Although most people survive a heart attackTrusted Source initially, the risk of death significantly increases over the following years.
In fact, 65% of peopleTrusted Source who have a heart attack over the age of 65 die within eight years of the initial incident. This is at least partly because while a person may survive an initial heart attack, the heart attack itself, which leads to the heart tissue being deprived of oxygen and then dying, does not regenerate in adult humans.
In a recent animal study, researchers identified a mechanism that allowed them to treat heart tissue and make healthy mice’s hearts more resilient before a heart attack.
The study’s results appear in Nature Cardiovascular Research.
Prof. James Leiper, Ph.D., Associate Medical Director at the British Heart Foundation and Professor of Molecular Medicine in the School of Cardiovascular and Metabolic Health at the University of Glasgow, U.K. told Medical News Today in an email:
“Most heart attacks are caused by coronary artery disease which can cause your coronary arteries to become narrowed. The narrowing is due to a gradual buildup of fatty deposits called atheroma. If a piece of atheroma breaks off, a blood clot forms around this to try and repair the damage to the artery wall. This clot can then block your coronary arteries causing the heart muscle to be starved of blood, oxygen, and vital nutrients, leading to heart muscle death.
The amount of damage to the heart muscle depends on the size of the area supplied by the blocked artery. As heart muscle is unable to regenerate it never fully repairs. Instead, scar tissue forms in place of healthy cardiac muscle.”
Cardiomyocytes are a type of cell in the heart that is responsible for the contraction of the muscle. This contraction of the muscle is essential for the heart to be able to squeeze blood around the body, in response to electrical signaling that maintains the heartbeat. When these cells are damaged in a heart attack, the heart loses some of its ability to squeeze blood around the body as effectively.
While cardiomyocytes are able to proliferate in human fetuses, this ability is lost in mature adult humans. It is believed this is partly due to an evolutionary trade-off that sees the ability of mature cardiomyocytes to proliferate decline with contractile strength. This means damage caused by events such as heart attacks can not be corrected.
The stages of maturation through which cardiomyocytes go from fetal to adult cells are the focus of much research. Because cardiomyocytes can not proliferate after the damage caused by a heart attack, research has been done on how cardiomyocytes can be dedifferentiated back a stage, to one where they are able to proliferate. Elucidating the mechanisms around this could provide information about how heart tissue damage could be reversed.
However, previous research into dedifferentiated cardiomyocytes has shown that deleterious and lethal effects of irreversible dedifferentiation occur. This is most likely due to the fact that dedifferentiated cells could become proliferative in a way that is similar to cancer.
It has been hoped that redifferentiation of cardiomyocytes back to the state they were in before differentiation, could avoid some of these complications. However, it has been unclear if the potential beneficial effects of previous differentiation to a more proliferative state would remain.
Researchers in Dr. Eldad Tzahor’s lab in the Weizmann Institute of Science Molecular Cell Biology Department, previously identifiedTrusted Source that when a particular protein ERBB2, coded for by the ERBB2 gene was over-expressed, dedifferentiation, occurred. However, the cardiomyocytes in this dedifferentiated, more proliferative state had a limited ability to contract. Researchers then observed that when overexpression was stopped, the cardiomyocytes underwent redifferentiation and went back to their original contractile ability, and cardiac performance improved.
In the lab’s latest research, led by Dr. Avraham Shakked, Ph.D., they sought to investigate the mechanism behind this gene and protein and the longevity of its effects. They showed that when a transgenic mouse that had its ERBB2 gene temporarily activated at 3 months old had a heart attack 5 months later, it recovered.
This demonstrated that redifferentiated cardiomyocytes maintained some of their proliferative, and therefore healing capacity.
This was the most exciting finding for the team, lead author Dr. Avraham Shakked told MNT in an interview:
“Perhaps the most exciting is the cardioprotective effect of this whole sequence of events that we weren’t really expecting to find or see at all, and actually that has the most potential impact at some point in the future.”
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The next steps for the team would involve elucidating the mechanism further. “One of the things that we’ll do is we’ll actually try and look into the mechanism behind that protection. Because if you can isolate the causative agent with a causative effect, then you don’t necessarily have to undergo a [dedifferentiation and redifferentiation] DR cycle, which could be quite invasive, or quite dramatic.
“If you know exactly what it was then you could probably be a lot more precise in achieving the same result,” he said.
The team had several hypotheses about what could be behind this mechanism and wanted to test them one by one, he said. Seeing if the findings could be replicated in non-transgenic mice or larger mammals, such as pigs, would be necessary before considering clinical applications in humans, he explained.
Prof. Mauro Giacca, Professor of Cardiovascular Sciences at King’s College London told MNT in an email: “The issue of understanding whether cardiomyocytes return to a physiological, differentiated state after being pushed to proliferate is a key question for clinical cardiac regeneration, and the results obtained by the Tzahor group in their elegant model are quite comforting in this respect. What was less expected is the issue of “rejuvenation” of these cardiomyocytes, which however makes a lot of sense, as replication requires extensive rearrangement of the epigenetic landscape of cardiomyocytes. This is an added bonus to the cardiac regeneration!”
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By Hannah Flynn on March 20, 2023 — Fact checked by Jill Seladi-Schulman, Ph.D.
A new study reports, for the first time, the effect of poor sleep on the longevity of a person’s cardiovascular health.
Researchers from the University of Sydney in Australia and the University of Southern Denmark analyzed the sleeping experiences and cardiovascular medical histories of 308,683 middle-aged adults.
The study found that sleep disorders are associated with a significant reduction in the number of years of cardiac, or heart, health a person experiences.
Included in the study were clinical sleep disorders such as insomnia and breathing-related disorders, as well as a range of other sleep-related issues, such as schedule/ chronotypeTrusted Source (sleep type) conflicts, snoring, and daytime sleepiness.
The two most common breathing-related sleep disorders considered in the study were central sleep apnea and obstructive sleep apnea.
The analysis revealed that breathing-related sleep disorders were linked to a shortening of a person’s heart-healthy lifespan by around 7 years.
The study appears in BMC MedicineTrusted Source.
For women, breathing-related sleep disorders were associated with a 7.32-year reduction in heart-healthy years, and 6.73 years for men.
People who slept poorly, according to the study’s definition, saw an average 2-year reduction in cardiac health.
The study explores the many types of sleep problems and their effect on heart health.
“Sleep is multidimensional and complex,” study co-author Prof. Emmanuel Stamatakis told Medical News Today.
“Our study suggests that it needs to be addressed holistically, and not to limit the discussion to, e.g., sleep duration only,” he noted.
The study’s authors hope it encourages cardiologists and other doctors to bring up the topic of sleep with patients, and work with them to resolve issues that may affect heart health in the long term.
Beyond its long-term health effects, poor sleep can impact people’s daily lives in many ways.
Being overtired increases the risk of accidents due to slower reaction times and lapses of attention, noted Dr. Jonathan Cedernaes, a sleep specialist from Uppsala University in Sweden, who was not involved in the study.
In addition, it may degrade a person’s daily physical performance, impair metabolic function, and promote inflammation, he added. Bad moods, irritability, and an inability to concentrate are all hallmarks of not getting enough sleep.
”We all suffer from poor sleep from time to time, but it’s when it becomes chronic that it may become an issue to worry about — that is when one should consider seeking professional help from healthcare providers,” said Dr. Cedernaes.
Prof. Stamatakis suggested that the especially negative association between breathing-related sleep disorders and cardiac health may have to do with common issues underlying both.
“Breathing-related sleep disorders are caused to a large extent by established cardiovascular risk factors such as obesity and physical inactivity,” he pointed out.
Sleep-disordered breathing can also worsen sleep all by itself, resulting in more fragmented, and thus less restorative, sleep, noted Dr. Cedernaes.
He added that poor sleep has also been linked to abnormal regulation of the cardiovascular system, including the heart and blood vessels, as well as increased inflammation, blood pressure dysregulation, and a disruption of the sympathetic nervous system.
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In the current study, the participants’ sleeping histories were either self-reported or submitted by clinicians. The two types of data were analyzed separately.
In research, there are always concerns about the accuracy of self-reported data. In this case, people may, for example, be asked to assess snoring they themselves do not hear. Prof. Stamatakis said that, nonetheless, self-reported sleep data generally capture the related health risks fairly well.
However, he cautioned that “[b]ecause of compromised accuracy, they [doctors] are bound to underestimate the true health consequences of poor sleep.”
Clinically observed breathing-related disorders reported by general practitioners or hospital doctors are less susceptible to measurement errors.
“This higher measurement accuracy is perhaps one of the reasons why breathing-related sleep disorders appear to have [such] dramatic effects on life expectancy and compromised cardiovascular health.”
– Prof. Emmanuel Stamatakis
The researchers assigned each individual a composite sleep score, ranking them as poor sleepers, intermediate sleepers, or healthy sleepers. Clinically diagnosed conditions — insomnia, sleep-related breathing disorders, and other sleep disorders — were considered separately.
Dr. Cedernaes applauded the use of multiple sleep questions in recording participants’ experiences, as it may make the capture of more forms of sleep disruption likely.
However, it is difficult to design a perfect sleep questionnaire, he pointed out. “For instance,” he said, “the questions don’t separate naps versus nighttime sleep, nor weekday versus weekend sleep.”
Dr. Cedernaes suggested that dividing existing inquiries into more specific subquestions may produce different results.
While this is the first study to specifically investigate a loss of healthy cardiovascular years due to sleep issues, its findings are supported by previous research, said Dr. Cedernaes. In addition, earlier studies have been backed up by well-controlled interventions.
Fortunately, it has also been shown that “extending sleep — or even taking a nap — can improve such parameters,” the researcher noted.
For people with sleep issues of any kind, the study underscores the value of partnering with one’s physician to identify solutions, especially if one is receiving cardiological care.
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