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C Cardiovascular Conditions

Cleft mitral valve: Overview, Causes, Symptoms, Diagnosis, and Treatment

January 10, 2026 Modified date: January 10, 2026

A cleft mitral valve is a congenital (present-from-birth) split or indentation in one leaflet of the mitral valve—the “gate” that controls blood flow from the left atrium to the left ventricle. The cleft itself is not always dangerous; what matters is whether it prevents the valve from sealing tightly. When the seal is incomplete, blood leaks backward with each heartbeat (mitral regurgitation), and the heart may gradually enlarge to compensate. Some people are diagnosed in infancy because of a heart murmur, while others remain undetected until adolescence or adulthood, when exercise intolerance, palpitations, or breathlessness becomes harder to ignore.

This article explains what a cleft mitral valve is, why it happens, who is at risk for complications, how it is diagnosed with modern imaging, and what treatment and long-term management usually look like.

What is a cleft mitral valve?
How a cleft causes mitral regurgitation
Causes and associated heart defects
Symptoms, complications, and red flags
How doctors diagnose it
Treatment and long-term management

What is a cleft mitral valve?

The mitral valve sits between the left atrium and left ventricle. It has two leaflets (anterior and posterior) that open and close with each heartbeat. A cleft mitral valve means one leaflet has an abnormal split that can extend toward the valve ring (annulus). Instead of meeting edge-to-edge like two cleanly aligned doors, the leaflet edges may leave a gap. The result can be a leak (mitral regurgitation), but the severity varies widely.

“Cleft” versus normal indentations

This topic can be confusing because the posterior mitral leaflet normally has scallops—natural separations that can look like small indentations. A true cleft is typically deeper and behaves differently: it can create a focused regurgitant jet, distort leaflet motion, or resist full coaptation (the moment the leaflets seal).

Clinicians therefore do not label every indentation as a cleft. They consider the depth, location, whether it reaches the annulus, and whether it clearly contributes to regurgitation.

Isolated cleft versus cleft with other defects

A cleft mitral valve may be:

Isolated: the cleft is the main structural issue.
Associated with other congenital heart disease: especially atrioventricular septal defect (AVSD) variants, atrial septal defect (ASD), ventricular septal defect (VSD), or abnormalities of the chordae/papillary muscles.

This distinction matters because associated defects can change symptoms, timing of surgery, and the surgical technique used.

Why some people feel fine for years

A mild cleft may leak only slightly, producing a murmur without major symptoms. The heart can often compensate for mild regurgitation for a long time. Symptoms tend to appear when regurgitation becomes moderate-to-severe, when the left atrium/ventricle enlarge, or when rhythm problems develop.

A useful perspective is that a cleft mitral valve is less a single diagnosis and more a spectrum—from an incidental imaging finding to a clearly symptomatic valve lesion requiring repair. The goal of evaluation is to place an individual patient accurately on that spectrum and plan follow-up accordingly.

How a cleft causes mitral regurgitation

Mitral regurgitation (MR) happens when blood flows backward from the left ventricle into the left atrium during contraction. In a cleft mitral valve, the backward flow usually occurs because the leaflet edges cannot meet and seal completely. Understanding the mechanics helps explain why symptoms vary and why some repairs are straightforward while others are more complex.

The key mechanical problem: imperfect coaptation

A healthy mitral valve closes in a broad, stable “seal zone.” A cleft reduces that seal in one segment, creating a weak spot. When ventricular pressure rises during systole, blood finds the path of least resistance—often through or adjacent to the cleft.

Several features influence how much leakage occurs:

Cleft size and depth: deeper or wider clefts typically leak more.
Leaflet tissue quality: thin, redundant, or restricted leaflet tissue can worsen the seal.
Chordae and papillary muscle geometry: abnormal chordal attachments can tether the leaflet or pull the edges apart.
Annular dilation: if the valve ring stretches, the leaflets must cover a larger opening, increasing leakage.
Left ventricular shape: dilation or altered contraction patterns can pull leaflets apart and magnify regurgitation.

Why MR can worsen over time

When MR becomes moderate-to-severe, the left atrium and left ventricle may enlarge to accommodate extra volume. This can become a feedback loop:

More regurgitation increases volume load.
Volume load enlarges chambers and stretches the annulus.
Annular dilation makes coaptation harder.
MR increases further.

This is why clinicians monitor not only symptoms but also objective markers: chamber sizes, regurgitation severity, pulmonary pressures, and rhythm changes.

What people often notice first

Early on, the body may compensate well. Symptoms typically emerge with exertion:

Breathlessness during activities that used to feel easy
Reduced stamina or slower recovery after exercise
Palpitations (especially if the left atrium enlarges and atrial fibrillation develops)
Fatigue that feels “cardiac” in quality—worse with activity, better with rest

In infants and young children, the signs can look different: poor weight gain, sweating with feeds, rapid breathing, or frequent respiratory infections.

Why imaging precision matters

MR from a cleft can be missed if imaging planes do not capture the cleft well. Modern three-dimensional echocardiography can map the valve “en face,” helping clinicians see exactly where the gap is and whether it is the dominant cause of regurgitation. That anatomical clarity often determines whether a catheter-based approach is feasible or whether surgical repair is the safer, more durable option.

Causes and associated heart defects

A cleft mitral valve is a congenital malformation—meaning it results from how the heart forms in early development. It is not caused by lifestyle factors, infections, or aging. That said, the clinical course can be influenced by later-life factors (blood pressure, rhythm disorders, pregnancy, endurance sports, and other stresses) that change how the valve and chambers handle volume.

How it develops

During fetal development, the mitral valve leaflets, chordae, and papillary muscles form through coordinated growth and remodeling of tissue in and around the atrioventricular canal. When leaflet formation or fusion is incomplete in a localized area, a cleft can remain. The anatomy can vary from a narrow “V-shaped” split to a broader gap that reaches toward the annulus.

Isolated cleft mitral valve

In an isolated cleft, the cleft is present without a common atrioventricular junction or classic atrioventricular septal defect anatomy. Isolated clefts are often discovered because of mitral regurgitation. They may involve:

The anterior leaflet (classically reported)
The posterior leaflet (less common, and sometimes mistaken for normal scallops without detailed imaging)
Rarely, complex patterns with multiple indentations

Because isolated clefts can be overlooked on standard two-dimensional views, many clinicians rely on transesophageal echocardiography (TEE) and 3D datasets when regurgitation seems “unexplained.”

Associated defects and why they matter

A cleft mitral valve is frequently discussed alongside other congenital defects, particularly:

Atrioventricular septal defect (partial/complete forms): cleft-like morphology can be part of the left AV valve structure in these lesions.
Atrial septal defect (ASD) or ventricular septal defect (VSD): these can change chamber sizes and flow patterns, affecting symptom timing.
Subvalvular anomalies: abnormal chordae, papillary muscle malposition, or tethering can amplify regurgitation and affect repair durability.
Left-sided obstructive lesions (less commonly): certain congenital syndromes cluster left-heart abnormalities.

When associated defects are present, treatment often aims to correct the broader circulation problem, not just the mitral valve.

Risk factors for progression are mostly mechanical

Because the cleft is congenital, “risk factors” for worsening typically relate to the valve’s mechanics and the heart’s response:

Moderate-to-severe MR at baseline
Annular dilation or rapid chamber enlargement
Elevated pulmonary pressures
New arrhythmias (especially atrial fibrillation)
Life stages with increased volume load (for example, pregnancy) when significant MR is present

A practical takeaway is that the cleft is not something you can prevent—but you can prevent avoidable consequences by monitoring MR severity and intervening at the right time, before the heart remodels in a way that is harder to reverse.

Symptoms, complications, and red flags

Symptoms from a cleft mitral valve usually come from mitral regurgitation and its effects on the left atrium, left ventricle, lungs, and rhythm stability. The same anatomical cleft can look very different clinically depending on the leak size and how long it has been present.

Common symptoms by age and stage

In older children and adults, common symptoms include:

Shortness of breath with exertion, sometimes progressing to breathlessness at rest
Reduced exercise tolerance, fatigue, and slower recovery after activity
Palpitations, skipped beats, or episodes of rapid heartbeat
Chest discomfort (often non-specific, but always worth evaluating)
Swelling of ankles/legs if heart failure develops

In infants and young children, watch for:

Poor feeding or tiring during feeds
Sweating with feeds, rapid breathing, or persistent fast heart rate
Poor weight gain or failure to thrive
Frequent respiratory infections or wheezing that does not fit the usual pattern

Complications clinicians monitor for

The key complications tend to fall into several categories:

Progressive chamber enlargement: especially left atrial enlargement, which can set the stage for arrhythmias.
Pulmonary hypertension: long-standing MR can raise pressures in the lungs, increasing risk and complicating surgery if delayed.
Arrhythmias: atrial fibrillation is a major turning point because it can worsen symptoms and reduce cardiac efficiency.
Heart failure: congestion, fluid retention, and declining function can appear if MR becomes severe or longstanding.
Endocarditis risk considerations: abnormal valves can be a site for infection, though routine antibiotic prophylaxis is not universal and depends on individual risk categories and prior history.

Red flags that need prompt medical evaluation

Seek urgent care if any of the following occur:

New or worsening shortness of breath at rest, especially with coughing, wheezing, or frothy sputum
Fainting, near-fainting, or sustained dizziness
Rapid, irregular heartbeat with weakness, chest discomfort, or breathlessness
Sudden swelling, rapid weight gain over days, or markedly reduced urine output
Fever with chills plus a new murmur, unexplained fatigue, or signs of infection (particularly if you have known valve disease)

What “stable” usually means

Stability is not the absence of symptoms—it is predictable symptoms with stable imaging, stable chamber sizes, and no new rhythm problems. Many people live well for years with mild MR and periodic monitoring. The tipping points that usually prompt a change in plan are worsening MR severity, progressive enlargement of chambers, rising pulmonary pressures, or the appearance of atrial fibrillation. Recognizing those changes early is often what preserves long-term heart function.

How doctors diagnose it

Diagnosis aims to answer two questions: (1) is there a true cleft (not a normal scallop indentation), and (2) how much does it matter physiologically—especially in terms of mitral regurgitation severity and cardiac remodeling. Modern imaging is central because a cleft can be easy to miss on limited views.

Clinical clues and the role of a murmur

Many patients enter evaluation because a clinician hears a murmur, often described as a systolic murmur at the apex. Symptoms may be absent or mild. In symptomatic patients, clinicians look for exertional breathlessness, palpitations, and signs of congestion.

A careful history often includes:

Timing and progression of symptoms
Exercise tolerance compared with prior baseline
Pregnancy plans or history (if applicable)
Prior congenital heart disease or childhood murmurs
Family history of congenital heart disease
Any past episodes suggesting arrhythmia

Transthoracic echocardiography is the starting point

A transthoracic echocardiogram (TTE) provides:

Valve anatomy and leaflet motion assessment
Quantification of MR (often multiparametric)
Left atrial and left ventricular size and function
Estimated pulmonary pressures
Screening for associated defects

However, TTE can miss a cleft if image quality is limited, if the cleft lies outside the best planes, or if the regurgitant jet is complex.

Transesophageal echocardiography and 3D imaging often clarify anatomy

TEE brings the probe closer to the mitral valve, improving resolution. Three-dimensional echocardiography can show the valve “from above,” allowing clinicians to identify:

Exact cleft location (anterior vs posterior leaflet; segment orientation)
Whether the cleft extends to the annulus
Coaptation gaps and how they change through the cardiac cycle
Multiple jets or combined mechanisms (cleft plus prolapse, tethering, or annular dilation)

This level of detail is often what surgeons and structural teams need to plan repair.

Additional tests when MR is significant

Depending on severity and patient age, clinicians may use:

ECG and ambulatory monitors to detect atrial fibrillation or frequent ectopy
Exercise testing to objectively measure functional limitation
Cardiac MRI when quantification of volumes and regurgitant fraction is needed or when echo windows are poor
In selected adults, coronary evaluation if surgery is planned and risk factors are present

A high-quality diagnostic workup does not end with “yes, there’s a cleft.” It defines the mechanism of MR, the stage of cardiac remodeling, and the safest path forward—monitoring, medical therapy, or repair.

Treatment and long-term management

Treatment depends on symptoms, MR severity, chamber remodeling, pulmonary pressures, and rhythm stability. Many patients do not need immediate surgery, but they do need a structured follow-up plan so intervention happens at the right moment—before the heart’s compensations become permanent.

When monitoring is appropriate

Monitoring is common when MR is mild and the heart chambers remain normal in size and function. A typical plan includes:

Periodic echocardiography at intervals tailored to MR severity and stability
Symptom tracking with attention to exertional capacity
Rhythm surveillance if palpitations occur or the left atrium is enlarged
Counseling about triggers that may expose progression (major endurance changes, pregnancy planning, untreated hypertension)

The goal is not frequent testing for its own sake; it is preventing “silent progression.”

Medical therapy: supportive, not corrective

Medications do not close a cleft. They are used to manage consequences:

Diuretics for congestion symptoms when present
Rate or rhythm management for atrial fibrillation or other arrhythmias
Blood pressure optimization (important because high afterload can worsen regurgitation volume)
In selected cases, therapy guided by heart failure principles if ventricular function declines

Clinicians also prioritize practical prevention: prompt treatment of respiratory infections, maintaining fitness within tolerance, and avoiding abrupt changes in activity when severe MR is present.

Surgical repair is the definitive treatment when needed

When MR is significant, symptoms progress, or the heart shows remodeling, mitral valve repair is generally preferred over replacement—especially in younger patients—because it preserves native tissue and avoids lifelong anticoagulation associated with many prosthetic valves.

Repair strategies may include:

Direct cleft closure with fine sutures (when tissue allows tension-free closure)
Leaflet augmentation (patch techniques) when the cleft is wide or tissue is deficient
Annuloplasty (supporting the valve ring) when annular dilation contributes
Chordal repair or papillary muscle adjustments if subvalvular anatomy drives the leak

Surgical planning relies heavily on detailed imaging to avoid creating stenosis (an overly tight valve) while eliminating regurgitation.

Special considerations in children and pregnancy

In children, timing balances symptom control, growth, and repair durability. Surgeons often aim to repair rather than replace, but the small size of structures and growth considerations can influence technique and reoperation risk.

In pregnancy, blood volume increases substantially. If MR is moderate-to-severe, pregnancy can worsen symptoms and reveal limited reserve. Pre-pregnancy counseling with cardiology is important to set expectations and plan monitoring.

When to seek care and what follow-up should include

Contact your clinician promptly for new breathlessness, reduced exercise tolerance, palpitations, fainting, swelling, or fever. Long-term management works best when follow-up is consistent and coordinated: periodic imaging, rhythm evaluation when appropriate, and early repair decisions based on objective markers—not only on how someone feels that month.

References

Disclaimer

This article is for educational purposes only and does not provide medical advice, diagnosis, or treatment. A cleft mitral valve can range from a mild finding to a condition that causes significant mitral regurgitation, arrhythmias, pulmonary hypertension, or heart failure. If you develop chest pain, fainting, severe shortness of breath, a new rapid or irregular heartbeat, fever with unexplained fatigue, or rapidly worsening swelling, seek urgent medical care. Always discuss testing, monitoring intervals, and treatment decisions with a qualified clinician who can assess your individual anatomy, symptoms, and overall risk.

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