Category: Cardiovascular Disease

Categories : Cardiovascular Disease New Compounds and TreatmentsTags :

An Experimental Drug to Prevent Post-heart Attack Heart Failure

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Scientists at UCLA have developed a first-of-its-kind experimental therapy that has the potential to enhance heart repair following a heart attack, preventing the onset of heart failure. After a heart attack, the heart’s innate ability to regenerate is limited, causing the muscle to develop scars to maintain its structural integrity. This inflexible scar tissue, however, interferes with the heart’s ability to pump blood, leading to heart failure in many patients – 50% of whom do not survive beyond five years.

The new therapeutic approach aims to improve heart function after a heart attack by blocking a protein called ENPP1, which is responsible for increasing the inflammation and scar tissue formation that exacerbate heart damage. The findings, published in Cell Reports Medicine, could represent a major advance in post-heart attack treatment.

The research was led by senior author Dr Arjun Deb, a professor of medicine and molecular, cell and developmental biology at UCLA.

“Despite the prevalence of heart attacks, therapeutic options have stagnated over the last few decades,” said Deb, who is also a member of the UCLA Broad Stem Cell Research Center. “There are currently no medications specifically designed to make the heart heal or repair better after a heart attack.”

The experimental therapy uses a therapeutic monoclonal antibody engineered by Deb and his team. This targeted drug therapy is designed to mimic human antibodies and inhibit the activity of ENPP1, which Deb had previously established increases in the aftermath of a heart attack.

The researchers found that a single dose of the antibody significantly enhanced heart repair in mice, preventing extensive tissue damage, reducing scar tissue formation and improving cardiac function. Four weeks after a simulated heart attack, only 5% of animals that received the antibody developed severe heart failure, compared with 52% of animals in the control group.

This therapeutic approach could become the first to directly enhance tissue repair in the heart following a heart attack; an advantage over current therapies that focus on preventing further damage but not actively promoting healing. This can be attributed to the way the antibody is designed to target cellular cross-talk, benefitting multiple cell types in the heart, including heart muscle cells, the endothelial cells that form blood vessels, and fibroblasts, which contribute to scar formation. 

Initial findings from preclinical studies also show that the antibody therapy safely decreased scar tissue formation without increasing the risk of heart rupture – a common concern after a heart attack. However, Deb acknowledges that more work is needed to understand potential long-term effects of inhibiting ENPP1, including potential adverse effects on bone mass or bone calcification. 

Deb’s team is now preparing to move this therapy into clinical trials. The team plans to submit an Investigational New Drug, or IND, application to the U.S. Food and Drug Administration this winter with the goal of beginning first-in-human studies in early 2025. These studies will be designed to administer a single dose of the drug in eligible individuals soon after a heart attack, helping the heart repair itself in the critical initial days after the cardiac event.

While the current focus is on heart repair after heart attacks, Deb’s team is also exploring the potential for this therapy to aid in the repair of other vital organs.

“The mechanisms of tissue repair are broadly conserved across organs, so we are examining how this therapeutic might help in other instances of tissue injury,” said Deb, who is also the director of the UCLA Cardiovascular Research Theme at the David Geffen School of Medicine. “Based on its effect on heart repair, this could represent a new class of tissue repair-enhancing drugs.”

Categories : Cardiovascular DiseaseTags :

Standing Time at Work can be Detrimental to Blood Pressure

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A Finnish study found that prolonged standing at work had a negative impact on the research participants’ 24-hour blood pressure. In contrast, spending more time sitting at work was associated with better blood pressure. The study suggests that the type of activity during working hours may be more relevant to 24-hour blood pressure than recreational physical activity.

Regular exercise is important for controlling blood pressure. In particular, more vigorous, aerobic exercise is effective for lowering blood pressure, but also everyday physical activity can have a beneficial impact. Previous studies have shown that exercise in leisure time is more beneficial for the cardiovascular system than physical activity at work, which can even be detrimental to health.

24-hour blood pressure important for cardiovascular health

In the Finnish Retirement and Aging study (FIREA) conducted at the University of Turku, the physical activity of municipal employees approaching retirement age was measured using thigh-worn accelerometers during working hours, leisure time, and days off.

In addition, the research participants used a portable blood pressure monitor that automatically measured their blood pressure every 30 minutes for 24 hours.

“Rather than any single measurement, 24-hour blood pressure is a better indication of how blood pressure stresses the heart and blood vessels throughout the day and night. If blood pressure is slightly high throughout the day and does not fall sufficiently even at night, blood vessels start to stiffen and the heart has to work harder to cope with the increased pressure. Over the years, this can lead to the development of cardiovascular disease,” says Doctoral Researcher Jooa Norha.

Take a break from standing during the workday

The latest results confirm previous findings that physical activity at work can be harmful to the heart and circulatory system.

In particular, prolonged standing can raise blood pressure as the body boosts circulation to the lower limbs by constricting blood vessels and increasing the pumping power of the heart.

“A standing desk can provide a nice change from sitting at the office, but too much standing can be harmful. It’s a good idea to take a break from standing during the work day, either by walking every half an hour or sitting for some parts of the day,” Norha recommends.

Recreational physical activity is also needed

In addition, the results of the study suggest that sedentary work in itself is not necessarily harmful to blood pressure.

Instead, researchers stress the importance of recreational physical activity for both office and construction workers.

“It is good to remember that being physically active at work is not enough on its own. Engaging in diverse physical exercise during leisure time helps to maintain fitness, making work-related strain more manageable. Similarly, employees with predominantly sedentary jobs should ensure that they get enough exercise during their leisure time,” Norha highlights.

Source: University of TYurku

Categories : Cardiovascular DiseaseTags :

The Factors Behind the Shifting Trends of Ischaemic Heart Disease and Stroke

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Incidence of stroke and ischaemic heart disease are declining around the world, except for in a handful of regions, according to research in the open access journal PLOS Global Public Health. Wanghong Xu of Fudan University and colleagues find that in East and West Sub-Saharan Africa, East and Central Asia and Oceania, ischaemic heart disease is increasing, which may be attributed to eight factors that include diet, high BMI, household air pollution and more.

Cardiovascular disease is a leading cause of death and disability worldwide, and ischemic heart disease and stroke accounted for 16% and 11% of total deaths in 2019 respectively. Over time both have decreased in incidence, but the distribution of this decline varies and in some regions there is an upward trend.

The team analysed global data from 1990-2019 for incidence of ischaemic heart disease and stroke and for exposure to 87 potential attributable factors. The authors describe the incidences and trends at a global, regional and national level, and find higher rates of ischaemic heart disease than stroke. Over three decades ischaemic heart disease reduced from 316 to 262 per 100 000 people and stroke declined from 181 to 151 per 100 000. The increases of ischaemic heart disease seen in some regions may be associated with the shifting distribution of eight factors: a diet high in trans-fatty acids; diet low in calcium; high BMI; household air pollution from solid fuels; non-exclusive breastfeeding; occupational ergonomic factors; vitamin A deficiency; and, occupational exposure to particulate matter, gases and fumes, which were determined by the World Bank income levels.

The results indicate how the potential socioeconomic development of some countries is affecting rates of cardiovascular disease and stroke, and that places experiencing rapid economic transitions – and rapidly changing lifestyle changes – may also be experiencing higher rates of disease. This study and provides insight into mechanisms involved and the potential for targeted interventions.

The authors add: “This study profiles the significantly different incidence trends of ischemic heart disease and stroke across countries, identifies eight potential contributors to the disparities, and reveals the pivotal role of socioeconomic development in shaping the country-level associations of the risk factors with the incidences of the two cardiovascular diseases.”

Provided by PLOS

Categories : Cardiovascular Disease Regenerative MedicineTags :

Human Hearts may Possess a Latent Ability to Regenerate Cardiomyocytes

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Right side heart failure. Credit: Scientific Animations CC4.0

After severe heart failure, the ability of the heart to heal by forming new cells is very low. But now Karolinska Institutet researchers found that, after use of a supportive heart pump, the capacity of a damaged heart to repair itself with new cardiomyocytes becomes significantly higher – even greater than that of a healthy heart. This study is published in the journal Circulation.

The ability of the human heart to renew itself by regenerating its muscle cells, myocytes, is very limited. But what happens to this capability when the heart is damaged by severe heart failure has been unknown.

Researchers at Karolinska Institutet have now discovered that after an injury, the rate of cell renewal is even lower than in a healthy heart. Standard-of-care for patients with advanced heart failure is a surgically implanted pump that helps propel blood, a so-called left ventricular assist device (LVAD).

Kick-starting repair

Surprisingly, the researchers found that patients with such a heart pump, who have shown significant improvement in their heart function, can regenerate heart muscle cells at a rate more than six times higher than in healthy hearts.

“The results suggest that there might be a hidden key to kick-start the heart’s own repair mechanism”, says Olaf Bergmann, senior researcher at the Department of Cell and Molecular Biology at Karolinska Institutet and last author of the paper.

The mechanism behind the effect is still unknown and there is not yet any hypothesis to explain it.

“It is difficult to say. In the existing data we cannot find an explanation for the effect, but we will now continue to study this process at a cellular and molecular level,” says Olaf Bergmann.

The findings open the possibility of developing new therapies for patients with serious heart conditions that stimulate the heart’s ability to repair itself after damage. This way, patients wouldn’t have to rely only on heart transplants or other kinds of long-term mechanical support.

“This offers some hope that the recovery after a heart incident can somehow be boosted,” says Olaf Bergmann.

Atomic bombs enable cell age estimation

It is generally difficult to determine the age of cells in the human body and to decide which cells are new and which are old. However, by using a method earlier devised by Jonas Frisén, professor of stem cell research at Karolinska Institutet, the group has been able to count the rate of renewal of myocytes in the heart. The method is based upon the fact that the percentage of radioactive carbon in the atmosphere, and subsequently in our cells, has steadily decreased since the nuclear test ban in 1963. For every following year, there is a little less radioactivity in newly formed cells, which means that they can be ‘dated’. 

Source: Karolinska Institute

Categories : Cardiovascular DiseaseTags :

Tirzepatide Found to Protect against Worsening Heart Failure

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Right side heart failure. Credit: Scientific Animations CC4.0

The diabetes drug tirzepatide can reduce the risk of death or worsening heart failure for patients with heart failure, preserved heart pump function and obesity, new research from UVA Health reveals.

Researchers tested the GLP-1 receptor agonist in the SUMMIT clinical trial, where a total of 731 patients with diastolic heart failure and a body mass index (BMI) of 30 or above were randomised to receive injections of either tirzepatide or a harmless placebo. The researchers then followed the patients for a median period of two years. Tirzepatide is also prescribed as a weight loss drug in certain countries.

During that time, 56 placebo recipients died or suffered worsening heart failure, compared with only 36 of those receiving tirzepatide. Participants taking tirzepatide also lost 11.6% of their body weight.

“This class of drugs continue to show benefits far beyond weight loss,” said researcher Christopher Kramer, MD, chief of UVA Health’s Division of Cardiovascular Medicine. “This drug will become an important part of the armamentarium for patients with obesity-related heart failure and preserved heart function.”

Obesity and heart failure

Obesity is a major contributing factor to heart failure, so Kramer and his collaborators in the SUMMIT trial wanted to see if tirzepatide, a weight-loss drug already approved by the federal Food and Drug Administration, could help. 

The trial found that tirzepatide offered substantial benefits for managing diastolic heart failure, reducing deaths, preventing hospitalizations and generally benefiting recipients’ health and quality of life. For example, recipients saw improvements in how far they could walk in six minutes, as well as substantial decreases in a biological indictor used to measure inflammation and predict risk of serious cardiovascular events.

Side effects seen in the tirzepatide group consisted of gastrointestinal issues such as nausea and diarrhea, and these were mostly mild or moderate, the researchers reported Saturday at a meeting of the American Heart Association in Chicago.

Tirzepatide Findings

Kramer, a cardiovascular imager, also led a magnetic resonance imaging substudy looking at how tirzepatide affected recipients’ heart structure and function. The researchers found beneficial reductions in both left ventricular mass (weight of the heart) and in the amount of surrounding fat tissue. The reduction in LV mass correlated with the reduction in body weight, as well as with decreases in left ventricular volumes.

“This drug is reversing the abnormal properties of the heart brought on by obesity,” Kramer said. “There is much more to these drugs than weight loss alone.”

The findings from these studies by Kramer and his fellow researchers from SUMMIT are being published simultaneous with the American Heart meeting in Chicago in four separate manuscripts, including the New England Journal of Medicine, Nature Medicine, Circulation and the Journal of the American College of Cardiology.

Source: University of Virginia Health System

Categories : Cardiovascular DiseaseTags :

A Link between Heart Shape and Cardiovascular Disease Risk

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Researchers from Queen Mary University of London and other universities have for the first time examined the genetic basis of the heart’s left and right ventricles using advanced 3D imaging and machine learning.

Prior research primarily focused on the heart’s size and volume and specific chambers. By studying both ventricles together, the team was able to capture the more intricate, multi-dimensional aspects of the heart shape.

This new approach of exploring shape has led to the discovery of new heart-associated genes and provided a better understanding of the biological pathways linking heart shape to cardiovascular disease.

Cardiovascular disease is among the leading causes of death in the UK and globally. The findings of this study could change how cardiac disease risk is evaluated. Genetic information related to heart shape can provide a risk score for heart disease, offering potentially early and more tailored assessment in clinical settings.

“This study provides new information on how we think about heart disease risk,” said Patricia B. Munroe, Professor of Molecular Medicine at Queen Mary and co-author of the study. “We’ve long known that size and volume of the heart matter, but by examining shape, we’re uncovering new insights into genetic risks. This discovery could provide valuable additional tools for clinicians to predict disease earlier and with more precision.”

The team used cardiovascular MRI images from over 40 000 individuals from the UK Biobank to create 3D models of the ventricles. Through statistical analysis, they identified 11 shape dimensions that describe the primary variations in heart shape.

Subsequent genetic analysis found 45 specific areas in the human genome linked to different heart shapes. Fourteen of these areas had not been previously known to influence heart traits.

“This study sets an important foundation for the exploration of genetics in both ventricles”, said Dr Richard Burns, Statistical Geneticist at Queen Mary. “The study confirms that combined cardiac shape is influenced by genetics, and demonstrates the usefulness of cardiac shape analysis in both ventricles for predicting individual risk of cardiometabolic diseases alongside established clinical measures.”

This research marks an exciting new chapter in understanding how genetics influence the heart and opens the doors to further studies on how these findings could be integrated into clinical practice, ultimately benefiting millions at risk of heart disease.

Source: Queen Mary University of London

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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Photo by Eren Li

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