Heart Conditions — Expert Guides

Rheumatic Heart Disease: A Preventable Condition Affecting Millions

May 31, 2026April 10, 2026

Key Points

Rheumatic heart disease is caused by repeated episodes of acute rheumatic fever, an abnormal immune response to streptococcal throat infection, that progressively damages the heart valves.
The causative organism is Group A Streptococcus, the same bacteria responsible for strep throat. In high-income countries, prompt antibiotic treatment prevents the inflammatory cascade. In low-resource settings, untreated infections lead to rheumatic fever and lasting valve damage.
The mitral valve is most commonly affected, producing stenosis or regurgitation that worsens with each recurrent episode of rheumatic fever. The aortic valve is the second most frequently involved.
Rheumatic heart disease remains the leading cause of acquired cardiovascular disease in children and young adults worldwide, predominantly affecting people in low and middle-income countries, including our nearest neighbour, Timor-Leste.
Prevention is straightforward and inexpensive: prompt antibiotic treatment of streptococcal throat infection, and long-term penicillin prophylaxis for those who have had rheumatic fever. The tragedy is one of access, not of medical complexity.

In Australian cardiology practice, rheumatic heart disease is a condition most cardiologists encounter rarely. A case here, a patient referred from overseas there. For many of my colleagues it exists mainly in textbooks, as a historical curiosity from an era before widespread antibiotic use.

But spend a week in the cardiac clinic at Hospital Nacional Guido Valadares in Dili, Timor-Leste, as I have, and the picture changes completely. You see young people in their twenties and thirties with severely damaged mitral valves. Children with significant valve disease. Patients who have never had access to the antibiotics that would have prevented everything they are now facing.

Rheumatic heart disease has not gone away. It has simply moved to places where we are less likely to see it, and where the people affected have less power to demand the attention their condition deserves. It remains the leading cause of acquired cardiovascular disease in children and young adults worldwide, affecting an estimated 40 million people and killing hundreds of thousands every year.

This article is about raising awareness of a condition that is preventable, treatable, and profoundly under-prioritised, and about the work being done to change that.

Heart Matters, Supporting the Timor-Leste Hearts Fund

The Timor-Leste Hearts Fund is Australia’s only medical NGO dedicated to life-saving heart surgery and heart health education for young people in Timor-Leste. Prof. Peter Barlis serves on the board and has worked on the ground in Dili supporting the Fund’s cardiac screening and skills training programs. Every donation makes a direct difference to a young person’s life.

Visit the Timor-Leste Hearts Fund →

The Causative Organism: Group A Streptococcus

A familiar bacteria with an unfamiliar consequence

Group A Streptococcus, Streptococcus pyogenes, is the bacteria responsible for strep throat. In Australia and other high-income countries, it is a common childhood infection that is diagnosed with a throat swab and treated with a course of antibiotics. Most children recover completely within days and never think about it again.

In settings where access to diagnosis and antibiotics is limited, or where poverty, overcrowding, and inadequate housing amplify the transmission and recurrence of streptococcal infections, the story is very different. When strep throat goes untreated or undertreated, some individuals mount an abnormal immune response. The immune system, primed to attack the streptococcal proteins, begins to cross-react with the body’s own tissues, including the heart. This is acute rheumatic fever.

Why the immune system attacks the heart

The mechanism of cardiac damage in rheumatic fever is molecular mimicry: proteins on the surface of Group A Streptococcus are structurally similar to proteins found in the human heart, particularly in the valve tissue. The immune system, mounting a response to the infection, cannot reliably distinguish between the bacterial proteins and the cardiac proteins. The resulting inflammatory attack damages the endocardium, the inner lining of the heart, and in particular the heart valves.

This is not a direct infection of the heart. The bacteria do not invade the cardiac tissue. It is the immune response itself, intended to protect the body, that causes the damage. This distinction matters because it explains why the damage continues even after the infection has resolved, and why recurrent streptococcal infections cause cumulative, progressive valve injury.

From Strep Throat to Heart Disease: The Disease Pathway

▶ The Progression of Rheumatic Heart Disease

Stage	What happens	Timeframe	Prevention window
Step 1	Group A strep throat infection. Sore throat, fever, swollen glands. Often mild or asymptomatic in young children.	Days	✓ Antibiotics here prevent everything that follows
Step 2	Acute rheumatic fever. Joint pain, fever, skin nodules, chorea (involuntary movements), and carditis (inflammation of the heart). Occurs 2 to 4 weeks after untreated strep infection in susceptible individuals.	2 to 4 weeks after infection	✓ Anti-inflammatory treatment limits cardiac damage
Step 3	Recurrent rheumatic fever. Each subsequent strep infection triggers another inflammatory attack on already-damaged valves. Damage is cumulative and progressive with each episode.	Months to years	✓ Penicillin prophylaxis prevents recurrence
Step 4	Chronic rheumatic heart disease. Scarring, thickening, and calcification of the valve leaflets produce stenosis (narrowing) or regurgitation (leaking), or both. Progressive valve dysfunction leads to heart failure, arrhythmia, and stroke.	Years to decades	Surgery or intervention required at this stage
Step 5	End-stage valve disease. Severe heart failure, pulmonary hypertension, atrial fibrillation, stroke risk. Without intervention, premature death, often in the third or fourth decade of life.	Decades	Prevention failed, surgical or palliative care only

How Rheumatic Fever Damages the Heart

Carditis: The Acute Inflammatory Phase

During an episode of acute rheumatic fever, inflammation can affect all three layers of the heart: the pericardium, myocardium, and endocardium. The endocarditis component, inflammation of the inner heart lining and valves, is responsible for the lasting structural damage. Small inflammatory nodules called Aschoff bodies form in the valve tissue. The valve leaflets become swollen and inflamed. In the acute phase, this can cause the valve to leak.

With prompt treatment and no recurrence, this acute inflammation may resolve without lasting damage. But with recurrent episodes, each one adds another layer of scarring, fibrosis, and calcification to the valve structure.

Valve Involvement: Which Valves and How

The mitral valve is by far the most commonly affected, involved in around 65 to 70% of cases of rheumatic heart disease. The aortic valve is the second most frequently affected, either in isolation or, more commonly, in combination with the mitral valve. The tricuspid and pulmonary valves are involved in a minority of cases and rarely in isolation.

Rheumatic damage produces two distinct valve abnormalities, either separately or together. Stenosis occurs when the valve leaflets fuse together along their edges, progressively narrowing the valve opening and restricting forward blood flow. Regurgitation occurs when scarring prevents the leaflets from closing completely, allowing blood to leak backwards. Many patients with longstanding rheumatic heart disease have elements of both.

Mitral Stenosis: The Signature Lesion

Mitral stenosis, narrowing of the mitral valve, is the signature lesion of rheumatic heart disease and is virtually unknown in high-income countries outside this context. As the valve area progressively narrows from a normal 4 to 6 square centimetres toward the critical threshold of below 1.5 square centimetres, blood backs up from the left atrium into the pulmonary circulation.

The consequences are progressive. Breathlessness develops, initially on exertion, then at rest. Pulmonary hypertension follows as the pressure backs up further. Atrial fibrillation becomes increasingly common as the left atrium dilates under chronic pressure overload, and in the context of mitral stenosis, AF carries a very high stroke risk from clot formation in the left atrial appendage. Heart failure follows. Without intervention, the trajectory is relentlessly downward.

This is the disease I see in young adults in Timor-Leste. A 28-year-old with severe mitral stenosis, in atrial fibrillation, breathless at minimal exertion. A picture that is largely absent from Australian cardiology practice but common across much of the developing world.

A Global Burden, and a Local Reality

The scale of the problem

Rheumatic heart disease affects an estimated 40 million people worldwide and causes approximately 300,000 deaths annually, the vast majority in low and middle-income countries in sub-Saharan Africa, South Asia, the Pacific Islands, and Southeast Asia. It disproportionately affects children and young adults in the prime of their lives, in communities that can least afford to lose productive members to preventable disease.

In Timor-Leste, Australia’s nearest neighbour, a country of approximately 1.3 million people that has only had independence since 2002, rheumatic heart disease remains one of the most significant cardiovascular burdens. Limited access to antibiotics for streptococcal infections, overcrowded housing conditions that facilitate strep transmission, and a healthcare system that is still developing its capacity to screen, diagnose, and treat cardiac disease all contribute to a burden that is entirely disproportionate to what should be possible with basic medical resources.

What I saw in Dili

During my time working with the cardiac team at Hospital Nacional Guido Valadares in Dili, the contrast with Australian practice was stark. Patients with valve disease that would have been identified and treated years earlier in Australia. Young people in heart failure from conditions that were preventable with antibiotics costing cents per course. Families who had no idea that a sore throat their child had years ago was the beginning of the heart disease now threatening their life.

The clinical skill and dedication of the local cardiologists working with the resources available to them is remarkable. The limitation is not knowledge or commitment. It is the infrastructure, the medication access, and the surgical capacity that simply do not yet exist within the country.

Mending Broken Hearts

The Timor-Leste Hearts Fund

Australia’s only medical NGO dedicated to life-saving heart surgery and heart health education for young people in Timor-Leste. Founded in 2010, the Fund partners with the cardiac clinic at Hospital Nacional Guido Valadares to screen patients, provide surgery for critical cases in Australia, and build local clinical capacity.

Key programs include penicillin prophylaxis for patients with known rheumatic heart disease, echocardiographic screening, clinical mentorship for local cardiologists, and advocacy for a health system that can one day manage this burden domestically.

Support the Timor-Leste Hearts Fund →

Prevention: The Power of a Simple Antibiotic

Primary Prevention: Treating Strep Throat

The most powerful intervention in the entire rheumatic heart disease chain is also the simplest: treating streptococcal throat infection promptly with antibiotics. A 10-day course of penicillin, or a single injection of benzathine penicillin G, eradicates the Group A Streptococcus and prevents the abnormal immune response that leads to rheumatic fever.

This is straightforward in a healthcare system with access to diagnosis and antibiotics. In settings without reliable access to either, it is the gap through which millions of lives fall.

Secondary Prevention: Penicillin Prophylaxis

For individuals who have already had acute rheumatic fever, preventing recurrence is the most important priority. Every subsequent streptococcal infection risks triggering another inflammatory attack on already-damaged valves. Long-term penicillin prophylaxis, typically monthly injections of benzathine penicillin G, prevents this recurrence and halts the progressive valve damage.

The Timor-Leste Hearts Fund’s penicillin prophylaxis programme is one of its most impactful initiatives, identifying patients with known rheumatic heart disease and ensuring they receive their monthly penicillin, protecting already-damaged valves from further deterioration. The cost of this intervention is minimal. The benefit to an individual’s cardiac trajectory is enormous.

Echocardiographic screening

One of the most significant advances in rheumatic heart disease management has been the recognition that echocardiography can identify subclinical rheumatic valve disease, damage that is present but not yet producing symptoms, in populations with high rheumatic fever rates. Screening programs in endemic regions can identify patients who would benefit from prophylaxis before their disease becomes clinically significant. The Fund supports this screening capacity at the National Hospital in Dili.

Treatment: When Prevention Has Failed

Medical management

For patients with established rheumatic heart disease, medical management focuses on controlling symptoms, preventing complications, and protecting against further rheumatic fever episodes. Diuretics manage fluid overload in patients with stenotic valves. Anticoagulation is essential in patients with mitral stenosis and atrial fibrillation to prevent stroke. Rate control for AF reduces symptoms and prevents further cardiac remodelling. Penicillin prophylaxis continues throughout.

Valve intervention

When rheumatic valve disease becomes haemodynamically significant, producing severe symptoms, pulmonary hypertension, or significant cardiac dysfunction, valve intervention is required. The options depend on the anatomy of the damage.

For mitral stenosis without significant regurgitation, percutaneous mitral balloon valvotomy, a catheter-based procedure that splits the fused leaflets, can produce excellent results and restore the valve to a functional state without open heart surgery. For more complex valve lesions, or when regurgitation is significant, surgical repair or replacement is necessary.

For patients in Timor-Leste who reach the threshold for surgical intervention, the Timor-Leste Hearts Fund coordinates their transfer to Australian hospitals where the surgery is performed, in many cases giving a young person a functional heart valve and decades of additional healthy life. The contrast between the trajectory without intervention and the outcome with it is one of the most dramatic in all of medicine.

Sitting in the outpatient clinic in Dili, seeing a 24-year-old woman with severe mitral stenosis, breathless climbing one flight of stairs, in AF, with a left atrium the size of a tennis ball, knowing that the strep throat she had at twelve years old caused all of this, and that a course of antibiotics would have prevented it entirely: that is the injustice of rheumatic heart disease in one consultation. The clinical complexity of what she now needs is significant. The simplicity of what would have prevented it is almost unbearable.

Professor Peter Barlis, Interventional Cardiologist & Board Member, Timor-Leste Hearts Fund

What You Can Do

Awareness is the first step. Rheumatic heart disease is not a condition confined to history or to distant countries. It is affecting millions of people right now, including young people in our own region, in communities without access to the medical infrastructure we take for granted.

For clinicians in high-income countries, particularly those seeing patients from endemic regions, maintaining a high index of suspicion for rheumatic valve disease in patients from sub-Saharan Africa, Southeast Asia, the Pacific Islands, and South Asia is important. A murmur in a young adult from an endemic region is rheumatic until proven otherwise.

For anyone who wants to make a direct contribution to changing the trajectory of this disease in one of our nearest neighbours, the Timor-Leste Hearts Fund offers a direct and efficient pathway to do so.

Key Facts About Rheumatic Heart Disease

Caused by Group A Streptococcus, the same bacteria as strep throat, via an abnormal immune response in susceptible individuals.
Affects an estimated 40 million people worldwide, predominantly in low and middle-income countries.
The mitral valve is most commonly affected, followed by the aortic valve.
Entirely preventable with prompt antibiotic treatment of strep throat and penicillin prophylaxis after rheumatic fever.
In Timor-Leste, the Timor-Leste Hearts Fund coordinates life-saving surgery, penicillin prophylaxis, screening, and clinical training.

Heart Matters Resource

When in Doubt, Get Checked Out

If you have a history of rheumatic fever, particularly if you grew up in a region where streptococcal infections were common and access to antibiotics was limited, a cardiac assessment including echocardiography is worth discussing with your doctor. Rheumatic valve disease detected early can be managed to protect against further deterioration.

Read: When in Doubt, Get Checked Out →

Conclusion

Rheumatic heart disease is the story of what happens when a preventable infection meets a healthcare system that cannot prevent it. The biology is well understood. The prevention is simple and cheap. The tragedy is one of access and equity, not of medical complexity.

Every course of antibiotics given to a child with strep throat in an endemic region is an act of cardiovascular prevention. Every monthly penicillin injection given to a young person with known rheumatic fever is a valve being protected from further damage. Every echocardiogram that identifies subclinical disease is a life being redirected away from the trajectory that brought so many patients to that clinic in Dili.

If this article has raised your awareness of rheumatic heart disease, the Timor-Leste Hearts Fund is one organisation doing direct work on it in our region. The links above will take you to their site if you wish to find out more.

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An Isolated Inferior Q Wave on Your ECG: Why It’s Usually Nothing to Worry About

May 31, 2026April 7, 2026

Key Points

Receiving an ECG report that mentions “possible old heart attack” or “cannot exclude prior infarction” is one of the most anxiety-provoking findings in cardiology, and in an otherwise fit, healthy person with no symptoms, it is almost always a normal variant that requires no treatment.
An ECG records the heart’s electrical activity from 12 different viewpoints around the chest and limbs. A Q wave is simply a small downward dip seen in some of these viewpoints. In certain positions, particularly one called lead III, a Q wave is extremely common in completely normal, healthy hearts.
Automated ECG software flags Q waves as “possible old heart attack” because it cannot apply clinical judgment. A cardiologist reviewing the same ECG in the context of a fit, symptom-free person will almost always reach a very different and reassuring conclusion.
A Q wave that genuinely indicates a previous heart attack must appear in multiple neighbouring viewpoints simultaneously and be accompanied by other supporting changes on the ECG. An isolated Q wave in a single viewpoint, with everything else completely normal, does not meet this standard.
If you have received a report like this and are anxious, that anxiety is entirely understandable. A clinical review with a cardiologist resolves this question quickly and in most cases definitively.

One of the most common referrals I receive, easily once or twice a week, is a fit, healthy, often younger person who has had an ECG for a routine reason and whose report has come back with a phrase like “possible old heart attack,” “Q waves, cannot exclude prior infarction,” or “inferior changes, clinical review advised.”

They arrive in my clinic worried. Some have been unable to sleep. Some have told their families. Some have already started researching heart attack symptoms they have never had. The phrase “old heart attack” in a document about their heart has landed with enormous weight.

In the overwhelming majority of these cases, when I look at the ECG myself, the finding is a small, isolated Q wave in a single ECG viewpoint, a completely normal variant with no clinical significance whatsoever, that tells me nothing concerning about the health of this person’s heart or coronary arteries.

This article exists to explain why, and to give people the information they need before that anxious wait even begins.

Understanding the ECG, a Brief Explanation

What an ECG actually records

An ECG, electrocardiogram, records the electrical activity of the heart using electrodes placed on the chest, arms, and legs. It does not take a picture of the heart. It records the tiny electrical signals that travel through the heart muscle with each beat, triggering the muscle to contract.

Because the electrodes are placed at different positions around the body, the ECG effectively looks at the heart’s electrical activity from 12 different angles, called leads or viewpoints. Each produces its own waveform on the paper trace, and together they give a detailed picture of how electrical signals are moving through the heart. We have a dedicated article on how the ECG works and what it shows on Heart Matters if you would like to understand the test in more depth.

What a Q wave is

Each heartbeat produces a characteristic shape on the ECG trace, a series of peaks and dips. A Q wave is simply a small downward dip at the beginning of the main electrical spike of each beat. In many of the 12 viewpoints, small Q waves are entirely normal, they reflect the normal direction in which the electrical signal travels through the heart at the start of each beat.

In certain viewpoints, particularly one called lead III, which looks at the heart from a specific angle determined by the position of the left arm and left leg electrodes, a Q wave is especially common as a normal finding. It can appear and disappear simply with a change in body position or a deep breath. It is not a sign of damage. It is a reflection of the angle at which that particular viewpoint happens to be looking at the heart.

What Would a Genuine Concern Actually Look Like?

When a heart attack damages an area of heart muscle permanently, that area becomes electrically silent, it no longer generates the normal electrical signals. The ECG viewpoints looking directly at that damaged area will show an abnormal Q wave as a result, deeper, broader, and more prominent than a normal variant Q wave.

But, and this is the critical point, a heart attack affecting any meaningful area of muscle will show these changes across multiple neighbouring ECG viewpoints simultaneously, not in just one. It will also typically be accompanied by other supporting changes in the same viewpoints, changes in the shape of the waveform, and changes in the pattern of recovery between beats.

An isolated Q wave appearing in just one viewpoint, with every other viewpoint completely normal and no supporting changes anywhere on the trace, does not fit this picture at all. It is simply not how genuine heart attack scarring presents on an ECG.

Why the Software Gets It Wrong

Modern ECG machines include automated interpretation software that analyses the trace and generates a written report. This software is useful, it can reliably identify certain patterns and flag them for clinical review. But it has an important limitation: it cannot think clinically.

When the software sees a Q wave in a particular viewpoint, it flags “possible old heart attack, clinical correlation recommended.” It cannot consider that the person is 32 years old and plays sport twice a week. It cannot consider that the Q wave is tiny and only visible in one viewpoint. It cannot consider that the person has never had any cardiac symptom in their life. It simply matches the pattern and generates the flag.

That flag is not a diagnosis. It is a prompt for a clinician to look at the full picture, and when a clinician does, the picture is almost always entirely reassuring.

In most of these referrals, one look at the ECG in the context of the patient in front of me resolves the question immediately. The report did its job. The clinical review does the rest.

— Prof. Peter Barlis, Interventional Cardiologist

Normal Variant vs Genuine Concern, Plain Language Guide

Feature	Almost certainly a normal variant	Worth investigating further
How many viewpoints show the Q wave	Only one viewpoint on the entire ECG	Multiple neighbouring viewpoints showing the same change
The rest of the ECG	Completely normal in every other respect	Other changes present in the same viewpoints
The person’s history	No cardiac symptoms ever, no risk factors, fit and active	History of chest pain, breathlessness, or cardiovascular risk factors
Does it change with breathing	Q wave reduces or disappears with a deep breath	Persistent regardless of position or breathing
Why the ECG was done	Routine, pre-employment, or incidental finding	ECG done because of symptoms or known cardiac history
Echocardiogram result	Normal heart structure and function throughout	Abnormal muscle movement in the area the Q wave viewpoints correspond to

What Investigation Is Actually Needed?

A clinical review, not a cascade of tests

The appropriate response to a report like this in an otherwise healthy person is a clinical review with a cardiologist, not an immediate referral for a stress test, a CT scan of the coronary arteries, or a coronary angiogram. A cardiologist looking at the ECG alongside your history and examination can in most cases answer the question definitively without any further testing at all.

If any uncertainty remains after that review, perhaps because there are some cardiovascular risk factors present, or because the ECG changes are borderline, an echocardiogram is the most efficient next step. This is an ultrasound of the heart that shows how the heart muscle is moving. If the muscle in the area corresponding to the Q wave viewpoint is moving completely normally, which it almost always is in these situations, that is powerful additional reassurance that no significant heart attack has occurred.

What you do not need

A fit, active, symptom-free person with no cardiovascular risk factors whose ECG shows an isolated Q wave in a single viewpoint, with everything else normal, does not need urgent investigation. They do not need to stop exercising while they wait for a result. They need a clinical review that puts the automated report in its proper context, and in most cases, that conversation is the only investigation needed.

If you have received a report like this, what to hold onto

An automated ECG report is generated by software, not a cardiologist. Its job is to flag things for clinical review, not to make diagnoses.
A Q wave appearing in just one ECG viewpoint, with everything else completely normal, is almost always a normal finding in an otherwise healthy heart.
A Q wave pattern that genuinely indicates a previous heart attack appears across multiple neighbouring viewpoints simultaneously, not in isolation.
A cardiologist reviewing your ECG alongside your history will almost always be able to give you a clear and reassuring answer, often without any further testing.
An echocardiogram, an ultrasound of the heart, is the most direct additional reassurance if any uncertainty remains after clinical review.

Heart Matters Resource

When in Doubt, Get Checked Out

If your ECG report mentions Q waves or a possible old heart attack and you are anxious about it, a cardiology review will answer the question efficiently and in most cases very reassuringly. Do not sit with that anxiety without getting it properly assessed.

Read: When in Doubt, Get Checked Out →

Conclusion

The automated ECG report that says “possible old heart attack” is one of the most anxiety-generating phrases in cardiology, and in a fit, healthy, symptom-free person it is almost always an over-call by software that cannot apply clinical judgment. The Q wave it has flagged is real. The interpretation it has placed on that finding is almost certainly wrong in this context.

A Q wave appearing in just one ECG viewpoint, with no other changes anywhere on the trace, in a person who has never had cardiac symptoms and has no significant risk factors, is a normal finding. It does not mean your heart is damaged. It does not mean you have had a heart attack. And it does not mean you need urgent investigation.

What it means is that you need a cardiologist to look at your ECG and your history together, and give you the reassurance that the software, by its nature, simply cannot provide.

A Living Legend of Interventional Cardiology: Professor Patrick Serruys

May 31, 2026April 6, 2026

heartmatters.com 2026 04 06T204658.338 1

Key Points

Professor Patrick Serruys is one of the most influential figures in the history of interventional cardiology, with over 3,500 peer-reviewed publications and 250,000 citations.
He introduced balloon angioplasty to the Netherlands in 1980 and performed the country’s first coronary stent implantation in 1986.
He helped pioneer drug-eluting stents, now the global standard of care, implanted in millions of patients every year.
In 2004, he performed the first percutaneous aortic valve replacement in the Netherlands, a procedure now known as TAVI.
He remains scientifically active today, continuing to shape the future of cardiovascular medicine.

Last week, I had the honour of presenting a lifetime achievement award to a man who shaped not only my career, but the entire field of interventional cardiology. Professor Patrick Serruys visited Sydney, and standing in front of him with that award in my hands, I found myself thinking about the extraordinary distance modern heart medicine has travelled, and how much of that journey he personally led.

Patrick was my PhD supervisor. He wrote the foreword to my book on heart stents. We continue to collaborate to this day. But this article is not really about my connection to him, it is about what his work means for patients. Because if you or someone you love has ever had a coronary stent, a drug-eluting stent, or a catheter-based heart valve procedure, there is a very real chance that the treatment you received exists in its current form because of Professor Serruys.

Where It All Began

Patrick Serruys published his first scientific paper in the British Heart Journal in 1978. He was working at the Thoraxcenter in Rotterdam, then a young institution that would become one of the most important centres of cardiovascular innovation in the world. From the very beginning, he was drawn to a question that would define his career: could blocked heart arteries be treated without open-heart surgery?

At the time, the answer was far from obvious. Coronary artery bypass surgery was the standard of care. The idea that a cardiologist could thread a thin catheter through the blood vessels, navigate to a blocked artery in the heart, and open it from the inside, without a single incision on the chest, was genuinely radical.

In September 1980, Professor Serruys introduced balloon angioplasty to Rotterdam. A small balloon on the tip of a catheter, inflated inside the narrowed artery to compress the blockage and restore blood flow. It worked. But it had a significant problem, the artery often narrowed again within months, a process called restenosis. For more than a decade, he led thirteen clinical trials attempting to solve this problem with medications. The results were disappointing.

The history of medicine is full of researchers who, faced with repeated setbacks, simply kept going. What distinguishes Professor Serruys is that each disappointment redirected his curiosity rather than diminishing it. The solution to restenosis, it turned out, was not a drug, it was a device.

The Stent That Changed Everything

In 1986, Professor Serruys performed the first coronary stent implantation in the Netherlands, just months after the very first procedures anywhere in the world. A coronary stent is a tiny mesh scaffold, deployed inside the artery to hold it open after balloon angioplasty. It was a transformative development. Restenosis rates fell. Patients did better.

But the stent itself still caused some degree of restenosis in a proportion of patients, because the metal triggered a healing response from the artery wall that could cause re-narrowing over time. The next challenge was clear: could the stent itself deliver medication directly to the artery wall to prevent this response?

By the late 1990s, working with colleagues in Rotterdam and São Paulo, Professor Serruys helped pioneer the first drug-eluting stents stents coated with medication that releases slowly into the surrounding tissue, dramatically reducing restenosis. In 2000, during one of cardiology’s most prestigious lectures, he predicted this technology would spread worldwide. It did. Drug-eluting stents are now the global standard of care for coronary intervention, implanted in millions of patients every year.

In 1994, he led the first randomised controlled trial directly comparing stenting with balloon angioplasty alone, published in the New England Journal of Medicine, which contributed to regulatory approval of coronary stents by the United States FDA that same year. If you want to understand the evidence behind the stent in your own chest, you can read more on our Coronary Artery Disease page.

Beyond the Stent

Even as stenting transformed interventional cardiology, Professor Serruys was already thinking about its limitations. A permanent metallic scaffold left forever inside a coronary artery troubled him. What if the scaffold could dissolve once its job was done, leaving the artery free and natural?

In 2006, he introduced fully biodegradable coronary scaffolds made from polylactic acid, the same material used in dissolvable surgical sutures, that provided the structural support of a stent during the critical healing period, then gradually disappeared over two to three years. The concept and early results were published in The Lancet and the New England Journal of Medicine. This remains an active and evolving area of research.

His curiosity never stayed confined to coronary arteries. In 2004, together with the pioneering French cardiologist Alain Cribier, he performed the first percutaneous aortic valve replacement in the Netherlands threading an artificial heart valve through the blood vessels and implanting it inside the diseased native valve, without open-heart surgery. This procedure, now known as TAVI, has since transformed the treatment of aortic stenosis and is now offered to tens of thousands of patients worldwide who previously had no good surgical option.

Professor Patrick Serruys presenting at Sydney Intervention 2026 — Professor Serruys presenting at Sydney Intervention 2026, his lecture on the future of coronary revascularisation included fifteen predictions for the field, published in the European Heart Journal.

The Scale of a Career

Numbers can feel abstract, but in this case they help convey something genuinely difficult to communicate in words. Professor Serruys has published more than 3,500 peer-reviewed scientific papers. His work has been cited more than 250,000 times by other researchers, placing him among the most cited medical scientists on the planet.

He has trained more than 400 interventional cardiologists and supervised more than 100 PhD candidates many of whom are now leading figures in the field in their own right. I am proud to count myself among them.

He is the author or co-author of 43 books and monographs, including three editions of the European Society of Cardiology’s flagship textbook of cardiovascular medicine. He holds an honorary doctorate in engineering from the University of Melbourne, a recognition that his contributions straddled the boundary between clinical medicine and biomedical engineering.

At the time of writing, he remains scientifically active at the University of Galway, where he established a research centre focused on advanced imaging and core laboratory science after his 36-year career at Erasmus University in Rotterdam. He cycles to the laboratory every day.

Professor Patrick Serruys and Prof. Peter Barlis at the University of Melbourne honorary doctorate ceremony 2016 — Professor Serruys receiving his honorary doctorate in engineering from the University of Melbourne in 2016, pictured with Prof. Peter Barlis.

What This Means for Patients

I am sometimes asked by patients why any of this history matters to them. The answer is simple. Every time a cardiologist threads a stent into a blocked coronary artery, a procedure that takes less than an hour, requires no general anaesthetic, and sends most patients home the same day, they are building on decades of work by researchers like Professor Serruys who refused to accept that open-heart surgery was the only answer.

The treatments we now consider routine were once considered impossible. They exist because of people who asked difficult questions, ran rigorous trials, published honest results, including failures, and kept pushing. Understanding that journey helps patients engage more confidently with their own care.

New Release 2026

Heart Stents: What You Need to Know

A comprehensive guide by Professor Peter Barlis, with a foreword by Professor Patrick Serruys. Published by Wiley.

Buy on Amazon →

Conclusion

Presenting that lifetime achievement award to Patrick last week, in Sydney, surrounded by colleagues whose careers he has shaped, was one of the genuine privileges of my professional life. The field of interventional cardiology owes him an enormous debt.

And so, indirectly, do the millions of patients whose lives have been changed by the treatments he helped bring into existence. If you have ever had a stent placed, a valve replaced without open-heart surgery, or benefited from any of the imaging technologies now used in the catheterisation laboratory, there is a very good chance that Professor Serruys played a role in making that possible.

That is a legacy worth celebrating, not just within cardiology, but for every patient who has sat in a recovery room, gone home the next morning, and returned to their life.

Professor Patrick Serruys receives a standing ovation at Sydney Intervention 2026 — Sydney Intervention 2026, a room full of cardiologists rises as Professor Serruys receives the lifetime achievement award.

How Atrial Fibrillation Is Treated: From Lifestyle to Ablation

May 6, 2026March 27, 2026

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Heart Health in Asian Populations

April 26, 2026March 26, 2026

Key Points

People of South Asian background, with ancestry from India, Pakistan, Bangladesh, Sri Lanka, and Nepal, tend to develop heart disease earlier than Western populations, often at lower body weights. The good news is that this risk is very well understood and very actionable with the right awareness and early assessment.
People of East Asian background, with ancestry from China, Japan, Korea, and Southeast Asia, have a different but equally important cardiovascular profile, with higher rates of stroke and blood pressure-driven heart disease. Again, this is a risk profile that responds very well to early identification and management.
Standard cardiovascular risk calculators used by doctors were developed mainly in Western populations and may underestimate risk in South and East Asian individuals, which is why proactively raising your background in a cardiovascular risk conversation is so valuable.
Diabetes develops at lower body weights in both South and East Asian populations than in Western populations, making blood sugar assessment important even in people who appear slim by standard measures.
Early engagement with your healthcare team, even without symptoms, is the single most effective step people from these communities can take. The earlier the conversation, the more options are available.

If you are of South Asian or East Asian background, this article is written specifically for you, and it carries a message that is ultimately optimistic, not alarming.

Yes, the evidence shows that people from these communities face cardiovascular risks that are not fully captured by standard medical tools designed for Western populations. But the reason to know this is not to worry, it is to act. Because the cardiovascular risks that affect South and East Asian populations are well understood, largely preventable, and highly responsive to early intervention.

The most powerful thing you can do with the information in this article is use it to start a more specific and more informed conversation with your doctor. That conversation, had early, before symptoms develop, is where the difference is made.

Why Standard Risk Tools Sometimes Miss the Picture

Doctors use scoring tools and calculators to estimate a patient’s risk of having a heart attack or stroke over the next ten years. These tools consider age, blood pressure, cholesterol levels, smoking history, and family history, and they are genuinely useful. But they were developed and tested primarily using data from white Western European and North American populations.

For people of South Asian or East Asian background, these tools can underestimate risk, sometimes significantly. The body weight thresholds, cholesterol ranges, and blood pressure cut-offs that signal concern in a Western patient do not always apply in the same way. The result is that some people from these communities are told their risk is low when a more targeted assessment would identify important factors worth addressing.

This is not a failure of medicine, it is a gap that is now well recognised and being actively addressed in cardiovascular research. Knowing about it puts you in a position to ask the right questions.

South Asian Communities, What the Evidence Shows

Who this section applies to

South Asian refers to people with family roots in India, Pakistan, Bangladesh, Sri Lanka, Nepal, and Bhutan. This is one of the largest communities in Australia, the United States, the United Kingdom, and Canada, and one that carries a cardiovascular risk profile that deserves specific attention and specific action.

Heart disease tends to arrive earlier

Coronary artery disease, the narrowing of the arteries that supply the heart with blood, tends to develop earlier in South Asian individuals than in Western populations. This is not inevitable, and it is not a reason for fatalism. It is a reason for earlier, more proactive engagement with cardiovascular risk assessment, because identifying and managing risk factors in your thirties or forties is far more effective than waiting for symptoms to appear.

The disease also tends to affect the smaller coronary arteries, which are harder to see on some investigations and more diffuse in its distribution. This is another reason why a thorough assessment, rather than a single test, gives the most complete picture.

Act Early

For people of South Asian background, starting cardiovascular risk conversations with your doctor in your thirties rather than waiting for symptoms is one of the most effective things you can do for your long-term heart health. Early assessment means early action, and early action produces the best outcomes.

Body weight, why standard measures can be misleading

The standard BMI, body mass index, thresholds used in Western medicine define overweight as a BMI above 25 and obese above 30. These thresholds were developed using data from Western populations and do not translate directly to South Asian individuals.

South Asian bodies tend to carry more fat around the abdomen, even at lower overall body weights, and this abdominal fat pattern is more strongly linked to metabolic problems like insulin resistance, high blood sugar, and abnormal cholesterol than fat carried elsewhere. As a result, a South Asian person with a BMI of 23 or 24, technically “normal weight” by standard measures, may already have a metabolic profile that warrants attention and management.

Waist circumference, the measurement around the middle, is a more useful indicator of this risk than BMI alone. If you are of South Asian background, asking your doctor to measure your waist circumference alongside your weight gives a more complete picture of your cardiometabolic health.

Diabetes, why it develops earlier and at lower weights

Type 2 diabetes, a condition where the body does not manage blood sugar properly, is two to four times more common in South Asian populations than in white Western populations, and it tends to develop at younger ages and lower body weights. This matters enormously for cardiovascular health because diabetes significantly amplifies the risk of heart disease and stroke when it is present.

The practical implication is that a blood sugar test, specifically an HbA1c, which gives a three-month average of blood sugar control, is worth requesting even if you are not overweight and have no obvious symptoms of diabetes. Identifying pre-diabetes or early diabetes early gives the best chance of reversing it before it affects the heart.

Lp(a), an inherited risk factor worth knowing about

Lipoprotein(a), usually written as Lp(a) and pronounced “L-P-little-a”, is an inherited particle in the blood that raises cardiovascular risk. It is not affected by diet, exercise, or standard cholesterol-lowering medications, and it is carried in elevated amounts by a higher proportion of South Asian individuals than most other populations.

Most people have never had their Lp(a) measured, because it is not part of standard cholesterol testing. But it is a simple blood test, needs only to be done once in a lifetime, and identifies an important risk factor that completely changes the management conversation when it is elevated. We have a dedicated article on Lp(a) and what it means for your heart on Heart Matters. If you are of South Asian background, particularly with a family history of early heart disease, asking your doctor about Lp(a) is one of the most valuable things you can do at your next appointment.

As someone of South Asian background myself, this is not an abstract clinical observation, it is something I see in my own extended family and community. The patients who arrive in my operating theatre with advanced coronary disease in their forties are often people whose risk was underestimated for years because the standard tools were not built with them in mind. Earlier conversations change outcomes. I have seen it.

— Prof. Jai Raman, Cardiothoracic Surgeon

East Asian Communities, What the Evidence Shows

Who this section applies to

East Asian refers to people with family roots in China, Japan, Korea, Taiwan, Hong Kong, and Mongolia. Southeast Asian encompasses Vietnam, Thailand, the Philippines, Indonesia, Malaysia, Cambodia, and neighbouring countries. While these are richly diverse populations with very different cultural and dietary traditions, they share some important cardiovascular patterns that are worth understanding.

Stroke, the priority risk to manage

East Asian populations generally have lower rates of coronary artery disease, blocked heart arteries, compared to South Asian or Western populations. This is genuinely positive and reflects the protective effects of traditional dietary patterns and historically lower rates of obesity in these communities.

However, stroke rates are higher, and this is the cardiovascular priority for East Asian populations. A stroke occurs when blood supply to part of the brain is interrupted, either by a blocked artery or a burst blood vessel. Both types are more common in East Asian populations than in Western ones, and both are strongly driven by high blood pressure, which is the most important cardiovascular risk factor to manage in these communities.

Blood pressure and salt, a particularly important connection

High blood pressure, or hypertension, is the dominant cardiovascular risk factor in East Asian populations, and it responds particularly strongly to dietary salt intake. Many traditional East Asian cuisines are naturally high in sodium, from soy sauce, fish sauce, miso, preserved vegetables, and processed foods, and this dietary pattern can contribute meaningfully to blood pressure elevation over time.

The good news is that this is one of the most modifiable risk factors available. Reducing dietary sodium, alongside medication where needed, produces very meaningful reductions in blood pressure and stroke risk. Having your blood pressure checked regularly, and monitoring it at home with a home blood pressure device, is one of the highest-value health habits for anyone of East Asian background. We have a dedicated article on monitoring blood pressure at home on Heart Matters.

Atrial fibrillation, a specific conversation worth having

Atrial fibrillation, or AF, is a common heart rhythm condition where the upper chambers of the heart beat irregularly rather than in a coordinated rhythm. When AF is present, blood can pool in the heart and form clots, which can travel to the brain and cause a stroke. We have a dedicated article on AF and stroke risk on Heart Matters.

In East Asian populations, the stroke risk associated with AF appears to be somewhat higher than in Western populations, which means the decision about whether to use blood-thinning medication to protect against stroke is particularly important. If you have been diagnosed with AF and are of East Asian background, having an explicit conversation with your cardiologist about your stroke risk and the best approach to managing it is very worthwhile.

Sleep apnoea at lower body weights

Obstructive sleep apnoea, a condition where breathing repeatedly stops and starts during sleep, is a significant but under-recognised cardiovascular risk factor. It is associated with high blood pressure, atrial fibrillation, and heart failure. Most people are aware that it is more common in people who are overweight, but in East and Southeast Asian populations, sleep apnoea develops at significantly lower body weights than in Western populations, due to differences in facial bone structure that affect the size of the upper airway.

This means that a lean East Asian person with heavy snoring, morning headaches, or unrefreshing sleep should be assessed for sleep apnoea regardless of their weight. We cover this in detail in our dedicated article on obstructive sleep apnoea and the heart.

Alcohol, an important note for East Asian individuals

Approximately one in three people of East Asian background carries a genetic variation that affects how the body processes alcohol. When alcohol is consumed, the body normally breaks it down through a series of steps. In people with this genetic variation, one of those steps does not work properly, causing a build-up of a toxic substance called acetaldehyde. This produces the characteristic facial flushing, redness of the face and neck, that many East Asian people experience after even small amounts of alcohol.

This flushing is not merely a cosmetic reaction. The acetaldehyde that builds up is a direct cardiovascular toxin and is also linked to an increased risk of certain cancers. For people of East Asian background who experience this flushing response, there is a particularly strong cardiovascular reason to keep alcohol consumption to a minimum. We discuss this further in our dedicated article on alcohol and the heart.

The Positive Picture, What Early Action Achieves

Everything described in this article is actionable. Every risk factor mentioned, blood pressure, blood sugar, Lp(a), sleep apnoea, cholesterol, dietary sodium, alcohol, can be identified with simple tests, and most can be meaningfully reduced with a combination of lifestyle changes and, where needed, medication.

The cardiovascular outcomes for South and East Asian patients who are identified early and managed proactively are excellent. The gap in outcomes between these populations and Western populations is not biological destiny, it is largely a consequence of later presentation and less targeted risk assessment. Change those two things, and the outcomes change with them.

The most important step is the first one: a conversation with your doctor that explicitly addresses your background and what it means for your cardiovascular risk assessment.

Background	Priority areas to discuss with your doctor	Key tests worth asking about
South Asian	Earlier cardiovascular risk assessment, diabetes screening at lower BMI, family history of early heart disease, abdominal weight distribution	Lp(a) blood test, HbA1c, waist circumference, full lipid profile, blood pressure
East Asian	Blood pressure control and home monitoring, dietary sodium, stroke risk if AF is present, sleep apnoea assessment, alcohol and the ALDH2 flushing response	Home blood pressure readings, HbA1c, sleep study if snoring or unrefreshing sleep, ECG if palpitations
Southeast Asian	Overlapping features from both groups above; rheumatic heart disease history if from an endemic region	Individualised based on specific background, discuss with your doctor what applies most to you

The patients I worry least about are the ones who come to see me early, before symptoms, before a crisis, and say “I know my background puts me at higher risk, so I want to understand where I stand.” That conversation, had in your thirties or forties, gives us every opportunity to protect your heart for decades to come.

— Prof. Peter Barlis, Interventional Cardiologist

A Note on Acculturation, Second and Third Generations

One pattern worth understanding is what happens as South and East Asian families become more established in Western countries across generations. First-generation immigrants often maintain the dietary patterns of their home country, which, particularly for East Asian families, can be quite protective. Second and third generations frequently adopt more Western eating habits, more processed food, more refined carbohydrate, less of the traditional plant-based and fermented foods, while sometimes losing awareness of the specific cardiovascular risks their background carries.

If you are a second or third-generation Australian, American, or British person of South or East Asian descent, the cardiovascular risk profile of your ethnic background applies to you just as much as it does to a first-generation immigrant. It is worth knowing about, and worth discussing with your doctor.

Questions to raise at your next appointment

Does my South Asian or East Asian background affect my cardiovascular risk, and does the standard risk calculator my practice uses account for this?
Should I have my Lp(a) measured? I understand it is elevated more commonly in people of South Asian background.
Can we check my waist circumference and HbA1c alongside my standard blood tests, even though I am not overweight?
I have AF, does my background affect my stroke risk or the best approach to anticoagulation for me?
I snore and wake feeling unrefreshed, should I be assessed for sleep apnoea regardless of my weight?

Free Download, Heart Matters

Our Heart Health Risk Factor Checklist covers 12 cardiovascular risk categories, a useful tool to complete before any appointment, to ensure the full picture is discussed and nothing important is overlooked.

Download the Risk Factor Checklist →

Heart Matters Resource

When in Doubt, Get Checked Out

If you are of South Asian or East Asian background and have not had a cardiovascular risk assessment that explicitly accounts for your ethnic background, that conversation with your doctor is one of the most valuable you can have. Start it today.

Read: When in Doubt, Get Checked Out →

Conclusion

The cardiovascular risks that affect South and East Asian communities are real, well understood, and highly manageable when identified early. The standard medical tools that doctors use every day were not built with your specific background in mind, which means you may need to be the one who brings this conversation to your appointment.

That is not a burden, it is an opportunity. The person who walks into their doctor’s office armed with this awareness, asks the right questions, and gets the right assessment is the person who gives themselves the best possible chance of a long and healthy life.

Your background is not your destiny. It is information, and information, acted on early, is one of the most powerful tools in cardiovascular medicine.

Understanding Ventricular Tachycardia: and Why Treatment Works

April 7, 2026March 10, 2026

Ventricular tachycardia is a fast heart rhythm originating in the lower chambers of the heart. With the treatments available today, most people do very well.

Obstructive Sleep Apnoea and the Heart: Why It’s So Often Missed

May 11, 2026March 6, 2026

Key Points

Obstructive sleep apnoea, often called OSA or simply sleep apnoea, is a condition where the airway repeatedly closes during sleep, causing breathing to stop briefly, sometimes hundreds of times a night. Most people have no idea it is happening.
Sleep apnoea is common. Around one in ten adults has the moderate-to-severe form with the clearest cardiovascular consequences, and rates are even higher when milder cases are included. The vast majority of people who have it have never been diagnosed.
The heart connections are significant and well established. Sleep apnoea is independently linked to high blood pressure, atrial fibrillation, heart failure, and increased risk of heart attack and stroke.
Symptoms include loud snoring, waking feeling exhausted despite adequate sleep, morning headaches, and significant daytime tiredness. Many people have subtle symptoms and do not recognise the pattern.
Treatment with CPAP, a small device that keeps the airway open during sleep, is highly effective and produces real cardiovascular benefits including better blood pressure control and reduced atrial fibrillation burden.

Most people who have sleep apnoea do not know they have it. They know they snore. They know they feel tired no matter how much they sleep. They know they wake with a headache some mornings. But they have put these things down to age, to stress, to being overweight, and the possibility that something specific and very treatable is happening during the night has never been raised.

Sleep apnoea sits at the junction of sleep health and heart health in a way that medicine has taken too long to fully recognise. It is not simply a snoring problem. It is a condition that stresses the cardiovascular system repeatedly through the night, and when it is identified and treated, the benefits extend well beyond simply sleeping better.

This article is for anyone who recognises the pattern described here, and for anyone managing a heart condition who has never been assessed for a sleep disorder that may be quietly working against their treatment.

What Is Sleep Apnoea?

What happens during the night

During sleep, the muscles throughout the body relax, including the muscles that support the soft tissues of the throat. In most people this relaxation is harmless. In people with obstructive sleep apnoea, the airway partially or completely collapses when those muscles relax, blocking the flow of air to the lungs.

When breathing stops, the level of oxygen in the blood begins to fall. The brain detects this and briefly rouses the person, just enough to restore muscle tone in the throat and allow breathing to restart, usually with a snort, gasp, or choking sound. The person rarely fully wakes and rarely remembers any of this. But it may happen dozens or even hundreds of times through the night, preventing the deep, restorative stages of sleep and leaving the person exhausted in the morning despite apparently adequate hours in bed.

How severity is measured

Sleep specialists measure the severity of sleep apnoea by counting the average number of breathing interruptions per hour of sleep. Mild sleep apnoea involves 5 to 15 events per hour. Moderate is 15 to 30. Severe is above 30, which means breathing is being interrupted more than once every two minutes throughout the night. In some people with untreated severe sleep apnoea, this happens every single minute of sleep, a level of overnight stress on the body that has very real cardiovascular consequences.

Recognising the Symptoms

Sleep apnoea has a recognisable pattern, but many of its features are easy to dismiss as something else. The symptoms below are the most useful to identify.

Symptoms to Recognise

Loud Snoring

Often loud enough to wake a partner. Not every snorer has sleep apnoea, but significant sleep apnoea is almost always accompanied by snoring.

Witnessed Pauses

A partner notices the person stop breathing and restart with a snort or gasp. If someone has told you this, it is one of the most important things to mention to your doctor.

Unrefreshing Sleep

Waking after a full night still feeling exhausted. Many people normalise this over years without realising it reflects a treatable condition.

Morning Headache

A dull pressure headache on waking that clears within an hour of getting up. Caused by overnight build-up of carbon dioxide in the blood.

Daytime Sleepiness

Struggling to stay awake during meetings, in front of the television, or while reading. Falling asleep at the wheel is a real risk in significant untreated sleep apnoea.

Nocturnal Palpitations

Each breathing pause triggers a stress surge that can disturb heart rhythm overnight, particularly relevant in atrial fibrillation.

If morning headaches or palpitations at night are a regular feature for you, our articles on morning headaches and the heart and why you feel your heart beating at night explore both connections in more detail.

Who Is at Risk?

Sleep apnoea is more common in men than women, though the gap narrows significantly after menopause. Carrying extra weight, particularly around the neck, is the most important modifiable risk factor, as it narrows the airway. Getting older, having a naturally narrow jaw, large tonsils, or a blocked nose all increase the likelihood of sleep apnoea developing.

But sleep apnoea is not exclusively a condition of overweight middle-aged men, and this assumption causes many people to go undiagnosed. Lean individuals, women, and younger people all develop sleep apnoea. People of East and Southeast Asian background develop it at lower body weights than Western populations due to differences in facial bone structure. The symptoms matter more than the stereotype. If the pattern fits, it is worth raising with your doctor regardless of what you weigh or what age you are.

Why Sleep Apnoea Matters for Your Heart

High blood pressure

Sleep apnoea is the most common identifiable cause of blood pressure that is difficult to control, where pressure stays high despite medication. The reason is that each time breathing stops during the night, the body’s stress response fires, raising the heart rate and tightening the blood vessels. This happens so many times through the night that the stress response carries over into the daytime, keeping blood pressure elevated around the clock.

For anyone whose blood pressure has been hard to bring under control despite treatment, asking about sleep apnoea is one of the most valuable steps available. Treating the sleep apnoea often produces blood pressure improvements that medication alone could not achieve.

Atrial fibrillation

Atrial fibrillation, an irregular heart rhythm that significantly increases stroke risk, is closely connected to sleep apnoea. The two conditions frequently coexist, and untreated sleep apnoea makes atrial fibrillation harder to treat and more likely to return after treatment. The overnight oxygen drops and stress surges from sleep apnoea irritate the heart’s electrical system in ways that promote irregular rhythm.

For anyone who has had cardioversion, an electrical reset of the heart rhythm, or catheter ablation to treat AF, treating sleep apnoea is now considered a standard part of protecting that result. Without it, the AF is significantly more likely to return.

Heart failure

In people with heart failure, where the heart is not pumping as efficiently as it should, sleep apnoea adds an additional burden on the heart through the night, at the very time the heart should be resting and recovering. Treating sleep apnoea in people with heart failure improves the heart’s pumping function and reduces the overnight stress load.

Heart attack and stroke risk

The repeated overnight stress that untreated sleep apnoea places on the blood vessels accelerates the build-up of plaque in the arteries, the same process that underlies heart attacks and strokes. Sleep apnoea is an independent cardiovascular risk factor, meaning it adds to risk over and above the conventional factors like blood pressure, cholesterol, and smoking.

Getting a Diagnosis: Simpler Than You Might Think

The sleep study

Diagnosing sleep apnoea requires a sleep study, but this is far simpler than most people imagine. The most common approach is a home-based study, a small portable monitor worn overnight in your own bed. It measures oxygen levels, breathing patterns, heart rate, and body position through the night. Most people sleep almost normally wearing it. The results are reviewed by a sleep specialist and used to determine whether sleep apnoea is present and how severe it is.

A formal in-laboratory sleep study, where the person sleeps overnight at a clinic with more detailed monitoring, is sometimes used for more complex cases, but the home study is the standard starting point for most people.

How to access a sleep study

Your GP or cardiologist can arrange a referral for a sleep study. If you have established cardiovascular disease, particularly high blood pressure that is hard to control, atrial fibrillation, or heart failure, and sleep apnoea has never been assessed, raising it proactively at your next appointment is worthwhile. Many people have been managing their heart condition for years without this important piece of the picture being investigated.

Treatment: What Works and What to Expect

CPAP: The Most Effective Treatment

CPAP, which stands for Continuous Positive Airway Pressure, is the most effective treatment for moderate to severe sleep apnoea. It involves wearing a mask during sleep that delivers a gentle, steady flow of air. This air pressure acts like a splint, keeping the airway open and preventing it from collapsing throughout the night.

Modern CPAP machines are much quieter and more comfortable than earlier generations. Many people are surprised by how unobtrusive they are in practice. The mask comes in several styles, and finding the right fit makes a significant difference to comfort. Most people go through an adjustment period of two to four weeks, and the vast majority who persist through that period find the improvement in their sleep, their daytime energy, and their overall wellbeing to be genuinely transformative.

The cardiovascular benefits of consistent CPAP use are real and measurable: better blood pressure control, reduced atrial fibrillation burden, improved heart function in heart failure, and lower overnight cardiovascular stress. For many people, CPAP treatment changes not just their sleep but their overall cardiac management picture.

Weight loss

For people who are overweight, meaningful weight loss reduces the severity of sleep apnoea significantly, and in some cases resolves it entirely. This is the most durable long-term solution. In practice, CPAP and weight loss often work together. The CPAP provides immediate protection while lifestyle changes work over time.

Sleeping position and dental devices

For milder sleep apnoea, particularly in people whose apnoeas mainly occur when sleeping on their back, simply learning to sleep on the side can make a meaningful difference. Custom dental appliances that gently advance the lower jaw during sleep are another option for people with mild to moderate sleep apnoea who cannot tolerate CPAP. They are made by a dentist with experience in sleep disorders and can be very effective in the right patient.

Sleep apnoea assessment is now a routine part of how I evaluate patients with high blood pressure, AF, and heart failure. When it is present and treated, the difference to their cardiac management can be substantial. Treating the heart condition without addressing the sleep apnoea is working with one hand tied behind your back.

Professor Peter Barlis, Interventional Cardiologist

Questions Worth Raising with Your Doctor

I snore heavily and wake feeling exhausted regardless of how long I sleep. Should I be assessed for sleep apnoea?
My blood pressure has been difficult to control despite medication. Could untreated sleep apnoea be a factor?
I have atrial fibrillation. Has sleep apnoea been assessed as part of my management?
I have heart failure. Should a sleep study be part of my investigation?
I have started CPAP but am finding it difficult to get used to. What support is available?

Heart Matters Resource

When in Doubt, Get Checked Out

If you recognise the pattern described in this article, or if your partner has raised concerns about your breathing during sleep, a sleep study is a straightforward, low-barrier investigation that can answer the question definitively. Raise it with your GP or cardiologist at your next appointment.

Read: When in Doubt, Get Checked Out →

Conclusion

Sleep apnoea is common, under-diagnosed, and very treatable. The connection to cardiovascular health is real and significant, and identifying it in someone managing high blood pressure, atrial fibrillation, or heart failure can genuinely change their clinical picture for the better.

The home sleep study is simple, the treatment is effective, and the improvement in how people feel, in their sleep, their energy, their capacity to engage with life, is one of the most consistent and satisfying outcomes in all of cardiovascular medicine.

If any of the symptoms in this article sound familiar, that conversation with your doctor is worth having. A good night’s sleep is not a luxury. For your heart, it is part of the treatment plan.

POTS: Understanding Postural Orthostatic Tachycardia Syndrome

April 18, 2026February 23, 2026

Key Points

POTS, Postural Orthostatic Tachycardia Syndrome, is a condition of the autonomic nervous system in which heart rate rises excessively on standing, producing symptoms that can be profoundly disabling.
The hallmark is a heart rate increase of 30 beats per minute or more within 10 minutes of standing, without a significant fall in blood pressure, accompanied by a characteristic symptom pattern.
Symptoms include dizziness, lightheadedness, palpitations, fatigue, brain fog, and near-fainting on standing, often dramatically improved by lying down, which is one of the most diagnostically telling features.
POTS is not rare, it predominantly affects women between the ages of 15 and 50, and is significantly under-diagnosed. Many patients spend years being told their symptoms are anxiety or deconditioning before receiving a correct diagnosis.
While POTS can be debilitating, a structured management approach, combining lifestyle strategies, physical reconditioning, and where needed medications, produces meaningful improvement in the majority of patients. Specialist clinic input is an important part of optimal care.

POTS is one of those conditions where the journey to diagnosis is often as difficult as the condition itself. Patients, most of them young, arrive in my clinic having seen multiple doctors, having been told their palpitations are anxiety, their fatigue is depression, their dizziness is nothing to worry about. Some have been told there is nothing wrong. Others have been given a diagnosis of chronic fatigue, fibromyalgia, or panic disorder, and while these may coexist, they are not POTS, and treating them alone leaves the underlying autonomic dysfunction unaddressed.

The relief that comes when POTS is finally named and explained, when a patient understands that their symptoms have a physiological basis that is measurable and treatable, is one of the more meaningful moments in a consultation. It does not make the condition less challenging. But it makes it navigable.

This article is for patients who suspect they may have POTS, who have recently been diagnosed, or who are trying to understand a condition that is often poorly explained. The message I want to convey from the outset is this: POTS is real, it is complex, it is frequently underestimated, and with the right approach, most people do meaningfully better.

What Is POTS?

The autonomic nervous system

The autonomic nervous system regulates the body’s automatic functions, heart rate, blood pressure, breathing, digestion, without conscious effort. When you stand up, it orchestrates an immediate response: blood vessels in the legs constrict to prevent blood pooling downward, and the heart rate adjusts to maintain adequate blood flow to the brain. In most people this happens seamlessly and invisibly.

In POTS, this orchestration is dysregulated. When standing, blood pools excessively in the lower body. The autonomic nervous system compensates with a disproportionate surge in heart rate, but this response is not fully effective, and the brain and upper body receive inadequate perfusion. The result is the characteristic symptom cluster of POTS: dizziness, palpitations, fatigue, and cognitive fog that appear on standing and improve dramatically on lying down.

The diagnostic criteria

The formal diagnostic criterion for POTS is a sustained heart rate increase of 30 beats per minute or more within 10 minutes of standing, or a heart rate exceeding 120 beats per minute on standing, in the absence of orthostatic hypotension (a significant fall in blood pressure on standing). In adolescents, the threshold is a rise of 40 beats per minute.

The key distinction from a simple faint or vasovagal episode is that in POTS, the blood pressure does not fall significantly, it is the heart rate that is the primary abnormality, compensating for inadequate venous return with a dramatic and sustained tachycardia.

What Does POTS Feel Like?

The upright-to-horizontal contrast

One of the most revealing features of POTS, both for diagnosis and for the patient’s own understanding, is how dramatically symptoms vary with position. Standing or sitting upright produces symptoms. Lying down relieves them, often within minutes. This positional dependence is so characteristic that many patients learn to structure their lives around it before they have any diagnosis, lying down after meals, avoiding prolonged standing, sitting rather than standing whenever possible.

When patients describe having to lie on the supermarket floor, or being unable to stand in the shower, or feeling well in bed but incapacitated within minutes of getting up, that history is POTS until proven otherwise.

The symptom cluster

Palpitations

Racing heart on standing, often the most alarming feature. The heart rate surge is real and measurable, not imagined.

Dizziness and lightheadedness

On standing, prolonged standing, or after meals. Reflects inadequate cerebral perfusion despite the compensatory tachycardia.

Profound fatigue

Not ordinary tiredness, a heavy, persistent exhaustion that does not resolve with rest and is worsened by upright activity.

Brain fog

Difficulty concentrating, slowed thinking, memory problems. Reflects reduced cerebral blood flow rather than a primary neurological disorder.

Near-fainting (presyncope)

The feeling of being about to faint, often without actually losing consciousness. Many patients faint eventually but presyncope is more common.

Other autonomic features

Nausea, sweating, temperature dysregulation, headache, and sleep disturbance are common, reflecting the broader autonomic nervous system dysfunction.

Who Gets POTS and Why?

Demographics

POTS predominantly affects women, around 80% of cases, typically between the ages of 15 and 50. The onset is often in adolescence or young adulthood. It is estimated to affect between one and three million people in the United States alone, making it considerably more common than many conditions that receive far greater clinical attention.

Triggers and associations

POTS can develop after a viral illness, a pattern that has been particularly well documented following COVID-19, where post-COVID POTS has been identified as one of the more prevalent long COVID manifestations. Other recognised triggers include significant physical deconditioning, pregnancy, surgery, trauma, and puberty. In some patients there is no identifiable trigger, the autonomic dysregulation appears to be constitutional.

Associated conditions include hypermobile Ehlers-Danlos syndrome, a connective tissue disorder characterised by joint hypermobility, which is found in a significant proportion of patients with POTS. Mast cell activation syndrome, autoimmune conditions, and small fibre neuropathy are also more common in the POTS population than in the general population. These associations are clinically important because they influence investigation and management.

Subtypes

POTS is not a single pathophysiological entity, several distinct subtypes have been described, each with different underlying mechanisms. Hypovolaemic POTS involves a reduced circulating blood volume. Neuropathic POTS involves partial autonomic denervation of the lower limb blood vessels. Hyperadrenergic POTS involves excessive sympathetic nervous system activity. Understanding the subtype, where this is possible, helps guide treatment selection. This is one of the reasons specialist clinic input is so valuable.

Diagnosis

The active stand test

The simplest diagnostic assessment is the active stand test, measuring heart rate and blood pressure after lying supine for 10 minutes, then at intervals over 10 minutes of standing. A sustained heart rate rise of 30 beats per minute or more (40 in adolescents), with symptoms, and without significant blood pressure fall, meets the diagnostic criteria.

Tilt table testing

For a more controlled assessment, or when the active stand test is inconclusive, a tilt table test is performed. The patient is strapped to a table that is tilted from horizontal to 70 degrees and held there for up to 45 minutes while heart rate and blood pressure are continuously monitored. This test is the gold standard for diagnosing POTS and other forms of orthostatic intolerance.

Further investigation

Blood tests assess for common associated conditions, thyroid function, anaemia, autoimmune markers, and plasma volume studies where available. A 24-hour Holter monitor documents the heart rate patterns throughout a normal day. Echocardiography confirms normal cardiac structure and function. Skin biopsy for small fibre neuropathy may be considered in specialist centres.

One of the most validating moments for a patient with POTS is seeing their own heart rate trace on a monitor, watching it jump from 70 to 130 beats per minute simply on standing. For someone who has been told for years that their symptoms are anxiety or deconditioning, seeing the objective evidence of what their body is doing is genuinely transformative. It changes the conversation from “is this real?” to “what are we going to do about it?”, and that is a much better conversation to be having.

— Prof. Peter Barlis, Interventional Cardiologist

Management

Why a specialist clinic matters

POTS is best managed by a multidisciplinary team with experience in autonomic disorders. In Australia, POTS clinics, typically combining cardiology, neurology, and physiotherapy, offer the comprehensive, coordinated approach that this condition requires. A cardiologist managing a patient with POTS in isolation can help, but the physiotherapy reconditioning programme, the dietary advice, the psychological support for coping with a chronic and often poorly understood condition, these are best provided by a team that has developed expertise in this specific patient group.

If you have been diagnosed with POTS and are not yet under the care of a specialist clinic, asking for a referral is a worthwhile conversation to have.

Non-pharmacological strategies, the foundation

The core of POTS management is non-pharmacological, and for many patients, these measures alone produce significant improvement.

Fluid and salt loading is fundamental. Increasing fluid intake to two to three litres of water per day and increasing dietary salt, in the absence of hypertension, expands circulating blood volume and reduces the degree of orthostatic pooling. Many patients notice improvement within days of implementing this consistently.

Compression garments, waist-high graduated compression stockings or abdominal binders, physically counteract blood pooling in the lower body on standing. They are unglamorous but effective, and most patients who use them consistently find them meaningful.

Physical reconditioning is one of the most impactful and most challenging elements of management. Deconditioning worsens POTS significantly, yet upright exercise is poorly tolerated in active POTS. The key is starting with recumbent exercise, rowing machines, recumbent cycling, swimming, that achieves cardiovascular conditioning without the orthostatic stress of being upright. Gradually, as tolerance improves, more upright exercise can be introduced. This process takes months and requires patience, but the functional gains are real and durable.

Practical behavioural strategies make a significant difference to daily functioning, elevating the head of the bed by 10 to 20 degrees, rising from lying slowly, avoiding prolonged standing, eating smaller and more frequent meals (large meals divert blood to the gut), and avoiding heat and dehydration.

Medications

When non-pharmacological measures are insufficient, several medications have evidence supporting their use in POTS. Fludrocortisone increases salt and water retention, expanding blood volume. Midodrine is a vasoconstrictor that increases peripheral vascular resistance and reduces pooling, it is taken in doses timed around upright activity and cannot be taken at night. Beta-blockers, particularly low-dose propranolol, reduce the heart rate surge on standing and can alleviate the palpitation component significantly, though they need to be used carefully as they can worsen fatigue. Ivabradine, a selective heart rate-slowing agent without the side effects of beta-blockers, has shown benefit in POTS and is increasingly used.

The right medication, and the right dose, varies significantly between patients and subtypes. This is another reason why specialist clinic input matters: the trial-and-error process of finding what works for an individual patient is better navigated with experience.

Pacing and long-term outlook

POTS is not a progressive condition in the way that heart failure or coronary artery disease is, it does not inevitably worsen over time. Many patients, particularly those who develop POTS in adolescence, improve significantly as they mature. Those who develop it after a trigger such as a viral illness often improve meaningfully once the underlying trigger resolves and they have completed a structured reconditioning programme.

The trajectory varies enormously between individuals, some recover to full functional capacity, others manage well with ongoing strategies, and some continue to find the condition significantly limiting. Managing expectations honestly while maintaining therapeutic optimism, and adjusting the management approach iteratively as the patient’s condition evolves, is the art of POTS management.

Questions worth asking at your next appointment

Has POTS been formally confirmed with an active stand test or tilt table test?
Is referral to a specialist POTS or autonomic clinic appropriate for my situation?
Am I implementing the foundational measures, fluid, salt, compression, reconditioning, consistently and correctly?
Could my POTS be associated with an underlying condition such as hypermobile EDS or an autoimmune process?
Is my current medication approach optimised, and are there alternatives worth considering?

Heart Matters Resource

When in Doubt, Get Checked Out

If you experience dizziness, palpitations, and profound fatigue on standing that relieves on lying down, and these symptoms have been attributed to anxiety or deconditioning without a formal assessment, asking your doctor about POTS is the right next step.

Read: When in Doubt, Get Checked Out →

Conclusion

POTS is a condition that deserves to be taken seriously, by patients, by the clinicians they see, and by the healthcare system that too often dismisses the symptoms before investigating them properly. It is not anxiety. It is not deconditioning, though deconditioning makes it worse. It is an autonomic nervous system disorder with a measurable, objective physiological signature and a range of treatments that meaningfully improve quality of life for most people who receive appropriate care.

The diagnostic journey is often long and frustrating. But a correct diagnosis changes everything, from the framing of the condition, to the management approach, to the patient’s own understanding of why their body responds the way it does.

If you have POTS, or suspect you might: you deserve a proper assessment, a clear explanation, and access to a management approach that goes beyond “drink more water and exercise more.” A specialist POTS clinic is the best environment in which to receive all of that. Ask for a referral if you have not already been offered one.

Conditions

POTS: Understanding Postural Orthostatic Tachycardia Syndrome

SVT: A Nasal Spray That Can Stop an Episode at Home

Heart Health During Pregnancy: What You Need to Know

Heart Attack vs Cardiac Arrest: What is the Difference?

Women’s Heart Health: Why It’s Different

What You Need to Know About Pacemakers

What Is Atrial Fibrillation and How Does It Increase Stroke Risk?

Heart Stent Unboxing: What’s Inside the Tiny Device That Keeps Arteries Open

First-Degree AV Block on Your ECG: What Does It Really Mean?

What Does a Left Bundle Branch Block (LBBB) Mean on an ECG?

When a Slow Heart Rate Is Not Normal: Understanding Bradycardia

Ventricular Ectopic Beats: What They Are and What They Mean

Takotsubo Cardiomyopathy: The Broken Heart Syndrome: and Why the Heart Heals

SCAD: Spontaneous Coronary Artery Dissection: What It Is and What to Expect

Recovering After a Heart Attack

The Causative Organism: Group A Streptococcus

A familiar bacteria with an unfamiliar consequence

Why the immune system attacks the heart

From Strep Throat to Heart Disease: The Disease Pathway

How Rheumatic Fever Damages the Heart

Carditis: The Acute Inflammatory Phase

Valve Involvement: Which Valves and How

Mitral Stenosis: The Signature Lesion

A Global Burden, and a Local Reality

The scale of the problem

What I saw in Dili

The Timor-Leste Hearts Fund

Prevention: The Power of a Simple Antibiotic

Primary Prevention: Treating Strep Throat

Secondary Prevention: Penicillin Prophylaxis

Echocardiographic screening

Treatment: When Prevention Has Failed

Medical management

Valve intervention

What You Can Do

When in Doubt, Get Checked Out

Conclusion

Related Reading

Understanding the ECG, a Brief Explanation

What an ECG actually records

What a Q wave is

What Would a Genuine Concern Actually Look Like?

Why the Software Gets It Wrong

Normal Variant vs Genuine Concern, Plain Language Guide

What Investigation Is Actually Needed?

A clinical review, not a cascade of tests

What you do not need

When in Doubt, Get Checked Out

Conclusion

More from Heart Matters

Where It All Began

The Stent That Changed Everything

Beyond the Stent

The Scale of a Career

What This Means for Patients

Conclusion

Why Standard Risk Tools Sometimes Miss the Picture

South Asian Communities, What the Evidence Shows

Who this section applies to

Heart disease tends to arrive earlier

Body weight, why standard measures can be misleading

Diabetes, why it develops earlier and at lower weights

Lp(a), an inherited risk factor worth knowing about

East Asian Communities, What the Evidence Shows

Who this section applies to

Stroke, the priority risk to manage

Blood pressure and salt, a particularly important connection

Atrial fibrillation, a specific conversation worth having

Sleep apnoea at lower body weights

Alcohol, an important note for East Asian individuals

The Positive Picture, What Early Action Achieves

A Note on Acculturation, Second and Third Generations

When in Doubt, Get Checked Out

Conclusion

More from Heart Matters

What Is Sleep Apnoea?

What happens during the night

How severity is measured

Recognising the Symptoms