Category: Cardiovascular Disease

Categories : Cardiovascular Disease PaediatricsTags :

Breaking up Sedentary Time with Light Exercise Lowers BP

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More than six sedentary hours per day from childhood through young adulthood may cause an excess increase of 4mmHg in systolic blood pressure, a new study shows. Continuously engaging in light physical activity (LPA) significantly mitigated the rise in blood pressure – while longer bouts of more vigorous exercise . The results were published in the prestigious Journal of Cachexia, Sarcopenia and Muscle.

In the present study, a collaboration between the Universities of Bristol and Exeter, and the University of Eastern Finland, 2513 children drawn from the Children of the 90s cohort were followed up from age 11 until 24 years. At baseline, the children spent six hours per day sedentary, six hours per day engaging in LPA, and approximately 55 minutes per day in moderate-to-vigorous physical activity (MVPA). At follow-up in young adulthood, nine hours per day were spent sedentary, three hours per day in LPA, and approximately 50 minutes per day in MVPA. 

The average blood pressure in childhood was 106/56mmHg which increased to 117/67mmHg in young adulthood, partly due to normal physiological development. Persistent increase in sedentary time from age 11 through 24 years was associated with an average of 4mmHg excess increase in systolic blood pressure. Participating in LPA from childhood lowered the final level by 3mmHg, but engaging in MVPA had no blood pressure-lowering effect. 

“Furthermore, when 10 minutes out of every hour spent sedentary was  replaced with an equal amount of LPA from childhood through young adulthood in a simulation model, systolic blood pressure decreased by 3mmHg and diastolic blood pressure by 2mmHg. This is significant, as it has been reported in adults that a systolic blood pressure reduction of 5mmHg decreases the risk of heart attack and stroke by ten percent,” says Andrew Agbaje, an award-winning physician and associate professor (docent) of Clinical Epidemiology and Child Health at the University of Eastern Finland.

The current study is the largest and the longest follow-up of accelerometer-measured movement behaviour and blood pressure progression in youth in the world. Measurements of blood pressure, sedentary time, LPA and, MVPA were taken at ages 11, 15, and 24 years. The children’s fasting blood samples were also repeatedly measured for low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, glucose, insulin, and high-sensitivity C-reactive protein. Heart rate, socio-economic status, family history of cardiovascular disease, smoking status as well as dual-energy X-ray absorptiometry measured fat mass and lean mass were accounted for in the analyses. 

“We have earlier shown that elevated blood pressure and hypertension in adolescence increase the risk of premature cardiac damage in young adulthood. The identification of childhood sedentariness as a potential cause of elevated blood pressure and hypertension with LPA as an effective antidote is of clinical and public health significance. Several MVPA-based randomised controlled trials in the young population have been unsuccessful in lowering blood pressure. We noted an MVPA-induced increase in muscle mass enhanced a physiologic increase in blood pressure explaining why earlier MVPA-based randomised clinical trials were unsuccessful,” says Agbaje.

Source: University of Eastern Finland

Categories : Cardiovascular Disease ExerciseTags :

Even Moderate Amounts of Exercise May Reduce Risk for Atrial Fibrillation

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Adding an extra hour every week of physical activity may lower the chance of developing the most common type of irregular heartbeat (arryhthmia) by 11%, a new study shows.

Led by researchers at NYU Langone Health, the investigation focused on atrial fibrillation. While past studies have linked exercise to reduced risk of this type of arrhythmia, nearly all of these analyses have relied on participants’ often inaccurate estimates of their own activity levels, the authors say.

To avert this flaw, the current study team used data recorded from the fitness tracker Fitbit to objectively measure physical activity in more than 6000 men and women across the United States. The results showed that those with higher amounts of weekly physical activity were less likely to develop atrial fibrillation. Notably, the researchers say, even modest amounts of moderate to vigorous exercise, which can range from taking a brisk walk or cleaning the house to swimming laps or jogging, were associated with reduced risk.

Specifically, study participants who averaged between 2.5 and 5 hours per week, the minimum amount recommended by the American Heart Association, showed a 60% lower risk of developing atrial fibrillation. Those who averaged greater than 5 hours had a slightly greater (65%) reduction.

“Our findings make clear that you do not need to start running marathons to help prevent atrial fibrillation and other forms of heart disease,” said preventive cardiologist Sean P. Heffron, MD, the study senior author. “Just keeping moderately active can, over time, add up to major benefits for maintaining a healthy heart,” added Dr Heffron, an assistant professor in the Department of Medicine at NYU Grossman School of Medicine.

Dr. Heffron notes that in the sole earlier study that used activity monitors to investigate atrial fibrillation, researchers provided Fitbit-style monitors to the participants and tracked them for only a week, an approach that may not have accurately captured their normal workout habits. The new investigation, which the authors say is the largest of its kind to date, assessed participants for a full year and included only those who already owned the devices.

A report on the findings will be presented at the annual meeting of the American Heart Association on November 16.

From data collected as part of the All of Us Research Program, the authors of the current study assessed physical activity in the subset (6086 people) who used a Fitbit device and permitted their Fitbit and electronic health records to be linked to their All of Us data. The team tracked activity information for a year as a baseline and then followed up for another five years to identify those who were diagnosed with atrial fibrillation. The researchers also took into account factors known to contribute to the condition, such as age, sex, and a history of high blood pressure.

“These results highlight the value of Fitbits and similar monitors in medical research,” said study lead author Souptik Barua, PhD, an assistant professor in the Department of Medicine at NYU Grossman School of Medicine. “By offering an objective way to measure exercise for years at a time, these tools can provide deeper insight into how different patterns of activity can impact health.”

For example, says Dr Barua, the research team next plans to explore whether working out in the morning or at night may have different effects on heart health.

He cautions that since many Fitbit owners in the study were college-educated White women, the investigation assessed a less-diverse group than that of the overall All of Us population. The program is now providing free devices to participants in underrepresented communities for future investigations.

Dr. Barua also cautions that the study was not designed to tell whether exercise alone directly reduced the risk of atrial fibrillation, nor to detect how that might come about or what other factors, such as income or educational status, might be in play in the reduced risk. However, the association between exercise “doses” and the development of the condition in the study participants was strong.

Source: NYU Langone Health / NYU Grossman School of Medicine

Categories : Cardiovascular Disease PaediatricsTags :

Adequate Sleep Significantly Reduces Hypertension Risk in Teens

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Adolescents who meet the recommended guidelines of nine to 11 hours of sleep per day were shown to have a significantly lower risk of hypertension, according to a new study from UTHealth Houston.  

Recently published in the Journal of the American Heart Association, the research revealed that adolescents had a 37% lower risk of developing incidents of high blood pressure by meeting healthy sleep patterns, and underscoring the importance of adequate sleep behaviour. The research further explored the impact of environmental factors potentially impacting sleep.  

“Disrupted sleep can lead to changes in the body’s stress response, including elevated levels of stress hormones like cortisol, which in turn can increase blood pressure,” said first author Augusto César Ferreira De Moraes, PhD, assistant professor in the Department of Epidemiology at UTHealth Houston School of Public Health. 

De Moraes and his team analysed data from 3320 adolescents across the US to investigate incidents of high blood pressure during nighttime sleep cycles. Scientists identified a rise in hypertension incidents over two data periods, 2018-2020 and 2020-2022, showing an increase from 1.7% to 2.9%. The data included blood pressure readings and Fitbit assessments, which measured total sleep time and REM sleep duration at night. The study’s design analysed covariates such as Fitbit-tracked sleep, blood pressure, and neighbourhood noise by residential geocodes, allowing for a thorough examination of environmental noise exposure for each participant. 

Neighbourhood/community noise was not significantly associated with the incidence of hypertension. Environmental factors, such as neighbourhood noise, point to the need for longer-term studies to investigate the relationship between sleep health and hypertension, particularly in relation to socioeconomic status, stress levels, and genetic predispositions. 

The study emphasises the importance of improved sleep behaviours and meeting recommendations. “Consistent sleep schedules, minimising screen time before bed, and creating a calm, quiet sleep environment can all contribute to better sleep quality,” advises Martin Ma, MPH, second author of the study and recent graduate of the school. “Although environmental noise didn’t directly affect hypertension in this study, maintaining a quiet and restful sleep environment is still important for overall well-being.” 

Source: University of Texas Health Science Center at Houston

Categories : Cardiovascular Disease Emergency MedicineTags :

Bystander CPR up to 10 Minutes after Cardiac Arrest may Protect Brain Function

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The sooner a lay rescuer (bystander) starts cardiopulmonary resuscitation (CPR) on a person having a cardiac arrest at home or in public, up to 10 minutes after the arrest, the better the chances of saving the person’s life and protecting their brain function, according to preliminary research to be presented at the American Heart Association’s Resuscitation Science Symposium 2024.

Cardiac arrest, which occurs when the heart malfunctions and abruptly stops beating, is often fatal without quick medical attention such as CPR to increase blood flow to the heart and brain. More than 357 000 out-of-hospital cardiac arrests happen each year in the US, with a 9.3% survival rate. “Our findings reinforce that every second counts when starting bystander CPR and even a few minutes delay can make a big difference,” said first author Evan O’Keefe, MD, a cardiovascular fellow at Saint Luke’s Mid America Heart Institute and the University of Missouri-Kansas City. “If you see someone in need of CPR, don’t dwell on how long they’ve been down, your quick actions could save their life.”

The study analysed nearly 200 000 cases of witnessed out-of-hospital cardiac arrest to determine whether initiating CPR within different time windows, compared to outcomes with no bystander CPR administered, made a difference in survival and brain function after hospital discharge.

“We found that people who received bystander CPR within the first few minutes of their cardiac arrest were much more likely to survive and have better brain function than those who didn’t,” O’Keefe said. “The longer it took for CPR to start, the less survival benefit one received. However, even when CPR was started up to 10 minutes after cardiac arrest, there was still a significant survival benefit compared to individuals who did not receive CPR from a bystander.”

Results also found: 

  • People who received CPR within two minutes of out-of-hospital cardiac arrest had an 81% higher rate of survival to release from the hospital and 95% higher rate of surviving without significant brain damage compared to people who did not receive bystander CPR.
  • Even people who received bystander CPR up to 10 minutes after cardiac arrest were 19% more likely to survive to hospital discharge and 22% more likely to have a favorable neurological outcome than those who did not receive bystander CPR at all.
  • For those who did not receive bystander CPR, about 12% survived to be released from the hospital, and more than 9% survived without significant brain damage or major disabilities. When bystander CPR was initiated more than 10 minutes after cardiac arrest, bystander CPR, compared to not receiving the lifesaving assistance, was no longer associated with improved survival.

“These results highlight the critical importance of quick action in emergencies. It suggests that we need to focus on teaching more people how to perform CPR, and we also need to emphasise ways to get help to those suffering cardiac arrest faster,” O’Keefe said. “This might include more widespread CPR training programs, as well as better public access to automated external defibrillators (AEDs) and improved dispatch systems.”

O’Keefe noted that future research could explore how technology (like apps that alert nearby trained bystanders or alert dispatchers to likely cardiac arrest) may help to reduce the time to first intervention, information that could be important for emergency dispatchers and policymakers in the development of public interventions for cardiac arrest.

“This study highlights the need for prompt recognition and treatment of cardiac arrest by bystanders. Time is of the essence when a cardiac arrest occurs, and late interventions can be as ineffective as no intervention. Community education and empowerment are critical for us to save lives,” said American Heart Association volunteer expert Anezi Uzendu, MD, an interventional cardiologist at the University of Texas Southwestern Medical Center in Dallas and a cardiac arrest survivor.

A limitation of the study includes that the average time of arrival for emergency medical technicians (EMTs) to the person having cardiac arrest was roughly 10 minutes. This means that in this study, the people who received bystander CPR 10 minutes after their cardiac arrest were likely being compared to a group receiving professional medical attention.

Study details and background:

  • The study identified 160 822 witnessed out-of-hospital cardiac arrests that occurred from 2013-2022.  Among the people whose data was analysed, the average age was 64 years old and about 34% were women.
  • Researchers used data from the Cardiac Arrest Registry to Enhance Survival (CARES), a national, web-based health registry focused on helping communities improve care for and survival of out-of-hospital cardiac arrest.
  • The research categorized time to initiation of bystander CPR in two-minute intervals and analysed the link between each time interval, compared to the group who did not receive CPR, with survival to hospital discharge and favourable neurological survival, or surviving with minor disabilities.

Source: American Heart Association

Categories : Cardiovascular Disease Mental HealthTags :

Beta Blockers may Also Cause Depression for Cardiac Patients

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Patients who have had a heart attack are typically treated using beta blockers. According to a Swedish study conducted earlier this year, this drug is unlikely to be needed for those heart patients who have a normal pumping ability. Now a sub-study at Uppsala University shows that there is also a risk that these patients will become depressed by the treatment.

“We found that beta blockers led to slightly higher levels of depression symptoms in patients who had had a heart attack but were not suffering from heart failure. At the same time, beta blockers have no life-sustaining function for this group of patients,” says Philip Leissner, a doctoral student in cardiac psychology and the study’s first author. The study was published in European Heart Journal Acute Cardiovascular Care.

Beta blockers are drugs that block the effects of adrenaline on the heart and have been used for decades as a basic treatment for all heart attack patients. In recent years, their importance has started to be questioned as new, successful treatments have begun to be developed. This is mainly the case for heart attack patients who do not suffer from heart failure.

The researchers wanted to look at the side effects of beta blockers, that is, whether they affect anxiety and depression levels. This is because older research and clinical experience suggests that beta blockers are linked to negative side effects such as depression, difficulty sleeping and nightmares.

Earlier this year, a major national study was conducted in Sweden, which found that those who received beta-blocking drugs were not protected from relapse or death compared to those who did not receive the drug. Leissner and his colleagues based their research on these findings and conducted a sub-study. It ran from 2018 to 2023 and involved 806 patients who had had a heart attack but no problems with heart failure. Half were given beta blockers and the other half were not. About 100 of the patients receiving beta blockers had been taking them since before the study, and the researchers observed more severe symptoms of depression in them.

“Most doctors used to give beta blockers even to patients without heart failure, but as the evidence in favour of doing so is no longer so strong, this should be reconsidered. We could see that some of these patients appear to be more at risk of depression. If the drug doesn’t make a difference to their heart, then they are taking it unnecessarily and at risk of becoming depressed,” adds Leissner.

Source: Uppsala University

Categories : Cardiovascular Disease Emergency MedicineTags :

Defibrillation Using 1/1000th the Energy could be Possible

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Researchers from Sergio Arboleda University in Colombia and the Georgia Institute of Technology in the US used an electrophysiological computer model of the heart’s electrical circuits to examine the effect of the applied voltage field in multiple fibrillation-defibrillation scenarios. Their research, published in the interdisciplinary journal Chaos, discovered that far less energy is needed than is currently used in state-of-the-art defibrillation techniques.

“The results were not at all what we expected. We learned the mechanism for ultra-low-energy defibrillation is not related to synchronisation of the excitation waves like we thought, but is instead related to whether the waves manage to propagate across regions of the tissue which have not had the time to fully recover from a previous excitation,” author Roman Grigoriev said. “Our focus was on finding the optimal variation in time of the applied electric field over an extended time interval. Since the length of the time interval is not known a priori, it was incremented until a defibrillating protocol was found.”

The authors applied an adjoint optimization method, which aims to achieve a desired result, defibrillation in this case, by solving the electrophysiologic model for a given voltage input and looping backward through time to determine the correction to the voltage profile that will successfully defibrillate irregular heart activity while reducing the energy the most.

Energy reduction in defibrillation devices is an active area of research. While defibrillators are often successful at ending dangerous arrhythmias in patients, they are painful and cause damage to the cardiac tissue.

“Existing low-energy defibrillation protocols yield only a moderate reduction in tissue damage and pain,” Grigoriev said. “Our study shows these can be completely eliminated. Conventional protocols require substantial power for implantable defibrillators-cardioverters (ICDs), and replacement surgeries carry substantial health risks.”

In a normal rhythm, electrochemical waves triggered by pacemaker cells at the top of the atria propagate through the heart, causing synchronised contractions. During arrhythmias, such as fibrillation, the excitation waves start to quickly rotate instead of propagating through and leaving the tissue, as in normal rhythm.

“Under some conditions, an excitation wave may or may not be able to propagate through the tissue. This is called the ‘vulnerable window,’” Grigoriev said. “The outcome depends on very small changes in the timing of the excitation wave or very small external perturbations.

“The mechanism of ultra-low-energy defibrillation we uncovered exploits this sensitivity. Varying the electrical field profile over a relatively long time interval allows blocking the propagation of the rotating excitation waves through the ‘sensitive’ regions of tissue, successfully terminating the irregular electric activity in the heart.”

Source: American Institute of Physics

Categories : Cardiovascular Disease ExerciseTags :

An Extra Five Minutes of Exercise a Day could Reduce Blood Pressure

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New research suggests that adding a small amount of daily physical activity, such as uphill walking or stair-climbing, may help to lower blood pressure. The findings were published in Circulation. 

Just five minutes of activity a day was estimated to potentially reduce blood pressure, while replacing sedentary behaviours with 20–27 minutes of exercise per day, including uphill walking, stair-climbing, running and cycling, was also estimated to lead to a clinically meaningful reduction in blood pressure. The study was done by experts from the ProPASS (Prospective Physical Activity, Sitting and Sleep) Consortium, an international academic collaboration led by the University of Sydney and University College London (UCL)

Joint senior author Professor Emmanuel Stamatakis, Director of the ProPASS Consortium said: “High blood pressure is one of the biggest health issues globally, but unlike some major causes of cardiovascular mortality there may be relatively accessible ways to tackle the problem in addition to medication.”

“The finding that doing as little as five extra minutes of exercise per day could be associated with measurably lower blood pressure readings emphasises how powerful short bouts of higher intensity movement could be for blood pressure management.”

The research team analysed health data from 14 761 volunteers in five countries to see how replacing one type of movement behaviour with another across the day is associated with blood pressure.

Each participant used a wearable accelerometer device on their thigh to measure their activity and blood pressure throughout the day and night. 

Daily activity was split into six categories: sleep, sedentary behaviour (such as sitting), slow walking, fast walking, standing, and more vigorous exercise such as running, cycling or stair climbing.

The team modelled statistically what would happen if an individual changed various amounts of one behaviour for another in order to estimate the effect on blood pressure for each scenario and found that replacing sedentary behaviour with 20-27 minutes of exercise per day could potentially reduce cardiovascular disease by up to 28 percent at a population level.

First author Dr Jo Blodgett from UCL said: “Our findings suggest that, for most people, exercise is key to reducing blood pressure, rather than less strenuous forms of movement such as walking.

“The good news is that whatever your physical ability, it doesn’t take long to have a positive effect on blood pressure. What’s unique about our exercise variable is that it includes all exercise-like activities, from running for a bus or a short cycling errand, many of which can be integrated into daily routines.

“For those who don’t do a lot of exercise, walking did still have some positive benefits for blood pressure. But if you want to change your blood pressure, putting more demand on the cardiovascular system through exercise will have the greatest effect.”

Professor Mark Hamer, joint senior author of the study and ProPASS Deputy Director from UCL, said: “Our findings show how powerful research platforms like the ProPASS consortium are for identifying relatively subtle patterns of exercise, sleep, and sedentary behaviour, that have  significant clinical and public health importance.”

Source: University of Sydney

Categories : Cardiovascular Disease Emergency MedicineTags :

Two Types of Bloodstream Access in Heart Attacks are Equally Effective

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There is no difference in the effectiveness of the two most commonly used methods for administering medication during out-of-hospital cardiac arrest, according to a large new clinical study published in NEJM.

This is shown in a large new clinical study from Aarhus University and Prehospital Services, Region Midtjylland, which compared two ways of accessing the bloodstream: a standard needle in a vein (venous catheter) and a so-called intraosseous needle, which is inserted into the bone marrow.

“When a person suffers cardiac arrest outside the hospital, it is crucial to quickly access the bloodstream to administer life-saving medication. We investigated which method is best,” explains Lars Wiuff Andersen, professor and physician at the Department of Clinical Medicine, Aarhus University, Prehospital Services, Region Midtjylland, and Aarhus University Hospital.

Venous catheter or intraosseous needle?

Until now, healthcare professionals have preferred using a venous catheter, but it can be difficult to place as veins may collapse during cardiac arrest.

The intraosseous needle, inserted either into the shinbone or upper arm, can be faster and easier to use in an emergency.

Therefore, it’s interesting to investigate the effectiveness of both methods, explains Lars Wiuff Andersen.

The study, based on data from nearly 1500 cardiac arrest patients across Denmark, showed that about 30 percent of patients in both groups had their blood circulation restored.

“The two methods proved to be equally effective in restoring blood circulation and saving lives. There was no difference in the patients’ survival or quality of life,” explains Mikael Fink Vallentin, associate professor at the Department of Clinical Medicine and Prehospital Services, Region Midtjylland, and co-lead author of the study.

May change guidelines

According to the researchers behind the study, the results may impact future guidelines, which previously recommended venous catheters as the first choice.

However, Lars Wiuff Andersen notes that it is too early to say exactly how the guidelines will change.

“Our data must be considered alongside a large clinical trial from the UK, which is being published simultaneously with our study. Combined, these two trials will likely influence guidelines for cardiac arrest treatment, but a thorough review of the results will be needed,” he says.

More unanswered questions

There are still several unanswered questions, especially regarding whether specific groups of cardiac arrest patients benefit more from one method than the other.

The researchers are continuing to analyse and compare their own data with data from the UK trial.

The Danish research team has already planned a new, large clinical trial to investigate which method is best for delivering electric shocks during cardiac arrest.

“We hope to gain even more answers on how to best save lives in cardiac arrest in the future,” says Lars Wiuff Andersen.

Source: Aarhus University

Categories : Cardiovascular Disease NeurologyTags :

Heart Attacks Trigger a Greater Need for Sleep to Promote Healing

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A heart attack can trigger a desire to get more sleep, allowing the heart to heal and reduce inflammation as a result of the heart’s special signals to the brain, according to a new Mount Sinai study. This is the first study showing how the heart and brain communicate via the immune system to promote sleep and recovery after a major cardiovascular event.

The novel findings, published in Nature, highlight the importance of increased sleep after a heart attack, and suggest that sufficient sleep should be a focus of post-heart-attack clinical management and care, including in intensive care, where sleep is frequently disrupted, along with cardiac rehabilitation.

“This study is the first to demonstrate that the heart regulates sleep during cardiovascular injury by using the immune system to signal to the brain. Our data show that after a myocardial infarction (heart attack) the brain undergoes profound changes that augment sleep, and that in the weeks following a myocardial infarction, sleep abundance and drive is increased,” says senior author Cameron McAlpine, PhD, Assistant Professor of Medicine (Cardiology), and Neuroscience, at the Icahn School of Medicine at Mount Sinai. “We found that neuro-inflammation and the recruitment of immune cells called monocytes to the brain after a myocardial infarction is a beneficial and adaptive response that increases sleep to enable heart healing and the reduction of damaging cardiac inflammation.”

The researchers from the Cardiovascular Research Institute at Icahn Mount Sinai first used mouse models to discover this phenomenon. They induced heart attacks in half of the mice and performed high-resolution imaging and cell analysis, and used implantable wireless electroencephalogram devices to record electrical signals from their brains and analyse sleep patterns. After the heart attack, they found a three-fold increase in slow-wave sleep, a deep stage of sleep characterized by slow brain waves and reduced muscle activity. This increase in sleep occurred quickly after the heart attack and lasted one week.

When the researchers studied the brains of the mice with heart attacks, they found that immune cells called monocytes were recruited from the blood to the brain and used a protein called tumour necrosis factor (TNF) to activate neurons in an area of the brain called the thalamus, which caused the increase in sleep. This happened within hours after the cardiac event, and none of this occurred in the mice that did not have heart attacks.

The researchers then used sophisticated approaches to manipulate neuron TNF signaling in the thalamus and uncovered that the sleeping brain uses the nervous system to send signals back to the heart to reduce heart stress, promote healing, and decrease heart inflammation after a heart attack. To further identify the function of increased sleep after a heart attack, the researchers also interrupted the sleep of some of the mice. The mice with sleep disruption after a heart attack had an increase in heart sympathetic stress responses and inflammation, leading to slower recovery and healing when compared to mice with undisrupted sleep.

The research team also performed several human studies. The first studied the brains of patients 1–2 days after a heart attack and found an increase in monocytes compared to people without a heart attack or other CVD, mirroring the mice findings. The next analysed the sleep of more than 80 heart attack patients during the four weeks post-event and followed them for two years. The patients were divided into good sleepers and poor sleepers based on the quality of their sleep during the four weeks post-heart attack. The poor sleepers had a worse prognosis; their risk of having another cardiovascular event was twice as high as good sleepers. Additionally, the good sleepers had a significant improvement in heart function while poor sleepers had no or little improvement. 

In another human study, the researchers analysed the impact of five weeks of restricted sleep in 20 healthy adults. Sleep was monitored using electronic devices and the participants kept a sleep diary. During the five-week study period, half the participants slept for the recommended seven to eight hours a night uninterrupted, while the other half restricted their sleep by 1.5 hours each night – either delaying bedtime or waking up early. After the study period, researchers analysed blood monocytes and found similar sympathetic stress signaling and inflammatory responses in the sleep-restricted group as those that were identified in mice.

Source: The Mount Sinai Hospital / Mount Sinai School of Medicine

Categories : Cardiovascular Disease Environmental EffectsTags :

Risk of Cardiovascular Disease Linked to Arsenic in Water

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Long term exposure to arsenic in water may increase cardiovascular disease and especially heart disease risk even at exposure levels below the US regulatory limit (10µg/L) according to a new study in Environmental Health Perspectives. This is the first study to describe exposure-response relationships at concentrations below the current regulatory limit and substantiates that prolonged exposure to arsenic in water contributes to the development of ischaemic heart disease.

The researchers, from Columbia University Mailman School of Public Health, compared various time windows of exposure, finding that the previous decade of water arsenic exposure up to the time of a cardiovascular disease event contributed the greatest risk.

“Our findings shed light on critical time windows of arsenic exposure that contribute to heart disease and inform the ongoing arsenic risk assessment by the EPA. It further reinforces the importance of considering non-cancer outcomes, and specifically cardiovascular disease, which is the number one cause of death in the US and globally,” said Danielle Medgyesi, a doctoral Fellow in the Department of Environmental Health Sciences at Columbia Mailman School. “This study offers resounding proof of the need for regulatory standards in protecting health and provides evidence in support of reducing the current limit to further eliminate significant risk.”

According to the American Heart Association and other leading health agencies, there is substantial evidence that arsenic exposure increases the risk of cardiovascular disease. This includes evidence of risk at high arsenic levels (> 100µg/L) in drinking water. The U.S. Environmental Protection Agency reduced the maximum contaminant level (MCL) for arsenic in community water supplies (CWS) from 50µg/L to 10µg/L beginning in 2006. Even so, drinking water remains an important source of arsenic exposure among CWS users. The natural occurrence of arsenic in groundwater is commonly observed in regions of New England, the upper Midwest, and the West, including California.

To evaluate the relationship between long-term arsenic exposure from CWS and cardiovascular disease, the researchers used statewide healthcare administrative and mortality records collected for the California Teachers Study cohort from enrollment through follow-up (1995-2018), identifying fatal and nonfatal cases of ischemic heart disease and cardiovascular disease. Working closely with collaborators at the California Office of Environmental Health Hazard Assessment (OEHHA), the team gathered water arsenic data from CWS for three decades (1990-2020).

The analysis included 98 250 participants, 6119 ischaemic heart disease cases and 9,936 CVD cases. Excluded were those 85 years of age or older and those with a history of CVD at enrolment. Similar to the proportion of California’s population that relies on CWS (over 90%), most participants resided in areas served by a CWS (92%). Leveraging the extensive years of arsenic data available, the team compared time windows of relatively short-term (3-years) to long-term (10-years to cumulative) average arsenic exposure. The study found decade-long arsenic exposure up to the time of a cardiovascular disease event was associated with the greatest risk, consistent with a study in Chile finding peak mortality of acute myocardial infarction around a decade after a period of very high arsenic exposure. This provides new insights into relevant exposure windows that are critical to the development of ischemic heart disease.

Nearly half (48%) of participants were exposed to an average arsenic concentration below California’s non-cancer public health goal < 1 µg/L. In comparison to this low-exposure group, those exposed to 1 to < 5 µg/L had modestly higher risk of ischaemic heart disease, with increases of 5 to 6%. Risk jumped to 20% among those in the exposure ranges of 5 to < 10 µg/L (or one-half to below the current regulatory limit), and more than doubled to 42% for those exposed to levels at and above the current EPA limit ≥ 10µg/L. The relationship was consistently stronger for ischemic heart disease compared to cardiovascular disease, and no evidence of risk for stroke was found, largely consistent with previous research and the conclusions of the current EPA risk assessment.

These results highlight the serious health consequences not only when community water systems do not meet the current EPA standard but also at levels below the current standard. The study found a substantial 20% risk at arsenic exposures ranging from 5 to < 10 µg/L which affected about 3.2% of participants, suggesting that stronger regulations would provide significant benefits to the population. In line with prior research, the study also found higher arsenic concentrations, including concentrations above the current standard, disproportionally affect Hispanic and Latina populations and residents of lower socioeconomic status neighbourhoods.

“Our results are novel and encourage a renewed discussion of current policy and regulatory standards,” said Tiffany Sanchez, senior author. “However, this also implies that much more research is needed to understand the risks associated with arsenic levels that CWS users currently experience. We believe that the data and methods developed in this study can be used to bolster and inform future studies and can be extended to evaluate other drinking water exposures and health outcomes.”

Source: Columbia University’s Mailman School of Public Health