heart attack and stroke prevention, aspirin is sometimes taken at low doses to lower the risk of blood clots, heart attacks, and strokes because it inhibits platelets’ production of TXA2.

Aspirin-treated mice experienced fewer metastases than control mice in the current study, which examined the mouse model of melanoma, an aggressive type of skin cancer. The aspirin allowed their T cells to kill cancer cells by releasing them from TXA2-induced suppression. According to a press release from Jie Yang, PhD, one of the study co-authors based at the University of Cambridge, It was a eureka moment when we found TXA2 was the molecular signal that activates this suppressive effect on T cells. Yang stated that before this, we were unaware of the significance of our findings in comprehending aspirin’s anti-metastatic action. It was a shocking discovery that led us in a completely different direction than we had originally intended.

Do the findings on aspirin and cancer also apply to people?
Yang emphasized the promise of the research team’s findings, pointing out that aspirin or other medications that might target this pathway might be more affordable than antibody-based treatments and, as a result, more widely available. However, the researchers caution that aspirin can have side effects and may not be suitable for everyone. Aspirin frequently causes indigestion, nausea, and irritation of the stomach or gut. Less frequent adverse effects include bruising, vomiting, stomach bleeding or inflammation, and worsening asthma symptoms. Rarely, it can result in hemorrhagic stroke, kidney failure, or brain bleeding, especially in people who take a daily dose.

The results were welcomed by Anton Bilchik, MD, PhD, a surgical oncologist who was not involved in this study. He is the Chief of Medicine and Director of the Gastrointestinal and Hepatobiliary Program at Providence Saint John’s Cancer Institute in Santa Monica, CA. However, he informed MNT that these findings must first be confirmed in clinical trials involving human subjects. It is necessary to assess aspirin as an adjuvant to immunotherapy and chemotherapy in patients with more advanced cancers as well as aspirin alone in patients with earlier cancers who are not candidates for these treatments.

The good news is that human clinical trials have begun. To determine whether aspirin can prevent or postpone the recurrence of early-stage cancers, the researchers will work with Ruth Langley, MD, professor of oncology and clinical trials in the MRC Clinical Trials Unit at University College London, who is in charge of the Add-Aspirin clinical trial. According to Langley, who was not involved in the current study, people should only begin taking aspirin on a doctor’s recommendation. A small percentage of people may experience severe side effects from aspirin, such as stomach ulcers or bleeding. She underlined that it is crucial to know which cancer patients are most likely to benefit and to always consult your doctor before beginning aspirin.

Medical Myths: All about cholesterol

Medical Myths: All about cholesterol

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Among all the substances found in our bodies, cholesterol is arguably the most well-known. Even though everyone is familiar with this fatty substance, there is a lot of misinformation about it. We shed some light on cholesterol in this article.

Since cholesterol is a necessary part of animal cell membranes, all animal cells synthesize it. Despite its unfavorable reputation, cholesterol is necessary for life. On the other hand, high blood levels of it raise the risk of cardiovascular disease. Plaques containing cholesterol and other materials, like fat and calcium, accumulate on the artery walls. This causes the blood vessels to narrow over time, which can result in complications like heart attacks and strokes.

The Centers for Disease Control and Prevention (CDC) estimate that 13% of Americans who were 20 years of age or older had high cholesterol in 2015–2016. According to estimates from the World Health Organization (WHO), elevated cholesterol levels cause 26 million deaths annually. It is not surprising that there is a lot of false information regarding cholesterol given its prevalence. So, to help us separate fact from fiction.

All cholesterol is bad
As indicated in the introduction, cholesterol is an essential part of membranes found in cells. In addition to playing a structural role in membranes, it is essential for the synthesis of bile acid, vitamin D, and steroid hormones. Therefore, even though high cholesterol raises the risk of disease, without cholesterol, life would not be possible.

Cholesterol is not harmful. In today’s modern world, an innocent bystander is being mistreated. Because our bodies were not made to survive in an environment where food was abundant, excess cholesterol will be stored in our bodies. And our blood vessels are frequently that deposit center, which is when it becomes harmful to us. In addition to its physiological roles, cholesterol’s mode of transportation influences whether or not it is harmful to health.

Lipoproteins are molecules made of protein and fat that transport cholesterol throughout the body. There are two primary methods of this transport. From the liver, low-density lipoprotein (LDL) transports cholesterol to cells, where it is utilized in a variety of functions. Because elevated blood levels of LDL cholesterol raise the risk of cardiovascular disease, people sometimes refer to LDL cholesterol as bad cholesterol. Since high-density lipoprotein (HDL) returns cholesterol to the liver, it is frequently referred to as good cholesterol. Once there, the body expels cholesterol, lowering the risk of cardiovascular disease.

I am a healthy weight, so I can’t have high cholesterol
Yes, you can, as Dr. Greenfield says. In actuality, our genetic makeup and the food we eat determine our cholesterol balance. For instance, a person may have a genetic predisposition to process cholesterol inefficiently from birth. He clarified that it has been dubbed familial hypercholesterolemia and that its frequency may be as high as 1 in 200 due to its genetic nature. Your genetic metabolism and the ratio of calories burned to calories consumed play a bigger role in weight. Dr. Paz agreed: Your cholesterol can be abnormal even if you have a healthy weight. The foods you eat, how much alcohol you drink, how much you smoke, and how often you exercise all have an effect on your cholesterol.

Furthermore, as Dr. Lajoie informed us, some overweight individuals may not have high cholesterol, while others who maintain a healthy weight may. She clarified that a person’s diet, exercise, sleep patterns, thyroid function, medications, and genetics all influence their cholesterol levels. She went on, Your age and your genetics are two more factors that can contribute to high cholesterol but that you cannot modify.

I would have symptoms if I had high cholesterol
This is an additional myth. According to Dr. Paz, high cholesterol typically doesn’t cause any symptoms. For this reason, it is advised to have blood tests regularly to check for high cholesterol. Your unique risk factors dictate when you should begin screening and how often.

When excessive cholesterol accumulation causes heart and blood vessel damage and blockage, the only symptoms that cholesterol can be linked to are the late symptoms. Angina (chest pain), a heart attack, or even abrupt death result from this. Dr. Lajoie reaffirmed that elevated cholesterol causes silent plaque accumulation in arteries, which worsens over time and can result in heart attacks or strokes.

If I eat lots of cholesterol, I will have high cholesterol levels
This subject is a little trickier to understand than one might think. According to Dr. Lajoie, cholesterol levels are not always directly correlated with the amount of cholesterol one consumes. Even if a person doesn’t consume much cholesterol, eating sugars or simple carbs can raise their blood pressure. She added, Compared to sedentary people, those who exercise are less likely to see elevations in cholesterol from eating cholesterol.

Our cholesterol levels will almost certainly rise if we eat more cholesterol. He gave the following explanation for this: You buy red meat, cheeses, and eggs at the grocery store, but you don’t go buy a package of cholesterol. Red meat has cholesterol and saturated fat. Since cholesterol is derived from animals, eating foods high in saturated fat will raise cholesterol overall as well as the bad, or LDL, cholesterol, which is then deposited in the arterial walls of our blood vessels.

Everyone should aim for the same cholesterol targets
Dismissed! According to Dr. Paz, your target cholesterol level depends on your risk of heart attack and stroke, which is determined by factors like age and high blood pressure, as well as whether you have a history of these conditions. That is untrue, according to cholesterol guidelines released by the National Lipid Association, the American College of Cardiology, and the American Heart Association (AHA). He went on to say that the LDL cholesterol, or bad cholesterol, should be less than 100 milligrams per deciliter (mg/dl) for those of us who have not experienced any cardiovascular issues. However, the LDL cholesterol target should be less than 70 mg/dl, if not lower, if you have a history of heart attacks, strokes, or other arterial vascular diseases, and especially if you have diabetes.

Only men need to worry about cholesterol levels
Despite being a persistent myth, this is untrue. Dr. Paz clarified: The CDC reports that between 2015 and 2018, the incidence of elevated total cholesterol in the U.S. adult population was 11.4 percent. In comparison to women, men were more likely than women to have high total cholesterol (10.5% versus 12.1%). Dr. Greenfield concurred that heart disease is an equal opportunity employer. He clarified that women start to accelerate their risk of heart disease and develop the same risk as men after losing the protective effects of estrogens. In actuality, more female heart attacks than male heart attacks are reported each year because women typically develop heart disease later in life and live longer. He also informed us that women are far more likely to die from heart disease than from breast cancer and that when they do suffer a heart attack, their prognosis is typically worse.

There’s nothing I can do about my cholesterol level
Fortunately, this is not accurate. Dr. Paz states that in addition to taking cholesterol-lowering drugs, you can lower your cholesterol by eating a healthy weight, exercising, quitting smoking, and consuming moderate amounts of alcohol. Dr. Greenfield concurred that there is a lot that can be done with an abnormally high cholesterol level. The first steps are always diet and exercise, and they are still very important. Statins are safe and highly effective at lowering cholesterol. The more recent statins have been around since 1987 and are thought to be safer, more effective, and have fewer side effects. And science is still coming up with new ideas. According to Dr. Greenfield, more recent injectable PCSK-9 inhibitors have also been demonstrated to significantly reduce cholesterol to previously unheard-of levels.

I take statins, so I can eat what I want
Dr. Greenfield started, Wouldn’t that be nice if it were true, but it’s not. You will put on weight if you overindulge in food and calories. Excessive weight gain, particularly around the abdomen, can lead to the development of metabolic syndrome, a prediabetic state. He went on: Statins do not help people lose weight. It is your responsibility to treat your body with respect, which includes what you eat, and your job to lower the bad LDL cholesterol.

I’m under 40, so I don’t need to have my cholesterol checked
Dr. Paz clarified that many, advise screening for elevated cholesterol as early as age 20, despite some disagreement regarding the optimal age to begin. Dr. Greenfield agreed the longer blood in your blood vessels has an excessively high cholesterol content, the higher your chance of developing cardiovascular disease in later life. According to the recommendations, a person’s first cholesterol test should be taken when they are a teenager, and if there is a strong family history, it should be taken earlier. He informed us that people with homozygous familial hypercholesterolemia should have their cholesterol checked starting at age 2.

Dr. Greenfield summarized her remarks as follows: I encourage my patients to ask questions and to do research on their medical conditions. But please be advised that a good portion of the polluted content is inaccurate and deceptive. He went on to visit reliable websites and trust the research presented by individuals who have devoted their lives to the treatment of heart disease.. Furthermore, anything that seems too good to be true or nonsensical is most likely not. Handle your body with reverence, not as if it were a theme park!

Reference:
https://www.medicalnewstoday.com/articles/medical-myths-all-about-cholesterol?utm_source=ReadNext#The-take-home-message

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Medical Myths: All about stroke

Medical Myths: All about stroke

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In this part of our series on medical myths, we explore common misconceptions regarding stroke. We address a number of common misconceptions, including whether a stroke is a heart condition and what to know about ministrokes and paralysis.

The Centers for Disease Control and Prevention (CDC) estimates that 610,000 Americans have their first stroke out of the over 795,000 who experience one each year in the United States. With 11 percent of deaths worldwide in 2019, stroke was the second most common cause of death. Stroke comes in three primary forms. The first type of stroke is the most prevalent, making up 87% of cases. It happens when an artery supplying the brain with oxygen loses its ability to carry blood. The second type of stroke is known as a hemorrhagic stroke, which is brought on by a brain artery burst that subsequently injures nearby tissues.

A transient ischemic attack (TIA), referred to as a ministroke, is the third stroke category. It occurs when there is a brief interruption in blood supply to the brain, usually lasting no longer than five minutes. Despite being extremely common, stroke is frequently misinterpreted. We consulted with Dr. Rafael Alexander Ortiz, chief of Neuro-Endovascular Surgery and Interventional Neuro-Radiology at Lenox Hill Hospital, to clear up misconceptions and deepen our understanding of the subject.

Stroke is a problem of the heart
Strokes occur in the brain, not the heart, although cardiovascular risk factors are linked to stroke risk. Dr. Ortiz told MNT that some people believe that heart problems are the cause of stroke. That’s not correct. A stroke is not a heart issue; rather, it is a brain issue brought on by an obstruction or rupture of cerebral arteries or veins. Heart attacks, which are brought on by a blockage in the blood supply to the heart rather than the brain, are sometimes confused with strokes.

Stroke is not preventable
According to Dr. Ortiz, the most prevalent risk factors [for stroke] are high blood pressure, smoking, high cholesterol, obesity, diabetes, head or neck trauma, and cardiac arrhythmias. A lot of these risk factors are modifiable through lifestyle choices. Regular exercise and a balanced diet help lower risk factors like diabetes, high blood pressure, obesity, and obesity. Stress and alcohol use are two more risk factors. A person’s chance of stroke may be decreased by making efforts to lessen or eliminate these lifestyle factors.

Stroke does not run in families
A person’s risk of stroke is increased by single-gene diseases like sickle cell disease. The risk of stroke may also be indirectly increased by genetic factors, such as an increased propensity for high blood pressure and other cardiovascular risk factors. Unhealthy lifestyle choices are likely to raise the risk of stroke in family members since families frequently share environments and lifestyles, particularly when combined with genetic risk factors.

Stroke symptoms are hard to recognize
The most common symptoms for stroke form the acronym F.A.S.T.
F: face dropping, when one side of the face becomes numb and produces an uneven smile
A: arm weakness, when one arm becomes weak or numb and, when raised, drifts slowly downward
S: speech difficulty, or slurred speech
T: time to call 911
Other symptoms of stroke include: The symptoms may include numbness or weakness in one or both eyes; confusion; trouble speaking or understanding speech; difficulty walking, including dizziness, loss of balance, and coordination; and severe headaches without a known cause.

Stroke cannot be treated
Dr. Ortiz clarified that there is a false belief that strokes are incurable and untreatable. Many stroke patients can have their symptoms reversed by emergency treatment with a clot-busting drug injection, minimally invasive mechanical thrombectomy for clot removal, or surgery, he noted. This is especially true if the patient arrives at the hospital early enough for the therapy (within minutes or hours since the onset of the symptoms). The chance of a positive result decreases with the duration of the symptoms. As a result, it’s imperative that at the first sign of a stroke, ie. He went on, “If you’re having problems speaking, double vision, paralysis, numbness, etc., call 911 to send an ambulance to the closest hospital.”. Additionally, studies reveal that people who visit within three hours of the onset of symptoms usually experience less disability three months later than people who arrive later.

Stroke occurs only in the elderly
One major risk factor for stroke is age. After age 55, the risk of stroke doubles every ten years. Strokes, however, can happen at any age. According to a study that looked at medical data, 34% of stroke hospitalizations in 2009 involved people under the age of 65. According to a 2013 review, young adults and adolescents account for 15% of all ischemic stroke cases. The most prevalent co-existing conditions in this age group, according to the researchers, were lipid disorders, obesity, diabetes, hypertension, and tobacco use all stroke risk factors.

All strokes have symptoms
Not every stroke has symptoms, and some studies indicate that strokes without symptoms occur far more frequently than strokes with symptoms. According to one study, of the approximately 11 million strokes that occurred in 1998, 770,000 had symptoms, while nearly 11 million did not. Evidence of these so-called silent strokes appears on MRI scans as white spots from scarred tissue following a blockage or ruptured blood vessel. When patients undergo MRI scans for symptoms like headaches, cognitive problems, or dizziness, silent strokes are frequently discovered. Even though they don’t have any symptoms, they should be treated in the same way as strokes that do. People who have silent strokes are more vulnerable to dementia, cognitive decline, and subsequent symptomatic strokes.

A ministroke is not so risky
According to Dr. Ortiz, the term “ministroke” has been misused because some people believe it to refer to small, low-risk strokes. That is untrue because a ministroke is actually a transient ischemic attack (TIA). This is not a minor stroke; rather, it is a warning sign that a major stroke could happen. He continued, “Any acute stroke symptom, whether temporary or persistent, requires emergency workup and management to prevent a devastating large stroke.

Stroke always causes paralysis
A stroke is one of the most common causes of permanent disability; however, not all stroke victims will become paralyzed or weak. Studies reveal that more than half of stroke survivors 65 and older have decreased mobility as a result of their stroke. However, many variables, including the location and extent of brain tissue damage, affect how a stroke affects a person in the long run. For instance, harm to the left brain will impact the right side of the body and vice versa. Effects of a stroke that happens on the left side of the brain might include memory loss, speech and language difficulties, paralysis on the right side of the body, and slow, cautious behavior. Paralysis may also happen, but on the left side of the body, if it impacts the right side of the brain. Other side effects could be memory loss, rapid and curious behavior, vision issues, or both.

Stroke recovery happens fast
After a stroke, recovery may take several months or even years. Many, though, might not fully recover. According to the American Stroke Association, of those who survive a stroke, 10% will recover almost completely, 10% will need care in a long-term facility or nursing home, 25% will recover with minor impairments, and 40% will experience moderate to severe impairments. Research indicates that there may be a critical window of 2-3 months following the onset of the stroke, during which intensive motor rehabilitation is more likely to result in recovery. During this time, some people might also be able to recover on their own. Although they are likely to occur much more slowly, improvements are still possible after this window and the 6-month point.

REFERENCES:
https://www.medicalnewstoday.com/articles/medical-myths-all-about-stroke?utm_source=ReadNext#10.-Stroke-recovery-happens-fast

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