Heart Conditions — Expert Guides

Aortic Dissection: The Chest Pain That Cannot Wait

July 17, 2026

Key Points

An aortic dissection is a tear in the wall of the aorta, the body’s main artery. It is a medical emergency, and every minute counts.
The warning sign is sudden, severe chest or back pain, often described as ripping or tearing, and often the worst pain a person has ever felt. It arrives at full intensity within seconds rather than building gradually.
Long term high blood pressure is the single biggest risk factor. Most people who have a dissection have had raised blood pressure for years.
Inherited conditions such as Marfan syndrome, and a family history of aortic aneurysm or unexplained sudden death, substantially increase risk and are a reason to ask about screening.
Dissection is easily mistaken for other conditions, and a normal ECG or normal blood test does not rule it out. If the pain fits the pattern, call 000.

Most cardiac emergencies announce themselves gradually. A heaviness in the chest that builds over minutes. A tightness that comes on with exertion and eases with rest. An aortic dissection does not behave this way. It arrives at full force, without warning, in people who felt perfectly well moments earlier.

It is the emergency that gives no notice. A person is well in the morning, well over lunch, and in cardiac arrest by the evening. That pattern is not a rare exception to how dissection behaves. It is characteristic of it.

Understanding what an aortic dissection is, who is at risk, and above all what it feels like, is the difference between a call to emergency services and a fatal delay.

What Is an Aortic Dissection?

The aorta is the largest blood vessel in the body. It leaves the heart, arches over the top of it, and travels down through the chest and abdomen, carrying every drop of blood the heart pumps out to the rest of the body. It is roughly the width of a garden hose, and it withstands enormous pressure with every heartbeat.

The wall of the aorta is made of three layers, bonded together. A dissection begins when the innermost layer develops a tear. Blood, travelling at high pressure, is forced into that tear and begins to push the layers apart, carving a false channel along the length of the vessel.

Once that channel opens, several things can go badly wrong at once. The false channel can compress the true one, starving organs of blood. It can extend into the branches that supply the brain, kidneys, or the heart muscle itself. It can rupture entirely. And if the tear is close to the heart, blood can leak into the sac that surrounds it, squeezing the heart until it can no longer pump.

The Two Types, and Why the Difference Matters

Doctors classify dissections by where the tear sits. This is not academic. The two types are treated in fundamentally different ways.

Type A dissections involve the ascending aorta, the section closest to the heart. These are surgical emergencies. The tear can extend backwards into the sac around the heart or shear off the arteries feeding the heart muscle, and either can cause sudden cardiac arrest. Type A dissections are taken directly to theatre.

Type B dissections are confined to the descending aorta, further down the chest. These are often managed initially with aggressive blood pressure control in intensive care, with a stent placed inside the vessel in selected cases. Surgery is not always the first step.

Type A

The tear involves the section of aorta nearest the heart. This is the more dangerous form and is treated as an immediate surgical emergency.

Type B

The tear is confined to the descending aorta, further from the heart. Often managed first with intensive blood pressure control, and sometimes a stent.

Why Time Matters

For an untreated Type A dissection, the risk of death rises with every hour that passes after the tear. This is why it is never something to wait out.

What It Actually Feels Like

This is the section worth remembering, because recognising the pain is what gets people to hospital in time.

The classic symptom is sudden, severe pain in the chest or back. Patients describe it as ripping, tearing, or being stabbed. It is frequently described as the worst pain of their life. Two features set it apart from most other chest pain.

First, the onset. It does not build. It is maximal within seconds. People can often tell you exactly what they were doing at the moment it began.

Second, it can move. As the tear extends along the vessel, the pain can travel, migrating from the front of the chest through to between the shoulder blades, or down into the abdomen.

Dissection can also present in ways that look like something else entirely. Stroke-like symptoms if the tear reaches the arteries to the brain. Abdominal pain. Fainting. A leg that suddenly turns cold and pale. In the most severe cases, the first sign is collapse. This was the pattern in the widely reported death of United States Senator Lindsey Graham in July 2026, whose office cited preliminary findings of an aortic dissection due to arteriosclerotic cardiovascular disease. He was 71, had recently returned from an overseas trip, and had shown no sign of being unwell.

Chest pain that arrives at full intensity in an instant, and is described as tearing or ripping, is not a wait and see symptom. It is a call an ambulance symptom.

Why Blood Pressure Sits at the Centre of This

The most important thing to understand about dissection is that in the majority of cases, it is the endpoint of a process that has been building quietly for years.

Every heartbeat sends a pulse of pressure through the aortic wall. Over decades, persistently high blood pressure stresses that wall, stiffening it and degrading the elastic tissue that holds the layers together. Add the plaque and inflammation of atherosclerosis, the same disease process that drives most heart attacks and strokes, and the wall becomes progressively less able to tolerate the pressure it is subjected to.

Chronic hypertension is the single biggest modifiable risk factor for aortic dissection, and it is present in the large majority of cases. This is the uncomfortable but hopeful part of the story. A condition that kills within minutes is driven, more than anything else, by a number that can be measured at home in 60 seconds and treated effectively.

The other well-recognised contributors are:

Age and sex. Dissection most commonly affects men in their 60s and 70s, though it can occur far younger, particularly where there is an inherited cause.
Smoking. Tobacco accelerates the arterial damage that weakens the aortic wall.
An existing aortic aneurysm. A vessel that has already enlarged is a vessel more likely to tear.
Stimulant drug use. Cocaine and amphetamines cause abrupt, extreme blood pressure surges.
Pregnancy. Uncommon, but a recognised period of increased risk in women with underlying aortic disease.

The Genetic Side, and When Family History Matters

Not every dissection is a story about decades of blood pressure. A meaningful minority occur in younger people whose aortas were structurally vulnerable from birth.

Inherited connective tissue conditions

Marfan syndrome is the best known. It affects the connective tissue that gives the aortic wall its strength, and people with Marfan syndrome can experience dissection in their 30s or 40s. Loeys-Dietz syndrome and vascular Ehlers-Danlos syndrome carry similar risk. These conditions often, though not always, come with recognisable physical features such as tall stature, long limbs and fingers, and problems with the lens of the eye.

Bicuspid aortic valve

Some people are born with an aortic valve that has two leaflets instead of the usual three. This is one of the most common congenital heart differences, and it is associated with weakness in the wall of the ascending aorta, independent of any valve problem. It is also relevant to aortic stenosis later in life.

Familial aortic disease with no syndrome attached

This is the group most often missed. Some families carry a tendency to aortic aneurysm and dissection without any of the classical syndromes and without any outward clues. The only signal is the family history itself.

If a parent, sibling, or child has had an aortic aneurysm, an aortic dissection, or an unexplained sudden death, that is worth raising with your doctor. Imaging can measure the size of the aorta long before it is in danger, and an aorta that is enlarging can be monitored, treated with blood pressure medication, and repaired electively. Elective repair is a very different proposition to emergency surgery on a tearing vessel.

Why It Is So Easily Missed

Aortic dissection is one of medicine’s great imitators, and this is worth understanding because it affects what you should do.

The standard tests used to assess chest pain, an ECG and a blood test for cardiac enzymes, can be entirely normal while the aorta is tearing. A chest X-ray is often unremarkable. The diagnosis usually rests on a CT scan of the aorta, and that scan only gets ordered if someone thinks to order it.

This has two practical implications. If you experience sudden tearing chest or back pain, say so in exactly those words to the paramedics and to the doctor in the emergency department. The description matters. And if you have a family history of aortic disease, say that too, unprompted. It changes how the pain in front of the doctor is interpreted.

It is entirely reasonable, in that situation, to ask directly whether an aortic dissection has been considered. Good clinicians will not be offended by the question.

What You Can Actually Do

The measures that protect the aorta are not exotic. They are the same measures that protect the rest of the cardiovascular system, applied consistently over years.

Know your blood pressure and treat it. If you have been prescribed medication for it, take it. This matters more than any other single action, and there is a great deal you can do alongside medication to help bring the numbers down.

Do not smoke. Treat raised cholesterol. Stay physically active. Understand your overall cardiovascular risk profile rather than any single number in isolation.

And know the alarm symptom. Sudden, severe, tearing chest or back pain, arriving at full intensity, in a person who was well moments before, is an emergency until proven otherwise. In Australia, call 000. Do not drive yourself. Do not wait to see whether it settles.

Conclusion

An aortic dissection is one of the few conditions in cardiovascular medicine where outcome is measured in minutes rather than hours or days. It is also, for most people, the final chapter of a much longer and much quieter story, one written by years of untreated blood pressure and arterial damage. That is the part that is within reach.

Take the blood pressure reading. Ask about the family history. And if the pain ever comes, sudden and tearing and unlike anything before it, do not talk yourself out of the phone call.

Cardiac Amyloidosis: The Stiff Heart Condition That’s Now Treatable

July 13, 2026

Cardiac amyloidosis is caused by misfolded proteins stiffening the heart muscle, and it is now treatable. Here is what patients need to know about this increasingly recognised and now treatable condition.

Demystifying Heart Failure: HFrEF, HFpEF and HFimpEF Explained

July 9, 2026

Key Points

Heart failure does not mean the heart has stopped or is about to. It means the heart is not pumping or filling as efficiently as it should, and in many cases this can be treated and even improved.
The confusing letters (HFrEF, HFpEF, and the newer HFimpEF) all describe one thing: the ejection fraction, or how much blood the main pumping chamber squeezes out with each beat.
Cardiologists separate these types because the underlying problem and the best treatment differ. The same label points the whole team toward the right medicines.
HFimpEF (improved ejection fraction) is the hopeful category. It describes people whose heart function has recovered, and the key lesson is that the medicines usually need to continue.
A new international consensus, the Second Universal Definition of Heart Failure published in June 2026, reframes heart failure as a condition that can change over time, with more focus on catching it early.

You have been told you have heart failure, and within the same conversation you have heard HFrEF, HFpEF, and perhaps HFimpEF. It sounds like alphabet soup, and it arrives at exactly the moment you are least equipped to decode it. The good news is that these terms are far less frightening once you understand what they are actually measuring, and why your cardiologist cares about the difference.

This article breaks the language down into plain English: what heart failure really means, what those letters stand for, why the distinction matters for your treatment, and what a major new international definition, published in June 2026, changes for patients.

Start With What Heart Failure Actually Means

The name is one of the cruellest in medicine. “Failure” suggests something has stopped, or is about to. That is not what it means. Heart failure is a clinical syndrome in which the heart cannot pump or fill with blood as efficiently as the body needs, usually producing symptoms such as breathlessness, fatigue, and swelling in the legs and ankles.

Crucially, it is not a single disease and it is not a death sentence. It is a description of how the heart is performing, and modern treatment can stabilise it, ease symptoms, and in a meaningful number of people improve the heart’s function substantially. To understand the categories, you first need to understand one number.

The Number Behind the Letters: Ejection Fraction

Every time the heart’s main pumping chamber, the left ventricle, contracts, it squeezes a percentage of the blood inside it out to the body. That percentage is the ejection fraction, usually shortened to EF. It is measured most often on an echocardiogram, the heart ultrasound.

A normal left ventricle does not empty completely. A healthy EF sits somewhere around 55% to 70%. So an EF of 60% is normal, not a sign that 40% is being left behind in a worrying way. This is the single most misread number in a cardiology report, so it is worth pausing on: a lower EF means the pump is weaker, but the EF is only one part of the picture, and it is not the whole story of how you will feel or fare.

The Three Main Types, Explained

Heart failure is grouped by ejection fraction because that number, more than almost anything else, tells the cardiologist what kind of problem they are dealing with and which treatments are likely to help. Here are the categories you are most likely to hear.

HFrEF: heart failure with reduced ejection fraction

This is the “weak pump” type. The EF is reduced, conventionally 40% or below, meaning the left ventricle is not contracting forcefully enough. The heart muscle has usually been damaged or weakened, and the squeeze is impaired. HFrEF is the type with the largest body of evidence behind its treatment, and, importantly, the type where the right combination of medicines can make the biggest difference.

HFpEF: heart failure with preserved ejection fraction

Here the EF is preserved, conventionally 50% or above, so the pump looks normal on paper. The problem is not the squeeze but the relaxation and filling. A stiff left ventricle cannot relax properly between beats, so it fills poorly and pressure backs up, producing the same symptoms of breathlessness and swelling. HFpEF is more common in older adults, in women, and in people with long-standing high blood pressure, diabetes, or obesity. For years it was the harder type to treat, though that has changed recently.

HFimpEF: heart failure with improved ejection fraction

This is the newest and most hopeful category. It describes someone who started with a reduced EF (40% or below) and, with treatment, has seen it recover to above 40%. Their heart has improved. The vital message attached to this label, and the reason cardiologists coined it rather than simply calling the person “better,” is that the improvement is usually because of the medicines, not instead of them. Stopping treatment because the numbers look good is one of the most common ways people relapse.

You may also hear HFmrEF, heart failure with mildly reduced ejection fraction, describing the middle band where EF sits between 41% and 49%. Think of it as the territory between the reduced and preserved categories, treated with a foot in both camps.

HFrEF: reduced

The pump is weak. Ejection fraction 40% or below. The muscle is not squeezing hard enough. Strong evidence exists for treatment that helps the heart recover.

HFpEF: preserved

The pump looks normal (EF 50% or above) but the ventricle is stiff and fills poorly. More common with age, in women, and with high blood pressure or diabetes.

HFimpEF: improved

Started reduced, now recovered above 40%. The good-news category, with one rule: the medicines that produced the recovery usually need to continue.

Why Cardiologists Bother Splitting Hairs

It is a fair question. If the symptoms are similar, why label the types at all? The answer is that the underlying mechanics are genuinely different, and so is the treatment that works. A medicine proven to save lives in a weak, reduced-EF heart may do little for a stiff, preserved-EF heart, and vice versa. The category is not bureaucratic tidiness. It is the shorthand that points your whole care team toward the treatments most likely to help you, and away from ones that will not.

Getting the category right also shapes what your cardiologist watches over time, from your BNP blood test to repeat scans that track whether your EF is holding steady, worsening, or improving.

The table below sets the three types side by side. It is a map, not a diagnosis, and your own cardiologist remains the person who reads it onto your particular heart.

Feature	HFrEF (reduced)	HFpEF (preserved)	HFimpEF (improved)
Ejection fraction	40% or below	50% or above	Was 40% or below, now above 40%
Core problem	A weak squeeze	A stiff chamber that fills poorly	A previously weak heart that has recovered
More common in	People with prior muscle damage or a weakened heart	Older adults, women, and people with high blood pressure or diabetes	People treated early and effectively for HFrEF
Treatment focus	The four pillars of medicine, built up together	Treating the drivers, plus SGLT2 inhibitors	Continuing the medicines that produced the recovery
Outlook message	Strong evidence that treatment helps	Improving fast as new evidence arrives	The hopeful category, if treatment continues

The label is not there to frighten you. It is there to make sure the right medicine reaches the right heart.

What Causes Each Type

The causes overlap, but they cluster differently across the categories, and identifying the cause is often as important as measuring the EF.

Reduced-EF heart failure most often follows damage to the heart muscle: a previous heart attack that has left a weakened area, longstanding uncontrolled blood pressure, disease of the heart muscle itself (the cardiomyopathies), heart rhythm problems such as atrial fibrillation, valve disease, or, in some people, alcohol and certain toxins.

Preserved-EF heart failure tends to grow out of years of a heart working against stiffening and pressure: chronic high blood pressure, diabetes, obesity, obstructive sleep apnoea, and ageing itself. Less commonly, an infiltrative condition such as cardiac amyloidosis stiffens the muscle, which matters because some of these causes now have specific treatments.

Improved-EF heart failure, by definition, starts as the reduced type and gets better, usually because the cause was treatable and the treatment worked. That is precisely why the medicines are rarely a temporary measure.

How Each Type Is Treated

This is where the categories earn their keep. The following is a general map, not a prescription. The right combination, and every dose, is individual, and only your own cardiologist can advise what is right for you.

For reduced-EF heart failure, the modern approach uses four classes of medicine together, often called the four pillars or quadruple therapy. In broad terms these are a medicine that relaxes and protects the blood vessels and heart (an ACE inhibitor, an ARB, or the combination agent Entresto), a beta-blocker, a mineralocorticoid receptor antagonist such as spironolactone, and an SGLT2 inhibitor. Used together and built up carefully, this combination has transformed outcomes over the past decade.

For preserved-EF heart failure, the picture has brightened considerably. SGLT2 inhibitors now have good evidence here too, which was not the case a few years ago. Beyond that, the priority is treating the drivers: controlling blood pressure and diabetes, managing weight, addressing sleep apnoea, and using diuretics to clear the fluid that causes congestion and breathlessness. Treating the specific cause, where there is one, matters more in this group than in any other.

For improved-EF heart failure, the treatment is, in most cases, to keep going. Trials have shown that stopping the medicines once the heart has recovered often allows the weakness to return. The recovery is best understood as the treatment succeeding, not as the illness disappearing, and the safest path is to maintain the therapy under your cardiologist’s guidance. Never stop a heart failure medicine without speaking to them first.

What the New 2026 Definition Changes

In June 2026, the world’s leading cardiovascular bodies, including the American Heart Association, the American College of Cardiology, the European Society of Cardiology, and the World Heart Federation, published the Second Universal Definition of Heart Failure, simultaneously in the journals JACC, Circulation, the European Heart Journal, and Global Heart. The American Heart Association has also released a plain-language summary for patients. It updates the first such definition from 2021, and although the document is written for clinicians, several of its changes matter to patients.

64 million
adults worldwide are estimated to live with heart failure, a number driven up by ageing populations and rising rates of high blood pressure, diabetes, and obesity.
American Heart Association, June 2026

First, it moves away from rigid cut-off numbers for ejection fraction and acknowledges that a normal EF differs by sex, age, and ethnicity, while keeping the familiar reduced, preserved, and improved categories as practical guides. Second, it puts far greater emphasis on catching heart failure early, before symptoms appear, so that prevention and treatment can start sooner. Third, and perhaps most reassuringly, it formally describes heart failure as a dynamic condition that can improve, go into remission, or progress, rather than a fixed, one-way diagnosis. The document is intended to be the foundation for the next major heart failure guideline, expected in 2027.

For a patient, the takeaway is encouraging: the field increasingly sees heart failure not as a static verdict but as a condition to be caught early, categorised accurately, and, in many people, improved.

Questions Worth Asking at Your Next Appointment

Which type of heart failure do I have, and what does that mean for my treatment?
What is my ejection fraction, and has it changed since my last echocardiogram?
Am I on the right combination of medicines for my specific type?
Are there conditions contributing to my heart failure, such as blood pressure, diabetes, or weight, that we should be managing more closely?
What symptoms should prompt me to contact the team between appointments?

Heart Matters Resource

When in Doubt, Get Checked Out

New breathlessness, unusual tiredness, or swelling in the legs are worth having assessed early. Heart failure is far more treatable when it is picked up sooner rather than later.

Read: When in Doubt, Get Checked Out →

Conclusion

The terminology around heart failure sounds far more alarming than the reality for most people. HFrEF, HFpEF, and HFimpEF are simply three ways of describing how well the heart’s main chamber is pumping and filling, and each points toward a different and increasingly effective set of treatments. The letters are a tool for getting you the right care, not a measure of how worried you should be.

If you have been given one of these labels, the most useful thing you can do is understand which type you have, take the medicines as prescribed even if you feel well, and keep the conversation with your cardiologist going. Heart failure is more treatable today than at any point in medical history, and, as the newest category reminds us, it can genuinely improve.

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

July 7, 2026

SCAD is a heart attack caused by a tear in the artery wall, not cholesterol. It mostly affects healthy women in their 40s and 50s, and the recovery outlook for most people is genuinely positive.

How to Measure Your Blood Pressure at Home

July 5, 2026

High blood pressure rarely causes symptoms, which is why measuring it regularly matters. This guide covers how to choose the right monitor and how to get accurate readings at home.

AI in Cardiology: What It Means for Your Heart, and What It Cannot Do

June 14, 2026

Key Points

Artificial intelligence is already being used in cardiology, quietly and carefully, in ways that are genuinely improving patient care.
AI does not replace your cardiologist. It gives them better tools, more time, and sharper information to make decisions with you.
From reading ECGs to analysing intracoronary imaging, planning complex procedures, and assessing heart valves, AI is being applied across almost every area of heart medicine.
Neural networks are already shortening the time taken to analyse complex imaging, making procedures faster and more accurate.
The goal is the same as it has always been: getting the right treatment to the right patient.

If you have heard the term artificial intelligence, or AI, mentioned in the context of medicine, and been unsure whether to find it exciting or unsettling, you are not alone. The term carries a lot of weight in public conversation, and not always in reassuring directions.

So let us be clear about something from the outset. The AI being developed and applied in cardiology is not about replacing doctors, or making decisions by algorithm, or removing the human relationship at the heart of medicine.

It is about giving cardiologists better tools. Tools that can process more information more quickly, spot patterns that are difficult for the human eye to detect, and help ensure that every patient benefits from the full weight of accumulated medical knowledge, not just the experience of the individual clinician in front of them.

As one of the leading figures applying AI to cardiovascular research and daily clinical practice, my view is clear. AI is here to help improve workflow, and that efficiency creates more face-to-face time with patients. Not less.

What Do We Actually Mean by AI in Cardiology?

AI is a broad term that encompasses several different technologies. In cardiology, the most relevant are machine learning, where a computer learns to recognise patterns by analysing large amounts of data, and deep learning, a more sophisticated version that can analyse complex images such as heart scans with remarkable accuracy.

Neural networks, modelled loosely on the structure of the human brain, sit at the heart of many of these systems. They are capable of identifying patterns in imaging data at a speed and consistency that no human analyst could match.

These are not futuristic concepts. They are already in use in hospitals and catheterisation laboratories around the world, often in ways that patients would not notice. They run quietly in the background, helping clinicians interpret information faster and more accurately than would otherwise be possible.

Speaking at the 2026 European Association of Percutaneous Cardiovascular Interventions Summit in Munich, I described AI as transforming cardiology at a pace that is genuinely unprecedented, having been at the forefront of applying machine learning to some of the largest datasets in coronary disease research, including the SYNTAX trial, which followed 1,800 patients for 10 years.

But alongside that enthusiasm, I was equally clear about the caution required. To trust an AI estimation more than clinical expertise, we have to be certain it has been proven in outcomes studies. Progress, but never at the expense of safety. That balance, genuine excitement tempered by rigorous caution, is precisely what patients should expect from the doctors leading this field.

Where Is AI Already Making a Difference?

The clearest way to understand where AI sits in modern cardiology is to follow the journey a patient takes, from the moment a problem is first suspected through to the treatment decision and beyond. At every stage of that journey, AI is already at work.

How AI Works in Cardiology

From data to clinical decision

Data Input

ECG readings, CT scans, echo images, blood tests, and your medical history are gathered, the raw information about your heart.

Neural Network

Trained on millions of examples, the AI identifies patterns in that information that are invisible to the human eye.

Analysis

Risk scores, measurements, plaque characterisation, and predictions are produced in seconds rather than hours.

Your Cardiologist

Reviews the AI output alongside clinical judgement and makes the final decision with you.

AI informs. Your cardiologist decides.

Stage 1: before you ever reach a specialist

AI is already working before most patients know they have a problem. Tools trained on millions of ECG recordings can now detect patterns associated with heart attacks, irregular rhythms, and structural heart disease with accuracy that matches experienced clinicians. Some of these tools are built into smartwatches and portable devices, bringing ECG analysis into patients’ own homes.

In resource-limited parts of the world, AI-powered digital stethoscopes and portable devices are allowing patients in communities without specialist cardiologists to be assessed and triaged to a standard that previously required a fully equipped hospital. A patient who would once have waited months to see a specialist, or never seen one at all, can now have their heart rhythm analysed, their valve function assessed, and their cardiovascular risk stratified using tools that fit in a small case.

This matters more than almost any other application of AI in medicine. The burden of cardiovascular disease falls most heavily on low- and middle-income countries, precisely the places with the fewest cardiologists, the least access to imaging equipment, and the longest distances between patients and the hospitals that could help them.

AI does not fix those structural problems. But it does mean that a community health worker in a rural clinic, equipped with a smartphone and a portable ECG device, can now make a triage decision that would previously have required a trained cardiologist. The technology does not replace the specialist. It extends their reach to places they cannot physically be.

Stage 2: investigating your heart

Once a problem is suspected, you will be referred for tests. This is where AI is already embedded most deeply in clinical practice.

Computed tomography coronary angiography, or CTCA, uses X-ray technology to produce detailed images of the coronary arteries. AI and machine learning are now being used to interrogate these datasets far beyond what conventional analysis could achieve. The presence, extent, and characteristics of plaque can be assessed with a granularity that helps your clinical team make better-informed decisions before you ever reach the procedure room.

The echocardiogram, the ultrasound of the heart, is one of the most widely used diagnostic tools in cardiology. Machine learning algorithms can now assist in assessing heart valve function with impressive accuracy. What is particularly striking is that the benefit is greatest for less experienced operators. A sonographer early in their training, using an AI-assisted system, can achieve diagnostic accuracy that would previously have required years of experience.

In some centres, robotic echocardiography systems guided entirely by AI are now acquiring images without a sonographer needing to hold the probe at all, opening up access to high-quality cardiac imaging in areas where specialist staff are scarce.

Stage 3: planning your procedure

When treatment is needed, AI is transforming how your clinical team prepares. Computational fluid dynamics, or CFD, combines your imaging data with mathematical modelling of blood flow to simulate how blood actually moves through your coronary arteries, and how different treatment strategies will change that flow. The procedure can effectively be planned and rehearsed virtually before it is performed.

This goes further still with what might be called a digital twin: a precise virtual replica of your specific heart and coronary anatomy, built from your own imaging data. Different treatment approaches can be tested on this model, complications anticipated, and the optimal strategy identified, all before you enter the operating theatre.

I am actively collaborating with Professor Peter Barlis and his team, and at the Peter Barlis Laboratory we have been using AI to simulate blood flow at bifurcation points, the branching junctions where blockages are most technically challenging to treat, with the goal of improving precision and safety for each individual patient.

“Where is AI most useful in cardiology? Preplanning. Planning is everything.”

Prof. Patrick Serruys, Interventional Cardiologist

Stage 4: in the procedure room

Once you are in the catheterisation laboratory, AI is present in real time. Intracoronary imaging techniques such as optical coherence tomography (OCT) and intravascular ultrasound (IVUS) look inside the coronary arteries during procedures and generate large amounts of imaging data. Neural networks can now analyse this data at a speed that would have been unimaginable a decade ago. They characterise plaque, identify high-risk features, and predict the result of a stenting procedure, all in the time it takes to complete the procedure itself.

AI is also reading the angiogram in real time as your cardiologist works, automatically measuring the degree of narrowing, the length of the blockage, and the appropriate stent size. A randomised clinical trial has shown that AI-guided angiography analysis produces results comparable to the most detailed imaging techniques available. This is AI genuinely in the room, providing an objective second opinion at the most critical moment of the procedure.

Stage 5: choosing your treatment

Perhaps the most directly relevant application of AI for patients is in the decision between stenting and bypass surgery. Rather than a broad population-based recommendation, machine learning models applied to the SYNTAX trial dataset were able to distinguish meaningfully between patients who looked similar on the surface but whose predicted outcomes differed significantly depending on which treatment they received.

Research Spotlight

The blood tests that turned out to matter more than anyone realised

When the SYNTAX trial dataset was analysed using machine learning, two findings stood out. C-reactive protein, a blood test that measures inflammation, and haemoglobin levels, which reflect anaemia, both emerged as powerful predictors of long-term outcomes after heart treatment. Neither had featured prominently in conventional cardiology risk scoring.

A further surprise was gamma-glutamyl transferase, a liver enzyme routinely measured in blood tests but not traditionally associated with heart outcomes. The machine learning model identified it as a significant predictor of 10-year outcomes. I was initially sceptical, but the finding held up in external validation across thousands of additional patients. It turns out this enzyme is a marker of oxidative stress, which does have a meaningful impact on plaque build-up and heart function.

These are not exotic tests. They are measurements taken routinely in almost every patient undergoing cardiac assessment. What AI revealed is that information we were already collecting was telling us more than our existing models were capturing.

What This Means for You

Not one answer for everyone. A different answer for each person.

When the machine learning model was applied to individual patients in the SYNTAX dataset, it identified three distinct groups. For some patients, stenting and bypass surgery were predicted to produce essentially the same outcome, genuine clinical equipoise, where patient preference should play a larger role in the decision. For others, it predicted a clear advantage for bypass surgery. And for a smaller group, stenting was the stronger option.

The goal is not to have an algorithm make the decision. It is to give your heart team better information so that when they sit down with you to discuss your options, the recommendation they make is as precisely tailored to your specific situation as possible.

The quieter wins: less paperwork, more conversation

One of the less dramatic but genuinely meaningful applications of AI in medicine is the reduction of administrative burden. Cardiologists, like all doctors, spend a significant portion of their working day on documentation, dictating notes, completing forms, and reviewing records. AI-assisted tools can take notes during consultations, generate clinical summaries, and help organise information so that less time is spent on administration and more time is available for the patient in the room.

There is also a more personal dimension that is rarely discussed: what AI means for the conversation between you and your doctor. When a cardiologist tells you that an AI algorithm has analysed your scan, or that a machine learning model has helped inform the recommendation for stenting over surgery, you deserve to understand what that means and who is ultimately responsible for the decision.

The answer to that last question has not changed. Your cardiologist is responsible. AI informs; it does not decide. The shared decision between you and your clinical team remains at the centre of your care, and no algorithm changes that.

AI and Your Heart Team

One of the most important things to understand about AI in cardiology is that it does not work in isolation, and it was never designed to. The Heart Team model, where your cardiologist and cardiac surgeon review your case together before making a recommendation, is precisely where AI adds the most value. The scoring tools, the imaging analysis, the risk predictions, all of this information is brought to that meeting, discussed, and weighed alongside things that no algorithm can measure: your preferences, your circumstances, your priorities.

Traditionally, a Heart Team meeting has centred on reviewing your angiogram images on a screen, measuring segments of arteries by eye, and debating the best approach based on accumulated experience.

AI is transforming this in a concrete and visible way. Machine learning can now process your coronary imaging data and assess your arterial anatomy with a speed and precision that was not previously possible, producing accurate measurements of vessel segments, identifying the location and extent of blockages, and predicting how different stenting or bypass strategies are likely to perform in your specific anatomy.

Extended reality takes this further still. Building on work developed at the CORRIB Research Centre at the University of Galway, coronary imaging data can now be converted into a three-dimensional hologram that the entire Heart Team can explore together before any procedure begins. Rather than looking at flat images on a screen, your cardiologist and cardiac surgeon can examine a three-dimensional model of your coronary arteries, rotate it, fly through it, and measure it in precise detail. The intervention can be planned virtually before you have entered the operating theatre or the catheterisation laboratory.

This has been demonstrated in real surgical cases, including the planning of complex multi-vessel bypass operations, where holographic measurements guided decisions about which vessels to bypass and which grafts to use.

The conversation that follows is still deeply human. The decision that emerges from it is still yours to make, with your team, together. What AI and extended reality change is the quality and precision of the information on the table when that conversation happens.

What AI Cannot Do, and Why That Matters

It is just as important to be clear about the limitations of AI in cardiology as it is to acknowledge its promise. Leading clinicians in this field are the first to make this point.

AI models are trained on data from past patients. They are powerful at identifying patterns within that data, but they cannot handle what they have never seen, and they require retraining as medical knowledge evolves. A model trained predominantly on data from one type of patient population may perform less well when applied to a different population. This is why external validation across diverse groups is essential before any AI tool is used in clinical practice.

There are also important questions about data privacy, about the transparency of AI decision-making, and about ensuring that the benefits of these tools are available equitably, not just to patients in well-resourced healthcare systems.

One of the most honest concerns in this field is what researchers call the black box problem. Many AI models can tell you what conclusion they have reached, but cannot easily explain how they reached it. A neural network that identifies a high-risk plaque on a CT scan may do so with impressive accuracy, but it cannot always show the clinician its reasoning in the way that a human expert can. Different AI platforms applied to the same imaging data can sometimes reach different conclusions.

Understanding where AI is reliable, where it is uncertain, and where it requires human oversight is not a weakness of the technology. It is the essential work of responsible implementation.

Perhaps most importantly: AI does not know you. It does not know that you are frightened, or that you have a strong preference for a less invasive approach, or that your recovery will be shaped by circumstances that no dataset could capture. That knowledge belongs to your cardiologist, your cardiac surgeon, and your clinical team. The human relationship at the centre of medicine, the conversation, the trust, the shared decision, is not something that any algorithm replaces.

What This Means for You as a Patient

If you are a cardiac patient today, or if someone you love is, the most reassuring thing I can say is this. The cardiologists caring for you are not waiting passively for AI to arrive. They are actively using and evaluating these tools, carefully, with the same rigour they apply to any new treatment or technology.

The ECG you had may have been read with the assistance of an AI algorithm. The scan images of your heart may have been processed by software that flags findings for a radiologist or cardiologist to review. The risk assessment your team carried out before recommending treatment may have drawn on scoring tools developed using machine learning on large patient datasets. The intracoronary images taken during your procedure may have been analysed by neural networks that helped guide exactly where and how a stent was placed.

None of this happened instead of your doctor’s judgement. It happened alongside it, giving them better information, faster, so that the decision they made with you was as well-informed as possible.

That is what AI in cardiology is for. Not to alarm. Not to replace. Simply to help the people caring for your heart do their jobs a little better, and to give you, as a patient, the benefit of everything medicine has learned.

Conclusion

AI in cardiology is not a glimpse of some distant future. It is already in the room with you, in the ECG software that flagged your rhythm, in the imaging analysis that helped your team measure your arteries, in the risk scoring that informed your treatment plan. None of it has changed who is responsible for your care, and none of it has removed the human conversation at the heart of medicine.

What it has done is sharpen the information your cardiologist works with, shorten the time between question and answer, and extend the reach of expert care to places it could not previously go. The realistic futures, as I often put it, are arriving faster than anyone anticipated. The question is no longer whether AI will reshape how we care for patients with heart disease. It already has. The question is how thoughtfully, how rigorously, and how equitably we carry that forward.

References

Serruys PW. AI in Cardiovascular Imaging and Interventions: Boon or Bane? Presented at the EAPCI Summit, Munich, February 2026. Reported by TCTMD.
Ninomiya K, Serruys PW et al. Can Machine Learning Aid the Selection of Percutaneous vs Surgical Revascularization? Journal of the American College of Cardiology, 2023;82:2113 to 2124.
Serruys PW et al. 10 Years of SYNTAX: Closing an Era of Clinical Research After Identifying New Outcome Determinants. JACC: Asia, 2023.
American Heart Association Scientific Advisory on AI in Cardiovascular Medicine, 2025.

Aortic Stenosis: When the Heart’s Gateway Narrows

June 10, 2026June 7, 2026

The aortic valve opens and closes 100,000 times a day. When it begins to narrow, the heart pays the price. Here is how aortic stenosis develops, how it is diagnosed, and how modern treatment, from open surgery to TAVR, restores flow.

Patent Foramen Ovale (PFO): What the “Hole in the Heart” Finding Really Means

June 4, 2026June 4, 2026

Key Points

A patent foramen ovale (PFO) is a small opening between the two upper chambers of the heart, present in roughly one in four adults, that simply did not seal after birth the way it usually does.
The vast majority of PFOs cause no symptoms and are found by chance. For most people, a PFO needs no treatment at all.
In a smaller group of patients, particularly those who have had a cryptogenic stroke (a stroke with no identified cause), a PFO may be the route by which a small clot crossed from the right to the left side of the heart and travelled to the brain.
In selected patients after a cryptogenic stroke, PFO closure (a minimally invasive catheter procedure) lowers the risk of a further stroke and is now supported by strong trial evidence.
Migraine with aura has a well-recognised association with PFO, though the relationship is complex, and closing a PFO for migraine alone is not currently standard practice.

A patent foramen ovale is one of those findings that can sound alarming when it is first mentioned. A hole in the heart, discovered on an echocardiogram, is not a phrase anyone wants to hear. And yet for most people who have one, it is entirely inconsequential. It requires no treatment, no monitoring, no change to how you live, and nothing you need to act on.

The reassurance I give most patients with a PFO is simple. You have a structural variation that around one in four adults share. In the vast majority of cases it is a finding rather than a diagnosis, something noted and filed, not something that needs managing.

Where it does become clinically relevant, mainly in the setting of an unexplained stroke in a younger person, is a separate and important conversation. But that conversation starts from a very different clinical picture than an incidental echo finding in someone who is otherwise well.

What Is a PFO?

Normal Circulation Before Birth

Before birth, the lungs are not yet doing their job. Rather than breathing, the baby receives oxygen-rich blood from the placenta. To bypass the lungs while they are still at rest, the circulation of every developing baby includes a small opening between the two upper chambers of the heart, called the foramen ovale. Blood passes straight through it from the right side to the left, skipping the lungs entirely.

At birth, the first breath opens the lungs, blood flow through them rises sharply, and the pressure in the left upper chamber climbs above that of the right. This change in pressure presses a small flap of tissue against the opening and seals it. In most people this seal becomes permanent over the first months of life, as the two layers of tissue gradually fuse.

What is a Patent Foramen Ovale?

A small unsealed opening in the wall between the upper chambers of the heart

Patent Foramen Ovale

An unsealed flap between the upper chambers, present in about 1 in 4 adults

~25%

of adults have a PFO, and most never know

Echo

Usually found by chance on an echocardiogram

Closure

Considered in selected stroke patients

heartmatters.com, patient education

When It Doesn’t Close

In around 25 to 27% of adults, roughly one in four, this fusion does not fully happen. The flap stays unsealed, leaving a potential channel between the two upper chambers that can open at moments of raised pressure on the right side of the heart, such as straining, coughing, or bearing down. This is a patent foramen ovale.

It is not a defect in the usual sense of the word. The heart formed normally, and the closure process simply did not finish. It causes no structural problem, no pressure abnormality, and no effect on how the heart works in the great majority of people who have one.

How Is a PFO Found?

Most PFOs are discovered by chance, on an echocardiogram done for another reason, such as looking into palpitations, a murmur, or as part of a stroke assessment. On a standard echocardiogram a PFO can be hard to see directly. A bubble study, in which a small amount of agitated saline is injected into a vein while you gently bear down, shows the PFO by revealing tiny bubbles crossing from the right chamber to the left. A transoesophageal echocardiogram gives the most detailed picture of a PFO’s size and shape.

Does It Actually Matter? The Context Question

The Incidental PFO, by Far the Most Common Situation

An incidental PFO, found in someone who has not had a stroke, has no neurological symptoms, and is otherwise well, needs no treatment. No blood thinners, no antiplatelet medicine beyond anything already needed for another reason, no closure procedure, and no restriction on activities including diving in most cases (high-altitude diving is a more nuanced discussion worth having with your cardiologist).

The most important thing I tell patients in this situation is that the finding does not change your risk in any way that matters clinically. One in four adults has one, and most go their whole lives without ever knowing.

PFO and Cryptogenic Stroke, the Association That Matters

About 30% of ischaemic strokes have no clear cause even after thorough investigation. These are called cryptogenic strokes. In younger patients who have had a cryptogenic stroke, a PFO is found more often than chance alone would explain, which suggests that in these individuals the PFO may have been the route through which the stroke happened.

The likely mechanism is called paradoxical embolism. A small clot forms in the venous system, often in the leg veins, travels to the right side of the heart, and crosses through the PFO into the left side at a moment of raised pressure, from where it can travel to the brain. This can happen without any obvious sign of a deep vein clot beforehand.

When a brain scan shows several small areas of stroke in different regions, suggesting clots arriving from a single source, a PFO assessment becomes particularly important. This is one reason prolonged heart monitoring for atrial fibrillation often goes hand in hand with a PFO assessment after a cryptogenic stroke. Both conditions can produce a similar pattern of stroke and need to be carefully told apart.

Three landmark randomised trials (RESPECT, CLOSE, and REDUCE) showed that closing a PFO in carefully selected patients after a cryptogenic stroke significantly lowers the risk of another stroke compared with antiplatelet medicine alone. This evidence has made PFO closure a standard recommendation for suitable patients after a cryptogenic stroke, typically those under 60 with a sizeable PFO and no other identified cause for the stroke.

Migraine With Aura

There is a well-documented link between PFO and migraine with aura. A PFO is more common in people who have migraine with aura than in the general population, and some people report fewer migraines after a PFO is closed. However, the trial evidence for closing a PFO specifically to treat migraine is mixed, and closure is not currently recommended for migraine with aura in someone who has not had a stroke. This remains an area of active research, and it is a reasonable thing to ask your cardiologist about if it affects you.

What PFO Closure Involves

PFO closure is a catheter-based procedure, with no open heart surgery involved. A thin tube is passed through a vein in the groin and guided up into the right upper chamber of the heart. With the help of echocardiography and X-ray guidance, a small device shaped like two discs is positioned across the opening, with one disc resting on each side of the wall. Over the following months, the body’s own tissue grows over the device and seals the opening permanently.

The procedure usually takes 30 to 60 minutes under sedation or light general anaesthesia, and most people go home the next day. Antiplatelet medicine is taken for a period afterwards, typically about six months, while the device becomes covered by the heart’s own lining. The long-term results are excellent, and device-related complications are very uncommon.

1 in 4
adults has a patent foramen ovale, making it one of the most common structural variations of the heart. For the great majority it is entirely harmless and needs no treatment.
American Heart Association

Clinical Situation	Typical Approach	Why
Incidental PFO, no stroke, no symptoms	Reassurance, no treatment needed	One in four adults has one; the risks of closing it outweigh any benefit
Cryptogenic stroke, under 60, no other cause found	PFO closure, strongly considered	Trial evidence shows a meaningful drop in further strokes
Cryptogenic stroke, over 60	Individualised, blood thinners often preferred	Other possible mechanisms more likely; benefit of closure less clear
Migraine with aura, no stroke history	No closure, not standard practice	Evidence not yet sufficient; trials ongoing
Decompression illness in divers	Individualised assessment	A careful, case-by-case discussion with a specialist

The most important conversation I have with patients who have a PFO is about context. The finding can be the same in two people. The significance can be entirely different. Context is everything.

Prof. Peter Barlis, Interventional Cardiologist

Questions Worth Asking at Your Next Appointment

My PFO was found by chance. Do I need any treatment, monitoring, or change to how I live?
I have had a stroke with no identified cause. Is my PFO likely to have been involved, and could I be a candidate for closure?
What do the size and shape of my PFO mean for my risk? Are all PFOs the same?
I dive recreationally. Does having a PFO change my risk, and should I adjust how I dive?
I have migraine with aura. Is there a link with my PFO, and is closure something I should consider?

Heart Matters Resource

When in Doubt, Get Checked Out

If you have been told you have a PFO and are unsure what it means for you, particularly if you have had a neurological event, a cardiology review to put the finding in context is the right next step.

Read: When in Doubt, Get Checked Out →

Conclusion

A patent foramen ovale is perhaps the cardiac finding that most needs to be put in context. In the great majority of people who have one, and a quarter of all adults do, it is entirely harmless, needs no intervention, and is nothing you need to act on.

In a carefully defined group of patients, those who have had a cryptogenic stroke at a younger age with no other identifiable cause, closing a PFO is a worthwhile step with strong evidence behind it. The procedure is safe, effective, and minimally invasive.

The key, in the end, is context. The very same finding can mean completely different things depending on the clinical picture in which it is discovered. Your cardiologist’s role is to place that finding in its proper frame, and where that frame is reassurance, the reassurance should be complete and confident.

What is a Muscle Bridge?

June 2, 2026May 31, 2026

Key Points

A myocardial bridge, often just called a muscle bridge, is a common and usually harmless variant present from birth, where a short stretch of a coronary artery dips down and runs through the heart muscle instead of sitting on the surface. Most people who have one will never know and never need treatment.
In a minority of people, a bridge can cause genuine symptoms, most often chest pain or tightness brought on by exertion or stress. These patients deserve to be taken seriously rather than reassured by default.
A standard angiogram often underestimates a bridge. Confirming whether a bridge is actually causing symptoms usually needs more detailed assessment, including intravascular ultrasound and specialised stress testing.
Most symptomatic bridges are managed well with medication, usually beta-blockers or calcium channel blockers. A small, carefully selected group with severe, persistent symptoms may benefit from an operation called surgical unroofing.
A large 2026 study from Stanford, published in the European Heart Journal, found that for this selected group, surgical unroofing produced lasting relief from angina five years later, with a low complication rate.

You have a muscle bridge. Many people hear that sentence for the first time lying on an angiogram table, nod along, and leave none the wiser. It is rarely explained in much depth, partly because for most people it carries no consequence at all, and partly because the few it does affect need a longer conversation than a results appointment allows.

A myocardial bridge is one of the most common variations in human heart anatomy. The overwhelming majority cause no symptoms, need no treatment, and carry no meaningful risk. For a smaller group of people, though, a bridge can be a real and treatable cause of angina, and telling those two groups apart is what good assessment is for.

This article explains what a muscle bridge actually is, why most are harmless, how the troublesome minority are identified, and what the newest evidence says about treating them.

What a Myocardial Bridge Actually Is

The coronary arteries, the vessels that supply blood to the heart muscle itself, normally run along the outer surface of the heart, sitting on top like rivers on a landscape. A myocardial bridge is a stretch where one of these arteries takes a short detour and tunnels down through the heart muscle before surfacing again on the other side.

The band of muscle lying over the tunnelled segment is the “bridge.” The buried portion of artery is sometimes called the tunnelled segment. It is present from birth, which means a bridge is a variation in how the heart formed rather than something that develops, wears in, or is caused by lifestyle. Around 97% of bridges occur in the same vessel, the left anterior descending artery, which runs down the front of the heart.

Diagram comparing a normal coronary artery running along the heart surface with a myocardial bridge, where the artery dips down through the heart muscle and is squeezed with each heartbeat. — In a normal artery, blood flows freely along the heart’s surface. In a myocardial bridge, the artery dips down and runs through the heart muscle for a stretch, and the overlying muscle squeezes that segment with each heartbeat.

The reason a bridge can matter comes down to mechanics. Every time the heart contracts, the muscle squeezes. If a segment of artery is buried inside that muscle, it gets squeezed too, narrowing with each beat. The heart does most of its own blood supply during the relaxation phase between beats, and in a bridge the squeeze can linger into that phase, slightly delaying the artery from springing back open. When the heart is calm and beating slowly, this rarely matters. When the heart beats fast, during exertion, stress, or strong emotion, the relaxation phase shortens, and the lingering squeeze has proportionally more effect. This is why bridge symptoms, when they occur, are so often tied to exertion.

Why Most Bridges Cause No Trouble

The single most important thing to understand about muscle bridges is how common they are, and how rarely they cause problems. The numbers vary enormously depending on how you look for them, which is itself revealing.

Up to 1 in 4
people may have a myocardial bridge when hearts are examined closely, yet only a small fraction ever experience symptoms from it.
Imaging and autopsy studies, summarised in European Heart Journal, 2026

On a standard coronary angiogram, bridges turn up in only a few percent of people. On detailed imaging such as CT coronary angiography, the figure is much higher, and when hearts are examined directly the prevalence rises further still, into the range of one in five to one in four. The gap between these numbers tells the story: most bridges are shallow, short, and functionally silent. They are found incidentally, if they are found at all, and they sit quietly for a lifetime.

So if you have been told you have a bridge and you have no symptoms, the most likely situation by far is that the bridge is an anatomical footnote rather than a problem. It does not need fixing, and in most cases it does not need anything beyond the awareness that it is there.

When a Bridge Does Cause Symptoms

A minority of people with a bridge experience real symptoms, most commonly chest pain or tightness that comes on with exertion or stress and eases with rest. Some describe breathlessness, and some report that episodes last noticeably longer than a typical bout of exertional chest pain. Whether a particular bridge causes symptoms depends on several features working together.

Length of the bridge

A longer tunnelled segment means more of the artery is subject to the muscle’s squeeze with each beat. Longer bridges are more likely to be functionally significant than short ones.

Depth of the tunnel

How deeply the artery is buried in the muscle matters. A deeper bridge is compressed more forcefully, so deeper bridges tend to have a greater effect on blood flow than superficial ones.

Heart rate and exertion

A fast heart rate shortens the relaxation phase when the artery would normally recover. This is why bridge symptoms typically appear during exercise, stress, or strong emotion rather than at rest.

Coronary spasm

Bridges frequently sit alongside a tendency for the artery to spasm, or tighten suddenly. Spasm can drive symptoms independently of the bridge itself and changes how the condition is treated.

Endothelial function

The artery lining near a bridge is often under abnormal mechanical stress, which can impair its ability to relax and widen on demand. This contributes to symptoms in many bridge patients.

Plaque just upstream

The disturbed blood flow around a bridge tends to encourage fatty plaque to build up in the artery just before it, which can add its own contribution to symptoms and risk.

Because several of these factors often coexist, a bridge that looks modest on a picture can still be the source of meaningful symptoms, and a bridge that looks dramatic can sit silent. Anatomy alone does not settle the question. This is the central difficulty in managing bridges, and it shapes everything about how they are investigated.

Why a Bridge Is Harder to Diagnose Than It Sounds

It would be reasonable to assume that if a bridge shows up on an angiogram, the picture tells the whole story. In practice it rarely does. A standard coronary angiogram is good at finding flow-limiting blockages, but it has low sensitivity for bridges and tells you little about how deep a bridge is, how long it is, or whether it is actually responsible for a person’s symptoms.

When symptoms and anatomy do not obviously line up, cardiologists turn to more detailed assessment. Intravascular ultrasound, a tiny ultrasound probe threaded into the artery, is considered the most reliable way to confirm a bridge and measure its length and depth precisely. To judge whether the bridge is functionally significant, meaning it genuinely restricts flow under stress, specialised measurements are taken while the heart is pushed to work harder with a medication called dobutamine. Standard pressure-wire measurements used for ordinary blockages are not adequate for assessing a bridge, which is part of why bridge assessment is a specialised undertaking.

A particular pattern on a stress echocardiogram, a transient buckling in one part of the heart wall with the tip of the heart spared, can also raise suspicion of a bridge non-invasively. The broader point for patients is that confirming a bridge as the cause of symptoms is a deliberate, layered process, not a single glance at an angiogram.

Finding a bridge and proving that the bridge is the cause of someone’s pain are two very different things. Most bridges are bystanders. The clinical skill lies in identifying the minority that are genuinely to blame, and treating that group properly without over-treating everyone else.

Heart Matters editorial

How Symptomatic Bridges Are Treated

Medication comes first

For the large majority of people whose bridge does cause symptoms, medication is the first and usually the only treatment needed. The two mainstays are beta-blockers and calcium channel blockers. Both work in part by slowing the heart and easing the force of each contraction, which lengthens the relaxation phase and reduces the squeezing effect on the bridged artery. They can be very effective, and many people are managed comfortably on them for years.

One counter-intuitive point is worth knowing. Nitrates, which are a standard reliever for ordinary angina, are often used with caution in bridge patients and can sometimes make symptoms worse rather than better. If you have a bridge and find that a nitrate spray does not help your chest pain in the way you would expect, or seems to aggravate it, that is worth mentioning to your cardiologist rather than dismissing.

When an operation is considered

A small, carefully selected group of patients continue to have severe, life-limiting symptoms despite the best medication can offer, and have a bridge that has been confirmed as genuinely significant on detailed testing. For this group, a surgical option exists. The preferred operation is called surgical unroofing, in which the surgeon carefully divides the band of muscle lying over the tunnelled artery, freeing the vessel to return to the surface where it belongs.

Two other approaches, placing a stent inside the bridged segment or performing a coronary artery bypass, have generally proved less satisfactory for bridges specifically, which is why unroofing has become the favoured operation in suitable patients. It is important to stress that this is a treatment for a minority within a minority. The vast majority of people with a bridge will never come close to needing it.

What the Latest Research Shows

Until recently, a fair question about unroofing was whether its benefits lasted. Earlier work had shown good results at six months, but long-term evidence was thin. A 2026 study from Stanford University, published in the European Heart Journal, has now provided the most substantial answer to date.

The researchers followed 218 patients who had undergone surgical unroofing of a significant bridge in the left anterior descending artery after medication had failed to control severe angina. The patients were relatively young, with a median age of 49, and around 60% were women. They were followed for a median of five years.

Nearly 9 in 10
patients reported a meaningful, lasting improvement in their angina five years after surgical unroofing, with episodes typically falling from weekly to monthly.
Pargaonkar et al., European Heart Journal, 2026

Across every measure of symptoms and quality of life, patients reported significant and durable improvement, and most needed fewer anti-anginal medications afterwards than before. When the surgical patients were compared with a closely matched group who had a similarly significant bridge but were managed with medication alone, the surgical group showed greater relief from physical limitation and from the frequency of their angina. Importantly, the operation proved safe in experienced hands, with a low rate of major cardiac events over the follow-up period and none of those events attributed to the surgery itself.

The practical message for patients is measured rather than dramatic. For the specific, carefully selected group with a confirmed significant bridge and severe symptoms that medication cannot control, surgical unroofing is now backed by solid long-term evidence as a worthwhile option. It is not a treatment for an incidental finding, and it is not a first step. It is a well-supported last resort for those who genuinely need it.

The Bridge Is Rarely the Whole Story

One of the most useful insights from the recent research is that a bridge often travels with company. In the Stanford group, who were of course a highly selected population with difficult symptoms, almost all had a small build-up of fatty plaque in the artery just upstream of the bridge, and the great majority showed evidence of coronary spasm or of an artery lining that did not relax normally on testing.

This matters for two reasons. First, it explains why a few patients still have some symptoms even after a technically successful unroofing: if spasm or lining dysfunction was contributing, removing the muscle band does not address that part of the problem, and ongoing medication may still be needed. Second, the tendency for plaque to form just before a bridge is part of why attention to general cardiovascular risk, including the standard modifiable risk factors, remains relevant even when the headline issue is a structural one present from birth.

Heart Matters Resource

When in Doubt, Get Checked Out

If you have been told you have a muscle bridge and you are experiencing chest pain, breathlessness, or symptoms on exertion, those symptoms are worth a proper conversation with your cardiologist rather than assuming the bridge is harmless.

Read: When in Doubt, Get Checked Out →

Conclusion

A myocardial bridge is, for most people, exactly what it usually sounds like when a cardiologist mentions it in passing: a common quirk of heart anatomy that asks nothing of you and changes nothing about your life. If you have one and no symptoms, that is almost certainly where the story ends.

For the minority who do have symptoms, a bridge is a real and treatable condition. The key is careful assessment to confirm whether the bridge is genuinely the cause, sensible use of medication for the many, and a well-evidenced surgical option held in reserve for the few who need it. If you have a bridge and symptoms that affect your daily life, the right next step is not to worry alone but to have it properly evaluated, because the difference between a harmless bystander and a treatable problem is exactly the kind of question modern cardiology is now well equipped to answer.

Conditions

Patent Foramen Ovale (PFO): What the “Hole in the Heart” Finding Really Means

What is a Muscle Bridge?

White Coat Hypertension: When Your BP Spikes at the Doctor’s

Stroke and TIA Explained

Hypertrophic Cardiomyopathy: What HCM Actually Means

Stents or Bypass Surgery: How Your Heart Team Decides

Single, Double, Triple, Quadruple Bypass: What Does the Number Mean?

Does a Coffee a Day Keep AF at Bay?

Iron Deficiency and the Heart

SVT (Supraventricular Tachycardia) Explained: Causes and Treatment

Rheumatic Heart Disease: A Preventable Condition Affecting Millions

How to Lower Blood Pressure Naturally

Possible Old Heart Attack on ECG? What Q Waves Mean

A Living Legend of Interventional Cardiology: Professor Patrick Serruys

How Atrial Fibrillation Is Treated: From Lifestyle to Ablation

What Is an Aortic Dissection?

The Two Types, and Why the Difference Matters

What It Actually Feels Like

Why Blood Pressure Sits at the Centre of This

The Genetic Side, and When Family History Matters

Inherited connective tissue conditions

Bicuspid aortic valve

Familial aortic disease with no syndrome attached

Why It Is So Easily Missed

What You Can Actually Do

Conclusion

Related Reading

Start With What Heart Failure Actually Means

The Number Behind the Letters: Ejection Fraction

The Three Main Types, Explained

HFrEF: heart failure with reduced ejection fraction

HFpEF: heart failure with preserved ejection fraction

HFimpEF: heart failure with improved ejection fraction

Why Cardiologists Bother Splitting Hairs

What Causes Each Type

How Each Type Is Treated

What the New 2026 Definition Changes

When in Doubt, Get Checked Out

Conclusion

Related Reading

What Do We Actually Mean by AI in Cardiology?

Where Is AI Already Making a Difference?

Stage 1: before you ever reach a specialist

Stage 2: investigating your heart

Stage 3: planning your procedure

Stage 4: in the procedure room

Stage 5: choosing your treatment

The quieter wins: less paperwork, more conversation

AI and Your Heart Team

What AI Cannot Do, and Why That Matters

What This Means for You as a Patient

Conclusion

References

Related Reading

What Is a PFO?

Normal Circulation Before Birth

When It Doesn’t Close

How Is a PFO Found?

Does It Actually Matter? The Context Question

The Incidental PFO, by Far the Most Common Situation

PFO and Cryptogenic Stroke, the Association That Matters

Migraine With Aura

What PFO Closure Involves

When in Doubt, Get Checked Out

Conclusion

Related Reading

What a Myocardial Bridge Actually Is

Why Most Bridges Cause No Trouble

When a Bridge Does Cause Symptoms

Why a Bridge Is Harder to Diagnose Than It Sounds

How Symptomatic Bridges Are Treated

Medication comes first

When an operation is considered

What the Latest Research Shows

The Bridge Is Rarely the Whole Story

When in Doubt, Get Checked Out

Conclusion

Related Reading

Stay Informed