Tag: heart failure

Categories : Cardiovascular DiseaseTags :

SGLT2 Inhibitors may be Effective for All HF Ejection Fractions

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Researchers presented new evidence that SGLT2 inhibitors may benefit a wide range of patients with heart failure (HF). At the ESC Congress 2022 in Barcelona, and in simultaneous publications in The New England Journal of Medicine and The Lancet, physician-scientists presented late-breaking research from the largest trial to date of heart failure patients with mildly reduced or preserved ejection fraction (EF).

They showed that dapagliflozin, which had previously been shown to benefit patients with heart failure with reduced ejection fraction (HFrEF), is likely to also reduce cardiovascular death and hospitalisation for patients with mildly reduced or preserved EF, for whom therapeutic options are limited. A meta-analysis that included two clinical trials further strengthened the evidence that this class of drugs may provide protection for a wide range of heart failure patients.

Scott Solomon, MD, at the Brigham, presented results from the AstraZeneca-funded DELIVER trial, a randomised, placebo-controlled trial of dapagliflozin among patients with heart failure with mildly reduced or preserved EF.

“In the largest and most inclusive trial of heart failure with mildly reduced or preserved ejection fraction, we found that treatment with the SGLT2 inhibitor dapagliflozin can benefit patients across the full spectrum of heart failure,” explained Dr Solomon. “These findings establish SGLT2 inhibitors as foundational treatment for patients living with heart failure, regardless of ejection fraction, to help prevent hospitalisation and morbidity and to extend meaningful survival and improve health-related quality of life. These are the outcomes that matter most to patients and to clinicians – to keep patients feeling well and living longer.”

Muthiah Vaduganathan, MD MPH, also at the Brigham, presented results from a pre-specified meta-analysis of DELIVER and EMPEROR-Preserved, a large-scale clinical trial of empagliflozin, funded by Boehringer Ingelheim and Eli Lilly.

“Our meta-analysis, encompassing more than 12 000 patients, provides a summary of the totality of the evidence and drives home the message that, when it comes to heart failure, this is a therapy for all,” said Dr Vaduganathan. “These trials included patients across a broad range of ages, race, functional class, sex and medical histories, but regardless of individual characteristics, they benefited consistently from this treatment.”

Dapagliflozin is a sodium-glucose co-transporter-2 (SGLT2) inhibitor, which causes the body to excrete sugar in urine. As well as blood glucose control in diabetes, SGLT-2 inhibitors have been shown to provide significant cardiovascular and kidney disease benefits. The DELIVER trial was designed to determine whether dapagliflozin would decrease cardiovascular morbidity and mortality in patients with heart failure with mildly reduced or preserved EF.

The international trial enrolled patients aged 40 or older and had symptomatic HF with an EF of greater than 40%, including mildly reduced ejection fraction and preserved EF, as well as patients who had previously had reduced EF that had improved to greater than 40%, and in both the outpatient and inpatient setting. More than 6000 participants were randomised to receive dapagliflozin or placebo and followed for a median of 2.3 years. The primary endpoint was a composite of cardiovascular death or worsening heart failure.

Dapagliflozin significantly reduced the primary composite endpoint by 18 percent. In the dapagliflozin group, 11.8% experienced worsening heart failure compared to 14.5% of the placebo group. Cardiovascular death in these groups occurred in 7.4 % and 8.3% of participants, respectively. Key secondary outcomes were also significantly reduced, including total heart failure hospitalisations and total symptom burden.

The meta-analysis used data from DELIVER and EMPEROR-Preserved, with a composite of cardiovascular death or first hospitalisation for heart failure. SGLT2 inhibitors were found to reduce primary outcome risk by 20%. Effects were consistent across subgroups by age, sex, race, body mass index, systolic blood pressure, history of various medical conditions and more.

The team further incorporated data from additional clinical trials with SGLT2 inhibitors, including those performed with dapagliflozin and empagliflozin in patients with HFrEF, and in patients from a clinical trial of the SGLT1/2 inhibitor sotagliflozin. Taken together, the evidence with all these data suggest that patients across the full spectrum of HF benefit from this class of drugs, regardless of EF or care setting.

Limitations were noted by the authors. Black patients made up less than 5% of the patients enrolled in DELIVER; the COVID pandemic limited symptom assessment after March 2020; and subgroups in the trial were underpowered. However, findings were consistent across prespecified subgroups.

“There are more than 64 million people worldwide affected by heart failure, half of whom have mildly reduced or preserved ejection fraction,” said Dr Solomon. “Our goal is to rigorously and scientifically evaluate potential treatments so that we can provide the best evidence-based care to help them lead longer, healthier lives.”

Source: Brigham and Women’s Hospital

Categories : Cardiovascular DiseaseTags :

Salt Restriction May Worsen HF with Preserved Ejection Fraction

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Salt restriction has long been held to be a key component of heart failure treatment, but cutting back too much may actually worsen the outcomes for people with preserved ejection fraction, suggests research published in Heart.

The findings indicate that younger people and those of black and other ethnicities seem to be most at risk.

Salt restriction is frequently recommended in heart failure guidelines, but the optimal restriction range (from less than 1.5g to less than 3g daily) and its effect on patients with heart failure with preserved ejection fraction (HFpEF) is less clear as they have often been excluded from relevant studies.

HFpEF, which accounts for half of all heart failure cases, occurs when the lower left chamber of the heart (left ventricle) isn’t able to fill properly with blood (diastolic phase), so reducing the amount of blood pumped out into the body.

In a bid to explore the association with salt intake further, the researchers drew on  secondary analysis of data from 1713 people aged 50 and above with heart failure with preserved ejection fraction who were part of the TOPCAT trial.

A phase III, randomised, double-blind, placebo-controlled study, this trial was designed to find out if the drug spironolactone could effectively treat symptomatic heart failure with preserved ejection fraction.

Participants were asked how much salt they routinely added to the cooking of staples, such as rice, pasta, and potatoes; soup; meat; and vegetables, and this was scored as: 0 points (none); 1 (⅛tsp); 2 (¼tsp); and 3 (½+tsp).

They were followed up for an average of three years for the primary endpoint, a composite of death from cardiovascular disease or admission to hospital for heart failure plus aborted cardiac arrest. Secondary outcomes were all cause mortality and cardiovascular disease mortality plus hospitalisation for heart failure.

Around half the participants (816) had a cooking salt score of zero: more than half of them were men (56%) and most were of white ethnicity (81%). They weighed significantly more and had a lower diastolic blood pressure (70 mm Hg) than those with a cooking salt score above zero (897).

They had also been admitted to hospital more often for heart failure, were more likely to have type 2 diabetes, poorer kidney function, to be taking meds to control their heart failure, and to have a reduced left ventricular ejection fraction (lower cardiac output). 

Participants with a cooking salt score above zero were at significantly lower risk of the primary endpoint than those whose score was zero, mainly driven by the fact that they were less likely to be hospitalised for heart failure. But all-cause mortality or CVD mortality was no higher than those whose cooking salt score was zero.

Those aged 70 or younger were significantly more likely to benefit from adding salt to their cooking than were those older than 70 in terms of the primary endpoint and admission to hospital for heart failure. 

Similarly, those of black and other ethnicities seemed to benefit more from adding salt compared with white participants, although the numbers were small.

Gender, previous hospitalisation for heart failure, and the use of heart failure meds weren’t associated with heightened risks of the measured outcomes and cooking salt score.

This is an observational study, and as such, can’t establish cause. Not all relevant data from the TOPCAT trial were available, while the cooking salt score was self-reported, acknowledge the researchers. And reverse causation, whereby people with poorer health might have been advised to further restrict their salt intake, can’t be ruled out. 

Lower sodium intake is usually associated with lower blood pressure and a reduced risk of cardiovascular disease in the general public and in those with high blood pressure. It is thought that it reduces fluid retention and the triggering of the hormones involved in blood pressure regulation.

But restricting salt intake to control heart failure is less straightforward, say the researchers. It may prompt intravascular volume contraction, which could, in turn, reduce congestion and the requirement for water tablets to ease fluid retention. 

But the researchers pointed out that the that the volume of plasma in the blood, an indicator of congestion, wasn’t significantly associated with cooking salt score – suggesting that low sodium intake didn’t ease fluid retention in people with heart failure with preserved ejection fraction.

“Overstrict dietary salt intake restriction could harm patients with [heart failure with preserved ejection fraction] and is associated with worse prognosis. Physicians should reconsider giving this advice to patients,” they conclude.

Source: EurekAlert!

Categories : Ageing GenderTags :

Losing their Y Chromosome Shortens Men’s Lifespans

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DNA repair
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As many men age, they lose their Y chromosome, which causes heart muscle to scar and can lead to deadly heart failure, new research from the shows. The finding, which appears in Science, may help explain why men die, on average, several years younger than women.

University of Virginia School of Medicine researcher Kenneth Walsh, PhD, says the new discovery suggests that men who suffer Y chromosome loss – estimated to include 40% of 70-year-olds – may particularly benefit from an existing drug that targets dangerous tissue scarring. The drug, he suspects, may help counteract the harmful effects of the chromosome loss – effects that may manifest not just in the heart but in other parts of the body as well.

On average, women live five years longer than men in the United States. The new finding, Prof Walsh estimates, may explain nearly four of the five-year difference.

“Particularly past age 60, men die more rapidly than women. It’s as if they biologically age more quickly,” said Prof Walsh. “There are more than 160 million males in the United States alone. The years of life lost due to the survival disadvantage of maleness is staggering. This new research provides clues as to why men have shorter lifespans than women.”

Many men begin to lose their Y chromosome in a fraction of their cells as they age, especially in smokers. The loss occurs predominantly in cells that undergo rapid turnover, such as blood cells. However, Y chromosome loss does not occur in male reproductive cells, so it is not inherited by the children of men who exhibit Y chromosome loss. It has been observed that men who suffer Y chromosome loss are more likely to die at a younger age and suffer age-associated maladies such as Alzheimer’s disease. This new research however is believed to be the first hard evidence that the chromosome loss harms men’s health.

Walsh and his team used CRISPR gene-editing technology to develop a special mouse model to better understand the effects of Y chromosome loss in the blood. The loss accelerated age-related diseases, made the mice more prone to heart scarring, leading to earlier death. But more than just the results of inflammation, there was complex series of responses in the immune system, leading to fibrosis throughout the body. This tug-of-war within the immune system, the researchers believe, may accelerate disease development.

The scientists also looked at the effects of Y chromosome loss in human men. They conducted three analyses of data compiled from the UK Biobank, a massive biomedical database, and found that Y chromosome loss was associated with cardiovascular disease and heart failure. As chromosome loss increased, the scientists found, so did the risk of death.

The findings suggest that targeting the effects of Y chromosome loss could help men live longer, healthier lives. One treatment option might be a drug, pirfenidone, approved in the US for the treatment of idiopathic pulmonary fibrosis. The drug is also being tested for the treatment of heart failure and chronic kidney disease, two conditions for which tissue scarring is a hallmark. Based on his research, Walsh believes that men with Y chromosome loss could respond particularly well to this drug, and other classes of antifibrotic drugs that are being developed, though more research will be needed to determine that.

At the moment, doctors have no easy way to determine which men suffer Y chromosome loss. Prof Walsh’s collaborator Lars A. Forsberg, of Uppsala University in Sweden, has developed an inexpensive polymerase chain reaction (PCR) test that can detect Y chromosome loss, but the test is largely confined to his and Prof Walsh’s labs. Prof Walsh, however, can foresee that changing: “If interest in this continues and it’s shown to have utility in terms of being prognostic for men’s disease and can lead to personalised therapy, maybe this becomes a routine diagnostic test,” he said.

“The DNA of all our cells inevitably accumulate mutations as we age. This includes the loss of the entire Y chromosome within a subset of cells within men. Understanding that the body is a mosaic of acquired mutations provides clues about age-related diseases and the aging process itself,” said Walsh, a member of UVA’s Department of Biochemistry and Molecular Genetics. “Studies that examine Y chromosome loss and other acquired mutations have great promise for the development of personalised medicines that are tailored to these specific mutations.”

Source: University of Virginia Health System

Categories : Cardiovascular Disease Surgeries & ProceduresTags :

Post-operative AF Linked to Risk of Hospitalisation for Heart Failure

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Associations between post-operative atrial fibrillation and incident heart failure hospitalisations. Credit: European Heart Journal

A study of over three million patients found that people who develop an atrial fibrillation (AF) after undergoing surgery have an increased risk of subsequent hospitalisation for heart failure.

The study, which is published in the European Heart Journal, showed that the risk of hospitalisation for heart failure among patients who developed AF after surgery increased regardless of whether or not the surgery was for a heart condition.

Among 76 536 patients who underwent heart surgery, 18.8% developed post-operative AF and the risk of hospitalisation for heart failure increased by a third compared to patients who did not develop AF. Among 2 929 854 patients without a history of heart disease who had surgery for non-heart-related conditions, 0.8% developed AF and the risk of hospitalisation for heart failure doubled.

The study’s first author, Dr Parag Goyal, Associate Professor of Medicine at Weill Cornell Medicine, said: “Our study, which to our knowledge is the largest study to date, shows that post-operative atrial fibrillation is associated with future heart failure hospitalisations. This could mean that atrial fibrillation is an important indicator of underlying but not yet detected heart failure; or it could mean that atrial fibrillation itself contributes to the future development of heart failure. While this study could not specifically address which of these mechanisms are at play, our hope is that this study will inspire future work into exploring the underlying mechanism seen in our important findings.

“Regardless of the mechanism, our study shows that post-operative atrial fibrillation is clearly an important entity that merits attention and incorporation into decision making. Most importantly, patients and doctors need to be more vigilant about heart failure symptoms among patients who develop post-operative atrial fibrillation. Those who do develop the condition may require more aggressive treatments for other risk factors for heart failure, such as high blood pressure, diabetes and narrowing of the arteries.”

Post-operative AF occurs in up to 40% of patients undergoing heart surgery and 2% of patients undergoing non-cardiac surgery. Doctors have tended to view it as a benign event, triggered by the stress of the surgery – but evidence is emerging that post-operative AF is linked to longer term problems such as stroke and death from any cause. Until now, there has been limited evidence regarding its association with subsequent heart failure.

For the current, retrospective study, the researchers collected data on hospital health claims from 2016 to 2018, adjusting for factors that could affect the results such as age, sex, race, insurance status, medical history and body mass index.

Study limitations include its observational nature which can only establish association, not causation. The study relies on administrative claims data and medical codes to identify medical conditions; it lacks more detailed information like management strategies for post-operative AF, and on the function and size of the left ventricle, which could affect the likelihood of developing AF.

The researchers hope to conduct further studies to understand the underlying mechanism and to investigate ways of preventing future hospitalisations for heart failure among patients who develop post-operative AF.

The researchers wrote in the conclusion that “In the meantime, clinicians should be aware that POAF [post-operative AF] may be a harbinger of HF.”

In an accompanying editorial, Dr Melissa Middeldorp and Professor Christine Albert, both from the Smidt Heart Institute at Cedars-Sinai, California, USA, write: “These data add to a growing body of literature suggesting that POAF is not just a transient response to surgery but may be reflective of underlying atrial and myocardial structural changes that not only predispose to the acute AF event but to other potentially related adverse cardiovascular events, such as HF hospitalisation.”

They write that further studies are needed for a better understanding of the mechanisms involved in placing people at greater risk of AF and post-operative heart failure is needed in order to reduce hospitalisation and deaths after surgery.

“With a greater understanding of patients’ full risk factor profile, we may advocate for early aggressive intervention at the initial manifestation of POAF, to improve outcomes and reduce rehospitalisation following cardiac and non-cardiac surgery,” they concluded.

Source: European Society of Cardiology

Categories : Cardiovascular Disease Metabolic DisordersTags :

New SGLT-2 Inhibitors Could Reduce Heart Failure Risk in Diabetes

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A study published in Annals of Internal Medicine has suggested that the new SGLT-2 inhibitors may be viable as a first-line treatment in patients with type 2 diabetes, with reduced odds of hospitalisation for heart failure compared to those receiving metformin.

In cardiovascular outcome trials among adults with type 2 diabetes (T2D), sodium-glucose co-transporter 2 inhibitors (SGLT-2i) have shown therapeutic promise, including reduced risk of hospitalisation for heart failure compared to placebo. However, SGLT-2i have mainly been evaluated as a second-line treatment – metformin is generally given as a first-line, antidiabetic treatment.

In this new study, researchers from the Brigham and Women’s Hospital compared cardiovascular outcomes among adults with T2D who initiated first-line treatment with either metformin or SGLT-2i. For the study, 8613 patients receiving SGLT-2i were matched to 17 226 patients receiving metformin.

The researchers reported that that patients receiving SGLT-2i showed a similar risk for myocardial infarction, stroke, and all-cause mortality, and a lower risk for hospitalisation for heart failure compared with patients who received metformin. The risk for adverse events was similar except for an increased risk for genital infections compared with those receiving metformin.

“Our results suggest that SGLT-2i may be considered as first-line treatment for patients with T2D and cardiovascular disease or who are at increased risk for cardiovascular events,” said lead author HoJin Shin, BPharm, PhD, of the Division of Pharmacoepidemiology and Pharmacoeconomics. “However, more evidence from randomised clinical trials or observational studies will help us to identify patients who would benefit most from using SGLT-2i as first-line type 2 diabetes treatment.”

Source: EurekAlert!

Categories : Cardiovascular Disease VaccinesTags :

In Flu Season, Vaccine Reduces Cardiovascular Events in Heart Failure

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A randomised controlled trial showed that people with heart failure receiving an annual flu shot had lower rates of pneumonia and hospitalisation on a year-round basis and a reduction in major cardiovascular events during peak flu season – but not year-round.

The study, presented at the American College of Cardiology’s 71st Annual Scientific Session, is the first randomised controlled trial to assess the benefits of the flu vaccine in people with heart failure, who face a high risk of cardiovascular events. It was conducted in countries across Asia, Africa and the Middle East where getting a flu shot is not commonplace.

Lead author Mark Loeb, MD, said: “Although our prespecified endpoints were not significant, our data suggest that there’s a clinical benefit [to getting a flu shot] given the clear reduction in pneumonia, moderate reduction in hospitalisation and reduction in vascular events and deaths during periods of peak influenza. When taken together with previous trials and observational studies, the collective data demonstrate there is a substantial benefit to receiving a flu vaccine for people with heart failure.”

Heart failure is a condition in which the heart becomes too weak or stiff to pump blood effectively. Previous studies have shown that people with heart disease or cardiovascular risk factors face an elevated risk of complications when they contract influenza, but there has been a lack of evidence on whether flu vaccines can help to mitigate this risk specifically in people with heart failure.

The trial enrolled 5129 patients with heart failure in 10 countries where flu vaccines are not common. Participants did not routinely get flu shots and had previously received a flu shot no more than once during the three years preceding the trial. Participants were randomised to receive a flu shot or a placebo annually for up to three years, though they could still get a flu shot outside of the trial. Researchers tracked health outcomes for a median of 2.9 years. The trial’s primary endpoint was a composite of death from cardiovascular causes, non-fatal heart attack or non-fatal stroke. Its co-primary endpoint included a composite of any of these events plus hospitalisation for heart failure.

Overall, the composite primary endpoint occurred in 691 participants and 1470 experienced the composite co-primary endpoint. When analysed on a year-round basis there was no significant difference in the rates of these events between those who had received a flu vaccine and those who had not.

Separate analyses of hospitalisation, pneumonia and other respiratory outcomes however found that rates of pneumonia were 42% lower and hospitalisations were down 15% among those who received a flu shot.

The flu vaccine arm showed a significant reduction in the first primary endpoint, as well as reductions in all-cause death and cardiovascular death, when the analysis was limited to periods of peak influenza circulation. When influenza circulation was low, no significant difference was seen.

The researchers accounted for the differences in influenza circulation seasons. Based on these results, researchers said the flu vaccine did help to protect patients from influenza complications, including cardiovascular events.

“Many of the effects we found during peak flu circulation disappeared outside of it,” Dr Loeb said. “There’s no biological explanation for that other than influenza infections.”

While the study was conducted in countries where the flu vaccine is either not widely available or not common to receive, Dr Loeb said the results could likely be generalisable even in countries where flu vaccine uptake is higher. Study participants were allowed to get a flu vaccine outside of the study, but Dr Loeb said that there was no impact on the findings as very few did so. He added that the study was stopped early in four countries due to the COVID pandemic.

Loeb said that additional trials and large-scale observational studies could further clarify the health benefits of influenza vaccination in people with cardiovascular disease.

“I think this study offers an important message about vaccines generally – that it is important to do randomised controlled trials in populations that historically haven’t had a very high uptake of vaccines,” Dr Loeb said. “These types of [research] gaps have to be filled.”

Source: American College of Cardiology

Categories : Cardiovascular DiseaseTags :

Micronutrients Could Replenish Mitochondria in Cardiac Cells

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There is convincing evidence that micronutrients, such as iron, selenium, zinc, copper, and coenzyme Q10, can impact the function of cardiac cells’ energy-producing mitochondria to contribute to heart failure according to a review published in the Journal of Internal Medicine.

Research has established a relationship between poor cardiac performance and metabolic perturbations, including deficits in substrate uptake and utilisation, reduction in mitochondrial oxidative phosphorylation and excessive reactive oxygen species production. Together, these disturbances result in depletion of cardiac adenosine triphosphate (ATP) and loss of cardiac energy. Delivering more energy substrates such as fatty acids to the mitochondria will be worthless if the mitochondria can’t turn them into fuel. 

Micronutrients are required to efficiently convert macronutrients to ATP. However, studies have shown that up to 50% of patients with heart failure have deficiencies in one or more micronutrients. “Micronutrient deficiency has a high impact on mitochondrial energy production and should be considered an additional factor in the heart failure equation,” the authors argued. Their findings suggest that micronutrient supplementation could represent an effective treatment for heart failure.

“Micronutrient deficiency has a high impact on mitochondrial energy production and should be considered an additional factor in the heart failure equation, moving our view of the failing heart away from ‘an engine out of fuel’ to ‘a defective engine on a path to self-destruction’,” said co–lead author Nils Bomer, PhD, of the University Medical Center Groningen, in The Netherlands.

An accompanying editorial suggests a large trial to see if there is indeed a clinical benefit.

Source: Wiley

Categories : Cardiovascular Disease Metabolic DisordersTags :

A Surprising Benefit of Dapagliflozin in Patients with Heart Failure

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Dapagliflozin, widely used to treat type 2 diabetes, was shown to improve symptoms and physical limitations in patients with heart failure with preserved ejection fraction, according to clinical trial results reported in Nature Medicine.

Heart failure with preserved ejection fraction (HFpEF) occurs when the heart’s lower left chamber is unable to fill with blood properly. The condition accounts for approximately half of all heart failure cases and disproportionally affects older individuals. Patients with HFpEF can experience a host of debilitating symptoms linked to cardiometabolic abnormalities, including physical limitations, impaired cognition and poor quality of life. Life expectancy is also reduced for patients with this diagnosis, with 50% of patients with the diagnosis not expected to survive more than five years.

Finding ways to improve patients’ health and developing or identifying therapeutic interventions that not only reduce hospitalisation but also improve patient survival is key, the researchers said, but at present there are no available treatments that improve patient survival for patients with HFpEF.

Previous studies have shown that sodium glucose cotransporter 2 (SGLT2) inhibitors – which inhibit SGLT2 receptor proteins produced by the kidneys and are used to treat type 2 diabetes – reduces risk of cardiovascular death and heart failure-related hospitalisation in patients with HFpEF.

For this trial, the researchers measured patient-reported symptoms, physical limitations and function in patients with HFpEF who were taking dapagliflozin, an SGLT2 inhibitor drug.

A total of 324 patients with HFpEF, 56.8% women, were randomised to receive either dapagliflozin or placebo for 12 weeks and at the end of the trial were evaluated using the Kansas City Cardiomyopathy Questionnaire Clinical Summary Score, a measure of heart failure-related health status.
“It’s important to note the percentage of women that were enrolled in this study because usually women are under-enrolled in clinical trials,” pointed out study co-author Professor Sadiya Khan.

Compared to the placebo group, an overall improvement in patient-reported symptoms, physical limitations and exercise function was seen in the dapagliflozin group. Adverse events were also similar between both groups, the authors reported.

“It was definitely surprising and very exciting to see such a stark difference between the treatment group and the placebo group, that there was this clear separation that happened even over a short period of time,” Prof Khan said, adding that next steps will be to investigate dapagliflozin’s precise molecular mechanisms that enable its effectiveness.

Source: Northwestern University

Categories : Cardiovascular DiseaseTags :

Heart Failure Risk Further Increased by Aspirin Use

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Aspirin may increase heart failure risk in at-risk people
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Aspirin use is associated with a 26% higher risk of heart failure in people with at least one risk factor for it, according to a study published today in ESC Heart Failure. Risk factors included smoking, obesity, hypertension, high cholesterol, diabetes, and cardiovascular disease.

“This is the first study to report that among individuals with a least one risk factor for heart failure, those taking aspirin were more likely to subsequently develop the condition than those not using the medication,” said study author Dr. Blerim Mujaj of the University of Freiburg, Germany. “While the findings require confirmation, they do indicate that the potential link between aspirin and heart failure needs to be clarified.”

The influence of aspirin on heart failure is controversial, and so the study sought to investigate its association with heart failure incidence in people with and without heart disease and assess whether it is related to a new heart failure diagnosis in at-risk individuals.

The analysis included 30 827 individuals at risk for developing heart failure who were enrolled from Western Europe and the US into the HOMAGE study. The definition of “at risk” included one or more of the following: smoking, obesity, hypertension, high cholesterol, diabetes and cardiovascular disease. Participants were aged 40 years and older and were free of heart failure at baseline. Aspirin use was recorded at enrolment and participants were classified as users or non-users. Participants were followed-up for the first incidence of fatal or non-fatal heart failure requiring hospitalisation.

Average participant age was 67, 34% were women, and at baseline, a total of 7,698 participants (25%) were taking aspirin. During the 5.3-year follow-up, 1330 participants developed heart failure.

The investigators assessed the association between aspirin use and incident heart failure after adjusting for factors including demographic variables, medical history and medication. Taking aspirin was independently associated with a 26% raised risk of a new heart failure diagnosis.

For consistency, the researchers repeated the analysis after matching aspirin users and non-users for heart failure risk factors. In this matched analysis, aspirin was associated with a 26% raised risk of a new heart failure diagnosis. After excluding patients with a history of cardiovascular disease, in 22 690 participants (74%) without cardiovascular disease, aspirin use was still associated with a 27% increased risk of incident heart failure.

Dr Mujaj noted that “this was the first large study to investigate the relationship between aspirin use and incident heart failure in individuals with and without heart disease and at least one risk factor. Aspirin is commonly used – in our study one in four participants were taking the medication. In this population, aspirin use was associated with incident heart failure, independent of other risk factors.”

He concluded that “large multinational randomised trials in adults at risk for heart failure are needed to verify these results. Until then, our observations suggest that aspirin should be prescribed with caution in those with heart failure or with risk factors for the condition.”

Source: European Society of Cardiology

Categories : Cardiovascular DiseaseTags :

A Year of Exercise Reverses Heart Failure Signs

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In a small study, a year of exercise training helped to maintain or increase the youthful elasticity of the heart muscle among people in late middle age showing early signs of heart failure.

Published in Circulation, the research reinforces the notion that “exercise is medicine,” an important shift in approach, according to the researchers.

The study focused on heart failure with preserved ejection fraction, which is characterised by stiffening of the heart muscle and high pressures inside the heart during exercise. Once established, the condition is largely untreatable and causes fatigue, excess fluid in the lungs and legs, and shortness of breath.

“It is considered by some to be one of the most important virtually untreatable diseases in cardiovascular medicine,” said senior author Dr Benjamin Levine,  professor of internal medicine at UT Southwestern and director of the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Dallas. “So, of course, if there are no therapies, then the most important thing to do is to figure out how to prevent it from happening in the first place.”

In previous studies, prolonged exercise training was shown to improve heart elasticity in younger people, but was ineffective for heart stiffness in people 65 and older. The researchers decided to see if committed exercise could improve heart stiffness in healthy, sedentary men and women ages 45 to 64.

The study recruited 31 participants who showed some thickening of the heart muscle and an increase in blood biomarkers associated with heart failure, even though they had no other symptoms such as shortness of breath.

Eleven were randomly assigned to a control group and prescribed a program of yoga, balance and strength training three times a week. The rest were assigned to an individually tailored exercise regimen that gradually ramped up until the participants were doing intensive aerobic interval training for at least 30 minutes at least twice a week, plus two to three moderate-intensity training sessions and one to two strength training sessions each week. 

After one year, the group assigned vigorous exercise training showed a physiologically and statistically significant improvement in measures of cardiac stiffness and cardiorespiratory fitness, compared to no change in the control group.

The results suggest late middle age may be a “sweet spot” for using exercise to prevent heart failure with preserved ejection fraction, before the heart gets too stiff, Prof Levine said. He compared the heart muscle to an elastic band: a new one stretches easily and snaps right back.

“That’s a youthful cardiovascular system,” he said. “Now, stick it in a drawer and come back 30 years later—it doesn’t stretch, and it doesn’t snap back. And that’s one of the things that happens to the circulation, both the heart and the blood vessels as we age, particularly with sedentary aging.”

However, the study cannot determine if the participants will still go on to develop heart failure. This question will have to be addressed by larger studies. Furthermore, it is difficult for people to adhere to an exercise program, and the intensive intervention studied may be difficult and expensive to replicate on a large scale.

Source: American Heart Association