Category: Cardiovascular Disease

Categories : Cardiovascular Disease COVIDTags :

Study Explains a Link between COVID and Increased Cardiovascular Risk

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A study published in the journal Nature Cardiovascular Research shows that SARS-CoV-2 can directly infect the arteries of the heart and cause the fatty plaque inside arteries to become highly inflamed, increasing the risk of heart attack and stroke. The findings may help explain why certain people who get COVID have a greater chance of developing cardiovascular disease, or if they already have it, develop more heart-related complications.

In the National Institutes of Health (NIH)-funded study, researchers focused on older people with atherosclerotic plaque, who died from COVID. However, because the researchers found the virus infects and replicates in the arteries no matter the levels of plaque, the findings could have broader implications for anybody who gets COVID.

“Since the early days of the pandemic, we have known that people who had COVID have an increased risk for cardiovascular disease or stroke up to one year after infection,” said Michelle Olive, PhD, acting associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH. “We believe we have uncovered one of the reasons why.”

Though previous studies have shown that SARS-CoV-2 can directly infect tissues such as the brain and lungs, less was known about its effect on the coronary arteries. Researchers knew that after the virus reaches the cells, the body’s immune system sends in macrophages to help clear the virus. In the arteries, macrophages also help remove cholesterol, and when they become overloaded with cholesterol, they morph into a specialised type of cell called foam cells.

The researchers thought that if SARS-CoV-2 could directly infect arterial cells, the macrophages that normally are turned loose might increase inflammation in the existing plaque, explained Chiara Giannarelli, MD, PhD, associate professor in the departments of medicine and pathology at New York University’s Grossman School of Medicine and senior author on the study. To test their theory, Giannarelli and her team took tissue from the coronary arteries and plaque of people who had died from COVID and confirmed the virus was in those tissues. Then they took arterial and plaque cells – including macrophages and foam cells – from healthy patients and infected them with SARS-CoV-2 in a lab dish. They found that the virus had also infected those cells and tissues.

Additionally, the researchers found that when they compared the infection rates of SARS-CoV-2, they showed that the virus infects macrophages at a higher rate than other arterial cells. Cholesterol-laden foam cells were the most susceptible to infection and unable to readily clear the virus. This suggested that foam cells might act as a reservoir of SARS-CoV-2 in the atherosclerotic plaque. Having more build-up of plaque, and thus a greater number of foam cells, could increase the severity or persistence of COVID.

The researchers then looked at the predicted inflammation in the plaque after infecting it with the virus. They observed the release of inflammatory cytokines, also known to promote the formation of even more plaque. The cytokines were released by infected macrophages and foam cells. The researchers said this may help explain why people who have underlying plaque buildup and then get COVID may have cardiovascular complications long after getting the infection.  

“This study is incredibly important as it adds to the larger body of work to better understand COVID,” said Olive. “This is just one more study that demonstrates how the virus both infects and causes inflammation in many cells and tissues throughout the body. Ultimately, this is information that will inform future research on both acute and Long COVID.”

Though the findings conclusively show that SARS-CoV-2 can infect and replicate in the macrophages of plaques and arterial cells, they are only relevant to the original strains of SARS-CoV-2 that circulated in New York City between May 2020 and May 2021. The study was conducted in a small cohort of older individuals, all of whom had atherosclerosis and other medical conditions; therefore, the results cannot be generalised to younger, healthy individuals.

Source: National Institutes of Health

Categories : Cardiovascular Disease ExerciseTags :

Yoga Therapy Improves Quality of Life and Cardiovascular Function

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Yoga therapy and lifestyle modifications have been shown to improve heart failure (HF) patients’ quality of life and enhance their cardiovascular function. A new study, presented at the American College of Cardiology Asia 2023 conference, examines the long-term outcomes of yoga therapy to determine the benefit of adding yoga therapy as a complementary treatment in the management of HF. After 12 months, participants with HF receiving yoga therapy continued to show improvement in left ventricular systolic function as well as quality of life.

The study included 75 heart failure patients (aged 30–70 years old) at a tertiary care centre in South India, who underwent coronary intervention, revascularisation or device therapy within in the previous six to 12 months. All of the patients included in the study were less than or equal to New York Heart Association (NYHA) Class III and had been on optimised medical therapy for at least 6 months to 12 months, and had a left ventricular ejection fraction (LVEF) of < 45%.

The interventional group included 35 participants (31 men and 4 women) and 40 (30 men and 10 women) were in the non-interventional (control) group. The interventional group received yoga therapy and guideline-directed medical therapy, while the control group only continued with standard guideline-directed medical therapy. Echocardiographic parameters were compared at various follow-ups to see the impact of yoga therapy on heart failure patients.

“Yoga is a combination of mind-body techniques, which is a set of physical exercises [asana] with breathing techniques [pranayama], relaxation and meditation that can be effectively used to stimulate physical and mental well-being,” said lead author Ajit Singh, PhD, research scientist for the Indian Council for Medical Research at Kasturba Medical College & Hospital, Manipal Academy of Heart Education in Manipal, India. “Our patients observed improvement in systolic blood pressure and heart rate compared to patients who were on medication without yoga.”

Participants in the yoga group were taken to the Department of Yoga at the hospital and an experienced yoga therapist taught selected yoga therapy like pranayama, meditation and relaxation techniques. Each session lasted around 60 minutes and participants were supervised for one week at the training centre before being asked to continue self-administered yoga at home. Those in the yoga group were advised to perform yoga at least five days a week for 12 months. At the training centre all the participants were taught together to perform the same steps, but individual support was available.

Researchers measured quality of life improvements using the World Health Organization Quality of Life questionnaire, which uses 26 questions to evaluate quality of life in four aspects: physical, psychological, social and environmental health. The participants completed the questionnaire at enrolment, as well as at 24 weeks and 48 weeks of follow-up. According to the researchers, the study showed participants in the yoga group had improvement in endurance, strength, balance, symptom stability and quality of life. They also observed that while patients improved physically and psychologically, there was no improvement in social and environmental health.

Echocardiographic parameters did not show any significant differences between the two groups at baseline. At both the six- and 12-month follow-up, improved biventricular systolic function was seen in the interventional (yoga) group compared to the control group. The interventional group also showed substantial improvement in functional outcomes as assessed by NHYA classification.

“This study proves that the addition of yoga therapy to standard medical management of heart failure leads to an improvement in left ventricular systolic function and quality of life in heart failure patients,” Singh said. “Hence, yoga therapy may improve physical well-being and left ventricular function among heart failure patients on guideline-directed optimal medical therapy.”

Source: American College of Cardiology

Categories : Cardiovascular Disease Obstetrics & GynaecologyTags :

Study Links Hot Flashes to Cardiovascular Risk Factors

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It has long been known that hot flashes are linked to a number of adverse health effects. Emerging data suggests an association between them and cardiovascular disease. A new study is the first to link physiologically assessed hot flashes with heightened systemic inflammation – a risk factor for cardiac disease. Study results will be presented during the 2023 Annual Meeting of The Menopause Society in Philadelphia September 27-30.

Vasomotor symptoms, more often referred to as hot flashes, are one of the most common symptoms identified during the menopause transition, with roughly 70% of midlife women reporting them. Not only do they interfere with a woman’s quality of life, but they have also been related to physical health risks, such as cardiovascular disease.

Previous research linking hot flashes with heightened systemic inflammation has relied on self-reporting to document the frequency and severity of the hot flashes. These self-reports of hot flashes are limited as they ask women to recall hot flashes over weeks or longer and may be subject to memory or reporting biases. A new study that included 276 participants from the MsHeart study, however, utilised sternal skin conductance to physiologically assess hot flashes and tested whether more frequent physiologically assessed hot flashes are associated with heightened system inflammation.

While large increases in inflammatory markers indicate acute infection or clinical disease, small and sustained increases of markers of inflammation that are in the physiologically normal range are predictive of later disease risk. For example, small and/or sustained increases in inflammatory biomarkers (conceptualised as heightened levels of systemic inflammation) have been related to plaque development and atherosclerotic cardiovascular disease.

Based on the results, the researchers concluded that physiologically assessed hot flashes during wake were associated with higher levels of a high-sensitivity C-reactive protein, even after adjusting for potential explanatory factors such as age, education, race/ethnicity, body mass index, and oestradiol.

The results will be presented during the Annual Meeting of The Menopause Society as part of the presentation entitled “Physiologically measured vasomotor symptoms and systemic inflammation among midlife women.”

“This is the first study to examine physiologically measured hot flashes in relation to inflammation and adds evidence to a growing body of literature suggesting that hot flashes may signify underlying vascular risk and indicate women who warrant focused cardiovascular disease prevention efforts,” says Mary Carson, MS, lead author from the Department of Psychology at the University of Pittsburgh.

“Since heart disease is the leading cause of death for women in the US, studies like these are especially valuable,” adds Dr Stephanie Faubion, medical director of The Menopause Society. “Healthcare professionals need to ask their patients about their hot flash experiences as they not only interfere with their quality of life but may also indicate other risk factors.”

Source: EurekAlert!

Categories : Cardiovascular Disease Obstetrics & GynaecologyTags :

Ground-breaking Progress in Identifying the Root Cause of Preeclampsia

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Researchers report in Nature Communications that they have made ground-breaking progress towards identifying the root cause and potential therapy for preeclampsia. They identified a toxic protein, cis P-tau, in the blood and placenta of preeclampsia patients. This protein is also linked to the development of memory loss after brain injury or Alzheimer’s.

The pregnancy complication affects up to 8% of pregnancies globally and is the leading cause of maternal and foetal mortality due to premature delivery, complications with the placenta and lack of oxygen. It also disproportionately affects women of certain races.

According to the study, led by Drs Kun Ping Lu and Xiao Zhen Zhou at the University of Western Ontario, and Drs Surendra Sharma and Sukanta Jash at Brown University, cis P-tau is a central circulating driver of preeclampsia.

“The root cause of preeclampsia has (so far) remained unknown, and without a known cause there has been no cure. Preterm delivery is the only life-saving measure,” said Lu, professor of biochemistry and oncology at Schulich School of Medicine & Dentistry.

“Our study identifies cis P-tau as a crucial culprit and biomarker for preeclampsia. It can be used for early diagnosis of the complication and is a crucial therapeutic target,” said Sharma.

In 2016, Sharma, a leading preeclampsia researcher, and his team had identified that preeclampsia and diseases like Alzheimer’s had similar root causes related to protein issues. This research builds on that finding.

Until now, cis P-tau was mainly associated with neurological disorders like Alzheimer’s disease, traumatic brain injuries (TBI) and stroke. This association was discovered by Lu and Zhou in 2015 as a result of their decades of research on the role of tau protein in cancer and Alzheimer’s.

An antibody developed by Zhou in 2012 to target only the toxic protein while leaving its healthy counterpart unscathed is currently undergoing clinical trials in human patients suffering from TBI and Alzheimer’s Disease. The antibody has shown promising results in animal models and human cell cultures in treating the brain conditions.

The researchers were curious whether the same antibody could work as a potential treatment for preeclampsia. Upon testing the antibody in mouse models they found astonishing results.

“In this study, we found the cis P-tau antibody efficiently depleted the toxic protein in the blood and placenta, and corrected all features associated with preeclampsia in mice. Clinical features of preeclampsia, like elevated blood pressure, excessive protein in urine and foetal growth restriction, among others, were eliminated and pregnancy was normal,” said Sharma.

Sharma and his team at Brown have been working on developing an assay for early detection of preeclampsia and therapies to treat the condition. He believes the findings of this study have brought them closer to their goal.

Preeclampsia, genetics and the brain

Recent research has also thrown light on preeclampsia’s long-term impacts and possible links to brain health.

“Research has shown that women of certain races have genes that could possibly lead to higher than average blood pressure levels, eventually creating conditions for preeclampsia during pregnancy. However, it’s also true that in many low socio-economic countries there’s no registry to record PE cases. So, its link to other environmental factors is still unclear,” said Sharma.

“Preeclampsia presents immediate dangers to both the mother and foetus, but its long-term effects are less understood and still unfolding,” said Sharma. “Research has suggested a heightened risk of dementia later in life for both mothers who have experienced preeclampsia and their children.” However, the causal link between preeclampsia and dementia is not known.

The researchers say this new study has pinpointed a potential underlying cause of the complex relationship between preeclampsia and brain health.

“Our study adds another layer to this complexity. For the first time, we’ve identified significant levels of cis P-tau outside the brain in the placenta and blood of preeclampsia patients. This suggests a deeper connection between preeclampsia and brain-related issues,” said Jash, the lead author of the study.

As researchers delve deeper, how our bodies respond to stress is also emerging as a potential factor in the onset of preeclampsia.

“Although genetics play a role, factors like stress could be an important piece of the puzzle. Understanding how stress and other environmental factors intersect with biological markers like cis P-tau may offer a more complete picture,” said Jash, assistant professor of molecular biology, cell biology and biochemistry (research) and paediatrics (research) at Brown.

A stress-response enzyme called Pin1

In 1996 and 1997, Lu and Zhou made the ground-breaking discovery of Pin1, which turns out to be a stress-response enzyme. This is a specific protein in the cells that becomes active or changes its behaviour in response to stressors, such as environmental challenges, toxins or physiological changes.

“Pin1 plays a pivotal role in keeping proteins, including the tau protein, in the functional shape during stress. When Pin1 becomes inactivated, it leads to the formation of a toxic, misshapen, variant of tau — cis P-tau,” said Zhou, associate professor, pathology and laboratory medicine at Schulich Medicine & Dentistry.

Interestingly, Pin1 is a key player in cancer signalling networks, turning on numerous cancer-causing proteins and turning off many cancer-suppressing ones. Found in high levels in most human cancers, it’s particularly active in cancer stem cells, which are thought to be central to starting and spreading tumours and are hard to target with existing treatments.

“Essentially, when Pin1 is activated, it can lead to cancer. On the other hand, when there’s a decrease or deactivation in Pin1, it results in the formation of the toxic protein cis P-tau, which leads to memory loss in Alzheimer’s and after TBI or stroke. Now, we’ve uncovered its connection to preeclampsia as well,” said Zhou.

“The results have far-reaching implications. This could revolutionise how we understand and treat a range of conditions, from pregnancy-related issues to brain disorders,” said Lu.

Source: University of Western Ontario

Categories : Cardiovascular Disease Metabolic DisordersTags :

New Research Points to Clot Lysis Protein for Cholesterol Control

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While high levels of low-density lipoprotein (LDL) can be reduced by drugs such as statins, reducing the risk of myocardial infarction and stroke, risk still remains in the form of other cholesterols. New research published in the journal Science describes how manipulating a protein involved in blood clot lysis could help bring cholesterol levels even more under control.

Heart disease remains a leading cause of death worldwide, despite advances in cholesterol-lowering medication such as proprotein convertase subtilisin-kexin type 9 inhibitors, which were approved by the FDA in 2015. One clinical trial following patients taking proprotein convertase subtilisin-kexin type 9 inhibitors demonstrated a benefit while also revealing an opportunity for improvement as the absolute risk reduction was considered modest at 1.5%.

“It is clear that there is more going on than just what statins and these newer inhibitor drugs can control,” says Ze Zheng, MBBS, PhD, MCW assistant professor of medicine. “More therapies are needed, and to get them we need to know more about other sources of risk for heart disease, especially heart attacks and strokes.”

So-called “bad cholesterol” is carried by apolipoprotein B (apoB) which forms well-structured particles with lipids and proteins. These particles serve as stable vehicles for transporting lipids such as cholesterol in the bloodstream. These lipid-rich particles mostly include very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL). Current cholesterol-lowering reduce mainly LDL levels, which though important to control, is not the only risk factor for heart disease. In fact, the other lipoproteins in the same group as LDL are not reduced by much with available treatments. Dr Zheng and her team are investigating how to reduce levels of other members of this family of lipoproteins, especially VLDL.

“With my background in lipid metabolism, I found myself consistently checking lipid levels even during studies regarding blood clot lysis and how an impairment in the body’s ability to remove blood clots affects the risk of blood vessel blockages,” Dr Zheng adds. “I was just naturally curious about it, and I noticed that a protein I was studying may have an effect on the amount of circulating cholesterol.”

In prior research, Dr Zheng has helped define a new cellular source of this protein, tissue-type plasminogen activator (tPA), and its role in breaking down blood clots and preventing blood vessel blockages. To understand its potential influence on cholesterol levels, her team used a gene-editing technique to stop liver cells from producing tPA in mice prone to blood vessel plaque formation. The scientists found that the mice developed increased lipoprotein-cholesterol in this experiment, and then validated the findings in follow-up studies using human liver cells and a type of rat liver cell known to produce VLDL in a way similar to human liver cells. With these and other experimental results, Dr Zheng and her team have demonstrated a new, important role that liver tPA influences blood cholesterol levels while underscoring a meaningful connection between the liver, heart and blood vessels.

“After defining this new role for tPA, we turned our attention to the question of how it changes blood cholesterol levels,” notes Wen Dai, MD, research scientist, Versiti Blood Research Institute.

The liver contributes to the majority of the “bad” apoB-lipoproteins by making VLDL. The team focused on whether and how tPA impacts the process of VLDL assembly in the liver. Microsomal triglyceride transfer protein (MTP) is required for the assembly of VLDL due to its role carrying lipids to the apoB. The scientists determined that tPA binds with the apoB protein in the same place as MTP. The more tPA is present, the fewer opportunities MTP has to connect with apoB and catalyse the creation of new VLDL. Essentially, MTP tries to pass a cholesterol to apoB, but tPA interferes with this pocess.

“Based on our prior research, we knew it also was critical to look at tPA’s primary inhibitor,” Dr. Zheng says.

Plasminogen activator inhibitor-1 (PAI-1) is known to block the activity of tPA. Scientists also have found a correlation between PAI-1 levels in blood and the development of disease due to plaque formation and blockages in blood vessels. The team found that higher levels of PAI-1 reduced the ability of tPA to bind with apoB proteins, rendering tPA less effective at competing with MTP to prevent VLDL production. Returning to the biological gridiron, PAI-1 might be a decoy receiver that distracts tPA until MTP connects with apoB for a big gain. The team studied this interaction in human subjects with a naturally occurring mutation in the gene carrying the code for PAI-1. The researchers found that these individuals, as predicted, had higher tPA levels and lower LDL and VLDL levels than individuals from the same community who did not have the same mutation.

“We are investigating therapeutic strategies based on these findings regarding tPA, MTP and PAI-1,” Dr Zheng notes. “I think we may be able to reduce the residual cardiovascular risk that has persisted even as treatment has advanced.”

Source: Medical College of Wisconsin

Categories : Cardiovascular DiseaseTags :

Brain Haemorrhage Risk Factor could be Transmissible via Blood Transfusion

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A major study led by researchers at Karolinska Institutet suggests that a possible cause of spontaneous brain haemorrhage could be transmitted via blood transfusion. At the same time, it is very unlikely that anyone should suffer a brain haemorrhage after receiving donated blood, according to the study findings which are published in JAMA.

A common cause of spontaneous, recurring brain haemorrhages is the vascular disease cerebral amyloid angiopathy (CAA), in which proteins accumulate along the small blood vessels of the brain. Several studies have shown that CAA can be transferred from one individual to another through neurosurgery and probably via treatment using a certain type of growth hormone.

Few affected individuals

This new study led by researchers from Karolinska Institutet shows that patients who have received blood from donors who later suffered recurring brain haemorrhages are more than twice as likely to suffer a brain haemorrhage themselves.

The findings suggest that some factor that can give rise to spontaneous brain haemorrhages can be spread through blood transfusion. However, as only 0.1% of the donors in the study subsequently suffered recurring brain haemorrhages there were consequently only a few affected patients.

“Blood transfusions are relatively common, which makes possible negative effects an important public health issue,” says the study’s last author Gustaf Edgren, researcher at the Department of Medicine, Karolinska Institutet (Solna) and specialist physician at Södersjukhuset. “However, in this case, it’s very unlikely that you’d suffer a brain haemorrhage from something transmitted through a transfusion.”

CAA could be transmissible

According to the researchers, the most important implication of the study is instead that it adds further support to the hypothesis that CAA can be transmitted between individuals, which, if true, can have consequences in several fields.

The study drew on the data of more than a million patients the Swedish-Danish transfusion database SCANDAT, which contains data on blood donors and patients receiving a transfusion from the 1970s onwards. The primary analyses were conducted in Sweden and then repeated with the Danish data, with almost identical results.

Confirmation needed

The researchers now hope to corroborate the hypothesis that the link between brain haemorrhage and blood transfusion concerns CAA. They will therefore be examining samples from the Danish Blood Donor Study biobank to see if they can identify aberrant proteins associated with the disease.

The plan is also to obtain CAT and MR scans from the affected donors and patients to see if they might also be able to support the hypothesis.

“This study does not demonstrate causality, so the observed increase in risk could depend on other factors,” says the study’s first author Jingcheng Zhao from Dr Edgren’s group at Karolinska Institutet. “More research is needed to confirm our findings and understand the potential underlying mechanism.”

Source: Karolinska Institutet

Categories : Cardiovascular Disease Implants and ProsthesesTags :

Redo Transcatheter Procedure is a Reasonable Treatment for Select Patients

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Cedars-Sinai investigators have shown that redo transcatheter aortic valve replacement (TAVR) procedures are both safe and effective when compared with situations in which patients with similar risk profiles undergo the same procedure for the first time.

The novel findings, which appear in The Lancet, are significant because recent randomised clinical trials have shown that TAVR is a meaningful treatment option for both younger and lower-risk surgical patients.

“We now know that redo TAVR with balloon-expandable valves may be a reasonable treatment for failed TAVR procedures in select patients,” said Raj Makkar, MD, Cedars-Sinai’s vice president of Cardiovascular Innovation and Intervention and the study’s senior author. “This is increasingly important, as the patients treated with TAVR are younger than they were a decade ago, meaning they will likely need a repeat procedure at some point in their lifetime.”

At both the 30-day post-procedure mark and at one year, Makkar’s team found no difference between redo TAVR or first-time TAVR in terms of death or stroke rates.  

“Our findings also suggest that redo TAVR was associated with a significant improvement in quality of life,” said Makkar, who is also the associate director of the Smidt Heart Institute at Cedars-Sinai, director of the Interventional Cardiology Division in the Department of Cardiology, and the Stephen R. Corday, MD, Chair in Interventional Cardiology.

Transcatheter aortic valve replacement is a procedure that replaces a diseased aortic valve with a man-made valve. The procedure is now the standard treatment for patients with symptomatic severe aortic valve stenosis (narrowing of the artery).

The research team accessed a national database of all consecutive patients undergoing commercial TAVR in the US. Among the 350 591 patients who underwent TAVR between November 2011 and December 2022, 1320 individuals required redo procedures. The patients who underwent a repeat procedure had a mean age of 78 years old. About 58% were male and 42% female. 

“Fixing damaged valves is something in which we excel at the Smidt Heart Institute,” said Eduardo Marbán, MD, PhD, professor and executive director of the Smidt Heart Institute. “Our finding that TAVR can be redone safely is yet another step in establishing this as the default technology for aortic valve disease.”

Interventionalists in the Smidt Heart Institute at Cedars-Sinai have successfully completed more than 6000 minimally invasive transcatheter aortic valve replacements to date, with more than 650 performed in fiscal year 2022.

Source: Cedars-Sinai

Categories : Cardiovascular Disease Environmental EffectsTags :

Cold Weather may Make Blood Pressure Control More Challenging

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Blood pressure among patients diagnosed with hypertension appeared to slightly increase and rates of systolic blood pressure being controlled during an outpatient visit appeared to slightly decrease during winter months, according to a new study presented at the American Heart Association’s Hypertension Scientific Sessions 2023.

Previous research has found that blood pressure varies with the seasons of the year, most of which is systolic blood pressure. The study authors sought to understand whether blood pressure control, defined in this study as less than 140/90mmHg among patients with hypertension, varied by season.

“Despite the smaller degree of systolic blood pressure variation in comparison to previous studies on seasonality in blood pressure, we were surprised to observe a large degree of change in blood pressure control between winter and summer months,” said lead study author Robert B. Barrett, a software engineer at the American Medical Association in Greenville, South Carolina. “Individuals with hypertension or values near the range of hypertension may benefit from periodic blood pressure monitoring and improvements in physical activity and nutritional patterns during winter months to offset adverse effects from seasonal blood pressure changes.”

The researchers reviewed electronic health records for 60 676 adults treated for hypertension between July 2018 and June 2023 at six health care centres. Each participant remained on their originally prescribed classes of antihypertensive drugs throughout the review period. The centres ranged from small health centres or clinics to large academic medical centres. Seasonal blood pressure readings were analysed to assess variations in blood pressure control during the northern hemisphere’s winter vs summer months (December through February vs June through August, respectively) as part of an American Medical Association-supported, quality-improvement program for clinicians and health care centres. Study participants were an average age of 62 years old; 52.3% identified as white race; 59.7% identified as female.

The analysis of the health records found that, on average, participants’ systolic blood pressure increased by up to 1.7mmHg in the winter months compared to the summer months. In addition, they found that blood pressure control rates decreased by up to 5% during the winter months.

Future directions for investigation might include analysing the frequency of heart disease and deaths during each season, the authors noted.

The study’s limitations include that the electronic health records did not capture a complete health history for each participant and that information collected for each patient was retrieved only from the institution where they were treated.

Source: American Heart Association

Categories : Cardiovascular DiseaseTags :

High Blood Pressure When Lying Down Linked to Increased Cardiovascular Risk

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People who had high blood pressure while lying flat on their backs had a higher risk of heart attack, stroke, heart failure or premature death, according to new research presented at the American Heart Association’s Hypertension Scientific Sessions 2023.

The autonomic nervous system regulates blood pressure in different body positions; but gravity may cause blood to pool when seated or upright, and the body is sometimes unable to properly regulate blood pressure during lying, seated and standing positions, the authors noted.

“If blood pressure is only measured while people are seated upright, cardiovascular disease risk may be missed if not measured also while they are lying supine on their backs,” said lead study author Duc M. Giao, a researcher and a 4th-year MD student at Harvard Medical School in Boston.

To examine body position, blood pressure and heart health risk, the researchers examined health data for 11 369 adults from the longitudinal Atherosclerosis Risk in Communities (ARIC) study. The data on supine and seated blood pressure was gathered during the enrolment period, ARIC visit 1, which took place between 1987–1989. Participants had their blood pressure taken while briefly lying down at a clinic. The average age of participants at that time was 54 years old; 56% of the group self-identified as female; and 25% of participants self-identified as Black race. Participants in this analysis were followed for an average of 25 to 28 years, up through ARIC visit 5, which includes health data collected from 2011–2013.

The researcher’s findings included:

  • 16% of participants who did not have high blood pressure (130/80 mm Hg or higher) while seated had high blood pressure while lying supine (flat on their backs), compared to 74% of those with seated high blood pressure who also had supine high blood pressure.
  • In comparison to participants who did not have high blood pressure while seated and supine, participants who had high blood pressure while seated and supine had a 1.6 times higher risk of developing coronary heart disease; a 1.83 times higher risk of developing heart failure; a 1.86 times higher risk of stroke; a 1.43 times higher risk of overall premature death; and a 2.18 times higher risk of dying from coronary heart disease
  • Participants who had high blood pressure while supine but not while seated had similar elevated risks as participants who had high blood pressure while both seated and supine.
  • Differences in blood pressure medication use did not affect these elevated risks in either group.

“Our findings suggest people with known risk factors for heart disease and stroke may benefit from having their blood pressure checked while lying flat on their backs,” Giao said.

“Efforts to manage blood pressure during daily life may help lower blood pressure while sleeping. Future research should compare supine blood pressure measurements in the clinic with overnight measurements.”

The study’s limitations included that it focused on adults who were middle-aged at the time of enrolment, meaning the results might not be as generalizable to older populations, Giao said.

Source: American Heart Association

Categories : Cancer Cardiovascular DiseaseTags :

Exercise Stress Tests Pick up More than Just Cardiovascular Problems

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The exercise stress test, which involves treadmill exercise test with electrocardiogram (ECG), is one of the most familiar tests in medicine. While exercise testing typically is focused on diagnosing coronary artery disease, a recent study from Mayo Clinic finds that exercise test abnormalities, such as low functional aerobic capacity, predicted non-cardiovascular causes of death such as cancer in addition to cardiovascular-related deaths. These new findings are published in Mayo Clinic Proceedings.

The exercise stress test is noninvasive, easily available and provides important diagnostic information. In addition to the ECG itself, the test produces data on functional aerobic capacity, heart rate recovery and chronotropic index, the standardised measure of heart rate during exercise that reflects age, resting heart rate and fitness.

“In our exercise testing cohort, non-cardiovascular deaths were more frequently observed than cardiovascular deaths,” says Thomas Allison, PhD, MPH, director of Mayo Clinic’s Integrated Stress Testing Center and the study’s senior author. “Though this was a cardiac stress test, we found that cancer was the leading cause of death, at 38%, whereas only 19% of deaths were cardiovascular. Exercise test results including low exercise capacity, low peak heart rate, and a slow recovery of the heart rate after exercise test were associated with increased mortality.”

The study looked at 13 382 patients who had no baseline cardiovascular issues or other serious diseases and who had completed exercise tests at Mayo Clinic between 1993 and 2010, then were followed closely for a median period of 12.7 years.

The findings suggest that clinicians should focus not only on ECG results but on data in the exercise test results such as low functional aerobic capacity, low chronotropic index and abnormal heart rate recovery. Patients should be encouraged to increase their physical activity if these results are atypical, even if the ECG results show no significant cardiovascular-related risk, Dr Allison says.

Source: Mayo Clinic