Category: Cardiovascular Disease

Categories : Cardiovascular DiseaseTags :

New Approach to Address Cardiac Disease in Rheumatoid Arthritis

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A new approach to address cardiac disease in rheumatoid arthritis (RA) patients has been developed.

Currently patients suffering from RA are also particularly susceptible to diastolic dysfunction, a type of cardiac deficiency which may lead to heart failure, resulting in a higher mortality rate among such patients.
To address this unmet clinical need, researchers from Queen Mary’s William Harvey Research Institute (WHRI) responded by developing an experimental model of cardiomyopathy in inflammatory arthritis.

After several attempts, the researchers finally hit upon the right model by characterising experimental animals with arthritis. The animals developed cardiac diastolic dysfunction, recapitulating the symptoms presented by RA patients. Diastolic dysfunction means the heart is able to contract as normal but unable to dilate properly, ultimately leading to heart failure over time.

Professor Mauro Perretti, lead study author and Professor of Immunopharmacology at Queen Mary University of London said, “As is often the case, the description of a valid model of disease can open new vistas on pathogenic mechanisms as well as on novel therapeutic approaches. At present, the cardiomyopathy of patients affected by rheumatoid arthritis is not treated, and on top of this, current anti-rheumatic drugs (eg biologics or steroids) may even worsen it. As such there is an urgent therapeutic need to intervene and treat, if not cure, the cardiomyopathy of patients affected by rheumatoid arthritis.”

“The broad area of cardiac inflammation is largely unexplored. At the WHRI we have several groups addressing experimental and translational work on several syndromes of the heart. Thus, there is work on myocarditis, on diabetes-induced cardiomyopathy and now with this study, the cardiomyopathy of inflammatory arthritis. The WHRI at Queen Mary University of London is a place of excellence to study cardiac inflammation in all its multiple faces, thanks also to our partnership with the Barts Heart Centre at Barts Health NHS Trust.”

The study was published in PNAS.

Source: EurekAlert!

Categories : Cardiovascular DiseaseTags :

Strong Adherence to Stroke Medication is Crucial

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A new study emphasises the importance of survivors of first-time stroke or transient ischaemic attack (TIA) to take medications on an ongoing basis, highlighting long-term associations with survival.

Stroke is the second leading risk of death worldwide, with In 2016, the average lifetime risk of stroke after 25 for the global population was 24.9%. Nearly half of all survivors of stroke are expected to experience a recurrent cardiovascular event within 10 years. Specific medications help to prevent this long-term risk, but adherence to these agents is often suboptimal among patients.

The study, published in Stroke, demonstrates the importance of medication adherence after stroke to maximise survival, even for patients with near-perfect adherence. These findings are in support of targeted initiatives to maximise medication adherence after stroke/TIA, such as implementation of medication reminder systems, mobile health technologies, increased follow-up by clinicians or complex behaviour change programs.

Drawing from Australian databases, the study enrolled 8363 adult patients who survived a first stroke or TIA between July 2010 and June 2014, with follow-up for a further three years. For patients with one-year adherence above 60%, each 10% improvement in adherence was associated with a 13-15% reduction in mortality risk. These results suggest that aiming for an arbitrary adherence target of 80% may be inappropriate as maximal survival benefits were observed closer to 100% adherence.

The study’s lead author, Associate Professor Monique Kilkenny, said continued use of secondary prevention medications can be improved with several factors: provision of medication on hospital discharge, regular contact with a primary care physician, and specialist physician contact.

“These findings represent important implications for practice by highlighting the value of efforts to improve medication adherence post-stroke/TIA, even among patients with near-perfect adherence,” said Associate Professor Kilkenny.

“Our findings provide evidence in support of targeted initiatives to maximise medication adherence after stroke/TIA and there is considerable scope for further interventions to improve medication adherence.”

Source: Monash University

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Study Links Poor Sleep to Arrhythmias

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A large observational study linked poor sleep to arrhythmias, although genetic risk factors for rhythm problems appeared to lessen the association.

The results, published in the American College of Cardiology, show that best self-reported sleeps (getting 7-8 hours etc) had a 29% lower risk of developing atrial fibrillation or flutter and a 35% lower risk of bradyarrhythmia compared with those with the worst sleep patterns (eg, being a night owl, sleeping too little, snoring, and having insomnia or daytime drowsiness).

The ventricular arrhythmia risk fell away after demographic, lifestyle, and genetic risk factors were accounted for.

Together with previous research linking a healthy sleep pattern to reduced cardiovascular disease and heart failure risks, the findings, according to the researchers, “emphasise the importance of improving the overall sleep behaviours in the prevention of cardiovascular disease at an early stage among the high-risk populations”.

Being reversible, the findings support the idea of better sleep for arrhythmia prevention.

“However, rest assured, we must not yet lose sleep over their findings,” cautioned Alan Kadish, MD, and Jason Jacobson, MD, in an accompanying editorial. They drew attention to a number of limitations, making the findings more theoretical than currently practicable.

Despite the study’s more sophisticated approach, “a major limitation is that arrhythmia diagnoses were obtained from diagnostic codes,” they noted. Furthermore, arrhythmias are subject to significant variability.
Arrhythmia prevention doesn’t mean cardiovascular disease prevention, they added. “[N]ot all arrhythmias have the same significance, and many are the consequence (not cause) of cardiovascular disease,” they wrote. “Alternatively, sleep disorders and arrhythmias may both simply be indicators of declining health overall and not causally linked.”

The researchers proposed potential mechanisms of action including disrupted autonomic nervous balance of sympathetic nervous and vagal outflows and metabolic changes.

The editorialists pointed out the interesting finding that genetic predisposition to atrial fibrillation significantly modified the associations. Good self-reported sleep and low genetic risk together presented a 46% lower risk of atrial fibrillation than a poor sleep pattern plus high genetic risk.

Progressively poorer sleep health scores were associated with higher incidences of atrial fibrillation and bradyarrhythmias.

Sleeping 7 to 8 hours per day, infrequent or no insomnia, and no frequent daytime sleepiness were each linked to lower arrhythmia risk.

Source: MedPage Today

Categories : Cardiovascular Disease Medical Research & TechnologyTags :

Is Heart Pump Development Dead in the Water?

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At an annual meeting of the Heart Failure Society of America (HFSA), heart failure specialists agreed that recalling the HeartWare heart pump was good but debated whether its departure leaves the field of mechanical circulatory support (MCS) dead in the water.

In June, Medtronic stopped sales of its HeartWare Ventricular Assist Device (HVAD), citing excess neurological events and mortality with the device. As a result, Abbott’s HeartMate 3 became the only FDA-approved, durable left ventricular assist device (LVAD) on the market.

“Competition breeds innovation. When competition is absent or minimal, there is little incentive for corporations to innovate,” said Jennifer Cowger, MD, MS, of Henry Ford Hospital in Detroit, during the annual scientific meeting.

“While I believe the removal of the HVAD from the market was the ethical thing to do, unless we as a field start embracing MCS technology and change our messaging to the general cardiology community, our field is going to be viewed as niche to referring cardiologists and we’re going to face irrelevance and we’re going to have bad times ahead,” she added.

However Nancy Sweitzer MD, PhD, of the University of Arizona in Tucson, disagreed, pointing out that there are plenty of advances on the horizon.

Nine companies worldwide are developing heart pumps for this $3-4 billion market, Dr Sweitzer noted. Several devices under investigation — implantable ones with no external component — will probably proceed to first-in-man trials in the next year, she said. “There’s a lot of money if you do this well,” she added

Internal competition alone may be enough to advance the field, Sweitzer argued, citing Thoratec’s HeartMate II superseding their old HeartMate XVE.

“They put their own device up against their own device. So I would argue that corporate competition isn’t necessary when the stakeholders realize that we need to get better at this. I think the companies in this space realize there’s a huge unmet need here if we develop a really good MCS that was truly portable, gave people excellent quality of life, and had lower complications,” she said.

Yet given the pace of LVAD research, “in the next decade, we have cause for concern in the MCS field,” Dr Cowger countered.

Both debaters suggested that MCS technology shouldn’t stop at HeartMate 3, even with its relatively impressive performance.

“Outcomes on HeartMate 3 are not the outcomes we really want for these patients. There are still innumerable complications. Hospitalization rates are extraordinarily high in these patients post-implant even if they’re successful implants. They bleed, they get infected, they get strokes. That still happens,” noted Dr Sweitzer.

Innovation issues aside, Dr Cowger pointed out that HeartMate 3 is also much larger than the HVAD, and the smaller device’s loss leaves a gap for patients. She said negative media views had not helped the recent “sense of apathy and loss of enthusiasm for MCS”.

“Physicians don’t want to use technology that will harm or be perceived to harm patients,” she said, noting that sentiment has shifted from “VADs are sexy, cool” to “we would not choose LVADs over [heart] transplant.”

Source: MedPage Today

Categories : Cardiovascular Disease Neurodegenerative DiseasesTags :

Unexpected Cognitive Effect of ARNI Therapy in Heart Failure

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Despite fears about cognitive decline in heart failure patients taking angiotensin receptor-neprilysin inhibition (ARNI), an observational study found that the drug instead had a protective effect.

Adults with systolic heart failure taking sacubitril/valsartan (Entresto) starting from 2015–2019 had fewer neurocognitive diagnoses up to 5 years later compared with a those staying on angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) alone.

  • Alzheimer’s disease: 1.11% on ARNI vs 1.24% on ACE inhibitors/ARBs
  • Dementia: 4.18% vs 6.49%
  • Cognitive decline: 11.82% vs 14.53%

On the basis of the PARAGON-HF trial,  sacubitril/valsartan won a broad heart failure indication, reaching into the normal ejection fraction range, for prevention of cardiovascular death and hospitalisation.

“Experimental studies with sacubitril/valsartan have fueled theoretical concerns about neurocognitive side effects, but long-term clinical data are scarce,” noted Prabhjot Grewal, MD, of Stony Brook University Hospital in New York, who reported the findings for the Heart Failure Society of America annual virtual meeting.

She explained that neprilysin inhibition by sacubitril could theoretically inadvertently interfere with the degradation of beta amyloid in the central nervous system, where neprilysin is expressed, in addition to the kidneys where it is most abundant.

However there are many factors in cognitive decline in heart failure, such as the circulatory deficit itself; vascular dementia resulting from comorbidities such as hypertension and vascular disease; and Alzheimer’s disease or Lewy body dementia. By ameliorating heart failure and improving blood pressure, drugs such as ACE inhibitors and sacubitril/valsartan could protect cognition, according to Mandeep Mehra, MBBS, MSc, of Brigham and Women’s Hospital and Harvard Medical School in Boston.

“Thus, even if a drug like sacubitril may cause worsening of one type of cognitive decline, it may be counterbalanced by positive effects on other domains since the reasons for cognitive decline in such patients are almost always multi-factorial and the signals may therefore be obfuscated in general analyses,” explained Mehra, who was not involved in the study.

The authors acknowledged that the observational study lacked systematic characterisation, and also leaves room for residual confounding despite propensity matching.

“This is why we require a prospective study that includes mechanistic end points (degree of beta amyloid protein deposition) in concert with functional outcomes (sensitive measures of cognitive decline) while ensuring that sufficient time is allowed to be evaluated since these are slow and subtle effects,” Mehra said, adding that the PERSPECTIVE trial will likely publish findings in 2022.

Source: MedPage Today

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Worse Lung Function Linked to Sudden Cardiac Death

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A new study found that people with modest but measurably worse lung function are more likely to suffer sudden cardiac death (SCD).

SCD is death due to a cardiovascular cause that occurs within one hour of the onset of symptoms. A sudden cardiac arrest occurs when the heart stops beating or is not beating sufficiently to maintain perfusion and life. There are often no previous warning signs, and is thought to be responsible for around 20% of all deaths in Europe.

The study was presented at the ERS International Congress by Dr Suneela Zaigham of Lund University. She said: “Although sudden cardiac deaths are common, we don’t know enough about who is at risk in the general population. There are links between lung and heart health, so we wanted to investigate whether measurable differences in lung function could offer clues about the risk of sudden cardiac death.”

The study involved 28 584 middle-aged participants with no known heart problems. All took part in spirometry tests where they were asked to blow into a machine to measure how well their lungs were working. Over the following approximately 40 years, researchers recorded any SCDs (death on the day of a coronary event) or any non-fatal coronary events (coronary events where people survived the first 24 hours)

They found that measurably lower lung function in middle-aged people (one standard deviation lower in the amount of air they could blow out in one second, which equates to around 0.8 litres) was more strongly associated with suffering a SCD (a 23% increase in risk) than a non-fatal coronary event (an 8% increase in risk) later on in life. The pattern of risk remained even in people who had never smoked.

Dr Zaigham said: “We believe this is the first study to directly compare the risk of sudden cardiac death and non-fatal coronary events and their links with lung function in the general population.

“Our findings suggest that testing people’s lungs when they are middle-aged and healthy could help spot those who have a higher risk of sudden cardiac death. This could enable people to take steps to potentially reduce the risk of this devastating event.”

A limitation of the study is that risk questionnaires were administered at the start of the study and these factors could have changed. The researchers next seek to see whether SCD could be prevented by testing lung function as part of current cardiovascular risk assessment. They plan to explore the link between lung function and SCD further to see if heart abnormalities, variable blood pressure or genetic causes are involved.

Source: European Respiratory Society

Categories : Cardiovascular Disease Diet and NutritionTags :

Added Potassium Salt Substitute Greatly Cuts CVD Risk

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Replacing table salt with a low-sodium, added potassium ‘salt substitute’ significantly reduces rates of stroke, heart attack and death, one of the largest dietary intervention studies ever conducted.

Presented at the European Society of Cardiology Congress in Paris, and simultaneously published in the New England Journal of Medicine, the results also showed that there were no harmful effects from the salt substitute, such as hyperkalaemia.

High sodium intake and low potassium intake are widespread. Both are linked to hypertension and increased risks of stroke, heart disease and premature death. Using a salt substitute – where part of the sodium chloride is replaced with potassium chloride – addresses both problems at once. Salt substitutes are known to lower blood pressure but their effects on heart disease, stroke, and death were unclear, until now.

Lead researcher, Professor Bruce Neal of The George Institute for Global Health, said that the benefit could prevent millions of early deaths with the widespread adoption of salt substitutes.

“Almost everyone in the world eats more salt than they should.  Switching to a salt substitute is something that everyone could do if salt substitutes were on the supermarket shelves,’’ he said.

“Better still, while salt substitutes are a bit more expensive than regular salt, they’re still very low-cost – just a few dollars a year to make the switch.”

“As well as showing clear benefits for important health outcomes, our study also allays concerns about possible risks.  We saw no indication of any harm from the added potassium in the salt substitute.  Certainly, patients with serious kidney disease should not use salt substitutes, but they need to keep away from regular salt as well,” added Professor Neal.

The Salt Substitute and Stroke Study enrolled 21 000 adults with either a history of stroke or poorly controlled blood pressure from 600 villages in rural areas of China from 2014 to 2015.

Participants in intervention villages were provided enough salt substitute to cover all household cooking and food preservation requirements – a daily amount of 20g per person. Those in the other villages continued using regular salt.

Over five years’ average follow up, more than 3000 participants had a stroke. Use of salt substitute reduced stroke risk by 14 percent, total cardiovascular events (strokes and heart attacks combined) by 13 percent and premature death by 12 percent.

Professor Neal said that as salt substitutes are relatively cheap (US$1.62 per kg vs US$1.08 per kg for regular salt in China), they are likely very cost effective.

“Last year, a modelling study done for China suggested that about 400 000 premature deaths might be prevented each year by national uptake of salt substitute. Our results now confirm this. If salt was switched for salt substitute worldwide, there would be several million premature deaths prevented every year,” he said.    

“This is quite simply the single most worthwhile piece of research I’ve ever been involved with. Switching table salt to salt substitute is a highly feasible and low-cost opportunity to have a massive global health benefit.”

As a result of the study, George Institute researchers are calling for salt manufacturers to embrace salt substitution, the promotion of salt substitutes by governments, and the use of substitute salt by consumers.

Source: George Institute for Global Health

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A Glass of Wine Raises Atrial Fibrillation Risk

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A single glass of wine can rapidly increase the risk of atrial fibrillation, according to new research published in Annals of Internal Medicine.

The study provides the first evidence that alcohol consumption significantly increases the chance of the heart rhythm condition occurring within a few hours, and is contrary to the notion of a cardioprotective effect of alcohol.

“Contrary to a common belief that atrial fibrillation is associated with heavy alcohol consumption, it appears that even one alcohol drink may be enough to increase the risk,” said Gregory Marcus, MD, MAS, professor of medicine in the Division of Cardiology at UCSF.

“Our results show that the occurrence of atrial fibrillation might be neither random nor unpredictable,” he said. “Instead, there may be identifiable and modifiable ways of preventing an acute heart arrhythmia episode.”

Atrial fibrillation (AF) is the most common heart arrhythmia seen clinically, but until now research has largely focused on risk factors and treatments for the disease, rather than what can trigger episodes. Large studies have established that chronic alcohol consumption can be a predictor for AF, and Marcus and other scientists have demonstrated that it is linked to increased risk for a first diagnosis of atrial arrhythmias.  

The research centered on 100 patients with documented AF who consumed at least one alcoholic drink a month, but without substance use disorders, certain allergies, or changing medications.

Each participant wore an electrocardiogram (ECG) monitor for roughly four weeks, pressing a button whenever they had a standard-size alcoholic drink. They were also all fitted with a continuously recording alcohol sensor. Blood tests reflecting alcohol consumption over the previous weeks were periodically administered. Participants consumed a median of one drink per day throughout the study period.

Researchers found that an AF episode was associated with two-fold higher odds with one alcoholic drink, and three-fold higher odds with two or more drinks within the preceding four hours. Increased blood alcohol concentration was also associated with AF episodes.

Study limitations included patients possibly forgetting to press their monitor buttons or minimising the number of button presses due to embarrassment, although these considerations would not have affected alcohol sensor readings. The study was also limited to those with established AF, not to the general population.

“The effects seem to be fairly linear: the more alcohol consumed, the higher the risk of an acute AF event,” said Prof Marcus. “These observations mirror what has been reported by patients for decades, but this is the first objective, measurable evidence that a modifiable exposure may acutely influence the chance that an AF episode will occur.”

Source: University of California – San Francisco

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When Damaged Hearts Struggle to Heal

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By analysing a certain protein that forms new blood vessels following a heart attack or unstable angina the long term-survival of heart patients could be predicted.

The study, published in PLOS ONE, has shown the presence or absence of a gene variant for the protein (vascular endothelial growth factor [VEGF]-A) can help predict the long-term survival chances in males who have experienced an acute coronary event.

Dr Barry Palmer of the Massey University School of Health Sciences said that the human body’s ability to recover from severe health events such as heart attacks is aided by its capacity for new blood vessel creation.

“Measuring an individual’s ability to restore blood circulation after a serious, life-threatening health event, may be useful in choosing treatment options and timing of specialist or GP visits. It may also have implications for susceptibility to other complex diseases, such as cancer.

“We showed testing for a VEGF-A gene variant from a patient’s blood was a useful predictor of how long these patients survived after their heart disease event. This association was most obvious in non-diabetic patients.”

The study reported on 1927 patients from the Coronary Disease Cohort Study in New Zealand, of which 30 percent had at least one previous episode of serious heart disease.

In a subgroup, the researchers also investigated the utility of measuring VEGF-A protein itself from 550 heart patients.

It has long been known that VEGF-A plays a role in helping cancer tumours to grow by increasing their blood supply, Dr Palmer said.

“In the heart disease field, it’s been suggested that high levels of VEGF-A might be a good thing to help grow new blood vessels around clogging or blocked arteries. The research so far has led to some controversy with some reports showing that more VEGF-A in the bloodstream is associated with better outcome in heart disease.

“While others, including our study, show high levels of VEGF-A after a heart event is linked to worse outcomes. An explanation for this could be that high VEGF-A levels may signal hearts under stress struggling to restore heart function, but not always rescuing function enough to save badly damaged hearts,” Dr Palmer added.

“High levels of VEGF-A in the blood may be being churned out to try and grow new blood vessels in a badly damaged heart, but may not be enough for the patients with the most damaged hearts. About 40 percent more of patients with high VEGF-A are dying within eight years of their original admission to hospital.

“After adjusting for seven other relevant measurements, patients with 10-fold higher levels of VEGF-A, measured shortly after their health event, had approximately twice the risk of death during the follow-up period.”

Source: Massey University

Categories : Cardiovascular Disease Expert OpinionTags :

‘Every Guideline We Write Is Out of Date’ Quips ESC as New Data Emerges

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Just as the European Society of Cardiology (ESC) unveiled their new guidelines for the treatment of heart failure, along came some data that the guideline’s authors hint will cause the work to be revised.

The guidelines, which appear in the European Heart Journal, state that so far, there is no treatment shown to reduce mortality and morbidity in patients with heart failure with preserved ejection fraction, however there are positive results from the EMPEROR-Preserved study showing that treatment with empagliflozin robustly reduced hospitalisation risk.

“Every guideline we write is out of date a few days after it’s published. I’m, of course, exaggerating a little bit, but guidelines are dynamic documents. They represent what we know at the time that they’re written and then new information comes out and they have to be updated, and that takes time,” Milton Packer, MD, of Baylor University Medical Center in Dallas, told MedPage Today.

“It’s a process, and we all understand that process; there is no real concept of finality here. We do the best we can with the data we have. And so these guidelines coming won’t represent the results of the EMPEROR-Preserved trial, but the next one will,” Dr Packer added.

Carlos Aguiar, MD, of Hospital Santa Cruz in Lisbon, agreed: “We also know that these new indications do need to go through the regulatory authorities, so it does take some time for the whole process to be concluded.”

“We do need to wait for those approvals also from the regulatory agencies in their reviews for physicians to be able to implement this in clinical practice,” he told MedPage Today.

However, the writers of the 2021 guideline did tweak the comprehensive algorithm for the treatment of heart failure, the highlights of which include:

  • Right heart catheterisation should be considered in patients in whom heart failure is thought to be due to constrictive pericarditis, restrictive cardiomyopathy, congenital heart disease, and high-output states. It may be considered in selected patients with heart failure with preserved left ventricular ejection fraction (LVEF) to confirm the diagnosis.
  • In patients with chronic heart failure with reduced LVEF, dapagliflozin (Farxiga) or empagliflozin are recommended to reduce hospitalisation and mortality risk. As a Class I recommendation, it is based on evidence gleaned from randomised clinical trials.
  • Vericiguat (Verquvo) may be considered in patients with New York Heart Association (NYHA) class II to IV heart failure after worsening with treatment with an angiotensin inhibitor, a beta-blocker, and a mineralocorticoid receptor antagonist, to reduce the risks of cardiovascular mortality or heart failure hospitalisation.
  • For treatment of heart failure with midrange LVEF — a change in term from “mildly reduced” ejection fraction — to reduce hospitalisation and mortality risk, the guidelines suggest a number of treatments including angiotensin inhibitors, beta-blockers, mineralocorticoid receptor antagonists, and the combination agent sacubitril/valsartan but none have strong clinical trial evidence (Class IIb)  .
  • For patients with heart failure with preserved ejection fraction, the current guidelines recommend (Class I evidence) screening for and treatment of aetiologies, as well as cardiovascular and non-cardiovascular comorbidities.
  • After hospitalisation for heart failure, the guidelines recommend (Class I evidence) that patients be carefully evaluated to exclude persistent signs of congestion before discharge and to optimise oral treatment, and that evidence-based oral medical treatment be administered before discharge. An early follow-up visit is recommended at 1 to 2 weeks after discharge to assess signs of congestion and drug tolerance, and to start and/or uptitrate evidence-based therapy.
  • The SGLT2 inhibitors canagliflozin (Invokana), dapagliflozin, empagliflozin, ertugliflozin (Steglatro), and sotagliflozin are recommended in patients with heart failure and type 2 diabetes at risk of cardiovascular events to reduce hospitalisations for heart failure, major cardiovascular events, end-stage renal dysfunction, and cardiovascular death. The SGLT2 inhibitors dapagliflozin, empagliflozin, and sotagliflozin are recommended in patients with type 2 diabetes and heart failure with reduced ejection fraction (Class I evidence). The DPP-4 inhibitor saxagliptin (Onglyza) is not recommended in patients with heart failure (Class III evidence).

Source: MedPage Today