Colleagues pay tribute to highly respected Dr Singh
Dr Surendra Singh. Photo: supplied
Monday, 27 May 2024. The passing of esteemed cardiologist Dr Surendra Singh (11 April 1955 – 16 May 2024) at the age of 69 after a short illness is a tremendous loss to healthcare in KwaZulu-Natal, the communities he served and everyone who knew him.
“We wish to express our sincere condolences to Dr Singh’s wife, Professor Shanta, and his children Rajiv, Ameet and Rhea,” said Netcare uMhlanga Hospital general manager Wendy Beato.
“We mourn the passing of an exceptional healthcare professional and a man of stature. Dr Singh was highly respected and much loved by his colleagues, patients and the staff and management of Netcare uMhlanga Hospital, where he has practised for several years.
“Dr Singh will be deeply missed by all who had the privilege to know him,” she says.
After qualifying as a cardiologist in 1990, Dr Singh embarked on a journey during which he harnessed the power of his knowledge to heal others. Known for this brilliance both as a man and a doctor, he possessed a rare combination of exceptional expertise, humility and deep caring.
“Dr Singh’s dedication to his patients was evident throughout his career, and he continued to provide much valued service at Netcare uMhlanga Hospital until he became ill. His passing leaves a deep void for all who knew him and the countless patients whose lives he touched throughout his career.
“Dr Singh’s legacy as a caring healthcare provider and respected cardiologist will endure. Through his considerable dedication and expertise, he improved and saved lives while inspiring a new generation of healthcare professionals. His passion for healing and deep commitment to his patients will be forever remembered. Although his time with us was cut short, the impact of his life’s work will continue to be felt for many years to come,” Beato concluded.
Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health
Changes in the gut microbiome have been implicated in a range of diseases including type 2 diabetes, obesity, and inflammatory bowel disease. Now, a team of researchers has found that microbes in the gut may affect cardiovascular disease as well. In a study published in Cell, the team has identified specific species of bacteria that consume cholesterol in the gut and may help lower cholesterol and heart disease risk in people.
Researchers at the Broad Institute of MIT and Harvard along with Massachusetts General Hospital analysed metabolites and microbial genomes from more than 1400 participants in the Framingham Heart Study, a decades-long project focused on risk factors for cardiovascular disease.
The team discovered that bacteria called Oscillibacter take up and metabolise cholesterol from their surroundings, and that people carrying higher levels of the microbe in their gut had lower levels of cholesterol. They also identified the mechanism the bacteria likely use to break down cholesterol. The results suggest that interventions that manipulate the microbiome in specific ways could one day help decrease cholesterol in people. The findings also lay the groundwork for more targeted investigations of how changes to the microbiome affect health and disease.
“Our research integrates findings from human subjects with experimental validation to ensure we achieve actionable mechanistic insight that will serve as starting points to improve cardiovascular health,” said Xavier, who is a core institute member and a professor at Harvard Medical School and Massachusetts General Hospital.
Postdoctoral researcher Chenhao Li and research scientist Martin Stražar, both in Xavier’s lab, were co-first authors on the study.
Cholesterol cues
In the past decade, other researchers have uncovered links between composition of the gut microbiome and elements of cardiovascular disease, such as a person’s triglycerides and blood sugar levels after a meal. But scientists haven’t been able to target those connections with therapies in part because they lack a complete understanding of metabolic pathways in the gut.
In the new study, the Broad team gained a more complete and detailed picture of the impact of gut microbes on metabolism. They combined shotgun metagenomic sequencing, which profiles all of the microbial DNA in a sample, with metabolomics, which measures the levels of hundreds of known and thousands of unknown metabolites. They used these tools to study stool samples from the Framingham Heart Study.
“The project outcomes underline the importance of high-quality, curated patient data,” Stražar said. “That allowed us to note effects that are really subtle and hard to measure and directly follow up on them.”
More than 16 000 associations between microbes and metabolic traits were found, one of them particularly strong: People with several species of bacteria from the Oscillibacter genus had lower cholesterol levels than those who lacked the bacteria. The researchers found that species in the Oscillibacter genus were surprisingly abundant in the gut, representing on average 1 in every 100 bacteria.
The researchers then wanted to figure out the biochemical pathway the microbes use to break down cholesterol. To do this, they first needed to grow the organism in the lab. Fortunately, the lab has spent years collecting bacteria from stool samples to create a unique library that also included Oscillibacter.
After successfully growing the bacteria, the team used mass spectrometry to identify the most likely byproducts of cholesterol metabolism in the bacteria. This allowed them to determine the pathways the bacteria uses to lower cholesterol levels. They found that the bacteria converted cholesterol into intermediate products that can then be broken down by other bacteria and excreted from the body. Next, the team used machine-learning models to identify the candidate enzymes responsible for this biochemical conversion, and then detected those enzymes and cholesterol breakdown products specifically in certain Oscillibacter in the lab.
The team found another gut bacterial species, Eubacterium coprostanoligenes, that also contributes to decreased cholesterol levels. This species carries a gene that the scientists had previously shown is involved in cholesterol metabolism. In the new work, the team discovered that Eubacterium might have a synergistic effect with Oscillibacter on cholesterol levels, which suggests that new experiments that study combinations of bacterial species could help shed light on how different microbial communities interact to affect human health.
Microbial messages
The human gut microbiome remains mostly unmapped, but the team believes they have paved the way for the discovery of other similar metabolic pathways impacted by gut microbes, which could be targeted therapeutically.
“There are many clinical studies trying to do faecal microbiome transfer studies without much understanding of how the microbes interact with each other and the gut,” Li said. “Hopefully stepping back by focusing on one particular bug or gene first, we’ll get a systematic understanding of gut ecology and come up with better therapeutic strategies like targeting one or a few bugs.”
“Because of the large number of genes of unknown function in the gut microbiome, there are gaps in our ability to predict metabolic functions,” Li added. “Our work highlights the possibility that additional sterol metabolism pathways may be modified by gut microbes. There are potentially a lot of new discoveries to be made that will bring us closer to a mechanistic understanding of how microbes interact with the host.”
Managing circadian rhythms through intense light and chronologically timed therapy can help prevent or treat a variety of circulatory system conditions including heart disease, according to a new study published in Circulation Research.
“The impact of circadian rhythms on cardiovascular function and disease development is well established,” said the study’s lead author Tobias Eckle, MD, PhD, professor of anaesthesiology at the University of Colorado School of Medicine.
“However, translational preclinical studies targeting the heart’s circadian biology are just now emerging and are leading to the development of a novel field of medicine termed circadian medicine.”
The senior author is Professor Tami A. Martino, PhD, distinguished chair in molecular and cardiovascular research at the University of Guelph in Ontario, Canada.
The study reviews current circadian medicine research, focusing on the use of intense light therapy following surgery, utilizsng light to treat cardiac injury, exploring how cardiovascular disease can differ between men and women and administering drugs at specific times of day to coincide with the body’s internal clock to speed healing.
It also urges more aggressive use of this therapy in humans, rather than relying on mostly animal models.
“There are literally millions of patients who could benefit from this,” Eckle said.
“The treatments are almost all low-risk. Some involve using light boxes and others use drugs that are already on the market.”
Circadian rhythms significantly influence how the cardiovascular system operates. Timing is everything. Blood pressure and heart rates follow distinct patterns, peaking during the day and ebbing at night. When this is disrupted, it leads to worse cardiovascular disease outcomes including myocardial infarction and heart failure. Light is critical in maintaining the proper balance and functioning of the body. Shift employees who may work night hours then day hours often have worse cardiac outcomes.
Eckle, who has studied circadian rhythm and health for years, said intense light can help heal the body after heart surgery while protecting it from injury during surgery, including reducing the chances of cardiac ischemia.
According to the researchers, when light hits the human eye it is transmitted to the suprachiasmatic nucleus, a structure in the brain’s hypothalamus that regulates most circadian rhythms in the body.
Intense light stabilizes the PER2 gene and increases levels of adenosine, which blocks electrical signals in the heart that cause irregular rhythms, making it cardiac protective.
Eckle has used light therapy with patients after surgery and seen positive results including lower levels of troponin, a key protein whose elevation can signal a heart attack or stroke.
Given the mounting evidence that intense light and timed drug treatments are effective, he said, it is time to move forward with more clinical trials.
“Circadian rhythms play a crucial role in cardiovascular health, influencing the timing of onset and severity of cardiovascular events and contributing to the healing process from disease,” Eckle said. “Studies in humans are clearly required. Regarding intense light therapy, chronotherapy and restricted feeding are low-risk strategies that should be tested sooner than later.”
Cleveland Clinic researchers have identified a new pathway that contributes to cardiovascular disease associated with high levels of niacin, a common B vitamin previously recommended to lower cholesterol.
The team, led by Stanley Hazen, MD, PhD, reported in NatureMedicine that they had found a link between 4PY, a breakdown product from excess niacin, and cardiovascular disease. Higher circulating levels of 4PY were strongly associated with development of heart attack, stroke and other adverse cardiac events in large-scale clinical studies.
The researchers also showed in preclinical studies that 4PY directly triggers vascular inflammation which damages blood vessels and can lead to atherosclerosis over time. The study also details genetic links between 4PY and vascular inflammation.
The findings provide a foundation for potential new interventions and therapeutics to reduce or prevent that inflammation.
“What’s exciting about these results is that this pathway appears to be a previously unrecognised yet significant contributor to the development of cardiovascular disease,” said Dr Hazen, Chair of Cardiovascular and Metabolic Sciences at Cleveland Clinic’s Lerner Research Institute and Co-Section Head of Preventive Cardiology in the Heart, Vascular & Thoracic Institute.
“What’s more, we can measure it, meaning there is potential for diagnostic testing. These insights set the stage for developing new approaches to counteract the effects of this pathway.”
Niacin (vitamin B-3) is very common in a Western diet. “For decades, the United States and more than 50 nations have mandated niacin fortification in staple foods such as flour, cereals and oats to prevent disease related to nutritional deficiency,” said Dr Hazen.
Yet one in four subjects in the researchers’ patient cohorts appear to be getting too much, and had high levels of 4PY, which appears to contribute to cardiovascular disease development.
Dr. Hazen compares our intake of niacin as multiple taps pouring water into a bucket.
Once that bucket is filled, it begins to spill over. The human body then needs to process that spill-over and produce other metabolites, including 4PY.
“The main takeaway is not that we should cut out our entire intake of niacin – that’s not a realistic approach,” said Dr Hazen.
“Given these findings, a discussion over whether a continued mandate of flour and cereal fortification with niacin in the US could be warranted.”
Dr. Hazen notes broader use of over-the-counter supplements made with different forms of niacin have also become popular because of presumed anti-aging purposes.
He adds that patients should consult with their doctors before taking over-the-counter supplements and focus on a diet rich in fruit and vegetables while avoiding excess carbohydrates.
The new findings also might help explain why niacin, one of the first treatments prescribed to lower LDL cholesterol, is no longer a go-to treatment for for this.
Eventually niacin was shown to be less effective than other cholesterol-lowering drugs and was associated with other negative effects and higher mortality rates in previous research.
“Niacin’s effects have always been somewhat of a paradox,” Dr Hazen said.
“Despite niacin lowering of cholesterol, the clinical benefits have always been less than anticipated based on the degree of LDL reduction. This led to the idea that excess niacin caused unclear adverse effects that partially counteracted the benefits of LDL lowering. We believe our findings help explain this paradox. This illustrates why investigating residual cardiovascular risk is so critical; we learn so much more than what we set out to find.”
The study authors note that long-term investigations are needed to assess the effect of chronic elevation of 4PY levels on atherosclerosis and other phenotypes.
University of Pittsburgh Schools of Medicine researchers uncovered a fundamental mechanism that controls the body’s response to limited oxygen and regulates blood vessel disease of the lung.
By combing through genomes of more than 20 000 individuals in the US, France, England and Japan and combining the results with molecular studies in the lab, the team discovered a shared genetic trait that could predict a higher risk of pulmonary hypertension and its more severe form, pulmonary arterial hypertension, and influence the development of drug therapies that target the body’s response to limited oxygen. The findings were published in Science Translational Medicine.
“This new level of knowledge will help identify people who may be at a higher genetic risk of pulmonary hypertension and jump-start precision medicine practices to offer customised treatments,” said senior author Stephen Chan, MD, PhD.
Pulmonary hypertension encompasses a range of conditions of various causes that manifest in high blood pressure in the arteries of the lung and the right side of the heart.
The disease is accompanied by a decreased supply of oxygen to the lung tissue and the blood, is chronic and deadly, and its molecular origins and genetic background remain unsolved.
Using a combined approach of genomics and biochemistry, the Chan lab found a gene pair that had an important function in regulating blood vessel metabolism and disease.
This gene pair included a long non-coding RNA molecule – a messenger that facilitates the transformation of the body’s genetic code into protein products – and a protein binding partner, and their interaction was frequently active in cells exposed to low oxygen compared to normal cells.
Taking the findings a step further, the team discovered that a single DNA letter change directing expression of this RNA-protein pair under low oxygen conditions was associated with a higher genetic risk of pulmonary hypertension across diverse patient populations.
According to Chan, pulmonary hypertension is a borderline orphan disease, and the limited number of patients with pulmonary hypertension makes it challenging to find genetic variations that are rare but still impactful enough to eclipse individual differences.
With that in mind, Pitt scientists turned to collaborators around the globe and to public research datasets to ensure that the findings are relevant across a diverse global population.
Chan hopes that his findings will spur the development of targeted therapies relevant to oxygen sensitivity in blood vessel lining and that their pending patent application will contribute to the growth on an entirely new field of epigenetic and RNA drug therapeutics that work not by manipulating the genome but by changing how it is being read.
Only concerted multi-disciplinary collaboration and research will stem the tide of diabetes and diabetes-linked cardiovascular disease (CVD), the latter currently the leading cause of death locally and worldwide, claiming 17.9 million lives annually1.
This was the consensus among some of the world’s leading cardiologists and researchers gathered at the SA Heart Association’s annual congress aptly themed: ‘The Cardiac Collaboration,’ which took place at the Sandton Convention Centre in Johannesburg from 26-29 October this year.
Globally, CVD takes more lives than TB, HIV and malaria combined, while 215 South Africans are killed by CVD every day – with 80% of CVD and strokes being preventable.1,2 The prevalence of diabetes has also increased in South Africa, from 4.5% in 2010 to 12.7% in 2019. Of the 4.58 million people aged 20-79 years who were estimated to have diabetes in 2019, 52.4% were undiagnosed.3
With diabetes being a key driver of CVD – especially in Africa (with limited access to novel drugs and the prevalence of sugar-rich, poverty-driven lifestyles), the mutual consensus at this year’s congress was that collaboration is key.
Dr Zaheer Bayat, Chairperson of the Society for Endocrinology, Metabolism and Diabetes of South Africa (SEMDSA), told delegates that endocrinologists and cardiologists would have to work together to improve outcomes for diabetic patients, 30% of whom suffered cardiovascular events. He warned that a 134% increase of people living with diabetes was predicted over the next two decades, translating into a dramatic surge in chronic kidney disease, cardiovascular disease, blindness, and amputations.
Dr Bayat said he intends appealing for mass diabetes screening to find the 52% of people whom researchers estimate are undiagnosed. Ideally, this should be followed by access to cheaply acquired, effective new glucose-lowering drugs.
“The reality is that this country cannot afford all the new treatments for everyone – not private funders, not government. So, drugs are not really a solution – the best solution is to change lifestyle and prevent disease in the first place,” said Dr Bayat.
“We’re here to fight for our patients, not our pockets. Can we afford to have 52% of our patients not knowing they’re diabetic? People who should be contributing to our economy are living with diabetes and eventually dying,” he asserted.
Dr Bayat also said that globally, First World countries such as the USA and Sweden are reducing myocardial infarctions, strokes, and amputations, because they’re doing all the right things together. This included adopting a healthy lifestyle, effective management of sugar, blood pressure and cholesterol and smoking cessation.
“However, here in South Africa with private healthcare representing 15% of healthcare delivery but consuming 50% of the spend and the public sector representing 85% of the population and consuming the other half – we’re not doing nearly as well. With only 200 cardiologists in the country (one per 190 000 population), and even less nephrologists, we need to join together and change the trajectory of diabetes. We must work together to reduce morbidity and mortality,” said Dr Bayat.
According to the SA Heart Association, this graphically illustrates the importance of a multi-disciplinary approach, the very reason why the conference was called ‘The Cardiac Collaboration.’
The SA Heart Association has already begun forging formal ties with other academic societies and next year, it hopes to join and host joint sessions with collaborative meetings to connect a multidisciplinary team in order to achieve a well-rounded balance of care.
A study published in the journal Nature Cardiovascular Research shows that SARS-CoV-2 can directly infect the arteries of the heart and cause the fatty plaque inside arteries to become highly inflamed, increasing the risk of heart attack and stroke. The findings may help explain why certain people who get COVID have a greater chance of developing cardiovascular disease, or if they already have it, develop more heart-related complications.
In the National Institutes of Health (NIH)-funded study, researchers focused on older people with atherosclerotic plaque, who died from COVID. However, because the researchers found the virus infects and replicates in the arteries no matter the levels of plaque, the findings could have broader implications for anybody who gets COVID.
“Since the early days of the pandemic, we have known that people who had COVID have an increased risk for cardiovascular disease or stroke up to one year after infection,” said Michelle Olive, PhD, acting associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH. “We believe we have uncovered one of the reasons why.”
Though previous studies have shown that SARS-CoV-2 can directly infect tissues such as the brain and lungs, less was known about its effect on the coronary arteries. Researchers knew that after the virus reaches the cells, the body’s immune system sends in macrophages to help clear the virus. In the arteries, macrophages also help remove cholesterol, and when they become overloaded with cholesterol, they morph into a specialised type of cell called foam cells.
The researchers thought that if SARS-CoV-2 could directly infect arterial cells, the macrophages that normally are turned loose might increase inflammation in the existing plaque, explained Chiara Giannarelli, MD, PhD, associate professor in the departments of medicine and pathology at New York University’s Grossman School of Medicine and senior author on the study. To test their theory, Giannarelli and her team took tissue from the coronary arteries and plaque of people who had died from COVID and confirmed the virus was in those tissues. Then they took arterial and plaque cells – including macrophages and foam cells – from healthy patients and infected them with SARS-CoV-2 in a lab dish. They found that the virus had also infected those cells and tissues.
Additionally, the researchers found that when they compared the infection rates of SARS-CoV-2, they showed that the virus infects macrophages at a higher rate than other arterial cells. Cholesterol-laden foam cells were the most susceptible to infection and unable to readily clear the virus. This suggested that foam cells might act as a reservoir of SARS-CoV-2 in the atherosclerotic plaque. Having more build-up of plaque, and thus a greater number of foam cells, could increase the severity or persistence of COVID.
The researchers then looked at the predicted inflammation in the plaque after infecting it with the virus. They observed the release of inflammatory cytokines, also known to promote the formation of even more plaque. The cytokines were released by infected macrophages and foam cells. The researchers said this may help explain why people who have underlying plaque buildup and then get COVID may have cardiovascular complications long after getting the infection.
“This study is incredibly important as it adds to the larger body of work to better understand COVID,” said Olive. “This is just one more study that demonstrates how the virus both infects and causes inflammation in many cells and tissues throughout the body. Ultimately, this is information that will inform future research on both acute and Long COVID.”
Though the findings conclusively show that SARS-CoV-2 can infect and replicate in the macrophages of plaques and arterial cells, they are only relevant to the original strains of SARS-CoV-2 that circulated in New York City between May 2020 and May 2021. The study was conducted in a small cohort of older individuals, all of whom had atherosclerosis and other medical conditions; therefore, the results cannot be generalised to younger, healthy individuals.
It has long been known that hot flashes are linked to a number of adverse health effects. Emerging data suggests an association between them and cardiovascular disease. A new study is the first to link physiologically assessed hot flashes with heightened systemic inflammation – a risk factor for cardiac disease. Study results will be presented during the 2023 Annual Meeting of The Menopause Society in Philadelphia September 27-30.
Vasomotor symptoms, more often referred to as hot flashes, are one of the most common symptoms identified during the menopause transition, with roughly 70% of midlife women reporting them. Not only do they interfere with a woman’s quality of life, but they have also been related to physical health risks, such as cardiovascular disease.
Previous research linking hot flashes with heightened systemic inflammation has relied on self-reporting to document the frequency and severity of the hot flashes. These self-reports of hot flashes are limited as they ask women to recall hot flashes over weeks or longer and may be subject to memory or reporting biases. A new study that included 276 participants from the MsHeart study, however, utilised sternal skin conductance to physiologically assess hot flashes and tested whether more frequent physiologically assessed hot flashes are associated with heightened system inflammation.
While large increases in inflammatory markers indicate acute infection or clinical disease, small and sustained increases of markers of inflammation that are in the physiologically normal range are predictive of later disease risk. For example, small and/or sustained increases in inflammatory biomarkers (conceptualised as heightened levels of systemic inflammation) have been related to plaque development and atherosclerotic cardiovascular disease.
Based on the results, the researchers concluded that physiologically assessed hot flashes during wake were associated with higher levels of a high-sensitivity C-reactive protein, even after adjusting for potential explanatory factors such as age, education, race/ethnicity, body mass index, and oestradiol.
The results will be presented during the Annual Meeting of The Menopause Society as part of the presentation entitled “Physiologically measured vasomotor symptoms and systemic inflammation among midlife women.”
“This is the first study to examine physiologically measured hot flashes in relation to inflammation and adds evidence to a growing body of literature suggesting that hot flashes may signify underlying vascular risk and indicate women who warrant focused cardiovascular disease prevention efforts,” says Mary Carson, MS, lead author from the Department of Psychology at the University of Pittsburgh.
“Since heart disease is the leading cause of death for women in the US, studies like these are especially valuable,” adds Dr Stephanie Faubion, medical director of The Menopause Society. “Healthcare professionals need to ask their patients about their hot flash experiences as they not only interfere with their quality of life but may also indicate other risk factors.”
By HualinXMN – Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=133759262
According to results from the SELECT trial run by Novo Nordisk, semaglutide dramatically reduces the risk of major adverse cardiovascular events (MACEs) in addition to its obesity benefits. This is bolstered by the results of another trial, STEP-1, which also suggested significant reduction in future cardiovascular events. These results have captured the attention of researchers, who commented in Nature that they could change the practice of cardiology.
Semaglutide, sold in the US for the treatment of both obesity (Wegovy) and diabetes (Ozempic), is an agonist for glucagon-like peptide 1 (GLP-1), a hormone associated with appetite.
”It’s hard to think of other [drugs], apart from statins, that have shown such a profound effect,” says Martha Gulati, director of preventive cardiology at Cedars-Sinai Medical Center in Los Angeles, USA.
It was expected that semaglutide would have cardiovascular benefits through promoting weight loss, but evidence shows that drugs mimicking GLP-1 can improve fatty-acid metabolism and reduce inflammation, for example, says Gulati. “This is what’s so fascinating about these drugs. They work on the brain, the pancreas, the cardiovascular system, the gastrointestinal tract … There’s more to them than simply weight loss.”
Recent studies have been encouraging in terms of semaglutide’s benefits for reducing cardiovascular disease risk. Earlier this month, Novo Nordisk announced the headline results from the SELECT cardiovascular outcomes trial. The double-blinded trial compared subcutaneous once-weekly semaglutide 2.4mg with placebo as an adjunct to standard of care for prevention of MACEs over a period of up to five years. The trial enrolled 17 604 adults aged 45 years or older with overweight or obesity and established cardiovascular disease (CVD) with no prior history of diabetes.
The trial showed 20% reduction in MACEs for people treated with semaglutide 2.4mg compared to placebo. The primary endpoint was a composite outcome of the first occurrence of MACE cardiovascular death, non-fatal myocardial infarction or non-fatal stroke. All three of these components contributed to the MACE reduction. 1270 first MACEs were accrued.
Expanding GLP-1 analogues to cardiovascular disease prevention may not be without challenges, as the European Medicines Agency opened investigations into semaglutide and liraglutide over reports of suicidal thoughts and self-harm.
A separate study based on the STEP 1 trial data found that 93 million adults in the US could benefit from semaglutide, from a combination of weight loss and reduced cardiovascular benefits. They estimate a reduction in relative risk of 18% with the drug.
Recreational drug use may be a factor in a significant proportion of admissions to cardiac intensive care, with various substances detected in 1 in 10 such patients, suggest the findings of a multicentre French study published online in the journal Heart.
Drug use was also associated with significantly poorer outcomes, with users nearly 9 times as likely to die or require emergency intervention as other heart patients while in hospital, and 12 times as likely to do so if they used more than one drug.
Recreational drug use is a known risk factor for cardiovascular incidents, such as a heart attack or abnormal heart rhythm (atrial fibrillation), explain the researchers. An estimated 275 million people around the globe indulged in this activity in 2022, a 22% increase on the figure for 2010, they add.
But it’s not clear how common recreational drug use is among patients admitted to hospital with heart problems, or to what extent this affects the likely course of their condition.
To try and find out, the researchers analysed the urine samples of all patients admitted to cardiac intensive care in 39 French hospitals during one fortnight in April 2021, with a view to detecting recreational drug use.
During this period, 1904 patients were admitted, 1499 of whom provided a urine sample – average age 63, 70% male. Of these, 161 (11%) tested positive for various recreational drugs, but only just over half (57%) of whom admitted to using.
Prevalence was even higher among the under-40s, 1 in 3 (33%) of whom tested positive for recreational drugs.
The most frequently detected substance was cannabis (9%), followed by opioids (2%), cocaine (just under 2%), amphetamines (nearly 1%), and MDMA or ecstasy (just over 0.5%).
Compared with other non-using heart patients, users were more likely to die or to require emergency intervention for events such as cardiac arrest or acute circulatory failure (haemodynamic shock) while in hospital: 3% vs 13% – especially if they had been admitted for heart failure or a particular type of heart attack (STEMI).
After adjusting for other underlying conditions, such as HIV, diabetes, and high blood pressure, users were nearly 9 times as likely to die or require emergency treatment.
While cannabis, cocaine, and ecstasy were each independently associated with these incidents, and single drug use was detected in nearly 3 out of 4 patients (72%), several drugs were detected in more than 1 in 4 (28%) users: these patients were at even greater risk, being 12 times as likely to die or require emergency treatment.
This is an observational study, so can’t establish that recreational drug use resulted in admission to cardiac intensive care. The researchers also acknowledge that the study was only conducted over 1 fortnight in April, so the findings might not be applicable to other months of the year or the longer term.
And they caution: “Although the strong association between the use of recreational drugs and the occurrence of [major adverse events] suggests an important prognostic role, the limited number of events requires caution in the clinical interpretation of these findings.”
But recreational drugs can increase blood pressure, heart rate, temperature, and consequently the heart’s need for oxygen, they explain.
And they conclude: “While the current guidelines recommend only a declarative survey to investigate recreational drug use, these findings suggest the potential value of urine screening in selected patients with acute cardiovascular events to improve risk stratification in [cardiac intensive care].”
In a linked editorial, doctors from London’s St Bartholomew’s Hospital and Queen Mary’s University of London reiterate that the study wasn’t designed to uncover a causal relationship. Larger studies would be needed to try and establish that.
But the study findings prompt two obvious questions, they suggest: “(1) Should patients admitted to intensive cardiac care units be screened for recreational drug use: and (2) What, if any, interventions might be implemented following a positive patient test result?”
Knowing that a patient had used recreational drugs might shed light on the cause of their condition and inform how it’s managed, they suggest. It might have other benefits too.
“A positive test result would provide an opportunity for counselling about the adverse medical, psychological, and social effects of drugs, and for the implementation of interventions aimed at the cessation of drug use,” they write.
But quite apart from the cost, screening raises issues of patient confidentiality and the potential for discrimination in how targeted screening might be applied, they say.
And they conclude: “There is a considerable way to go, however, before screening for recreational drug use can be recommended.”
