Acute aortic regurgitation

Article written and reviewed by Dr Luca Moretti

Acute aortic regurgitation is the sudden loss of diastolic competence of the aortic valve. When regurgitation is severe, blood returns into a left ventricle that has had no time to dilate or increase its compliance: filling pressure rises rapidly, forward output falls, and pulmonary edema, ischemia and shock may develop. It is a hemodynamic syndrome distinct from chronic aortic regurgitation, not simply a more symptomatic version of the same lesion.

Diagnosis is difficult because the classic findings of chronic regurgitation - a dilated ventricle, wide pulse pressure, bounding pulses and a long diastolic murmur - may be absent: rapid equalization between aortic and ventricular pressure makes the murmur short and sometimes faint. In the presence of sudden pulmonary edema, hypotension and an apparently nonstenotic valve, acute aortic regurgitation must therefore be actively sought without waiting for textbook signs.

The two causes that must be excluded immediately are infective endocarditis and type A aortic dissection, both capable of causing complications extending far beyond the valve and requiring an urgent surgical pathway. In this setting, pharmacological stabilization serves as a bridge to control of the mechanical lesion, not as definitive therapy.

Causes and anatomy of the lesion

Infective endocarditis may perforate a cusp, destroy its free edge, rupture a fenestration or cause flail through tearing. Infection may extend to the annulus, forming an abscess, pseudoaneurysm or fistula, and may reach the conduction system. Large vegetations may also embolize to the brain, spleen, kidneys or coronary arteries.

Hemodynamic severity does not depend on the visible size of the vegetation: a small perforation in an unfavorable position may create a large orifice, whereas mobile vegetations may intermittently interfere with coaptation. Negative blood cultures also do not exclude endocarditis when previous antibiotics, fastidious microorganisms or inadequate culture techniques reduce sensitivity.

Type A dissection causes regurgitation through different mechanisms: acute root dilation with commissural separation, detachment of a commissure, prolapse of the flap through the orifice or extension toward the annulus. The valve may be anatomically normal and regain competence after commissural resuspension and root reconstruction; in other situations replacement is necessary.

Sudden chest or interscapular pain, pulse deficit, blood pressure difference, a new neurological deficit or malperfusion support the diagnosis of dissection, but none is mandatory. Tamponade, coronary ischemia from ostial involvement and acute regurgitation may dominate the clinical picture and mask pain.

Blunt chest trauma may tear a cusp or commissure, sometimes with delayed diagnosis if the initial regurgitation is not fulminant. Penetrating injuries are rare and often associated with multiple cardiac injuries. The history should include high-energy accidents, sternal compression and recent procedures.

Iatrogenic causes include cusp injury during septal or mitral surgery, TAVI, ablation procedures, ventricular septal defect interventions and complex catheterization. After TAVI, massive paravalvular regurgitation, embolization, malposition, annular rupture or coronary obstruction may cause instability; the mechanism guides post-dilation, a second device, closure or surgery.

A bioprosthesis may develop sudden leaflet tear, endocarditis or thrombosis; a mechanical prosthesis may become obstructed by thrombus or pannus, causing regurgitation or obstruction. In this setting, Doppler findings should be compared with the baseline examination and integrated with fluoroscopy or CT when time and stability permit.

Less common causes include destructive aortitis, rupture of a fenestration or of a sinus of Valsalva aneurysm, and complications of mechanical support devices. Etiologic diagnosis is not merely descriptive: it determines antibiotics, the extent of surgery, the need for debridement and treatment of the aorta.

Regurgitation may arise on a previously normal valve or worsen a chronic lesion. In the latter case the ventricle is already dilated, but the new loss of coaptation produces an increment that exceeds its reserve. The distinction between acute-on-chronic disease affects interpretation of chamber size: a large cavity does not justify excluding a recent emergency.

The cause also modifies extracardiac risk. In endocarditis, emboli, infective aneurysms and metastatic foci should be sought; in dissection, cerebral, coronary, visceral and peripheral malperfusion. This information should not delay correction of shock, but it changes cannulation, cerebral protection, antibiotics and the operative sequence.

Pathophysiology and clinical presentation

The regurgitant volume is abruptly added to pulmonary venous return and enters a ventricle that is still normal in size and lies on the steep portion of the pressure-volume curve. Consequently, even modest increases in volume produce large rises in pressure, rapidly bringing left ventricular end-diastolic pressure close to aortic pressure and above atrial pressure.

When ventricular pressure exceeds atrial pressure before the onset of systole, the mitral valve closes prematurely. Premature mitral valve closure partly protects the pulmonary circulation from direct reflux but shortens filling and reduces output. If pressure continues to rise, diastolic mitral regurgitation into the atrium may develop.

Because total stroke volume does not increase enough to compensate for regurgitation, the forward component falls and a sympathetic response with tachycardia and vasoconstriction is activated. Moderate tachycardia shortens diastole and limits regurgitant volume, but increases oxygen demand; marked vasoconstriction, however, raises afterload and worsens the proportion of blood returning to the ventricle.

Aortic diastolic pressure falls while ventricular pressure rises: the coronary perfusion gradient narrows from both sides. Tachycardia, hypotension and increased wall stress promote ischemia even in the absence of coronary artery disease. Coronary involvement by dissection or septic emboli may add a true myocardial infarction.

Atrial and pulmonary capillary pressures rise and cause interstitial and alveolar edema. Atrial compliance is insufficient to buffer the acute increase. Hypoxia and acidosis worsen contractility and pulmonary vascular resistance, creating a vicious circle that may progress to right ventricular dysfunction and multiorgan failure.

Sudden dyspnea is the most common manifestation. The patient may present with orthopnea, diffuse crackles, frothy sputum, hypoxemia and marked respiratory distress. An initial chest radiograph may show no cardiomegaly because the ventricle is not dilated; congestion may be asymmetric and mistaken for pneumonia.

Signs of hypoperfusion include hypotension, a weak pulse, cold skin, oliguria, confusion and elevated lactate. Pulse pressure may be normal or reduced. Tachycardia is common, whereas an unusually low heart rate may worsen regurgitation or indicate involvement of the conduction system.

The diastolic murmur is often short, early and soft. Rapid decline of the pressure difference truncates the murmur; a third heart sound and an apical mid-diastolic murmur may be present. In noisy pulmonary edema and in a ventilated patient, auscultation is even less sensitive.

Fever, chills, petechiae, embolic lesions, new atrioventricular block and immunologic phenomena suggest endocarditis. Tearing pain, syncope, neurological deficits, tamponade or malperfusion suggest dissection. The absence of fever or pain does not exclude these diagnoses, particularly in older, immunocompromised or already treated patients.

In older and frail patients, presentation may be limited to delirium, hypotension or worsening renal function. During pregnancy and postpartum, pain and dyspnea require attention to dissection, especially in patients with aortopathy. After a cardiac procedure, sudden difficulty weaning from support or a new jet should be considered iatrogenic until proven otherwise.

Clinical severity may fluctuate with blood pressure and heart rate. A vasodilator may temporarily attenuate the jet and improve oxygenation without reducing the anatomical defect; a hypertensive crisis may do the opposite. Imaging reports should document the hemodynamic state at the time, and a decision should not be reversed because of transient improvement achieved in intensive care.

Urgent diagnosis

The initial approach simultaneously addresses airway, breathing and circulation. ECG, oxygen saturation, blood pressure in both arms when possible, venous access, blood gas analysis, complete blood count, renal and liver function, lactate, troponin and chest radiography are obtained without delaying bedside echocardiography. If infection is suspected, at least three sets of blood cultures are collected before antibiotics when this does not introduce a dangerous delay.

Transthoracic echocardiography identifies regurgitation, global function, ventricular dimensions, pulmonary pressure, the pericardium and gross signs of dissection or vegetation. A nondilated ventricle with a large jet and elevated pressures supports an acute process; a large ventricle suggests a pre-existing chronic component on which deterioration may have superimposed.

In severe acute regurgitation, the most alarming findings are:

• Premature mitral valve closure, particularly when marked.
• Diastolic mitral regurgitation due to reversal of the atrioventricular gradient.
• Short pressure half-time, often less than 200 ms, interpreted in context.
• Nondilated left ventricle despite extensive regurgitation.
• Prominent diastolic flow reversal in the descending aorta.
• Causal lesion such as perforation, flail cusp, vegetation, abscess or intimal flap.

Jet area alone may underestimate an eccentric or pressure-dependent lesion. Quantitative criteria validated in chronic disease are technically difficult and sometimes misleading in hemodynamic instability; the decision should integrate anatomy, hemodynamic signs, Doppler findings and the clinical picture. An orifice that is not extremely large can still be lethal in a stiff ventricle.

Transesophageal echocardiography provides superior resolution for vegetations, perforations, abscesses, prosthetic dehiscence and the proximal aorta. It is often the decisive test in the operating room or intensive care unit. Sedation, hypoxemia and instability require a prepared team; if dissection is evident and the patient is collapsing, TEE may be completed directly in the operating room.

When dissection is suspected, CT angiography from the aortic root to the iliac arteries is rapid and defines extent, branch involvement, malperfusion and procedural planning, provided transport is safe. TEE is preferable in a patient who is too unstable. Magnetic resonance imaging has excellent accuracy but generally has no role in the diagnosis of an unstable emergency.

Catheterization and aortography are not first-line tests and may delay intervention or propagate a dissection. Preoperative coronary angiography is omitted when the delay outweighs its benefit; CT or intraoperative assessment may replace it. An apparent acute coronary syndrome should not automatically lead to catheterization before dissection has been excluded.

Differential diagnoses include acute mitral regurgitation, septal rupture, ischemia with pulmonary edema, myocarditis, pulmonary embolism, ARDS and sepsis. Color Doppler and valve analysis distinguish the mechanism, but multiple lesions may coexist: a dissection may cause tamponade, regurgitation and ischemia in the same patient.

Invasive pulmonary capillary pressure measurement may show prominent waves and elevated pressure, but it is nonspecific and a pulmonary artery catheter should not precede echocardiography. If already in place, cardiac output and venous oxygen saturation help titrate bridging treatment. Placement carries risks and does not replace anatomical identification.

Lung ultrasound documents B-lines and pleural effusions and allows congestion to be followed, without distinguishing its cause. Focused ultrasound does not replace a complete valve study: an improperly set color box or an eccentric jet may be missed. Emergency care requires rapid acquisition and review by an experienced echocardiographer.

Stabilization and definitive treatment

A patient with severe acute regurgitation should be transferred immediately to a center with cardiac surgery. Arterial monitoring, selected central venous access, serial perfusion assessment and early communication with the surgeon, anesthesiologist, imaging team and infectious disease specialist reduce delays. The pathway should not wait for complete deterioration before being activated.

Oxygen, noninvasive ventilation or intubation treat hypoxemia, but anesthetic induction may precipitate collapse through vasodilation and loss of sympathetic tone. Positive-pressure ventilation reduces preload and afterload, with potentially beneficial or harmful effects depending on cardiac output. Hemodynamic preparation and the presence of experienced personnel are essential.

A titratable vasodilator such as nitroprusside may lower vascular resistance, increase forward stroke volume and reduce regurgitant volume if blood pressure permits. In hypotensive patients, dobutamine may support contractility and heart rate. Norepinephrine may be necessary to maintain a minimum perfusion pressure, but excessive vasoconstriction increases afterload.

Diuretics relieve congestion but do not correct the orifice and may further reduce output. A poor response is expected when pressures are driven by massive regurgitation. Therapy should be titrated to perfusion, oxygenation and echocardiographic findings, not to pursuit of an unattainable euvolemia before correction.

Bradycardia prolongs diastole and increases the time available for regurgitation. Beta-blockers are therefore not a treatment for isolated acute regurgitation. In dissection, however, reducing dP/dt and heart rate limits aortic wall stress: anti-impulse control is balanced against output and regurgitation within an immediate surgical strategy.

Intra-aortic balloon counterpulsation is contraindicated because diastolic inflation raises aortic pressure and regurgitant flow. Alternative mechanical support is complex: transvalvular devices may interfere with the valve or flap and ECMO increases afterload. In exceptional cases an experienced team may use these as a bridge with appropriate ventricular unloading, but they are not standard solutions.

Urgent surgery is the definitive treatment for severe acute regurgitation. In endocarditis it includes radical debridement, replacement or rarely repair, annular reconstruction if destroyed, and treatment of abscesses or fistulas. Prosthesis selection considers age, infection, anticoagulation and anatomy; no material eliminates the risk of reinfection without removal of infected tissue.

In dissection, the procedure treats the ascending aorta and restores valvular competence. If the cusps and root are salvageable, resuspension and supracoronary replacement may preserve the valve; root destruction or primary root disease requires root replacement, sometimes valve-sparing in expert hands. The priority is to eliminate the segment at risk of rupture and correct malperfusion and regurgitation.

Nonsevere acute regurgitation in a stable patient may be managed according to the cause, but requires close surveillance because perforations and aortic lesions may progress. In endocarditis, heart failure, uncontrolled infection and prevention of embolism are independent domains of the surgical indication. Timing also considers neurological complications and bleeding risk.

A nonhemorrhagic ischemic stroke does not necessarily mandate postponing surgery for weeks when heart failure or uncontrolled infection makes surgery lifesaving. Intracranial hemorrhage, infarct size and infective aneurysms change the balance. The decision requires neurology, brain imaging and cardiac surgery input, with close reassessment.

Interhospital transfer is a high-risk phase. It should occur with monitoring, titratable drugs, ventilation capability and direct communication with the receiving center; nonessential studies should not delay transfer. In dissection, control of pain and hemodynamic stress continues during transport without compromising output.

Complications, postoperative care and prognosis

The dominant immediate complication is cardiogenic shock. Hypotension, ischemia and acidosis further depress contractility; the rise in catecholamines increases vascular resistance and regurgitation. Serial lactate, urine output and perfusion assessment are more useful than a single apparently acceptable blood pressure reading.

Pulmonary edema may become refractory and require invasive ventilation. Elevated atrial pressure may produce functional mitral regurgitation and worsen congestion. After correction, the lungs may take time to clear edema and the inflammatory response, but the nondilated ventricle often recovers rapidly if ischemic injury has not occurred.

Reduced coronary perfusion causes subendocardial ischemia; coronary dissection, septic embolism and compression by an abscess cause focal injury. New ECG changes or arrhythmias should be interpreted together with anatomy. Atrioventricular block in aortic endocarditis suggests perianular extension and increases urgency.

Dissection may cause tamponade, stroke, mesenteric, renal or peripheral ischemia. In endocarditis, cerebral emboli, infective aneurysms, splenic infarction and glomerulonephritis may occur. These complications modify technique and timing, but often do not eliminate an indication driven by valvular heart failure.

After surgery, vasoplegic syndrome, bleeding, renal failure, stroke, heart block, arrhythmias and ventricular dysfunction may occur. Echocardiography verifies prosthetic or repair function, absence of leak, ventricular function and the pericardium. Antibiotics and microbiological monitoring continue according to the causative organism and infected material.

Without correction, the prognosis of severe acute regurgitation is very poor. Outcomes depend on the cause, duration of shock, age, neurological and multiorgan injury, and complexity of reconstruction. Early diagnosis before persistent hypotension provides the best chance of survival and recovery.

Post-discharge follow-up includes a baseline echocardiogram, aortic surveillance, monitoring of the prosthesis or repair, rehabilitation and endocarditis prevention. In survivors of dissection, the entire residual aorta requires lifelong imaging; after endocarditis, recurrent fever and new embolic signs require immediate evaluation.

Rehabilitation should consider deconditioning, intensive-care neuropathy and neurological or renal sequelae. Intensity is guided by ventricular function, stability of the repair and the residual aorta. Rapid hemodynamic recovery does not always coincide with functional recovery after prolonged shock.

Prevention of recurrence is etiologic: eradication of the source and oral health after endocarditis, blood pressure control and genetic assessment when indicated after dissection, and technical review after iatrogenic injury. The patient should receive documentation describing the cause, procedure, microorganism, prosthesis and imaging plan, because this information affects every future emergency.