Mitral valve

Article written and reviewed by Dr Luca Moretti

The mitral valve is an anatomical complex located between the left atrium and ventricle that allows diastolic filling and prevents backward flow during systole. Describing it as a simple valve is reductive because competence arises from the moment-to-moment interaction among the annulus, leaflets, commissures, chordae tendineae, papillary muscles and ventricular myocardium. A small lesion in one component may be compensated for by the others, whereas altered ventricular geometry may produce regurgitation even when the leaflets are structurally intact.

The mitral valve separates two chambers with a low pressure difference during diastole, but during systole it must withstand the pressure generated by the left ventricle. Its large opening area normally makes filling efficient; the broad leaflet surface and their zone of overlap provide a reserve of coaptation. This architecture explains why the clinical picture cannot be inferred from the appearance of a leaflet alone: chamber size, rhythm, blood pressure, contractility and loading conditions modify valve behavior.

The two fundamental hemodynamic abnormalities are mitral stenosis, in which diastolic passage is obstructed, and mitral regurgitation, in which part of systolic stroke volume flows backward into the atrium. The two lesions may coexist, especially in rheumatic heart disease or after repair, and their relative importance depends on flow, heart rate and chamber compliance.

The mitral valve is also particularly sensitive to cardiac geometry. Myocardial infarction, dilated cardiomyopathy, atrial fibrillation and atrial dilation may render a histologically normal valve incompetent; conversely, primary leaflet disease may progressively remodel the atrium, ventricle, pulmonary circulation and right heart. Assessment must therefore integrate anatomy, hemodynamics and prognostic significance.

Anatomy of the mitral apparatus

The mitral annulus is not a rigid fibrous circle. It has a three-dimensional saddle-shaped configuration, with higher points anteriorly and posteriorly and lower points at the commissures. Its anterior portion is in fibrous continuity with the aortic valve and trigones; the posterior portion is more muscular and deformable. During systole, the normal annulus decreases its area and accentuates its saddle shape, reducing leaflet stress.

The mitral annulus is also related to surgically vulnerable structures. Posteriorly lies the coronary sinus; at the right fibrous trigone, near the posteromedial commissure, runs the atrioventricular conduction system, while the circumflex artery may lie very close to the posterolateral annulus. Anteriorly, the mitral-aortic continuity forms the roof of the outflow tract. These relationships explain why annuloplasty, replacement and transcatheter procedures require careful planning for the risks of injury to adjacent structures and outflow tract obstruction.

The anterior leaflet occupies approximately one third of the annular circumference but has a broad surface and a semicircular shape. The posterior leaflet inserts along the remaining two thirds and is divided by indentations into scallops. Surgical nomenclature describes A1, A2 and A3 in the anterior leaflet and P1, P2 and P3 in the posterior leaflet, moving from the anterolateral to the posteromedial commissure. Segmental localization is the common language of the echocardiographer, surgeon and interventional cardiologist.

Both leaflets have a translucent zone and a distal rough zone where chordae insert and coaptation occurs; a basal zone is described in the posterior leaflet. The tissue is organized in layers rich in collagen, elastin and proteoglycans and covered by endothelium. Its composition is not passive: interstitial cells, matrix and mechanical forces participate in physiological and pathological remodeling.

The commissures are not merely junction points, but regions where the two leaflets converge and receive fan-shaped chordae. Commissural fusion is the characteristic morphological sign of rheumatic stenosis; a commissural lesion may generate an eccentric jet that is difficult to quantify. The three-dimensional “surgical” view allows the segments to be oriented as the operator sees them from the left atrium.

The chordae tendineae connect the leaflets to the papillary muscles and distribute load. Marginal chordae prevent eversion of the free edge; basal and intermediate chordae support the leaflet body. Strut chordae of the anterior leaflet are particularly robust. Elongation, rupture, retraction, fusion or calcification alter motion and coaptation through different mechanisms.

The anterolateral and posteromedial papillary muscles do not always correspond to two single bodies; they may consist of multiple heads. The anterolateral muscle generally receives a more redundant blood supply from the left anterior descending and circumflex territories, whereas the posteromedial muscle more often depends on a single territory, frequently the dominant right coronary artery. This difference contributes to the vulnerability of the posteromedial muscle to ischemic rupture.

Chordae from both papillary muscles distribute to both leaflets. Papillary contraction does not close the valve like a sphincter: it maintains the relationship between leaflets and ventricle while the annulus moves toward the apex and systolic pressure tends to push the leaflets into the atrium. Ischemia or papillary displacement can therefore cause tethering without rupture.

The inferolateral and anteroseptal ventricular walls, interpapillary distance and apical shape are part of the ventricular-mitral unit. In ischemic or dilative remodeling, the papillary muscles are displaced laterally and apically, the chordae pull the leaflets, and coaptation occurs below the annular plane. The lesion is functional, but the subvalvular apparatus is directly involved.

The left atrium and posterior annulus form another functional unit. Chronic atrial dilation, especially with atrial fibrillation, may enlarge the annulus beyond the adaptive capacity of the leaflets. If the ventricle remains relatively preserved, the result is atrial functional mitral regurgitation, which differs from the ventricular form in geometry and strategy.

Physiology, dynamics and mechanics

At the beginning of diastole, ventricular pressure falls below atrial pressure and the mitral valve opens. Ventricular relaxation and elastic recoil contribute to early filling and the E wave, whereas atrial contraction generates the A wave; at a normal heart rate, most filling occurs passively. As heart rate increases, diastole shortens and, for the same valve area, the gradient rises: this is one reason why tachycardia becomes particularly important in mitral stenosis.

Normal anatomical area is generally about 4-6 cm², sufficiently wide that the mean gradient is minimal. A moderate reduction may remain compensated at rest but become hemodynamically relevant during exercise, pregnancy, fever or anemia, when flow and heart rate increase. The gradient is therefore not a fixed property of the valve, but the result of orifice size and flow conditions.

Closure begins when ventricular pressure exceeds atrial pressure. The filling vortex, slowing of flow and ventricular contraction bring the leaflets closer together; rising pressure completes coaptation. The anterior and posterior portions overlap across a surface rather than meeting along a line. This coaptation reserve allows the valve to tolerate physiological variations in volume and shape.

Systolic forces tend to push the leaflets toward the atrium, while chordae and papillary muscles exert anchoring forces toward the ventricle. Stable competence requires a balance between closing forces, generated by the pressure gradient, and tethering forces, determined by ventricular geometry. Markedly reduced contractility decreases the former; dilation and papillary displacement increase the latter.

The saddle shape of the annulus helps reduce peak leaflet stress. When the annulus flattens, as occurs in several degenerative and functional forms, tension on leaflets and chordae increases; annuloplasty therefore aims not only to reduce diameter but also to restore a stable coaptation platform. The size and shape of the prosthetic ring must nevertheless be chosen to avoid iatrogenic stenosis and systolic anterior motion.

Continuity between the anterior leaflet and aortic root coordinates inflow and outflow. During diastole, the anterior leaflet moves away from the septum and opens inflow; during systole, it forms part of the posterior wall of the outflow tract. After repair, a tall posterior leaflet, a small ring or a hyperdynamic ventricle may shift the coaptation point anteriorly and cause SAM, or systolic anterior motion, with regurgitation and dynamic obstruction.

The subvalvular apparatus preserves ventricular shape. The older concept of replacement with complete resection of leaflets and chordae has been superseded by recognition that annulo-papillary continuity supports ventricular function and geometry. When the valve is replaced, chordal preservation is generally pursued when technically safe.

The valve responds to respiration, posture, blood pressure and circulating volume. Secondary regurgitation may decrease after diuresis and vasodilation or increase during exercise; primary regurgitation may appear less severe during hypotension or sedation. Assessment should record hemodynamic conditions and should not turn a single image into an immutable characteristic.

Aging modifies the complex through fibrosis, reduced elasticity and calcium deposition. Mitral annular calcification may extend to the leaflet bases, cause regurgitation, stenosis or both, and complicate repair, replacement and transcatheter anchoring. It is also a marker of atherosclerotic and metabolic burden, not necessarily the cause of every symptom.

Main diseases of the mitral valve

Clinical classification begins by distinguishing obstruction from regurgitation, acute from chronic presentation, and primary from secondary lesions. The same patient may move across categories: chronic chordal degeneration may culminate in acute rupture; cardiomyopathy may produce secondary regurgitation and later induce structural leaflet changes. Mechanism and stage must therefore be redefined over time.

Rheumatic stenosis results from commissural fusion, leaflet thickening and retraction of the subvalvular apparatus. The orifice assumes the typical doming appearance and progressively narrows. Increased atrial pressure causes dyspnea, atrial fibrillation, thrombosis and pulmonary hypertension. It is less common in high-income countries, but migration and health inequalities maintain its relevance.

Degenerative stenosis due to annular calcification is a different disease: the commissures are not fused and a calcific mass narrows the orifice from the leaflet bases. It often affects older adults with renal dysfunction, aortic disease and multiple comorbidities. Planimetry, gradient interpretation and therapeutic options require different criteria from rheumatic disease.

In primary mitral regurgitation, the cause lies in valvular or subvalvular tissue. Myxomatous degeneration, Barlow disease, fibroelastic deficiency, endocarditis, rheumatic disease, drugs and inflammatory diseases produce different anatomies. Repairability depends on the lesion, its extent and center experience.

Mitral valve prolapse denotes systolic displacement of one or both leaflets beyond the annular plane. It does not automatically mean severe regurgitation or Barlow disease. A flail leaflet, by contrast, has a free edge everted into the atrium because of chordal rupture or elongation and often generates a significant jet.

Myxomatous mitral valve disease encompasses a spectrum of matrix expansion and tissue redundancy. Barlow disease tends to involve multiple segments, with bulky leaflets, a dilated annulus and abnormal chordae; fibroelastic deficiency features thin tissue and a focal lesion, often chordal. Distinguishing phenotypes avoids generic descriptions and anticipates repair complexity.

In ventricular secondary mitral regurgitation, myocardial infarction or cardiomyopathy dilates the ventricle and makes it more spherical. The papillary muscles are displaced, the leaflets remain tethered and the annulus dilates. Regurgitation is both a consequence and an amplifier of heart failure; treatment of ventricular disease therefore precedes or accompanies any valve procedure.

The atrial form results mainly from enlargement of the atrium and annulus in atrial fibrillation or heart failure with preserved ejection fraction. The ventricle does not show the typical dilative remodeling of the ventricular form. An apparently restricted posterior leaflet and insufficient leaflet growth relative to annular enlargement may contribute to loss of coaptation.

Acute mitral regurgitation follows ischemic papillary rupture, chordal rupture, endocarditis or trauma. A nondilated, poorly compliant atrium cannot accommodate the regurgitant volume: pulmonary pressure rises abruptly, causing edema and shock, while the murmur may be brief or soft. It is an emergency distinct from compensated chronic disease.

Different organic etiologies leave different anatomical signatures. Endocarditis may perforate a leaflet, destroy a commissure, create vegetations or abscesses and rupture chordae; rheumatic heart disease often combines retraction and fusion, producing a mixed lesion; radiotherapy and some drug exposures induce thickening and retraction, whereas connective tissue disorders may promote prolapse. Recognizing the cause is essential because it changes both systemic risk and therapeutic strategy.

Mitral annular disjunction describes a systolic separation between the atrial-valvular junction and posterolateral ventricular myocardium. It is common in some myxomatous phenotypes and may be associated with exaggerated annular motion, fibrosis and arrhythmias, but does not by itself identify a malignant syndrome. Arrhythmic risk, regurgitation and the indication for valve intervention must be assessed separately.

Clinical assessment and imaging

The clinical history investigates dyspnea, reduced exercise tolerance, palpitations, edema, chest pain, syncope, embolism and previous rheumatic fever or endocarditis. Defining the course is essential: gradual adaptation leads many patients to reduce activity without recognizing themselves as symptomatic. Planned pregnancy, major surgery, atrial fibrillation and comorbidities influence the timing and mode of decision-making.

Auscultation complements but does not replace imaging. Stenosis produces an opening snap and an apical diastolic rumble, more evident in the left lateral position; chronic regurgitation typically generates an apical holosystolic murmur radiating to the axilla. Calcification, low output, high atrial pressure or an acute jet may attenuate classic signs.

Transthoracic echocardiography defines morphology and motion, jet direction, valve area or regurgitant orifice, gradients, volumes, ejection fraction, atrial size, pulmonary pressure and the right heart. Technical quality and hemodynamic conditions should be stated. A reliable conclusion arises from convergence of multiple parameters, not from a single measurement.

Transesophageal echocardiography provides higher resolution for segments, commissures, chordae, vegetations, thrombi and procedural planning. Three-dimensional imaging shows the atrial en face view and enables planimetry and geometric measurements. Sedation and reduced blood pressure may decrease regurgitation: an intraprocedural examination does not automatically replace the baseline study obtained under physiological conditions.

In stenosis, orifice planimetry, mean gradient, pulmonary pressure and commissural morphology form the core of assessment. In regurgitation, vena contracta, flow convergence, effective regurgitant orifice area, regurgitant volume, pulmonary venous Doppler, jet density and remodeling are integrated. Eccentric, multiple or late-systolic jets require particular caution.

The Carpentier classification describes leaflet motion: type I normal motion with annular dilation or perforation; type II excessive motion in prolapse or flail; type IIIa restricted motion in systole and diastole, typical of rheumatic retraction; type IIIb restricted systolic motion due to ventricular tethering. It is a mechanical grammar, not a complete etiological classification.

Exercise echocardiography is useful when symptoms and resting severity are discordant. It may document an increased gradient in stenosis, worsening secondary regurgitation, pulmonary pressure, contractile reserve and functional capacity. Meaning depends on the clinical question and should not be reduced to an isolated threshold.

Cardiac magnetic resonance measures ventricular volumes with high reproducibility and quantifies regurgitation by the difference between ventricular stroke volume and aortic flow. It is valuable when echocardiography is inconclusive and characterizes ischemic scar or fibrosis. Arrhythmias, devices and poor cooperation may limit it.

CT defines annular calcium, relationships with the circumflex and coronary arteries, annular dimensions, predicted neo-outflow tract and access routes. It is central to transcatheter planning but involves contrast and radiation. Catheterization is reserved for coronary disease and hemodynamic discrepancies that imaging does not resolve.

Electrocardiography and rhythm monitoring complement imaging by documenting atrial fibrillation, conduction disturbances and ventricular arrhythmias. BNP and NT-proBNP reflect wall stress but should be interpreted in light of age, rhythm and renal function; complete blood count, renal and hepatic function, hemolysis indices and infectious markers instead answer specific clinical questions. A valve diagnosis becomes meaningful only when placed within the overall patient profile.

Surveillance should use comparable measurements and, when possible, the same laboratory. Small variations may reflect technique or loading conditions; coherent changes in symptoms, volumes, function, pulmonary pressure and severity indicate progression. A useful report describes mechanism, severity, consequences and anatomical feasibility, not just grade.

Principles of treatment and follow-up

Treatment considers four questions: is the lesion truly severe, does it cause symptoms or damage, can it be corrected with durable benefit, and what is the risk of waiting compared with intervention? The decision is not equivalent to the availability of a technique. Biological age, frailty, life expectancy, preferences, concomitant diseases and functional goals belong to the same assessment.

Medical therapy controls consequences and associated conditions but rarely corrects a severe structural lesion. Diuretics reduce congestion, rate control prolongs filling in stenosis and heart failure therapy may reduce secondary regurgitation. Symptomatic improvement does not prove that the valve disease is no longer severe.

Atrial fibrillation requires rate or rhythm control, thromboembolic assessment and anticoagulation according to context. In clinically significant rheumatic stenosis, vitamin K antagonists remain the standard and DOACs are not equivalent. In nonrheumatic regurgitation, choice follows specific indications, renal function, bleeding risk and prosthetic status.

In rheumatic stenosis with favorable anatomy, percutaneous mitral commissurotomy separates fused commissures without implanting a prosthesis. Important commissural calcification, atrial thrombus, regurgitation greater than mild or absence of fusion reduce efficacy or safety. Degenerative calcific stenosis is not treated according to the same principle.

For primary degenerative regurgitation, durable surgical repair is preferred to replacement when performed at a center with a high probability of success and low mortality. Selective resections, neochordae, commissural repair and annuloplasty are combined according to the lesion. Preservation of tissue and the subvalvular apparatus should produce competence without stenosis or SAM.

Replacement is necessary when repair is not predictably durable, as in some rheumatic, calcific, infectious or complex multisegment disease. Mechanical and biological prostheses carry different profiles of durability, anticoagulation and reintervention. The choice is shared and should anticipate possible future procedures.

Transcatheter edge-to-edge repair brings leaflet margins together and creates a double orifice. It is established in selected patients with persistent secondary regurgitation despite optimized therapy and may be considered in severe high-risk primary disease with suitable anatomy. Benefit depends on patient selection, effective reduction of regurgitation and an acceptable residual gradient.

Other technologies include annuloplasty, transcatheter replacement and valve-in-valve or valve-in-ring implantation. In annular calcification, valve-in-MAC implantation remains high risk because of leak, embolization and outflow tract obstruction. These procedures require CT, simulation and expert centers; they are not equivalent to routine aortic TAVI.

The Heart Team brings together clinical cardiology, imaging, interventional cardiology, cardiac surgery, anesthesia and, when needed, heart failure, electrophysiology, geriatrics and infectious disease expertise. Its value lies not in a formal meeting but in shared verification of mechanism, risk, repairability, alternatives and bailout planning.

Follow-up after repair or replacement establishes an echocardiographic baseline and monitors residual regurgitation or stenosis, gradient, ventricular function, pulmonary pressure and the prosthesis. Fever, a new murmur, embolism, hemolysis or heart failure require earlier assessment. Endocarditis prophylaxis, oral hygiene and antithrombotic therapy depend on the procedure and guidelines.

Prognosis is excellent when a correctable lesion is treated before irreversible damage develops and without procedural complications. Ventricular dysfunction, marked atrial dilation, pulmonary hypertension, atrial fibrillation, tricuspid regurgitation, right ventricular dysfunction, renal disease, frailty and nondurable repair worsen outcome. Disappearance of the murmur does not necessarily coincide with complete biological recovery.

The most important principle is temporal: waiting for advanced symptoms may transform valve disease into multichamber cardiac disease. Intervening too early, however, exposes the patient to immediate risk, prosthesis implantation or reinterventions without demonstrated benefit. Competent surveillance and individualized decision-making aim to identify the window in which net benefit is greatest.