Cardiology News

According to one research, myocarditis following SARS-CoV-2 immunisation was uncommon but more common in younger guys, especially after the second mRNA-1273 (Moderna) vaccine, showing that vaccine type, age, and gender should all be considered when vaccinating.

The study was published in the Canadian Medical Association Journal (Canadian Medical Association Journal) “In this study, we found higher observed rates of myocarditis after receiving mRNA vaccines than expected, but absolute rates were low,” writes Dr. Naveed Janjua of the University of British Columbia’s School of Population and Public Health and the British Columbia Centre for Disease Control in Vancouver, BC, with coauthors.

Researchers looked at population health data from the BC COVID-19 Cohort, which includes more than 10.2 million doses of mRNA vaccinations given to persons aged 12 and above between December 15, 2020, and March 10, 2022. Almost 7 million doses of BNT162b2 (Pfizer-BioNTech) and 3.2 million doses of mRNA-1273 (Moderna) were administered. The researchers looked for persons who were hospitalised to the hospital or went to the emergency room due to myocarditis between 7 and 21 days after getting the vaccination.

The rate of myocarditis 21 days after vaccination was 1.37 per 100,000 participants, compared to an anticipated rate of 0.39 per 100,000 unvaccinated people. Males (rate: 2.15/100 000), those aged 18-29 (rate: 2.97/100 000), after the second dose (rate: 2.27/100 000 doses), and persons vaccinated with mRNA-1273 (Moderna) (rate: 1.75/100 000) had the greatest risks of myocarditis. The incidence was 22.9/100,000 doses among males aged 18-29 who got the mRNA-1273 (Moderna) vaccination. Myocarditis rates were decreased after the third dosage, especially among those aged 18 to 29.

“The overall rates of myocarditis per 100 000 doses were still very low for both vaccine products,” write the authors. However, they state that their findings “… support the preferential use of the BNT162b2 (Pfizer-BioNTech) vaccine over the mRNA-1273 (Moderna) vaccine for people aged 18-29 years.”

A US study estimated that per million second doses of mRNA SARS-CoV-2 vaccine administered to males aged 12-29 years, 11 000 COVID-19 cases, 560 hospital admissions, 138 ICU admissions, and 6 deaths from COVID-19 could be avoided, compared to 39-47 expected cases of myocarditis after SARS-CoV-2 vaccination.

“The benefits of vaccination against SARS-CoV-2 in reducing the severity of COVID-19, hospital admission and deaths far outweigh the risk of developing myocarditis. … Thus, continued vaccination of this group, along with monitoring of adverse events, including myocarditis, should remain the preferred strategy,” the authors conclude.

Aortic valve stenosis occurs when the aortic valve narrows, limiting blood flow from the heart to the artery and then to the rest of the body. It can cause cardiac failure in extreme circumstances. Identifying the illness in distant places can be challenging since it needs advanced technology and early stage diagnoses are difficult to get.

Researchers from the University of Kerala and the University of Nova Gorica in Slovenia published a method to discover valve failure using a complicated network analysis that is accurate, simple to use, and low-cost in the Journal of Applied Physics, published by AIP Publishing.

“Many rural health centers don’t have the necessary technology for analysing diseases like this,” said author MS Swapna, of the University of Nova Gorica and the University of Kerala, adding, “For our technique, we just need a stethoscope and a computer.”

The diagnostic technique is based on the noises made by the heart. While the mitral and tricuspid valves shut, the organ makes a “lub” noise, stops as ventricular relaxation occurs and blood flows in, and then makes a “dub” noise as the aortic and pulmonary valves close.

Swapna and her colleagues created a graph, or a complicated network of connected nodes, using heart sound data gathered over 10 minutes. The data was divided into portions, and each segment was represented on the graph by a node, or a single point. A line, or edge, was drawn between the two nodes if the sound in that piece of the data was comparable to another segment.

The network in a healthy heart exhibited two different groups of points, with many nodes remaining disconnected. A heart with aortic stenosis, on the other hand, has many more relationships and edges. “In the case of aortic stenosis, there is no separation between the lub and dub sound signals,” Swapna said.

The researchers examined the graphs using machine learning to identify individuals with and without illness, attaining a classification accuracy of 100%. Their approach evaluates the correlation of each point, making it more accurate than others, merely the intensity of the signal, and accomplishes so in less than 10 minutes. It might help with early-stage diagnosis.

So far, the procedure has only been evaluated with data and has not been tested in a clinical context. The writers are working on a mobile application that will be available worldwide. Their method might possibly be used to diagnose other diseases. “The proposed method can be extended to any type of heart sound signals, lung sound signals, or cough sound signals,” Swapna said.

Predictions of the disease’s future prevalence are a crucial component of health policy-makers budget preparation and of significant interest to persons with a family history of cardiovascular disease (CVD). Researchers from Japan have now forecast a decline in CVD incidence through 2040 using new statistical modelling techniques. Governments need projections of disease rates to determine how much money will be needed for healthcare in the future and for what health priorities. However, due to the wide range of variables that affect disease rates, it might be difficult to make precise projections.

According to a research that will be published in The Lancet Regional Health – Western Pacific, between 2020 and 2040, there may be a decrease in coronary heart disease (CHD) and stroke mortality in Japan. “Key elements that must be considered include population ageing and population growth or reduction,” says Eri Kiyoshige, the study’s principal author. “When it comes to cardiovascular problems, additional variables such as rising diabetes, cholesterol levels, and body mass index lately observed in Japan play a vital influence.” Previous research that attempted to predict future CHD and stroke in Japan did not take into account the country’s 47 prefectures.

As a consequence, in addition to more typical statistical modelling, the researchers employed a Bayesian age-period-cohort model that takes into consideration Japanese population estimates as well as the number of CHD and stroke fatalities in Japan from 1995 to 2019. (for all men and women over 30 years of age). These were used to population forecasts for the years 2020 to 2040 in order to anticipate changes in CHD and stroke mortality more precisely than traditional modelling could.

“This model predicted that the number of national-level cardiovascular deaths in Japan will decrease from 2020 to 2040,” says Chris Kypridemos, one of the authors of the study. “Rates are also predicted to decline in most prefectures over this same time period, although some regional differences are predicted in 2040.”

The findings indicate that considerable decreases in death rates in the Japanese population can be expected to compensate for the negative consequences of an ageing population. Furthermore, changes in population size will have only a minor impact at the national and regional levels.

However, as CVD deaths decline and life expectancy rises, there is likely to be an increase in healthcare spending for dementia and frailty, as well as a possibly higher burden of residential care, all of which must be considered when estimating overall future healthcare expenses. These findings are likely to help health policymakers make more accurate funding choices, thereby improving health care at the national and regional levels in Japan.

According to a Rutgers study of obese persons with nonalcoholic fatty liver disease (NAFLD) and morbid obesity (body mass index > 40), those who had bariatric surgery had considerably fewer serious cardiovascular events in the years that followed.
The findings were published in JAMA Network Open, and the Rutgers team revealed that obese individuals receiving bariatric surgery were roughly 50% less likely to experience adverse cardiovascular events such as heart attacks, angina, or strokes.

“The findings provide evidence in support of bariatric surgery as an effective therapeutic tool to lower elevated risk of cardiovascular disease for select individuals with obesity and NAFLD,” said Vinod K. Rustgi, Distinguished Professor of Medicine, clinical director of Hepatology and director of the Center for Liver Diseases and Liver Masses at Rutgers Robert Wood Johnson Medical School.

“These findings are extremely significant for a variety of reasons.” Heart disease is the top cause of mortality for both men and women in the United States, regardless of race or ethnicity. According to the Centers for Disease Control and Prevention, around 697,000 persons in the United States died from heart disease in 2020. NAFLD and its more advanced variant, NASH, are both fast rising forms of liver disease that can affect persons who use little to no alcohol. The illness is more frequent in persons with obesity and type 2 diabetes because too much fat is deposited in liver cells, causing an inflammatory state.

Researchers used the MarketScan Commercial Claims and Encounters medical insurance database to assess outcomes data from 2007 to 2017. Of the 230 million people covered, 86,964 persons aged 18 to 64 with obesity and NAFLD were found. The research group included of 68 percent females, 35 percent underwent bariatric surgery, and 65 percent got nonsurgical therapy.

Patients who underwent bariatric surgery had a 49 percent lower chance of experiencing serious cardiovascular events such as heart attacks, heart failure, or ischemic strokes. They were also considerably less likely to suffer from angina, atherosclerosis, or arterial blood clots.

According to the researchers, the relationship between bariatric surgery and lower risk of developing cardiovascular disease has never been investigated in such depth. There is mounting evidence that bariatric surgery, due to the weight loss it induces in patients, has significant health advantages. A study done by Rustgi and colleagues, which was published in the journal Gastroenterology in March 2021, found that bariatric surgery can considerably lower the incidence of cancer, particularly obesity-related malignancies, in obese persons with NAFLD. Colorectal, pancreatic, endometrial, thyroid, multiple myeloma, and hepatocellular carcinoma were among the malignancies studied.

“Although bariatric surgery is a more aggressive approach than lifestyle modifications, it may be associated with other benefits, such as improved quality of life and decreased long-term health care burden,” Rustgi said.

A bacterial infection of the heart or blood arteries affects 40,000-50,000 people in the United States each year, with a 30% death rate after one year. People who inject drugs (PWID) are more likely to be younger and to develop infected endocarditis as a result of microbes entering the circulation (IE).

Indeed, the current opioid crisis is most likely to account for the surge in IE cases among younger patients and PWID. According to a new study published in the Journal of Internal Medicine, the risk of dying from infected endocarditis has grown by a factor of two among young US residents between the ages of 15 and 44 during the last two decades.

Furthermore, PWID among young people who die from IE has risen to almost 20%. Investigators reviewed death certificate data from the US Centers for Disease Control and Prevention and determined the following rates per 100,000 individuals (with age-adjusted rates):

The entire US population’s IE death rate declined from 2.1 in 1999 to 1.8 in 2020, however young US citizens’ mortality rates more than doubled over that time, rising from 0.3 in 1999 to 0.6 in 2020.

The mortality rate among adults aged 15 to 34 increased from 0.1 to 0.3.

Young people were responsible for 10% of all IE fatalities in 2020, up from 6.8% in 1999.

The percentage of PWID among all patients who died from IE grew from 1.1 per cent in 1999 to 3.0per cent in 2020; the percentage among young people also increased, from 10.2 per cent in 1999 to 19.5 per cent in 2020.

“The number of young people in the US who die of infective endocarditis is increasing, and the ongoin opioid epidemic, specifically injectable drug abuse, appears to be a significant cause,” said corresponding author Polydoros Kampaktsis, MD, PhD, of the Columbia University Irving Medical Center.

According to recent study, when heart cells develop in mice, the number of communication routes known as nuclear pores falls drastically. While this may shield the organ from harmful signals, the researchers discovered that it may also hinder adult heart cells from renewing.

The study, which was published today in Developmental Cell, suggests that quieting communication between heart cells and their environment protects this organ from harmful signals associated with stresses such as high blood pressure, but at the expense of preventing heart cells from receiving signals that promote regeneration.

“This paper provides an explanation for why adult hearts do not regenerate themselves, but newborn mice and human hearts do,” said senior author Bernhard Kuhn, M.D., professor of pediatrics and director of the Pediatric Institute for Heart Regeneration and Therapeutics at Pitt School of Medicine and UPMC Children’s Hospital of Pittsburgh. “These findings are an important advance in fundamental understanding of how the heart develops with age and how it has evolved to cope with stress.”

While skin and many other tissues of the human body retain the ability to repair themselves after injury, the same isn’t true of the heart. During human embryonic and fetal development, heart cells undergo cell division to form the heart muscle. But as heart cells mature in adulthood, they enter a terminal state in which they can no longer divide.

To understand more about how and why heart cells change with age, Kuhn teamed up with fellow Pitt researchers and biomedical imaging experts Yang Liu, Ph.D., associate professor of medicine and bioengineering, and Donna Stolz, Ph.D., associate professor of cell biology and pathology and associate director of the Center for Biologic Imaging, to look at nuclear pores. These perforations in the lipid membrane that surround a cell’s DNA regulate the passage of molecules to and from the nucleus.

“The nuclear envelope is an impermeable layer that protects the nucleus like asphalt on a highway,” said Kuhn, who is also a member of the McGowan Institute for Regenerative Medicine. “Like manholes in this asphalt, nuclear pores are pathways that allow information to get through the barrier and into the nucleus.”

Using super-resolution microscopy, Liu visualized and counted the number of nuclear pores in mouse heart cells, or cardiomyocytes. The number of pores decreased by 63% across development, from an average of 1,856 in fetal cells to 1,040 in infant cells to just 678 in adult cells. These findings were validated by Stolz who used electron microscopy to show that nuclear pore density decreased across heart cell development.

In previous research, Kuhn and his team showed that a gene called Lamin b2, which is highly expressed in newborn mice but declines with age, is important for cardiomyocyte regeneration.

In the new study, they show that blocking expression of Lamin b2 in mice led to a decrease in nuclear pore numbers. Mice with fewer nuclear pores had diminished transport of signaling proteins to the nucleus and decreased gene expression, suggesting that reduced communication with age may drive a decrease in cardiomyocyte regenerative capacity.

“These findings demonstrate that the number of nuclear pores controls information flux into the nucleus,” explained Kuhn. “As heart cells mature and the nuclear pores decrease, less information is getting to the nucleus.”

In response to stress, such as high blood pressure, the nucleus of a cardiomyocyte gets signals that alter gene pathways, resulting in structural remodelling of the heart. This remodelling is a significant contributor to heart failure.

To investigate how nuclear pores contribute to this remodelling process, the researchers employed a mouse model of elevated blood pressure. Mice with fewer nuclear pores demonstrated decreased regulation of gene pathways implicated in detrimental cardiac remodelling. In addition, these mice showed greater cardiac function and lifespan than their counterparts with more nuclear pores.

“We were surprised at the magnitude of the protective effect of having fewer nuclear pores in mice with high blood pressure,” said Kuhn. “However, having fewer communication pathways also limits beneficial signals such as those that promote regeneration.”

A multidisciplinary team from the University of Texas at Arlington will conduct new research on how to improve the safety and effectiveness of medical procedures done on patients with inoperable enlarged hearts.

Jun Liao, associate professor of bioengineering, developed a controlled septal ablation for inoperable hypertrophic cardiomyopathy. The cash will be used to strengthen the research environment at UTA as well as provide undergraduate students with access to cutting-edge biomedical research opportunities.

“This project bridges bioengineering innovation to clinical need,” Liao said. “When (coinvestigator) Dr Pietro Bajona brought up the clinical challenges in septal ablation, we answered with a novel idea and started working on it. This collaborative research paves a new avenue to better health for patients with inoperable enlarged hearts.”

Professor Kytai Nguyen, an expert in nanofabrication, and Associate Professor Yi Hong, an expert in biomaterials, are co-investigators from UTA Bioengineering. Other associates include Dr Matthias Peltz, surgical director of cardiac transplant at UT Southwestern Medical Center, and Bajona, director of the Allegheny Health Network’s Hypertrophic Cardiomyopathy Program. Both doctors will contribute their clinical knowledge and viewpoints to the contemplated study.

In order to lessen a left ventricular outflow obstruction, Liao said patients with inoperable enlarged hearts undergo a technique known as alcohol septal ablation in which a portion of the overgrowth septal muscle is removed. However, problems can develop from drinking only pure alcohol, resulting in uncontrollable cardiac muscle destruction.

“The current procedure brings with it some risky complications,” Liao said. “There is about a 2% mortality rate, with complications such as ventricular fibrillation, possible heart attack and a complete heart block due to indiscriminate tissue destruction.”

Liao claimed that recent studies even used super glue for pure alcohol, which presented problems regarding long-term safety and effectiveness.

“Our goal is to design a novel nanoparticle ablation system to replace the pure alcohol procedure,” Liao said. “We want to achieve a controllable, localized tissue shrinkage leading to a safer ablation.”

According to the Cleveland Clinic, between 600,000 and 1.5 million Americans suffer from an enlarged heart.

“This research could have a significant impact on hypertrophic cardiomyopathy, a genetic disease that results in abnormal thickening of the ventricular muscle, particularly the septum,” said Michael Cho, professor and chair of the Department of Bioengineering. “The research highlights UT Arlington’s ability to collaborate with other clinical institutions and their specialities to drive forward translational and transformative research.”

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For decades, scientists in Berlin have been researching a bizarre hereditary illness that causes half of certain families’ members to have abnormally short fingers, hypertension and dangerously high blood pressure. Patients who are not treated frequently die of a stroke when they reach the age of 50.

The study’s findings were published in the journal Circulation. Researchers at the Max Delbruck Center (MDC) in Berlin discovered the cause of the disease in 2015 and were able to prove it five years later using animal models: a mutation in the phosphodiesterase 3A gene (PDE3A) causes its encoded enzyme to become overactive, affecting bone growth and causing blood vessel hyperplasia, resulting in high blood pressure.

Immune to hypertension-related damage

“High blood pressure almost always leads to the heart becoming weaker,” said Dr. Enno Klussmann, head of the Anchored Signaling Lab at the Max Delbruck Center and a scientist at the German Centre for Cardiovascular Research (DZHK). As it has to pump against a higher pressure, Klussmann explains, the organ tries to strengthen its left ventricle. “But ultimately, this results in the thickening of the heart muscle – known as cardiac hypertrophy – which can lead to heart failure greatly decreasing its pumping capacity.”

But in hypertension patients with shortened fingers and mutated PDE3A gene, this doesn’t happen. “For reasons that are now partly – but not yet fully – understood, their hearts appear immune to the damage that usually results from high blood pressure,” said Klussmann.

The study is the result of a collaboration between researchers at the Max Delbruck Center, Charite – Universitatsmedizin Berlin, and the DZHK. In addition to Klussmann, professors Norbert Hubner and Michael Bader from the Max Delbruck Center were involved as final authors, along with Dr. Sylvia Bahring from the Experimental and Clinical Research Center (ECRC) – a joint institution of Charite and the Max Delbruck Center. Together with 43 other researchers from Berlin, Bochum, Heidelberg, Kassel, Limburg, Lubeck, Canada, and New Zealand, the team has now reported its findings on the protective effects of the gene mutation – and why these results could change the way heart failure is treated in the future.

The publication has four first authors, three of whom conduct research at the Max Delbruck Center and one at the ECRC.

Two mutations with the same effect

The scientists performed their tests on human patients with hypertension and brachydactyly (HTNB) syndrome – i.e., high blood pressure and abnormally short digits – as well as on rat models and heart muscle cells. The cells were grown from specially engineered stem cells known as induced pluripotent stem cells. Before testing began, researchers altered the PDE3A gene in the cells and the animals to mimic HTNB mutations.

“We came across a previously unknown PDE3A gene mutation in the patients we examined,” reports Bahring. “Previous studies had always shown the mutation in the enzyme to be located outside the catalytic domain – but we have now found a mutation right in the center of this domain.” Surprisingly, both mutations have the same effect in making the enzyme more active than usual. This hyperactivity ramps up the degradation of one of the cell’s important signalling molecules known as cAMP (cyclic adenosine monophosphate), which is involved in the contraction of the heart muscle cells. “It is possible that this gene modification – regardless of its location – causes two or more PDE3A molecules to cluster together and thus work more effectively,” Bahring suspects.

The proteins stay the same

The researchers used a rat model – created with CRISPR-Cas9 technology by Michael Bader’s lab at the Max Delbruck Center – to try to better understand the effects of the mutations. “We treated the animals with the agent isoproterenol, a so-called beta-receptor agonist,” says Klussmann. Such medications are sometimes used in patients with end-stage heart failure. Isoproterenol is known to induce cardiac hypertrophy. “Yet surprisingly, this occurred in the gene-modified rats in a manner similar to what we observed in the wild-type animals. Contrary to what we expected, existing hypertension did not aggravate the situation,” reports Klussmann. “Their hearts were quite obviously protected from this effect of the isoproterenol.”

In further experiments, the team investigated whether proteins in a specific signaling cascade of the heart muscle cells changed as a result of the mutation and if so which ones. Through this chain of chemical reactions, the heart responds to adrenaline and beats faster in response to situations such as excitement. Adrenaline activates the cells’ beta receptors, causing them to produce more cAMP. PDE3A and other PDEs stop the process by chemically altering cAMP. “However, we found little difference between mutant and wild-type rats at both the protein and the RNA levels,” Klussmann said.

More calcium in the cytosol

The conversion of cAMP by PDE3A does not occur just anywhere in the heart muscle cell, but near a tubular membrane system that stores calcium ions. A release of these ions into the cytosol of the cell triggers muscle contraction, thus making the heartbeat. After the contraction, the calcium is pumped back into storage by a protein complex. This process is also regulated locally by PDE.

Klussmann and his team hypothesized that because these enzymes are hyperactive in the local region around the calcium pump, there should be less cAMP, inhibiting the pump’s activity. “In the gene-modified heart muscle cells, we actually showed that the calcium ions remain in the cytosol longer than usual,” said Dr. Maria Ercu, a member of Klussmann’s lab and one of the study’s four first authors. “This could increase the contractile force of the cells.”

Activating instead of inhibiting

“PDE3 inhibitors are currently in use for acute heart failure treatment to increase cAMP levels,” Klussmann explains. Regular therapy with these drugs would rapidly sap the heart muscle’s strength. “Our findings now suggest that not the inhibition of PDE3, but – on the contrary – the selective activation of PDE3A may be a new and vastly improved approach for preventing and treating hypertension-induced cardiac damage like hypertrophic cardiomyopathy and heart failure,” Klussmann said.

But before that can happen, he says, more light needs to be shed on the protective effects of the mutation. “We have observed that PDE3A not only becomes more active, but also that its concentration in heart muscle cells decreases,” the researcher reports, adding that it is possible that the former can be explained by oligomerization – a mechanism that involves at least two enzyme molecules working together. “In this case,” said Klussmann, “we could probably develop strategies that artificially initiate local oligomerization – thus mimicking the protective effect for the heart.”

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Physical activity intervention during chemotherapy is safe, increases long-term cardiorespiratory fitness, and alleviates some of the side effects of cancer treatment, according to research published in JACC: CardioOncology. If exercise is not possible during chemotherapy, the individual can participate in a post-treatment exercise programme to regain function.

One of the most important independent predictors of cardiovascular health is cardiorespiratory fitness, as measured by peak oxygen uptake (VO2peak). VO2peak drops by up to 25% during cancer treatment. Cancer treatment frequently has negative effects on the patient’s health-related quality of life (HRQoL), such as decreased cardiorespiratory fitness, increased fatigue, and cardiovascular morbidity. Physical activity has been shown to reduce these risks.

Exercise therapy has been linked to improved cardiorespiratory fitness, increased VO2peak, and a reduction in cardiovascular morbidity, cancer mortality, and overall mortality.

“Exercise is widely recognised as beneficial to cancer patients. However, there is insufficient evidence on the best time to start exercising for improving long-term cardiorespiratory fitness in cancer patients “Annemiek M.E. Walenkamp, MD, PhD, senior author of the study and a medical oncologist at University Medical Center Groningen in Groningen, the Netherlands, said

The ACT trial looked at the efficacy of exercise intervention during chemotherapy versus after treatment for improving long-term cardiorespiratory fitness.

The study included adult patients who had recently been diagnosed with breast cancer, colon cancer, testicular cancer, or B-cell non-Hodgkin lymphoma and were scheduled to receive curative chemotherapy. Between February 2013 and November 2018, trial participants were randomly assigned to a 24-week exercise intervention that began either during or after chemotherapy.

Rigorous exercise

Moderate to vigorous effort on a stationary bicycle, resistance training with weight machines and free weights, and badminton were all types of exercise. The difference in VO2peak one year after the intervention was the primary endpoint. At all time points, the secondary endpoints were VO2peak after chemotherapy and intervention, muscle strength, HRQoL, fatigue, physical activity, and self-efficacy.

The researchers discovered that the group that began exercise therapy during treatment reported less fatigue and increased physical activity, as well as a decrease in VO2peak, HRQoL, and muscle strength. Three months after chemotherapy, the group that started exercising after treatment had similar values to the group that started exercising during treatment. Regardless of timing, both groups returned to their baseline cardiorespiratory fitness one year after completing the exercise intervention.

“These findings suggest that the best time to exercise is during chemotherapy. When exercising during chemotherapy is not possible, starting a physical exercise programme after chemotherapy is a viable option “Walenkamp explained. “We hope that our findings will encourage health-care providers to advise patients on exercise interventions during anti-cancer treatment.”

The American College of Cardiology envisions a world in which knowledge and innovation improve cardiovascular care and outcomes. The mission of the College and its more than 56,000 members, as the professional home for the entire cardiovascular care team, is to transform cardiovascular care and improve heart health.

The ACC confers credentials on cardiovascular professionals who meet stringent qualifications and is a driving force behind the development of health policy, standards, and guidelines. In addition, the College offers professional medical education, disseminates cardiovascular research through its world-renowned JACC Journals, operates national registries to measure and improve care, and provides cardiovascular accreditation to hospitals and institutions.

The ACC’s JACC Journals are ranked among the top cardiovascular journals in the world in terms of scientific impact.

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Article by Dr. Viveka Kumar – Principal Director & Chief of CathLabs (Pan Max), Cardiac sciences, Max Super speciality hospital

Sudden Cardiac Arrests are caused by an aberrant disruption of electrical signals in the heart that results in arrhythmia, which is characterized by rapid, irregular heartbeats. The heart then stops beating, cutting off the blood supply throughout the body. This often occurs in 4-6 minutes, during which it is crucial to perform CPR (cardiopulmonary resuscitation) in order to aid the patient in improving his or her chances of survival while also protecting the body from any potential catastrophic harm.

Depending on the severity of the attack and the outcomes of the screening tests conducted to aid in the diagnosis of any underlying conditions that may have contributed to it, a majority of patients spend a few days in the hospital.

5 early signs & symptoms of cardiac arrest everyone should know are as follows:

1. Chest Pain/Discomfort in the chest

It is best to get an ECG done to diagnose the problem if you consistently experience chest pain, even when you are not exercising, heavy lifting, running, or doing any other vigorous activities.

2. Momentary loss of consciousness

A patient may occasionally experience brief unconsciousness as a result of their heartbeat constantly fluctuating, which, if ignored, can lead to cardiac arrest. To treat the same, immediate action is necessary before complications arise.

3. Breathlessness

As your lungs and heart work harder to supply energy, you should not be surprised if you suffer shortness of breath while performing intense tasks. However, if the same thing happens while performing routine, low-energy jobs, there may be a substantial probability that you will experience Sudden Cardiac Arrest.

4. Heart palpitations

Sudden or frequent heart palpitations might be a primary indicator of a Sudden Cardiac Arrest. It is important to have your heart examined to rule out any underlying diseases if you are experiencing arrhythmias.

5. Weakness and dizziness

There may be a high likelihood that someone is developing the danger of experiencing a Sudden Cardiac Arrest if they feel weak and unsteady all the time.

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