Prof. Peter Barlis

Professor Peter Barlis (MBBS, MPH, PhD, FESC, FACC, FSCAI, FRACP) is an Interventional Cardiologist and the founding editor of Heart Matters. With expertise in coronary artery disease, advanced cardiac imaging, and interventional cardiology — and fellowships of the European Society of Cardiology, the American College of Cardiology, and the Royal Australasian College of Physicians — he brings the highest level of clinical authority to everything published on this site. Heart Matters was founded on Professor Barlis's belief that patients who understand their condition are less frightened and better equipped to make decisions about their care. Every article on this site reflects that commitment.

Rheumatic Heart Disease: A Preventable Condition Affecting Millions

rheumatic heart disease
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.

Related Reading

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

heartmatters.com 2026 03 31T225746.389
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.

More from Heart Matters

A Living Legend of Interventional Cardiology: Professor Patrick Serruys

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.


Heart Stents: What You Need to Know by Prof. Peter Barlis

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.

More from Heart Matters: Coronary Artery Disease · Heart Stents Explained · TAVI, What to Expect · When in Doubt, Get Checked Out

Fatigue and the Heart: When Tiredness Is More Than Just Being Tired

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Key Points

  • Fatigue, persistent, disproportionate tiredness, is one of the most underappreciated cardiac symptoms, frequently attributed to stress, poor sleep, or ageing before a cardiac cause is considered.
  • When the heart is not pumping efficiently, the body diverts blood away from muscles and peripheral tissues to protect the brain and vital organs, producing the profound, heavy tiredness that characterises cardiac fatigue.
  • Cardiac fatigue is typically out of proportion to activity level, does not improve with rest in the way normal tiredness does, and is often accompanied by other symptoms such as breathlessness or ankle swelling.
  • Heart failure, significant valve disease, atrial fibrillation, and coronary artery disease can all present primarily as fatigue, particularly in women, older adults, and people with diabetes.
  • Fatigue that is new, progressive, or unexplained deserves investigation, not reassurance without assessment.

Fatigue is one of the great diagnostic challenges in medicine. It is almost universal, nearly everyone who sees a doctor mentions tiredness at some point. And because it is so common and so non-specific, it is often passed over quickly, attributed to lifestyle factors, and not investigated as systematically as it should be.

But cardiac fatigue has a quality that distinguishes it, and patients who have experienced it often describe it as unlike any tiredness they have felt before. It is heavy. It is persistent. It does not lift after a good night’s sleep. It limits what they can do in a way that feels disproportionate to how hard they are actually working.

Understanding the cardiac causes of fatigue, and the symptoms and patterns that should raise concern, is genuinely important, because fatigue is frequently the first and sometimes the only prominent symptom of significant cardiac disease.

Why the Heart Causes Fatigue

Reduced cardiac output

The heart’s primary job is to deliver oxygenated blood to every tissue in the body. When the heart is not pumping as strongly as it should, whether from a weakened heart muscle, a significant valve problem, or an irregular rhythm, the body’s tissues receive less oxygen and less fuel than they need to function normally.

The body responds with a hierarchy of protection: blood is directed preferentially to the brain and vital organs. Muscles, skin, and peripheral tissues receive less. The result is the muscular weakness, heaviness, and profound tiredness that patients with heart failure describe, the legs that feel like lead, the arms that tire carrying a bag of shopping, the effort required to do things that used to require no effort at all.

The body’s stress response

Heart failure also triggers a cascade of stress hormones and chemical signals, the body’s attempt to compensate for a struggling heart. Over time, these responses have their own side effects, including fatigue, muscle wasting, and a general sense of unwellness that goes beyond simple tiredness.

The slow onset

Cardiac fatigue typically develops gradually, so gradually that patients accommodate to it the same way they accommodate to progressive breathlessness. They stop doing things that tire them. They attribute the tiredness to getting older, to stress, to not sleeping well. By the time they present for assessment, significant cardiac compromise may already have been present for months.

One question I often ask is: “What were you able to do six months ago that feels harder now?”
These changes can be subtle and easy to dismiss as a natural part of aging.
It is always worth a conversation with your doctor, simple tests can offer clarity and help you get that spring back in your step.

Cardiac Conditions That Present Primarily as Fatigue

Heart failure

Fatigue is one of the cardinal symptoms of heart failure, often preceding breathlessness, particularly in the early stages. The reduced pumping capacity means that even modest exertion produces a degree of tiredness that feels out of all proportion to the effort involved. Many patients describe fatigue as their most limiting symptom, even when their heart scan results show significant changes.

Atrial fibrillation

AF reduces the heart’s efficiency in several ways, the irregular rhythm is less effective than a regular one, and a fast heart rate reduces the time for the heart to fill properly between beats. Many people with AF describe fatigue and reduced exercise tolerance as their most prominent symptoms, more so than palpitations.

Significant valve disease

Aortic stenosis in particular can present with fatigue as a predominant early symptom, before breathlessness, chest pain, or dizziness become apparent. The increased effort required to pump blood through a narrowed valve can produce significant fatigue well before other symptoms develop.

Coronary artery disease

In some people, particularly women, older adults, and those with diabetes, fatigue on exertion can be the main warning sign of reduced blood flow to the heart, even without any chest pain at all. Fatigue on exertion that is out of proportion to the effort involved, in someone with cardiovascular risk factors, should always prompt a conversation with your doctor.

Bradycardia and medication effects

A significantly slow heart rate, from the heart’s own natural pacemaker slowing down, a problem with the heart’s electrical system, or medication, reduces how much blood the heart pumps with each beat, and can produce profound fatigue. Beta-blockers, which are used widely in heart medicine, can cause fatigue as a side effect, sometimes to a degree that significantly impacts quality of life. If fatigue develops after starting a new cardiac medication, the timing connection is worth discussing with the prescribing team.

Heart failure

Reduced pumping capacity leads to muscle underperfusion, heavy, persistent tiredness that does not lift with rest.

Atrial fibrillation

AF reduces the heart’s efficiency. Many people with AF experience fatigue and reduced exercise tolerance more than palpitations.

Valve disease

Aortic stenosis can present as fatigue before more classic symptoms develop, the increased workload on the heart produces energy depletion.

Coronary artery disease

Fatigue on exertion can signal reduced blood flow to the heart muscle, particularly in women, older adults, and people with diabetes where chest pain may be absent.

Bradycardia

A significantly slow heart rate reduces how much blood the heart pumps and can produce profound tiredness, sometimes worsened by cardiac medications.

Non-cardiac causes

Anaemia, thyroid disease, diabetes, sleep apnoea, depression, all require consideration alongside cardiac causes, and may coexist.

Distinguishing Cardiac Fatigue

Several features help distinguish cardiac fatigue from the more common causes of tiredness, though ultimately investigation is needed to be certain.

Cardiac fatigue tends to be related to exertion, worse with activity, somewhat better with complete rest, but never fully resolved. It is disproportionate to the level of activity involved, tasks that should be easy feel exhausting. It is progressive, getting worse over weeks and months rather than fluctuating day to day. And it is often accompanied by at least one other cardiac symptom, breathlessness, ankle swelling, palpitations, or reduced exercise tolerance, even if that symptom is mild and has been attributed to other causes.

Investigation

The investigation of unexplained or progressive fatigue should include a full blood count for anaemia, thyroid function, kidney function, a blood sugar test for diabetes, and a BNP blood test, a simple marker that indicates how hard the heart is working. A standard heart tracing (ECG) assesses rhythm and rate. A heart ultrasound (echocardiogram) provides the most comprehensive picture, how well the heart is pumping, how the valves are working, and whether there are signs of pressure building up.

If the history suggests fatigue on exertion with cardiovascular risk factors, further tests to assess blood flow to the heart may follow. A sleep study may also be arranged if sleep apnoea is suspected, it is more common than it is diagnosed, and it is a significant and treatable cause of both fatigue and cardiac risk.

Questions worth asking at your next appointment

  • Could my fatigue have a cardiac cause, and what investigations would identify or exclude this?
  • I have been more tired since starting a new medication, could this be a side effect, and is there an alternative?
  • Is my fatigue related to my heart condition, or is it likely to have another explanation?
  • Should I have a heart strain blood test and a heart ultrasound as part of the workup?
  • Could sleep apnoea be contributing, and should I have a sleep study?

Free Download, Heart Matters

Our Heart Health Risk Factor Checklist covers 12 cardiovascular risk categories, a useful tool to bring to any appointment investigating unexplained fatigue, to ensure the full cardiovascular picture is considered.

Download the Risk Factor Checklist →

Heart Matters Resource

When in Doubt, Get Checked Out

Fatigue that is new, progressive, disproportionate to your activity level, or accompanied by any other cardiac symptom deserves investigation, not reassurance that it is simply age or stress.

Read: When in Doubt, Get Checked Out →

Conclusion

Fatigue is easy to dismiss and easy to over-explain. “You’re working too hard.” “You’re not sleeping well.” “It’s your age.” These explanations are sometimes correct, but they should be reached after appropriate investigation, not instead of it.

Cardiac fatigue is real, specific, and measurable. It responds to treatment, sometimes dramatically. Many patients who have lived with progressive fatigue for months describe the improvement after effective heart failure therapy or AF rate control as transformative, not just feeling better, but feeling like themselves again in a way they had stopped expecting.

If your fatigue is new, progressive, or qualitatively different from normal tiredness, particularly if it limits what you can do or is accompanied by any other cardiac symptom, that is the conversation worth having with your doctor.

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