This is a form of thickened heart muscle that is caused by a change in a gene called MYBPC3, that does not block the flow of blood out of the heart, and that is already causing symptoms [1,2,3].
This page provides general information. It does not replace advice from a doctor or another qualified healthcare professional.
The name is long because each part describes something different.
Hypertrophic cardiomyopathy. Cardiomyopathy means a condition of the heart muscle, and hypertrophic means thickened. So the muscular wall becomes thicker than it should be, usually in the left ventricle, the chamber that pumps blood to the body [2]. A thicker wall is a stiffer wall, so the heart does not relax and fill as easily between beats [1]. The term is used only where the thickening has no other explanation, such as long-term high blood pressure [2].
Non-obstructive. In some people the thickened wall gets in the way of blood leaving the heart. Doctors call this outflow tract obstruction and measure it as a pressure difference, or gradient, with 30 mm Hg or more counting as obstruction [4]. Non-obstructive means these gradients are absent. It is not the mild version: one large study found more frequent serious rhythm disturbances in this group than in people with obstruction [13].
MYBPC3-associated. Genes are instructions inside our cells. The MYBPC3 gene holds the instructions for a protein called cardiac myosin-binding protein C, found in heart muscle cells [3]. Muscle contracts because tiny overlapping filaments slide past each other, and this protein helps fine-tune how fast that happens [3]. When the gene is changed, cells make less of it than the heart needs, which is thought to cause the thickening and stiffness [3,8].
Symptomatic. Many people with HCM never notice anything. Symptomatic means a person already has symptoms, rather than being found by a scan while feeling well [4,24].
HCM affects approximately 1 in 500 people worldwide, and the British Heart Foundation quotes the same figure for the United Kingdom [2,15]. That estimate comes from heart imaging, so it counts people whose scans show the pattern. Fewer carry a formal diagnosis, since many have no symptoms and are never scanned. Forms not linked to a wider syndrome, the group covered here, likely account for more than half of cases [2].
MYBPC3 is the gene most commonly involved, accounting for roughly 40 to 50 percent of cases in which testing finds a cause [7].
How many people have the non-obstructive form is genuinely uncertain, and estimates conflict. The 2024 American guideline gives no figure, saying only that obstruction is present in a significant proportion, and that up to half of it is missed by a resting scan alone [4].
Founder variants, where one change is common in a population because it came from a shared ancestor, are known in the Netherlands, Finland, Iceland, Japan and India [9,10].
The cause is a change, or variant, in the MYBPC3 gene. Most changes shorten the protein or stop it being made, so the working copy cannot make up the difference and the heart runs short of it [8].
It is usually inherited in an autosomal dominant pattern, meaning one changed copy, inherited from one parent, is enough. Each child of an affected person has a 1 in 2 chance of inheriting it [4,15]. In some people the change is new and came from neither parent [2].
Inheriting the change does not mean a person will definitely develop the condition, which is called incomplete penetrance [2]. Among relatives known to carry a family change, estimates cluster around a half to two thirds, and are much lower for carriers found by chance during wider testing [1,7]. Penetrance depends on age too, so a normal heart check does not rule out developing it later [1].
Symptoms often appear in the teens or twenties, though they can begin at any age [1,2]. Common ones include:
Some people develop an irregular rhythm called atrial fibrillation, and a smaller number develop heart failure, meaning the heart struggles to keep up with the body’s needs [1,2].
There is also a raised risk of sudden cardiac death, when a dangerous rhythm stops the heart. Contemporary estimates put this at around 0.5 percent per year across HCM as a whole [12]. Each person’s own risk is estimated individually and reviewed every visit or two [5,14]. To do that, European guidance uses a calculator that estimates five-year risk from age, greatest wall thickness, left atrium size, the outflow gradient, family history of sudden cardiac death, short runs of a fast rhythm called non-sustained ventricular tachycardia, and unexplained fainting [11,14]. It is treated as an aid to a shared conversation, not a decision on its own [11].
When to seek urgent help. Call emergency services for fainting during or just after exercise, severe chest pain, sudden severe breathlessness, or a fast irregular heartbeat with dizziness. If someone collapses and is not breathing normally, start CPR and use a defibrillator if one is nearby.
A cardiologist leads the work-up, ideally at a center that sees a lot of HCM [5]. An echocardiogram, an ultrasound scan of the heart, is the main test [5]. In adults, HCM is usually defined as a maximum left ventricular wall thickness of 15 mm or more, or 13 to 14 mm where a close relative already has the diagnosis [1]. If the resting gradient is under 50 mm Hg, the scan is repeated with maneuvers such as standing or straining, and if nothing shows, with exercise [5].
An electrocardiogram, or ECG, records the heart’s electrical activity, and 24 to 48 hours of portable monitoring looks for rhythm problems [5]. Cardiac MRI helps where the echocardiogram is unclear and to judge risk [5]. Genetic testing is offered alongside a conversation with a genetic counselor, and a three-generation family history is taken [5]. Testing finds a cause in around 30 percent of people with HCM, rising to about 60 percent where there is a family history [1]. Diagnosis is often delayed, since early symptoms are easy to put down to being unfit.
There is no cure. Treatment eases symptoms, protects against dangerous rhythms and looks after the heart long term.
Medicines for symptoms. For symptomatic non-obstructive HCM with normal pumping function, first-line treatment is a beta blocker or a calcium channel blocker such as verapamil or diltiazem, which slow the heart and give it longer to fill [6].
A point worth being clear about. Cardiac myosin inhibitors are a newer class of medicine that reduces the over-forceful squeezing seen in HCM. Two are approved: mavacamten, in the United States in April 2022 and the European Union in June 2023, and aficamten, in the United States on 19 December 2025 and the European Union in February 2026 [16,17,19,20]. Both are approved only for symptomatic obstructive HCM, and neither is approved for the non-obstructive form anywhere [16,18,19]. As the maker of aficamten put it in May 2026, “There are no currently approved therapies for nHCM” [24].
Rhythm, clots and advanced disease. Where risk of sudden cardiac death is judged high enough, an implantable cardioverter-defibrillator is offered: a small device under the skin that can correct a dangerous rhythm [14]. Where atrial fibrillation is present, blood-thinning medicine lowers stroke risk [5]. Heart transplant is considered for the small number whose symptoms stay severe despite full treatment [5,6]. Regulatory approval is not the same as funding, so local availability differs.
Care works best through a specialist center [5]. Exercise is no longer something to give up. Current guidance encourages mild to moderate recreational exercise and does not support blanket bans on competitive sport, though intense sport should be discussed with a specialist [5]. High blood pressure, extra weight and sleep apnea can all worsen symptoms and are worth treating [1]. Pregnancy is usually well tolerated, with care shared between a cardiologist and a maternity team [1,5].
First-degree relatives, meaning parents, siblings and children, are encouraged to be checked [29]. Where the family gene change is known, relatives who carry it have an echocardiogram and ECG every one to two years, and where it is not known, every two to three years in childhood and every three to five years in adulthood [1]. A genetic diagnosis reaches into the whole family, and a specialist nurse or peer support group helps many people.
Clinical trials test whether a treatment works and is safe. Non-obstructive HCM is an active research area, since no approved medicine targets it [24]. Looking into one is a personal choice, and it helps to take it in steps.
Every trial has rules about who can take part, called eligibility criteria. Here they might include a confirmed HCM diagnosis, a confirmed MYBPC3 gene change, an outflow gradient low enough to count as non-obstructive, or a minimum result on an exercise test.
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Medicines that reduce over-forceful squeezing. Cardiac myosin inhibitors have now been tested in non-obstructive HCM, with mixed results. In April 2025 Bristol Myers Squibb reported that its mavacamten study missed both main goals, for exercise capacity and symptoms, and the results were published that September [21,22,23]. In May 2026 Cytokinetics reported that its aficamten study met both main goals, improving symptoms and exercise capacity compared with placebo [24]. Those results had not yet been published or presented at a meeting at the time of writing, and aficamten is not approved for non-obstructive HCM [24].
Approaches aimed at the gene itself. A gene therapy called TN-201 is being studied in symptomatic adults with MYBPC3-associated HCM. It delivers a working copy of the gene to heart muscle cells in one infusion, so the heart can make more of the missing protein [25,26]. This is an early, open-label study with no comparison group, and seven people had received it by a data cut in May 2026 [26]. The first-in-human report says plainly that longer follow-up is needed before anything can be said about how well it works [25]. It is investigational and not approved anywhere. Gene editing and RNA-based approaches remain at laboratory and animal stage [27].
Study status checked: 3 August 2026. Research moves and what is being studied changes. For current study information, use app.trialport.com.
In the United States, the Hypertrophic Cardiomyopathy Association offers support, advocacy and education, including intake calls, discussion groups and family-screening guidance [28,29]. The Children’s Cardiomyopathy Foundation supports families of affected children [32].
In the United Kingdom, Cardiomyopathy UK runs a free helpline staffed by specialist nurses, a genetic advice helpline, local groups and an online HCM support group [30,31]. The British Heart Foundation explains the condition clearly and runs a genetic information service that can point you to your nearest inherited heart conditions clinic [15].
In Australia and New Zealand, Cardiomyopathy Australia New Zealand offers peer support and information sessions [33], and the Cardiac Inherited Disease Group coordinates family screening across New Zealand [34].
Coverage elsewhere is uneven. The Global Heart Hub Cardiomyopathy Patient Network brings together 35 organizations across 19 countries and is the most practical starting point [35]. We could not confirm a cardiomyopathy-specific organization in the Middle East or Africa, and coverage in Asia and South America is thin. Where no local group exists, a specialist inherited heart conditions clinic is the next best contact for families.
What is the difference between obstructive and non-obstructive HCM?
In obstructive HCM the thickened muscle reduces blood flow out of the heart, and in non-obstructive HCM it does not [15]. Obstruction means a gradient of 30 mm Hg or more [4], and the difference changes which treatments are available [16,18].
Is it inherited, and should my family be tested?
Usually yes to the first. Each child of an affected person has a 1 in 2 chance of inheriting the change [4,15]. First-degree relatives are encouraged to have an echocardiogram and ECG, repeated over the years [1,29].
If I inherited the gene change, will I definitely get the condition?
No, penetrance is incomplete [2]. Among relatives known to carry a family change, roughly a half to two thirds go on to develop HCM, and the figure is much lower for people found by chance [1,7].
Is there a cure?
No. Treatment eases symptoms, protects against dangerous rhythms and looks after the heart long term [4,6]. Approaches aimed at the gene are being studied, not approved [25,26].
What is my life expectancy?
Most people with this group of conditions have a normal life expectancy [2]. Death rates across HCM overall are higher than in the general population, so regular follow-up matters [1]. Sudden cardiac death risk is around 0.5 percent per year across HCM [11,12].
Written by: trialport editorial team
Reviewed by: Keith Berelowitz, Founder and CEO, trialport
Reviewed on: 3 August 2026
Next review due: 3 August 2027
References last checked: 3 August 2026