Category: Cardiovascular Disease

Categories : Cardiovascular DiseaseTags :

Time to Rethink Beta Blockers as Secondary Prevention for Heart Attack Survivors?

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Secondary prevention after a heart attack, where beta blockers are used over the long term to curb the risk of further heart attacks or death, doesn’t seem to be warranted in patients who don’t have heart failure, suggests a large study published in the journal Heart.

The researchers found no difference in these risks between patients taking beta blockers more than a year after their heart attack and those not on these drugs.

Beta blockers are mostly used to manage abnormal heart rhythms, as well as angina and high blood pressure. They are routinely prescribed after a heart attack as secondary prevention to lower the risk of recurrence and other cardiovascular complications.

But it’s not clear if these drugs are warranted in patients who don’t have heart failure, or a potentially fatal complication of heart attack known as left ventricular systolic dysfunction (LVSD) beyond the first year.

Most of the current evidence is based on the results of clinical trials that predate major changes to the routine care of heart attack patients, explain the researchers.

The researchers drew on 43 618 adults who had had a heart attack between 2005 and 2016 that required hospital treatment, and whose details had been entered into the national Swedish register for coronary heart disease (SWEDEHEART).

None of these patients had heart failure or LVSD: 34 253 of them were prescribed beta blockers and were still on these drugs 1 year after hospital discharge; 9365 hadn’t been prescribed these drugs. Their average age was 64 and around 1 in 4 were women.

The researchers wanted to find out if there were any differences between the two groups in terms of deaths from any cause and rates of further heart attacks, revascularisation, or hospitalisation for heart failure.

The real time data showed that long term treatment with beta blockers wasn’t associated with improved cardiovascular outcomes during an average monitoring period of 4.5 years.

Some 6475 (19%) of those on beta blockers, and 2028 (22%) of those who weren’t, died from any cause, or had another heart attack, or required unscheduled revascularisation, or were admitted to hospital for heart failure.

After accounting for potentially influential factors, including demographics and relevant co-existing conditions, no significant difference was seen in rates of these events between the two groups.

As an observational study, it can’t establish cause. Additionally, despite being the largest study of its kind to date, the findings should be viewed in the context of certain limitations, acknowledge the researchers.

Patients weren’t randomised to treatment; only certain cardiovascular outcomes were included; there was no indication of how consistently patients took their drugs; nor any information on their health related quality of life.

And there were some differences between the two groups in respect of factors known to influence the risk of poor cardiovascular outcomes.

But, the researchers point out, beta blockers are associated with several side effects such as depression and fatigue, and it’s now time to reassess the value of long term treatment with these drugs in heart attack patients who don’t have heart failure or LVSD, they suggest.

In a linked editorial, Professor Ralph Stewart and Dr Tom Evans write: “Despite strong evidence that long-term beta-blockers can improve outcomes after [heart attack], it has been uncertain whether this benefit applies to lower risk patients who are taking other evidence-based therapies and who have a [normal functioning heart].”

They point out: “Recommendations on the duration of beta blocker therapy are variable or absent because this question was not specifically evaluated in clinical trials. Most patients take daily medications for many years after a [heart attack] because they believe they are beneficial.”

And they conclude: “[This] study raises an important question directly relevant to the quality of care –do patients with a normal [functioning heart] benefit from long term beta-blocker therapy after [heart attack]? To answer this question, more evidence from large randomised clinical trials is needed.”

Source: EurekAlert!

Categories : Cardiovascular Disease Obstetrics & GynaecologyTags :

Preterm Birth and Size Linked to Adult Fibrillation Risk

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A new study published in JAMA Pediatrics showed an association between being born preterm or large for gestational age and increased risks of atrial fibrillation later in life. Being small for gestational age at birth was only associated with an increased risk of atrial fibrillation up to the age of 18.

The incidence of atrial fibrillation in the young has increased over the past few decades, from low levels.

To date there have been little or mixed findings regarding the risk of atrial fibrillation in those with adverse birth outcomes. Atrial fibrillation increases the risk of stroke and other cardiovascular conditions, and is the most common form of cardiac arrhythmia. It mainly affects the middle-aged and the elderly. The estimated incidence in the young is low, 0.12 to 0.16%.

Low incidence in the young

A collaborative study involving researchers from Karolinska Institutet has now investigated the risk of atrial fibrillation according to preterm birth and foetal growth.

“Atrial fibrillation at a young age may involve a heavy socioeconomic burden for the affected individuals and we need to learn more about the underlying causes of the disease,” says first author Fen Yang, doctoral student at Karolinska Institutet. “Our findings may highlight the need to monitor and prevent the disease in individuals with an elevated risk of atrial fibrillation.”

“We found that individuals born preterm and those who were large for gestational age at birth had a slightly higher risk of developing atrial fibrillation up to middle-age than those with corresponding normal birth outcomes,” says principal investigator Krisztina László, associate professor at the Department of Global Public Health, Karolinska Institutet, and senior lecturer at the Department of Public Health and Caring Sciences at Uppsala University. “Individuals who were small for gestational age at birth had an increased risk of atrial fibrillation up to the age of 18, but not later in adulthood.”

The risk increase was 30% for individuals born preterm, 55% for individuals who were large at birth and 71% for individuals who were both preterm and large for gestational age at birth.

Eight million participants

The results of the study are based on statistical analyses of over eight million births from Danish (1978–2016), Finnish (1987–2014) and Swedish (1973–2014) medical birth registries who were followed for incident atrial fibrillation in the national patient and cause of death registries up to 2021. The results were compared with siblings in the same families. Since the study was observational, no causal relationships could be ascertained.

The researchers say that future studies may investigate the association between preterm birth, foetal growth, and the risk of atrial fibrillation up to old age.

Source: Karolinska Institutet

Categories : Cardiovascular Disease HIVTags :

Statins Trial in HIV Patients Ended Early Due to Efficacy

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Colourised scanning electron micrograph of HIV (yellow) infecting a human T9 cell (blue). Credit: NIH

A large randomised controlled trial into using statins in people with HIV and low-to-moderate cardiovascular risk was stopped early due to clear benefits, according to an update posted online in JAMA Network. Participants, who were taking 4mg pitavastatin calcium daily, saw a 35% reduction in risk with no significant difference in adverse events compared to placebo, according to the National Institutes of Health.

This recommendation came after a planned interim analysis of data from the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE) study, which enrolled 7769 participants, across 12 countries across Asia, Europe, North America, South America and Africa. Participants were aged 40–75 years, had 100 cells/mm3 of blood at enrollment, and had low-to-moderate traditional cardiovascular disease risk that would not typically be considered for statin treatment. 

It was not clear if statins would have the same effect in people living with HIV and who have premature cardiovascular disease despite having low-to-moderate traditional risk. The interim analysis was compelling enough that the study’s independent Data Safety and Monitoring Board recommended at its latest regular meeting that it be halted early given adequate evidence of efficacy.

The study participants are being notified of the findings and will continue to be monitored for several months. Study results from the review are expected to be published in the coming weeks.

Categories : Cancer Cardiovascular DiseaseTags :

Study Reveals Why Cancer Drugs Cause Cardiotoxicity

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While being effective at treating cancer, some cancer treatments can cause cardiotoxicity which can lead to heart failure – a phenomenon unexplained until now. An international study, published in the journal Science Advances, has identified proteins present in the blood that are linked to an increased risk of developing cardiac disease, including heart failure, and which are also affected by drugs used in cancer treatment.

The findings can explain how cancer drugs cause their damaging effects on the heart and could help to identify those at increased risk. In the long run, the researchers believe this will help to improve cancer treatments, with new drugs potentially being developed that can shrink tumours without affecting the identified proteins.

In addition, the study reveals new potential drug targets for treating heart diseases including heart failure. These may work by inhibiting proteins linked to higher disease risk, or activating proteins linked to lower risk.

The researchers first performed a genome-wide association study, searching through the DNA of nearly 37,000 people without heart disease enrolled in the UK Biobank study. This identified genetic variants linked to changes to the structure and function of the pumping chambers of the heart – the ventricles.

The researchers then pinpointed 33 proteins using Mendelian randomisation, coded for by these genetic variants, that are present in the blood and associated with the risk of developing several heart diseases. These included different types of heart failure, and atrial fibrillation (a common abnormal heart rhythm which increases the risk of stroke). Crucially, many of these proteins are the targets of drugs currently used to treat cancer.

Lead author Dr Floriaan Schmidt said: “The proteins identified in our study will help to accelerate future drug development, offering scientists a blueprint for new treatments for both cancer and heart diseases. This can help them to be more confident of the effects of the drugs that they design – whether that’s shrinking tumours without causing damage elsewhere or improving the heart’s pumping action.”

Professor Sir Nilesh Samani, Medical Director at the British Heart Foundation, said: “While there have been advances in treating cancer, one of the consequences has been a risk of heart damage from these drugs.

“This research points the way towards developing safer and more refined drugs so that, one day, worries about developing heart problems after cancer treatment might be a thing of the past.”

Source: University College London

Categories : Cardiovascular Disease Pain ManagementTags :

Researchers Quantify Risk Factors for Oral Diclofenac

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Safety concerns related to the widely used analgesic diclofenac may be tied to a little-studied drug-metabolising enzyme which can vary as much as 3000 times across individuals, according to new research published in the journal Clinical Pharmacology & Therapeutics.

The findings could be used to develop ways to identify those at risk of serious side effects from the drug. They may help determine safer dosing standards for specific populations, including women, young children and people of certain ethnicities.

Used to treat arthritis-associated pain and inflammation, diclofenac was available over-the-counter in the US until 2013, when the Food and Drug Administration restricted it to prescription-only use following reports of the drug causing heart damage. More than 10 million prescriptions per year are written for it in the US. It is also one of the most widely used non-steroidal anti-inflammatory drugs worldwide, and is still over-the-counter in many countries. 

“Most patients who are using diclofenac have arthritis, and many of them are at risk of heart disease,” senior author Bhagwat Prasad, an associate professor at Washington State University. “So there is a concern that taking diclofenac may be putting them at even greater risk of cardiovascular events such as heart attack and stroke.”

Previous findings by the WSU team had found a high degree of variability in the expression of UGT2B17, an enzyme that is a known player in diclofenac metabolism. They found that the enzyme is present at much lower levels in women than in men, which could explain the increased risk of heart damage seen in women taking diclofenac. The enzyme was also mostly absent in children under age 9 and discovered large ethnicity-based differences in the number of people who lack the gene for the enzyme altogether, which ranges from around 20% of Caucasians up to around 90% of Japanese people.

In this new study, the WSU researchers used human liver and intestinal samples along with computer modelling to quantify the degree to which this enzyme contributes to diclofenac metabolism relative to other related enzymes. They found it to be a major player, supporting the idea that low levels of the UGT2B17 enzyme may be the cause of heart damage tied to diclofenac use.

“No one knew why this heart toxicity is happening in some individuals,” said first author Deepak Ahire, a graduate student in the WSU College of Pharmacy and Pharmaceutical Sciences. “Our study showed, for the first time, that UGT2B17 is important in diclofenac metabolism and suggests that differences in UGT2B17 expression are what makes people’s response to diclofenac so variable, leading to toxicity in some whereas for others the drug simply does not work.”

Ahire said that their study found that this enzyme metabolises diclofenac mainly in the intestine, unlike other related enzymes that are active mostly in the liver. Thus the observed effects are limited to diclofenac tablets taken by mouth, which provides for the quickest absorption and pain relief.

The findings suggest genetic testing could help healthcare providers evaluate safety risks before prescribing diclofenac. Prasad also noted that drug regulatory authorities in countries where diclofenac is still available over the counter should consider doing efficacy testing to determine the optimal dose of the drug for their local market.

The WSU researchers are currently in the process of confirming their findings in a pilot clinical trial. Their next step would be to pursue collaborations with large hospitals to study the connection between diclofenac and heart damage in patients’ electronic medical records.

Source: Washington State University

Categories : Cardiovascular DiseaseTags :

Sedentary Time may Significantly Enlarge Teens’ Hearts

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Photo by Steinar Engeland on Unsplash

In adolescents, sedentary time may increase heart size three times more than moderate-to-vigorous physical activity, according to a paper published in the Scandinavian Journal of Medicine & Science in Sports. The British and Finnish researchers explored the associations of sedentary time, light physical activity, and moderate-to-vigorous physical activity with cardiac structure and function.

Recent World Health Organization reports and guidelines note that more than 80% of adolescents across the globe have insufficient physical activity per day. Physical inactivity has been associated with several non-communicable diseases in adults such as cardiovascular diseases, type 2 diabetes, and cancer. In the pediatric population, the majority of movement behaviour studies have focused on the effect of sedentary behaviour and physical activity on cardiometabolic health which includes blood pressure, insulin resistance, blood lipids, and body mass index.

There has been a gap in knowledge on the effect of sedentary time and moderate-to-vigorous physical activity on cardiac structure and function in large adolescent populations due to the scarcity of device-measured movement behaviour and echocardiography assessment in the pediatric population. A higher left ventricular mass, which indicates an enlarged or hypertrophied heart, and a reduced left ventricular function, which indicates decreased heart function, may in combination or independently lead to an increased risk of heart failure, myocardial infarction, stroke, and premature cardiovascular death.

The current study, which used data from the University of Bristol study Children of the 90s (also known as the Avon Longitudinal Study of Parents and Children) included 530 adolescents aged 17 years who had complete measurements of fat mass, muscle mass, glucose, lipids, an inflammation marker, insulin, smoking status, socio-economic status, family history of cardiovascular disease, echocardiographic cardiac function and structure measures, and accelerometer-based measure of sedentary time, light physical activity, and moderate-to-vigorous physical activity.

On average, adolescents spent almost 8 hours/day sedentary and about 49 minutes/day in moderate-to-vigorous physical activity in this new study. It was observed that both sedentary time and moderate-to-vigorous physical activity were associated with higher left ventricular mass. However, the increase in cardiac mass (3.8g/m2.7) associated with sedentary time was three times higher than the cardiac mass increase (1.2g/m2.7) associated with moderate-to-vigorous physical activity. This finding was observed in adolescents irrespective of their obesity status, ie among adolescents who had normal weight and those who were overweight or obese. Importantly, light physical activity was not associated with an increase in cardiac mass but was associated with better cardiac function estimated from left ventricular diastolic function.

“This novel evidence extends our knowledge of the adverse effects of sedentary time on cardiac health. It is known among adults that a 5g/m2 increase in cardiac mass may increase the risk of cardiovascular disease and death by 7–20%. Engaging in moderate-to-vigorous physical activity also slightly enlarged the heart but it seems an acceptable negative side effect considering several other health benefits of moderate-to-vigorous exercise. Hence, public health experts, health policymakers, high school administrators and teachers, paediatricians, and caregivers are encouraged to facilitate adolescent participation in physical activity to enable a healthy heart,” says Andrew Agbaje, a physician and clinical epidemiologist at the University of Eastern Finland.

Source: University of Eastern Finland

Categories : Cardiovascular DiseaseTags :

Scientists ‘Poke the Bear’ to Gain a Better Understanding of Blood Clotting

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It’s generally good advice not to “poke the bear” as they say, but that’s exactly what a multinational team of scientists have been doing, to discover the secrets of blood clotting. Hibernating bears, paralysed humans, and pigs kept in small enclosures all avoid dangerous blood clots, despite being immobile for extremely long periods.

Their new study published in Science shows that reduction of a key protein inhibits the formation of blood clots in all three mammal species when they are immobile for days, months or even years.

Passengers on long haul flights run the risk of developing deep vein thrombosis if they do not take some time to walk around and use compression socks. Some people are predisposed to blood clots, due to genetic factors.

Yet, when humans – and other mammals such as bears – are immobilised for a much longer period than a flight, the researchers found that a protein known as Hsp47 is reduced by 55 times. This could lead to new medicines to help those who have inherited blood clotting disorders that put them at risk for pulmonary embolism, heart attack, and stroke.

Professor Jon Gibbins led the work at the University of Reading. He said: “It seems counterintuitive that people who have severe paralysis don’t appear to be at higher risk of blood clots. This tells us that something interesting is happening. And it turns out that reducing levels of Hsp47 plays a key role in preventing clots, not just in humans, but in other mammals, including bears and pigs.

“When we see something like this in multiple species, that reinforces its importance. Having Hsp47 must have been an evolutionary advantage.”

Hsp47 is released by platelets – the sticky blood cells that trigger blood clotting.  Usually clotting is an important response to an injury, to prevent blood loss, and Hsp47 is one of the necessary ingredients to enable platelets to do their job. Examining the role of Hsp47 in clotting function the team found that when released into the blood of bears, mice and humans that it promoted conditions that may give rise to deep vein thrombosis.

Professor Gibbins said, “We aren’t totally sure how, but it appears that there is something about movement that keeps Hsp47 at an appropriate level. It could be that the mechanical forces involved in moving around actually have an impact on gene expression, dramatically increasing the amount of Hsp47 that circulates in the blood.”

The team took blood samples from bears in winter, while hibernating, and in summer, while awake and moving around. They also compared people who were immobilised with those who can move and walk. And finally, pigs kept in small pens were compared with others that were free to move around in barns. In all three cases, proteomics experiments showed that the absence of movement was associated with having far less Hsp47.

Professor Gibbins continued: “Now we know that Hsp47 is so important, we can begin to look for new or existing medicines that might be able to inhibit the function of this protein in blood clotting and protect mobile people who are prone to clots.”

Source: University of Reading

Categories : Cardiovascular Disease Diet and NutritionTags :

The Effectiveness of Salt Restriction in Primary Aldosteronism

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Results from a clinical trial published in the Journal of Internal Medicine reveal several health benefits of moderate salt restriction in patients on standard medical treatment for primary aldosteronism/ These included lowered blood pressure and reduced depressive symptoms. 

Primary aldosteronism – when adrenal glands produce excess aldosterone – is a common cause of secondary hypertension. The combination of aldosterone excess and high dietary salt intake leaves affected patients with a higher risk of cardiovascular disease than patients with hypertension from other causes. Mineralocorticoid antagonists are the main treatment of primary aldosteronism, but these medications do not completely normalise patients’ elevated cardiovascular risk.

Because elevated aldosterone and high dietary salt intake have detrimental effects on patients’ health, investigators wanted to find out whether salt restriction might benefit patients. In the non-randomised single-arm Salt CONNtrol trial that included 41 patients, moderate salt restriction reduced blood pressure and depressive symptoms without detectable adverse effects.

“The study shows that a moderate dietary salt restriction is feasible, when combined with a dedicated smartphone app for continuous motivation, and has a strong antihypertensive effect in patients with primary aldosteronism,” said corresponding author Christian Adolf, MD, of Ludwig Maximilian University of Munich, in Germany. “Our findings will help to improve care for patients with primary aldosteronism and, likely, also for subgroups of patients with essential hypertension.”

Source: Wiley

Categories : Cardiovascular Disease Emergency MedicineTags :

Better Survivor Outcomes One Year after Cardiac Arrest When Bystanders Perform Defibrillation

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Survivors of out-of-hospital cardiac arrest (OHCA) who received initial bystander defibrillation with a nearby automated external defibrillator (AED) reported better outcomes at 12 months after arrest compared with those initially defibrillated by paramedics, according to a new study from Monash University which appears in Heart.

The retrospective study recruited adult non-traumatic OHCA with initial shockable rhythms between 2010 and 2019. Survivors at 12 months after arrest were invited to participate in structured telephone interviews. Outcomes were identified using the Glasgow Outcome Scale-Extended (GOS-E), EuroQol-5 Dimension (EQ-5D), 12-Item Short Form Health Survey and living and work status-related questions.

Of 6050 patients, 3211 (53.1%) had a pulse on hospital arrival, while 1879 (31.1%) were discharged alive. Survival rates were highest with bystander defibrillation (52.8%), followed by dispatched first responders (36.7%) and paramedics (27.9%). Of the survivors, 1802 (29.8%) survived to 12-month post-arrest; of these 1520 (84.4%) were interviewed. 1088 (71.6%) were initially shocked by paramedics, 271 (17.8%) by first responders and 161 (10.6%) by bystanders. Bystander-shocked survivors reported higher rates of living at home without care (87.5%), upper good recovery (GOS-E=8) (41.7%) and EQ-5D visual analogue scale (VAS) ≥ 80 (64.9%) compared with first responder and paramedics, respectively. After adjustment, initial bystander defibrillation was associated with higher odds of EQ-5D VAS ≥ 80 (adjusted OR (AOR) 1.56), good functional recovery (GOS-E ≥ 7) (AOR 1.53), living at home without care (AOR 1.77) and returning to work (AOR 1.72) compared with paramedic defibrillation.

Categories : Cardiovascular Disease NeurologyTags :

Researchers Identify a Protein to Treat Intracerebral Haemorrhage

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Photo by cottonbro studio from Pexels

University of Helsinki and Taiwanese researchers have found a new way to remove waste from the brain after haemorrhage, using a protein called cerebral dopamine neurotrophic factor (CDNF).

Intracerebral haemorrhage, and bleeding into the brain tissue, is a devastating neurological condition affecting millions of people annually. It has a high mortality rate, with long-term neurological deficits experienced by many survivors. To date, no medication has been identified that supports brain recovery following haemorrhage.

In an international collaboration, researchers from the Brain Repair laboratory, University of Helsinki, together with their Taiwanese colleagues investigated whether CDNF, a protein being currently tested for Parkinson’s disease treatment, could be a potential treatment for brain haemorrhage.

Research suggests that CDBF also has therapeutic effects and enhances immune cell’s response after brain haemorrhage. The authors found that the administration of cerebral dopamine neurotrophic factor accelerates haemorrhagic lesion resolution, reduces brain swelling, and improves functional outcomes in an animal model of brain haemorrhage.

“Surprisingly, we found that cerebral dopamine neurotrophic factor acts on immune cells in the bleeding brain, by increasing anti-inflammatory mediators and suppressing the production of the pro-inflammatory cytokines that are responsible for cell signalling. This is a significant step towards the treatment of injuries caused by brain haemorrhage, for which we currently have no cure,” says Professor Mikko Airavaara, from University of Helsinki.

Dr.Vassileios Stratoulias from the Brain Repair laboratory comments, “It’s interesting to note that after a bleeding episode, the brain contains a lot of waste and debris. Cerebral dopamine neurotrophic factor encourages immune cells in the brain to consume and remove the waste and debris, which is essential for the brain’s recovery!.”

The administration of cerebral dopamine neurotrophic factor also resulted in the alleviation of cell stress in the area that surrounds the haematoma.

Finally, the researchers demonstrated that systemic administration of cerebral dopamine neurotrophic factor promotes scavenging by the brain’s immune cells after brain haemorrhage and has beneficial effects in an animal model of brain haemorrhage.

Source: University of Helsinki