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 endothelial cell health. Show all posts
Showing posts with label endothelial cell health. Show all posts

Saturday, June 1, 2024

New Research Could Help Explain Anger’s Link to Heart Attacks and Strokes

 

So it's not helpful getting vein bursting angry at your doctor for KNOWING NOTHING ON GETTING YOU 100% RECOVERED! You'll just have to hope comeuppance hits her/him when they are the 1 in 4 per WHO that has a stroke?  

If your doctor wrote three prescriptions to OT, PT and ST of E.T.(Evaluate and Treat) that means your doctor is no better than a trained chimpanzee as far as getting you recovered! You still have to remain calm.

New Research Could Help Explain Anger’s Link to Heart Attacks and Strokes

JAMA. Published online May 31, 2024. doi:10.1001/jama.2024.9776

Observational studies have associated anger with increased risks of myocardial infarction—heart attack—and stroke, but little has been known about the mechanism behind this phenomenon. Now, the results of a randomized clinical trial published in the Journal of the American Heart Association suggest that anger may affect blood vessel dilation, offering a possible explanation.

The researchers, supported by the National Institutes of Health (NIH), aimed to examine how negative emotions affect the blood vessels.

“This study adds to our body of knowledge that acute negative psychological events, such as stress or anger, can have real physiologic effects,” said cardiologist Glenn Levine, MD, a professor at Baylor College of Medicine who was not involved with the study.

The Backstory

Although there’s plenty of conversation around psychiatric conditions and physical health, Daichi Shimbo, MD, the study’s lead author and a cardiologist at Columbia University Medical Center, wanted to investigate the physiological influences of negative emotions that everyone experiences from time to time. “When we think about mental health, we think about severe chronic conditions like depression, anxiety, posttraumatic stress disorder, and so forth,” he said. “What we don’t talk about is negative emotions.”

After seeing data linking both short-term and long-term risk of heart disease to anger and sadness, he wondered what could cause this correlation. He worked with fellow researchers to design a study centering around 3 core emotions: anger, transient anxiety, and stress.

The Trial Design

The trial involved 280 participants between the ages of 18 and 73 years with no history of hypertension, diabetes, lipid imbalance, or mood disorders, who were assigned to various conditions designed to induce specific emotions:

• Either an anger or an anxiety recall task: participants were asked to recall an event that made them angry or anxious and talk about it for 8 minutes.

• A depressed mood task: participants were asked to read scripts off slides that became progressively sadder for 8 minutes.

• A neutral task: participants in this control group counted out loud for 8 minutes.

The recall tasks for anger and anxiety were based on validated methods designed to elicit the negative emotions felt at specific points in the participants’ lives.

“Obviously what may make you angry is different than what makes me angry,” Shimbo said. “There’s individual stimuli that cause people to have these negative emotions.”

The depressed mood task relied on the Velten Mood Induction Procedure, a validated measure for inducing sadness. Because the simple act of talking can affect blood vessel function, the control condition included a speaking component, but it was designed to be somewhat boring, Shimbo explained.

Researchers measured flow changes in the blood vessels of each participant’s dominant arm with a blood pressure cuff, an intravenous catheter, and a finger probe immediately after the negative emotion induction or the neutral task and then again after 3, 40, 70, and 100 minutes.

The Results

They found that:

• Blood vessel dilation was significantly reduced in the anger induction group compared with the control group.

• There was no statistically significant difference in blood vessel dilation between the anxiety or sadness induction conditions and the control group.

• Vessel impairment in the anger induction condition persisted for up to 40 minutes before returning to the baseline.

“This study suggests that a short episode of anger may be linked to vascular impairments or the ability of the vessels to dilate,” said Rebecca Campo, PhD, a social-health psychologist and program director at the NIH’s National Heart, Lung, and Blood Institute, which funded the work. “The idea is that if this is something that occurs frequently, it could be a precursor to the kind of long-term damage that can lead to heart attacks and strokes.”

It's important to note that the emotional induction lasted only 8 minutes and was on a scale between mild and moderate. Shimbo pointed out that this level of emotional annoyance is in line with what people experience every day and yet it impaired healthy blood vessel dilation for up to 40 minutes.

“I speculate if you’re a person who gets angry a lot, you’re chronically insulting your arteries,” he said. “I think over time it’s going to reach a point that it’s going to be chronically dysfunctional. And that’s the step toward getting atherosclerosis and heart disease.”

The Biological Mechanisms

Healthy blood vessels regularly undergo the process of vasodilation, where they widen to allow increased blood flow, helping to deliver oxygen and nutrients throughout the body. Part of this is dependent on the health of the endothelial cells, which line the blood vessels and release vasoactive factors.

Impairment of vasodilation, caused by the loss of normal endothelial function, promotes numerous processes that lead to the buildup of plaque in the arteries, known as atherosclerosis.

This study is one of the first to show that anger affects blood vessel function, and so the intermediary mechanisms that connect these variables aren’t yet fully understood. However, researchers proposed several potential pathways to explore in the future.

Levine hypothesized that the sympathetic nervous system’s activity plays a role.

“We can categorize things like anger and stress together,” he said. “We know in the short-term, episodes like that can increase adrenaline levels and sympathetic tone. Your heart rate goes up, your blood pressure goes up, your body releases adrenaline, and these can lead to increased oxygen demand by your heart. These can lead to constriction of your coronary arteries.”

But Shimbo, who codirects the Columbia Hypertension Center, is somewhat skeptical of this explanation because the increase in blood pressure in the study was similar for both the anxiety and anger conditions but only the latter was associated with impaired vasodilation.

In his view, a connection with the powerful vasoconstrictor endothelin 1, which is released when a person feels stress, is a more likely explanation. He noted it’s also possible that anger affects vascular function through the inflammatory cascade, the body’s process of responding to trauma by recruiting immune cells and chemical mediators.

The Takeaways

Based on the study, Shimbo said that cardiovascular researchers should distinguish between different negative feelings.

“I was surprised that sadness and anxiety didn’t have negative effects on blood vessel function and anger did,” he said. “I think that tells you that maybe we shouldn’t put all these negative emotions into one bucket.”

Although there’s still a lot to learn about the connection between anger and heart disease, the results of this study provide a basis for additional work.

“Controlled laboratory studies such as this are an important starting point for understanding basic biological mechanisms underlying emotions and health outcomes,” Campo said.

Campo also noted several limitations inherent to the study design. Although focusing on a relatively young and healthy population removes some confounding variables, the results are not widely generalizable.

“The participants were free of any cardiovascular disease; they weren’t taking any cardiovascular medication,” she said, adding that the study wasn’t conducted in a real-life setting and “didn’t examine populations at risk for health disparities.”

Additionally, the study did not examine the chronic effects of anger—but future work could try and tackle this issue. Shimbo is also interested in testing the impact of cognitive behavioral therapy on vascular function or finding a medication to reduce the physiological effects of anger.

In the meantime, clinicians can use these preliminary findings to advise patients on various anger management strategies to protect their long-term cardiovascular health.

For patients who “get chest discomfort when they get angered or stressed, this is a real phenomenon,” Levine said. “It’s not just in their mind. It is good to explore mechanisms where they can learn to better deal with situations that might cause stress, frustration, or anger.”

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Article Information

Published Online: May 31, 2024. doi:10.1001/jama.2024.9776

Conflict of Interest Disclosures: No disclosures were reported.

Wednesday, May 15, 2024

Anger damages blood vessel function, raising heart disease risk

 So it's not helpful getting vein bursting angry at your doctor for KNOWING NOTHING ON GETTING YOU 100% RECOVERED! You'll just have to hope comeuppance hits her/him when they are the 1 in 4 per WHO that has a stroke?  

If your doctor wrote three prescriptions to OT, PT and ST of E.T.(Evaluate and Treat) that means your doctor is no better than a trained chimpanzee as far as getting you recovered!

Anger damages blood vessel function, raising heart disease risk

In a recent study published in the Journal of the American Heart Association, a team of researchers investigated how provoked anger and negative emotions of sadness and anxiety affect endothelial cell health in an attempt to understand the association between core negative emotions and cardiovascular disease events.

Study: Translational Research of the Acute Effects of Negative Emotions on Vascular Endothelial Health: Findings From a Randomized Controlled Study. Image Credit: Tiko Aramyan / ShutterstockStudy: Translational Research of the Acute Effects of Negative Emotions on Vascular Endothelial Health: Findings From a Randomized Controlled Study. Image Credit: Tiko Aramyan / Shutterstock

Background

Cardiovascular disease events are often due to thrombus formations that occur after atherosclerotic plaques break off the arterial walls. These plaques are formed when lipids and other elements in the blood get deposited along the walls of the arteries. Substantial research efforts are dedicated to understanding the underlying mechanisms and determinants of the pathways leading to atherosclerosis.

However, since the 1950s, the link between psychosocial factors and the risk of incident cardiovascular disease events has also gained considerable interest, especially since Friedman and Rosenman found that highly competitive individuals who are work-driven, ambitious, aggressive, and time-conscious are at a higher risk of cardiovascular disease that people with other behavioral patterns.

Numerous studies have also found that acute anger is linked to an increased risk of cardiovascular disease events. However, the underlying mechanisms through which acute anger affects the development and progression of atherosclerosis and cardiovascular disease events remain understudied.

About the study

In the present study, the researchers examined how provoked anger and negative emotions of sadness and anxiety affect endothelial cell health. Vascular homeostasis is primarily regulated by the endothelium, and the endothelial cells are essential for maintaining the integrity of the vasculature and vascular tone. Furthermore, studies have found that dysfunction of the endothelium triggers the development of atherosclerosis and brings about the onset of cardiovascular disease events.

Research also indicates that tasks that cause mental stress, such as public speaking, affect endothelium-dependent vasodilation. A previous non-randomized study by the same team of researchers had also found that anger recall tasks, which involve recollection and reexperiencing prior events that provoked acute anger, have a significant impact on endothelial cell health in injuring endothelial cells, impairing endothelium-dependent vasodilation and disrupting the reparative capacity of endothelial cells.

The present single-blind, randomized controlled study enrolled close to 300 participants, who were randomized to four groups based on four conditions: anger recall tasks, depressive mood recall tasks, anxiety recall tasks, and a neutral emotional condition.

The pre-and post-assessments of endothelial cell health included detecting the circulatory levels of microparticles derived from endothelial cells to assess endothelial cell injury and evaluate flow-mediated endothelium-dependent vasodilation. Additionally, determining the circulatory levels of endothelial progenitor cells derived from the bone marrow provided information on the reparative capacity of endothelial cells.

Participants with chronic medical conditions, including any history of cardiovascular disease or coronary revascularization, as well as risk factors such as diabetes, dyslipidemia, and hypertension, were excluded. Actively smoking participants, those using over-the-counter dietary supplements and medications, or those with a history of personality disorder, mood disorder, or psychosis were also excluded from the study to avoid confounding the results.

Self-administered questionnaires were used to obtain information on cardiovascular disease risk factors, physical activity levels, alcohol consumption, tobacco exposure, and demographic characteristics.

Results

The results showed that even a short-term provocation of anger impaired endothelium-dependent vasodilation and had a negative impact on endothelial cell health. The study also reported that the tasks to induce negative emotions were extremely effective in provoking the required negative emotion, confirming the effectiveness of this procedure.

The researchers found that compared to neutral emotions, the feelings of provoked anger led to the impairment of the reactive hyperemia index score between 0 and 40 minutes. This score measures the excess of blood supply to a region or organ and is an indicator of endothelial function. The impairment in the score was also not observed beyond 40 minutes post-induction of anger, highlighting the acute effects of provoked anger on endothelial function.

Furthermore, compared to the neutral emotional condition, feelings of sadness or anxiety did not bring about any significant changes in the reactive hyperemia index score. The findings linked to provoked anger and the reactive hyperemia index score also did not change when adjusted for visual analog scale ratings, indicating that nonspecific feelings of sadness or anxiety did not influence the association between provoked anger and endothelial cell health. No changes were observed in the endothelial cell-derived microparticles and endothelial progenitor cells in relation to any of the emotion induction tasks.

Conclusions

Overall, the study found that provoked anger acutely impacted endothelial cell health by impairing endothelium-dependent vasodilation. Other negative emotions, such as sadness and anxiety, do not have a similar effect on endothelial function. These findings provide a better understanding of the biological mechanisms through which core negative emotions increase the risk of cardiovascular disease events.

Journal reference:
  • Daichi S., Cohen, M. T., McGoldrick, M., Ipek Ensari, Diaz, K. M., Fu, J., Duran, A. T., Zhao, S., Suls, J. M., Burg, M. M., & Chaplin, W. F. (n.d.). Translational research of the acute effects of negative emotions on vascular endothelial health: Findings from a randomized controlled study. Journal of the American Heart Association, DOI: 10.1161/JAHA.123.032698, https://www.ahajournals.org/doi/full/10.1161/JAHA.123.032698