Acute mitral regurgitation

Article written and reviewed by Dr Luca Moretti

Acute mitral regurgitation is a time-dependent hemodynamic syndrome, not simply a chronic form that is suddenly recognized. Within hours or days, a significant regurgitant orifice develops and directs blood into a left atrium that has had no time to dilate; left atrial and pulmonary capillary pressure rise abruptly while aortic output falls. Pulmonary edema and shock can therefore coexist even with a nondilated ventricle and an apparently normal ejection fraction.

Causes include papillary muscle rupture after myocardial infarction, degenerative chordal rupture, perforation or destruction due to endocarditis, trauma and iatrogenic injury. Acute regurgitation can also be functional, without structural rupture, when ischemia or sudden remodeling displaces the papillary muscles and prevents coaptation. Distinguishing a primary mechanical lesion from ischemic tethering is therefore essential because urgency, likelihood of recovery and the procedure differ.

The condition requires immediate activation of intensive cardiology care, imaging and cardiac surgery. Drugs and support devices can buy time, but stabilization does not cure a severe structural lesion. The 2025 ESC/EACTS guidelines indicate urgent surgical or transcatheter treatment in poorly tolerated severe acute primary mitral regurgitation; the transcatheter option remains reserved for selected patients in whom surgery is prohibitive or when it is used as a bridge.

Causes and anatomical mechanisms

Papillary muscle rupture is a rare but catastrophic mechanical complication of myocardial infarction, usually occurring within the first few days. The posteromedial muscle more often has a single blood supply from the posterior descending artery and is therefore more vulnerable than the anterolateral muscle, which receives blood from the left anterior descending and circumflex arteries. Even nonextensive inferior or posterolateral infarctions can cause papillary muscle rupture and regurgitation disproportionate to global ventricular dysfunction.

Rupture can involve one head or the entire muscle. Rupture of a head releases the chordae of one or more segments and produces a flail leaflet; complete rupture leaves a large portion of the valve uncontrolled and frequently leads to shock. Echocardiography may show a mobile mass, but the muscle is not always easy to visualize; an eccentric jet and a hypermobile leaflet after myocardial infarction should maintain a high index of suspicion.

Ischemia without rupture causes papillary muscle dysfunction and displacement, reduces closing forces and increases tethering. In this setting, regurgitation is secondary and may lessen after revascularization, afterload reduction and myocardial recovery; if it remains severe, however, it may continue to sustain edema or shock and make correction necessary. The term "ischemic" must therefore be supplemented by a description of the mechanism.

In myxomatous degeneration or fibroelastic deficiency, an elongated chord can rupture spontaneously and transform compensated prolapse into a flail leaflet. The extent of the rupture, the segment involved and atrial compliance determine the presentation, ranging from subacute dyspnea to fulminant edema. An atrium already dilated because of pre-existing regurgitation may blunt the pressure rise without making the lesion harmless.

In endocarditis, acute regurgitation may result from leaflet perforation, chordal rupture, annular abscess or prosthetic dehiscence, in a setting that combines bacteremia, embolic risk and progressive destruction. Highly mobile vegetations can interfere with coaptation even before perforation occurs. The absence of fever, particularly in an older patient or after antibiotics, is not sufficient to exclude infection.

Blunt chest trauma, endomyocardial biopsy, transcatheter procedures, aortic surgery, valve replacement and devices can damage leaflets, chordae or papillary muscles. After mitral valve repair, chordal rupture, ring dehiscence or partial detachment of an edge-to-edge device are specific mechanisms. Reconstructing the temporal relationship with the procedure guides imaging.

Rarer causes include spontaneous rupture of a papillary muscle in infiltrative or inflammatory diseases, lupus, congenital abnormalities and tumors. In every case, classification should describe the level of the lesion - annulus, leaflet, chord, papillary muscle or ventricle - and not be limited to jet severity.

A further distinction concerns acute regurgitation superimposed on chronic regurgitation. A patient with known prolapse may rupture a new chord: an already compliant atrium limits initial edema, but the increase in volume can precipitate heart failure and rapidly reduce reserve. The finding of a dilated atrium therefore does not justify classifying the episode as exclusively chronic; history and comparison with previous examinations reconstruct the new component.

Papillary muscle rupture should be distinguished from rupture of a chord attached to an ischemic papillary muscle. In the former, a muscular portion moves with the leaflet and necrotic tissue makes repair difficult; in the latter, the papillary muscle remains continuous and may provide an anchor. This anatomical difference changes the likelihood of preserving the valve and the safety of TEER.

Pathophysiology, presentation and differential diagnosis

During systole, a suddenly large portion of stroke volume enters the noncompliant atrium. A prominent v wave develops and is transmitted to the pulmonary veins and capillaries. Fluid crosses into the interstitium and alveoli, causing hypoxemia, reduced lung compliance and respiratory distress. Distribution may be asymmetric if the jet is directed selectively toward one pulmonary vein, sometimes mimicking unilateral pneumonia.

The ventricle ejects through two pathways: the aorta and the atrium. Total ejection fraction may be normal or hyperdynamic because the atrium offers low impedance, while forward stroke volume is inadequate. Arterial pressure and renal and coronary perfusion fall; acidosis and vasoconstriction increase afterload and regurgitation. Shock is therefore simultaneously mechanical and metabolic.

The typical presentation includes sudden dyspnea, orthopnea, sweating, hypoxemia and hypotension, but the clinical picture varies with the cause. After myocardial infarction, chest pain, electrocardiographic changes or cardiac arrest may predominate, whereas endocarditis is more often associated with fever, a new murmur, emboli and septic signs. A partial chordal rupture may instead produce increasing symptoms over several days and then worsen abruptly.

The apical murmur is often holosystolic and radiates to the axilla or base, but it may be short, decrescendo or faint when ventricular and atrial pressures equalize early. Low output during shock attenuates it further. The absence of an obvious murmur should not delay echocardiography in a patient with pulmonary edema after myocardial infarction.

Differential diagnoses include ventricular septal rupture, tamponade due to free-wall rupture, ischemic heart failure without a mechanical complication, pulmonary embolism, aortic dissection with regurgitation, pneumonia and ARDS. Septal rupture produces a left-to-right shunt and a parasternal murmur; pulmonary artery catheterization may show an oxygen saturation step-up. More than one mechanical complication can coexist.

ECG and troponins identify ischemia, but elevated troponin also occurs in shock. Chest radiography and lung ultrasound document edema without determining its cause. Complete blood count, renal and hepatic function, lactate, coagulation tests and blood gas analysis define organ injury and prepare for intervention. If endocarditis is suspected, at least three sets of blood cultures are obtained before antibiotics unless instability requires immediate treatment.

The pulmonary capillary wedge pressure tracing may show giant v waves, but this finding is not specific and may be absent. Catheterization should not delay imaging or the operating room; it is useful when hemodynamics and diagnosis remain uncertain or to guide complex support. In post-infarction papillary muscle rupture, urgent coronary angiography identifies the culprit artery and plans revascularization while maintaining a timeline compatible with valve correction.

Unilateral pulmonary edema, more often on the right, deserves particular attention. An eccentric jet directed toward the right superior pulmonary vein produces a regional pressure rise and a focal infiltrate; stress leukocytosis and low-grade fever may incorrectly reinforce a diagnosis of pneumonia. Rapid radiographic change after reduction of regurgitation and asymmetric pulmonary venous Doppler findings clarify the mechanism.

In shock, serial assessment should look for cerebral perfusion, peripheral temperature, capillary refill, urine output and lactate trends. Blood pressure restored with vasopressors does not necessarily mean adequate cardiac output. Likewise, disappearance of crackles after intubation does not demonstrate normalization of left atrial pressure.

Urgent echocardiography and quantification

Transthoracic echocardiography should be performed at the bedside without waiting for complete stabilization. It assesses the leaflets, chordae, papillary muscles, ventricular function and wall motion, right ventricle, pulmonary pressure, pericardium and possible septal defects. A focused examination can identify the emergency, but it should be followed by a complete acquisition as soon as possible.

Direct anatomical signs include a flail leaflet, mobile papillary muscle head, ruptured chord, perforation, vegetation or dehiscence; in the functional form, systolic restriction, papillary muscle displacement and ischemic wall-motion abnormalities predominate. Color Doppler often shows an eccentric jet that adheres to the wall because of the Coandă effect and may appear less extensive. In a patient in shock, therefore, a visually small jet does not at all exclude severe regurgitation.

Chronic quantification criteria cannot be transferred mechanically. The atrium and ventricle may be normal in size because they have not had time to remodel. EROA may be large, but PISA is unstable, nonhemispheric and variable during systole. Vena contracta, continuous-wave Doppler density and contour, pulmonary venous flow and stroke volume should be integrated with hemodynamic tolerance.

Pulmonary venous flow shows systolic reversal in the vein reached by the jet, while a vein not affected by the jet may appear normal. Estimated pulmonary pressure may be high; in advanced shock it may be low because of right ventricular failure. Ejection fraction overestimates contractile function and should not provide reassurance.

Transesophageal echocardiography is urgently indicated when transthoracic examination does not define the lesion, in patients receiving mechanical ventilation, in suspected endocarditis, in the presence of a prosthesis, or when surgery or TEER is being planned. Three-dimensional reconstructions localize the segment, extent of the flail, perforation and amount of tissue available. Sedation can reduce blood pressure and regurgitation: morphology remains decisive.

In endocarditis, transesophageal echocardiography looks for abscesses, fistulas and involvement of other valves. A negative initial study does not exclude infection when probability is high and should be repeated according to guidelines. Cardiac CT can further assess perivalvular complications; PET/CT is particularly useful for prosthetic valves, but no advanced test should delay life-saving surgery.

During stabilization, echocardiography is repeated after major changes in support. Vasodilators and ventilation reduce afterload and may decrease the jet, whereas vasoconstrictors increase it. Each image should be described in relation to blood pressure, drugs and mechanical support; otherwise, a transient reduction can be mistaken for resolution.

The echocardiographer should communicate immediately rather than simply produce a report. The site and extent of the lesion, likelihood of papillary muscle rupture, biventricular function, associated defects and possibility of repair are operational information. In an unstable patient, a vague conclusion such as "moderate-to-severe regurgitation" without a mechanism can delay definitive treatment.

Quantification must account for systolic duration. A very large but late-systolic orifice may generate less volume than a smaller holosystolic one; conversely, in papillary muscle rupture, regurgitation often occupies the entire systole. EROA and volume should therefore be interpreted together with the temporal profile rather than as interchangeable numbers.

Intensive stabilization and causal treatment

Treatment begins simultaneously with diagnosis. Oxygen, noninvasive ventilation or intubation correct hypoxemia and reduce the work of breathing; positive pressure lowers preload and afterload, but induction and ventilation can precipitate hypotension. Intubation should therefore be prepared by an experienced team with hemodynamic support available.

Intravenous diuretics reduce congestion when perfusion and volume status permit. In normotensive or hypertensive patients, nitroprusside lowers aortic impedance, favors forward output and reduces regurgitant volume. It is a titrated bridge under invasive monitoring, not definitive treatment, and is contraindicated in uncorrected hypotension.

In shock, norepinephrine can support blood pressure, while dobutamine or other inotropes increase output when necessary, while balancing the risk of tachycardia and greater myocardial oxygen consumption. Excessive vasoconstriction increases regurgitation, and indiscriminate fluid loading can worsen edema unless true hypovolemia is present. Treatment should therefore be guided by ultrasound, perfusion signs, lactate, urine output and, in selected cases, invasive hemodynamic monitoring.

The intra-aortic balloon pump reduces afterload and increases coronary perfusion, but it has no routine benefit in shock due to myocardial infarction and is now an exceptional support or bridge in selected mechanical complications. Impella can unload the ventricle but crosses the aortic valve and does not correct the regurgitant orifice; venoarterial ECMO increases afterload unless combined with unloading. The choice of mechanical support depends on anatomy, ventricular failure, the center and the definitive strategy.

In myocardial infarction, urgent revascularization is performed, but complete rupture is not repaired by PCI alone. In ischemic functional regurgitation without rupture, revascularization may permit recovery and reduction of regurgitation; if instability and severity persist, passive waiting is inappropriate. The emergency Heart Team must decide within hours.

In endocarditis, bactericidal antibiotics are started after blood cultures and adapted to the microorganism and susceptibility profile. Refractory edema, shock, uncontrolled infection or high embolic risk may require urgent surgery. Control of infection does not replace removal of destroyed tissue when valve mechanics are compromised.

Severe acute primary mitral regurgitation generally requires urgent surgery. Repair is preferred when it can provide a rapid and durable result, as in some localized degenerative chordal ruptures. In complete papillary muscle rupture, friable ischemic tissue and destructive endocarditis, replacement with preservation of the residual subvalvular apparatus is often safer. Concomitant revascularization and control of the infectious source are part of the procedure.

TEER has become a rescue option for patients considered inoperable or at extreme risk with graspable anatomy. It can rapidly reduce v waves and congestion, allow weaning from support, or serve as a bridge. Post-infarction registries show success in secondary forms and in partial papillary muscle rupture as well, but mortality and surgical conversion remain particularly high in papillary muscle rupture.

These data are observational and subject to selection of survivors and technically treatable cases. TEER does not remove infected tissue, does not reconstruct a necrotic papillary muscle and may make subsequent surgery more complex. It should be performed with expert imaging, cardiac surgery available and an exit strategy defined before transseptal puncture.

The timing of intervention balances resuscitation and progression. Correcting acidosis, hypoxemia and coagulopathy reduces risk, but waiting for complete normalization is impossible when a lesion is maintaining shock. The decision is dynamic: if vasopressor dose, lactate or respiratory support increase, the window for effective correction is closing.

The choice between repair and replacement must be pragmatic. Repair preserves geometry and avoids a prosthesis, but in an acute setting it must be performed rapidly and with high reliability; a complex reconstruction on necrotic tissue may instead fail. When necessary, replacement with preservation of the chordal apparatus provides immediate competence and may represent the safest strategy in shock, with the type of prosthesis then chosen according to age, bleeding, infection and the need for anticoagulation.

In post-infarction papillary muscle rupture, the specimen and operative appearance may show more extensive necrosis than suggested by echocardiography. Sutures must be anchored in viable tissue, and revascularization is integrated when appropriate. If rupture is partial and localized, repair may be feasible in experienced hands, but it should not prolong already critical cardiopulmonary bypass without a robust prospect of success.

In acute functional regurgitation, the absence of flail tissue sometimes permits a recovery strategy with revascularization, unloading and reassessment. The threshold for intervention depends on persistence of hemodynamic failure, not on a predetermined waiting period. Improvement under maximal support should be verified during controlled reduction of medications before the lesion is considered resolved.

Prognosis, complications and care after the acute phase

Prognosis depends on the cause, the amount of damage already accumulated and how rapidly effective valve competence is restored. Complete papillary muscle rupture has very high mortality because it combines infarction, edema, shock and tissue fragility; degenerative chordal rupture without shock more often permits repair, whereas endocarditis adds sepsis, emboli and a risk of recurrence. Age, renal function, lactate and duration of support reflect systemic severity and contribute to prognostic assessment.

Early complications include respiratory failure, arrhythmias, renal and hepatic ischemia, coagulopathy, stroke, infections and right ventricular failure. After surgery, low output, bleeding, conduction block, residual regurgitation or prosthetic dysfunction may occur. After TEER, surveillance focuses on single-leaflet device attachment, stenosis, atrial septal defect, hemolysis and a persistent jet.

Once the emergency has been overcome, echocardiography before discharge defines true ventricular function after elimination of the low-impedance pathway. Ejection fraction may decrease, an afterload mismatch phenomenon that does not necessarily indicate a new infarction. Heart failure treatment, revascularization, secondary prevention and rehabilitation are optimized.

In patients operated on for endocarditis, antibiotic therapy is completed and the source, complications and need for prophylaxis are assessed. In post-infarction patients, arrhythmic risk stratification is performed after the appropriate interval and recovery. Anticoagulation depends on the prosthesis, atrial fibrillation and other indications, not on the episode of acute regurgitation alone.

Early follow-up assesses symptoms, congestion, the wound or access sites, complete blood count, renal function and imaging. Thereafter, frequency depends on the prosthesis or repair, ventricular function and residual regurgitation. A patient rescued with bridge TEER should be reconsidered for definitive surgery when organ function and operative risk improve; "procedural success" does not automatically close the clinical pathway.

The discharge summary should clearly specify the mechanism, culprit artery or microorganism, type of repair, prosthetic material, residual regurgitation and gradient, and antithrombotic plan. These data are essential if the patient presents again with dyspnea, fever or hemolysis and make it possible to distinguish recurrence from post-infarction ventricular dysfunction.

The main opportunity to improve outcome is to reduce diagnostic delay. New dyspnea, hypotension or edema in the days after myocardial infarction should be considered a mechanical complication until excluded. Likewise, a patient with known prolapse who suddenly develops dyspnea or a febrile patient with new heart failure requires urgent echocardiography rather than deferred outpatient management.

Acute mitral regurgitation demonstrates the limitations of medicine based on a single number. Normal dimensions, preserved ejection fraction and a soft murmur can accompany maximal severity. Correct diagnosis integrates time, anatomy and hemodynamics; effective treatment uses stabilization to reach definitive correction, not to postpone it.