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Acute native aortic regurgitation: clinical presentation, diagnosis and management
  1. Jay Voit1,
  2. Catherine M Otto1,
  3. Christopher R Burke2
  1. 1Division of Cardiology, University of Washington, Seattle, Washington, USA
  2. 2Department of Cardiac Surgery, University of Washington, Seattle, Washington, USA
  1. Correspondence to Dr Christopher R Burke, Cardiac Surgery, University of Washington, Box 356310, Washington, USA; cburke22{at}uw.edu

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Learning objectives

  • To improve knowledge of the aetiology and clinical presentation of acute aortic regurgitation.

  • To discuss the diagnostic approach with suspected acute aortic regurgitation using complementary imaging techniques.

  • To understand basic principles in the management of acute aortic regurgitation including surgery.

Introduction

Acute native valve aortic regurgitation (AR) is a rapidly fatal condition resulting from the sudden loss of valve competency. Acute AR requires prompt intervention yet often is missed because the clinical presentation is not recognised. The large volume of retrograde diastolic flow into a left ventricle (LV) without compensatory dilation results in an abrupt decrease in cardiac output and increase in LV end-diastolic pressure (figure 1). Urgent surgical intervention to restore valve competency and treat the underlying cause is essential. Options for medical stabilisation or palliative care are limited. This review covers the aetiology, haemodynamics, clinical presentation, diagnosis, medical stabilisation and surgical management of patients with acute native valve AR.

Figure 1

Acute AR. Summary of the pathophysiology, clinical presentation, approach to diagnosis and treatment approach for patients with acute aortic valve regurgitation. AR, aortic regurgitation; AVR, aortic valve replacement; BP, blood pressure; CW, continuous wave Doppler ultrasound; CXR, chest X-ray; EDP, end-diastolic pressure; IABP, intra-aortic balloon pump; LV, left ventricle; LVAD, LV assist device; MR, mitral regurgitation; STJ, sinotubular junction of the aorta.

Aetiology

The aortic valve is a complex, three-dimensional (3D) structure that prevents retrograde blood flow from the aorta into the LV during diastole. The valve structure includes the three semilunar leaflets with support provided by the aortic sinuses and sinotubular junction.1 Each valve leaflet is attached in semicircular fashion to its associated sinus with central attachment of each leaflet just below the anatomic aortoventricular junction and commissural attachment at the sinotubular junction. Acute AR can arise from disruption of the valve leaflets themselves (primary AR) or of the aortic root defined as the annulus, sinuses, sinotubular junction and proximal ascending aorta (secondary AR).

The most common cause of primary acute native AR is bacterial endocarditis with destruction of leaflet tissue resulting in perforation, inadequate coaptation or a flail leaflet (table 1).2 3 Less often, a bulky vegetation prevents complete valve closure. Endocarditis also may be complicated by paravalvular abscess formation and aortocavitary fistula formation.4 Less common causes of primary acute AR include deceleration or blunt force chest trauma, spontaneous rupture of a congenital fenestration near the edge of the leaflet and iatrogenic complications.5 6 Fenestrations are focal areas of myxomatous degeneration located peripherally along valve commissure lines that can rupture, disrupting leaflet function.7 8 Iatrogenic complications include leaflet incompetence secondary to balloon aortic valvuloplasty, placement of a catheter across the aortic valve or a transaortic ventricular assist device.9–12

Table 1

Causes of acute aortic regurgitation

The most common cause of acute secondary AR is aortic dissection.2 Regurgitation results from: (1) dilation of the aorta resulting in central cusp non-coaptation, (2) dissection extending into the aortic sinus resulting in cusp prolapse or (3) intimal flap prolapse into the valve orifice preventing normal cusp closure.13 Patients with inherited connective tissue disorders, such as Marfan or Loeys-Dietz syndrome and those with a congenital bicuspid aortic valve typically present with chronic AR but also are at higher risk of aortic dissection than the general population and can present with acute AR.14 15 Rarely, aortic vasculitis results in acute AR, although these patients usually have a more chronic disease course.16–19

There are many important causes of AR in the non-native valve, like paraprosthetic AR after TAVI deployment, which this review does not cover.

Haemodynamics

Acute AR results in a typical haemodynamic cascade. Backflow of blood across the aortic valve in diastole leads to a decreased forward stroke volume and cardiac output because the normal-size LV has a fixed total stroke volume capacity. When the regurgitant volume, typically 50% or more of the total stroke volume, is subtracted from the total stroke volume, forward cardiac output can drop to less than ½ of normal with resultant systemic hypotension and cardiogenic shock. This differs from chronic AR in which the LV has slowly dilated over many years to compensate for the regurgitant volume allowing maintenance of a normal forward stroke volume despite a large regurgitation fraction (figure 2). A mixed haemodynamic profile with a larger LV size may be seen in patients with acute AR superimposed on chronic moderate AR, for example, a patient with a bicuspid aortic valve who develops endocarditis.

Figure 2

aAcute versus chronic aortic regurgitation (AR). The causes of acute (left) and chronic (right) AR differ significantly as shown by these examples of acute AR due to endocarditis and chronic AR due to a congenital bicuspid aortic valve. The Doppler AR jet width is related to severity, not acuity, but with acute AR, the left ventricle (LV) often is not dilated in contrast to the severely dilated and more spherical shape of the LV when chronic severe AR is present. The density of the continuous wave (CW) Doppler signal relative to antegrade flow reflects the severity of regurgitation. However, with acute AR, the diastolic slope of the AR signal is steep, which reflects the rapid rise in LV diastolic pressure and fall in aortic diastolic pressure, with nearly equalisation of pressure at end-diastole, due to the incompetence aortic valve and a non-compliant LV. The presence of holo-diastolic flow reversal in the proximal abdominal aorta in this example of acute AR is consistent with severe AR. Holo-diastolic flow reversal in the descending thoracic aorta, as in this example of chronic AR, may be seen with either moderate or severe regurgitation.

The acute backflow of blood into a normal size LV also results in a sudden increase in LV end diastolic pressure (LVEDP). This propagates upstream leading to elevated left atrial pressure, elevated pulmonary artery (PA) pressure and eventual right ventricular pressure overload and systolic dysfunction. These perturbations can be further exacerbated by pre-existing conditions, such as a stiff LV seen with hypertension or aortic stenosis.20 Acute compensatory mechanisms include increased adrenergic tone, resulting in tachycardia and hypercontractility.21 In contrast, with chronic AR, the LV has time to dilate and increase compliance so that LVEDP remains low even with severe AR.

Acute AR also adversely affects coronary blood flow. The low aortic diastolic pressure, high resting heart rate and augmented myocardial oxygen demand result in impaired resting coronary flow and diminished coronary flow reserve.22

Clinical presentation

Patients with acute AR typically present with pulmonary oedema or cardiogenic shock. Symptoms are non-specific and include shortness of breath, altered mental status, weakness and fatigue. At the bedside, tachypnoea, hypoxaemia, cool extremities and low urine output are common.23 In addition, patients may have symptoms due to the underlying cause of AR, such as fever or embolic events in patients with endocarditis or chest pain and unequal peripheral pulses in those with an aortic dissection.23 24 Features of the clinical history that should raise concern for acute AR include a personal or family history of aortic disease, hypertension, a bicuspid aortic valve or risk factors for endocarditis, including pre-existing valve disease or intravenous drug use.

Physical examination is challenging in patients with acute AR. In contrast to chronic AR, systolic blood pressure is low and pulse pressure may be narrow, because forward stroke volume is low. The typical high-pitched holo-diastolic murmur of chronic AR is absent. Instead, there is a brief soft low-pitched diastolic murmur due to rapid equalisation of aortic and LV diastolic pressures and a soft S1 due to premature closure of the mitral leaflet. Additionally, a loud P2 secondary to elevated pulmonary pressures, a diminished A2 due to leaflet non-coaptation and an S3 gallop can be heard. However, these findings are difficult to appreciate in a patient who is tachycardic and dyspnoeic or intubated.23

As might be expected, the presentation of acute cardiopulmonary collapse typically over-rides other considerations. These patients often are admitted to the critical care unit with an incorrect diagnosis of acute pulmonary failure or sepsis. Thus, it is incumbent on the clinician consider the possibility of acute AR in any patient with acute cardiopulmonary decompensation.

Diagnostic imaging

The key to prompt diagnosis of acute AR is imaging the aortic valve and aorta with echocardiography or CT, depending on the specific clinical presentation. In patients with suspected endocarditis, echocardiography allows rapid imaging of the aortic valve and sinuses, the presence and severity of AR, LV size and systolic function, and estimated pulmonary systolic pressures. When transthoracic echocardiography is non-diagnostic, it is appropriate to proceed to transoesophageal imaging.

In patients with suspected aortic dissection, the preferred initial imaging approach is contrast CT angiography of the aorta because it provides visualisation of the entire length of the aorta and branch vessels, facilitating surgical planning, and can be done quickly. Transoesophageal echocardiography (TOE) complements the CT data and is often used in the immediate preoperative and postoperative setting by qualified cardiac anaesthesiologists. With acute AR, the minimal number of tests needed for diagnosis and surgical planning are recommended to avoid unnecessary delays in definitive treatment.

Echocardiography

The echocardiographic examination starts with detailed imaging of the aortic valve leaflets to detect structural changes, such as perforation or vegetation, or abnormal motion including flail leaflet or failure of central coaptation (figure 2). Visualisation of the valve opening in systole in a short-axis two-dimensional or 3D view is used to determine if the valve is tricuspid or bicuspid and to examine the degree of leaflet thickening and calcification. When endocarditis is a clinical concern, TOE has a higher sensitivity than transthoracic echocardiography for detection of vegetations and diagnosis of paravalvular abscesses.

Next attention is directed towards the aorta, evaluating shape, size and for any evidence of dissection flap. Diameters at the annulus, or LV outflow tract, aortic sinuses, sinotubular junction and proximal ascending aorta are measured. More distal aortic segments including arch, descending thoracic and proximal abdominal are sometimes visualised with TOE, but typically some segments are missed and branch vessels are rarely seen.

Other key elements of the echocardiographic exam include mitral valve interrogation for high frequency diastolic fluttering of the anterior leaflet from an AR jet impact or early mitral valve closure due to a high LVEDP. The exam also includes evaluation of LV size and systolic function, which are typically normal in acute AR, pulmonary pressures and right ventricular function. Finally, attention should be made to the pericardial effusion which can indicate aortic dissection.21 25

Doppler findings in patients with acute AR differ significantly from those seen with chronic AR. Although the colour Doppler AR jet width fills much of the LV outflow tract, this finding may not be recognised because the lower velocities simulate normal LV inflow. The AR jet origin may provide clues about the cause of regurgitation; a central jet and stretched leaflets suggests aortic dilation, an eccentric jet suggests a flail leaflet and a jet originating on the leaflet itself suggests perforation. A colour Doppler vena contracta width >0.6 cm or a jet diameter >65% of LV outflow tract diameter is consistent with severe acute AR. Perhaps the quickest and most useful Doppler sign of acute severe AR is the presence of holo-diastolic flow reversal in the descending thoracic aorta that should be checked for early in the examination.26 Further quantitation is not needed in a patient with haemodynamic compromise.

Typically, the density of the continuous-wave Doppler AR signal in diastole equals the density of antegrade systolic flow, reflecting the large regurgitant volume. In addition, the diastolic slope of the AR signal is steep because there is rapid decline in aortic pressure with a rapid increase in LV pressure over the diastolic time interval. In fact, the end-diastolic velocity in patients with acute severe AR approaches zero as the aortic and LV pressures equalise. In contrast, in asymptomatic patients with chronic AR, even when severe, the continuous wave Doppler signal shows a flat diastolic slope and high end-diastolic velocity.26

Other supportive Doppler findings on echocardiographic imaging include diastolic mitral regurgitation in association with premature mitral valve closure and transmitral and pulmonary venous flow patterns consistent with a high LVEDP.27 28

Computed tomography

The use of ECG-gated multidetector CT (MDCT) angiography in acute AR is recommended as the initial test in patients with suspected aortic dissection given its high sensitivity/specificity (95%–98%) (figure 3).29 MDCT can be performed quickly, with a scan taking <1–5 s. The generated 3D data set allows for accurate reconstruction and quantification of an area of interest, even in oblique planes such as a tortuous aorta with a higher spatial resolution (<1 mm or 0.25–0.625 mm) compared with transthoracic echocardiogram (TTE) (1–3 mm).29 Orthogonal measurements from reconstructed images include diameter of the aortic annulus, aortic sinus, sino-tubular junction and ascending aorta. Other findings include presence or absence of an intimal flap, site of intimal tear, presence and degree of calcification, extent of dissection, involvement of branch vessels and contrast enhancement of the false lumen.30

Figure 3

CT imaging of aortic dissection with acute AR. Contrast CT imaging of the aorta with ECG-gating is the initial diagnostic step in most patients with acute aortic regurgitation secondary to aortic disease. CT imaging is rapidly available at most medical centres and provides accurate diagnosis of aortic dissection and other acute aortic syndromes. Standard tomographic images are obtained in coronal, sagittal and cross-sectional views as shown for the ascending aorta and left ventricle in panel A and the descending thoracic aorta in panel B. Full volume three-dimensional images of the aorta also can be generated and rotated as shown in panels C and D to show the relationship of aortic dilation and the dissection flap in relation to the sino-tubular junction, coronary ostia and aortic valve. In addition, the distal extent of the dissection and involvement of branch vessels is visualised. Cross-sectional images orthogonal to the long and short axis planes of the aortic root also can be used for accurate aortic dimension measurements. AR, aortic regurgitation.

If needed for clinical decision making, MDCT also can evaluate aortic valve leaflet morphology, including estimated leaflet number, calcification and size.30 Cine-mode imaging allows assessment of leaflet mobility, although requires higher radiation.29 Estimation of regurgitation severity can be performed via planimetry of an estimated regurgitant orifice area (EROA). There is reasonable correlation between CT planimetry of EROA and TTE Doppler-derived regurgitation severity, especially when AR is moderate to severe.30 31 LV size and function can be estimated via orthogonal measurements and help distinguish acute from chronic AR. Drawbacks to CT imaging include limited temporal resolution and lack of Doppler-derived haemodynamic data. It should be noted that after-hours CT service expertise with ECG-gated studies and retrospective imaging protocols is critical for proper study execution.

Other modalities

Cardiac magnetic resonance aortic angiography is rarely used in the evaluation of acute AR due to patient instability. Aortic aortography at the time of cardiac catherisation is appropriate if the initial diagnosis was an acute coronary syndrome, with coronary angiography suggesting propagation of an aortic dissection flap into the coronary artery, or when acute AR occurs intraprocedurally, for example, iatrogenic AR due to a catheter of ventricular assist device.

Patient stabilisation prior to surgical intervention

Surgical intervention is the only definitive therapy for acute regurgitation of a native aortic valve, although palliative care can be considered depending on the clinical situation and comorbid conditions. Medical stabilisation prior to intervention is challenging and a major goal should be to minimise the time to definitive therapy.32 Haemodynamic monitoring in the intensive care unit is recommended with careful titration of inotropic agents and vasodilators to augment cardiac output, support end-organ perfusion and reduce LVEDP.33 Together, these agents increase stroke volume (inotropes via contractility, vasodilators via afterload reduction), increase heart rate (inotropes via chronotropy) and decrease the regurgitant fraction (vasodilators via afterload reduction). Although beta-blockers are often administered with acute dissection when AR is not severe, they are contraindicated in acute severe AR due to their negative inotropic effects and longer diastolic interval, which results in greater severity of AR.33

Temporary mechanical support is not beneficial for management of patients with acute AR. Intra-aortic balloon pumps are contraindicated due to their inflation in diastole, which worsens the degree of AR.33 Similarly, the efficacy of LV-assist devices is blunted given the persistent retrograde filling of the LV via the incompetent aortic valve. Extracorporeal membrane oxygenation (ECMO) is theoretically feasible in acute AR as it can replace native cardiac output without dependence on valvular competency. It is, however, relatively contraindicated due to challenges with LV congestion resulting from aortic valve incompetence.34 Nevertheless, there have been rare case reports of ECMO being successfully used as bridge-to-intervention in patients with acute AR.35 36

Surgical management

Clinical experience supports the paradigm that prompt surgical intervention for patients with acute AR is lifesaving. Mortality rates for acute AR due to aortic dissection or endocarditis are extremely high and there are no other effective therapies, so that randomised controlled clinical trials of surgery versus no intervention are not possible or ethical. When feasible, valve or root repair is preferable to aortic valve replacement (AVR) (figure 4). Primary AR may be amenable to repair in the absence of significant leaflet destruction or paravalvular abscess. Secondary AR often is corrected by restoring the normal size and shape of the aorta, with preservation of the native aortic valve, either with resuspension or reimplantation. Currently, transcatheter aortic valve implantation is not recommended for treatment of patients with acute severe native AR.

Figure 4

Surgical management of acute AR. In patients with aortic pathology above the level of the aortic sinus causing acute AR, root repair with commissural resuspension and replacement of the ascending aorta is indicated (top). When aortic pathology extends into the aortic sinus or a genetic aortopathy is at play, replacement of the root with a graft and resuspension of the valve and reimplantation of the coronaries is preferred (middle). If the aortic valve itself is the aetiology of acute AR and unable to be repaired, then aortic valve replacement is performed (bottom). AR, aortic regurgitation.

Valve repair for acute severe primary AR

Primary acute severe AR most often is due to endocarditis, with leaflet tissue destruction and annular abscess formation. Thus, valve repair usually is not feasible and AVR continues to be the mainstay therapy for acute primary AR.

A few patients with acute primary AR may have valve anatomy amenable to valve repair. For example, the patient with a congenital fenestration in the leaflet that ruptures and extends into the load-bearing leaflet surface. Surgical repair of the aortic valve itself focuses on two main principles: aortic annular reduction (annuloplasty) and leaflet repair. Annuloplasty can be achieved in several ways and common techniques include external aortic ring or internal annuloplasty ring.37 38 Leaflet repair depends on the pathology encountered (perforation, prolapse and retraction). Perforation can be corrected with a patch repair. Prolapse can be addressed with plication, in which sutures are used to reduce the leaflet ‘length’ (or free margin length); this raises the ‘effective’ leaflet height, helping to increase leaflet coaptation.39 There is some enthusiasm for aortic valve leaflet reconstruction using a variety of materials such as autologous or bovine pericardium. However, there are significant concerns regarding the durability of this approach as pericardial aortic valve leaflet reconstruction tend to calcify over time and little is known about long-term durability.40 It must be noted that valve repair can result in longer cross-clamp time, which may be poorly tolerated by critically ill patients, thus the decision between repair and replacement must be highly individualised in this population.

Aortic repair for acute severe secondary AR

The common cause of secondary AR is acute type A aortic dissection with an intimal entry site in the proximal ascending aorta. Functionally, AR results from one of three pathologic states: (1) root dilation with normal leaflet motion and valve non-coaptation; (2) dissection into the aortic sinus with excessive leaflet prolapse; or (3) intimal flap prolapse into the valve coaptation zone with leaflet restriction.13 Typically, acute secondary AR resolves with resuspension of the aortic commissures and treatment of the ascending aortic dissection with reconstruction of the aortic root; it is rare that valve replacement is necessary.

In patients with dilation of the aortic sinuses, extension of the dissection flap into the sinuses or a known (or suspected) genetic aortopathy, stabilisation of the aortic annulus with replacement of the aortic sinuses and coronary reimplantation is needed. This classically involves a Bentall procedure, where both the aortic valve and sinuses are replaced, typically with a valved composite graft (either mechanical or biological valve). However, valve-sparing root replacement (VSRR) approaches can be done in experienced centres during type A dissection repair in patients with appropriate aortic valve anatomy and clinical condition. VSRR approaches include reimplantation of the aortic valve within a sinus graft (David procedure) or remodelling of the sinuses around the valve tissue (Yacoub procedure). VSSR has been shown to be safe during acute dissection and should be considered in young patients that require root replacement.31 The annulus is reduced and stabilised during VSRR by selection of graft size (smaller graft size leads to greater reduction in annular size). However, VSSR may not be feasible at less experienced centres and is more often performed as an elective procedure in patients with aortopathy and progressive aortic dilation.

Non-repairable aortic valve

In patients with acute primary AR due to infective endocarditis, it is critical to obtain a detailed assessment of valve anatomy and the paravalvular region because the presence of an aortic root abscess may significantly alter the surgical plan and choice of prosthetic valve. If significant aortic annular abscess and tissue destruction is present, a root replacement is typically mandated. A biological conduit, such as an aortic homograft or stentless bioprosthesis, is appealing in this situation and probably has a lower reinfection risk than prosthetic alternatives. In general, the patient is counselled on valve choice (mechanical vs bioprosthetic) as for any patient undergoing AVR. Additional demographic factors as well as psychosocial issues, including history of substance use and ability to adhere to anticoagulation, influence the decision of valve choice, but there is no convincing evidence that the risk of persistent infection is higher with a mechanical versus stented bioprosthetic valves. In fact, a recent meta-analysis suggests that patients with a stented bioprosthetic valve are at higher risk of endocarditis than patients with a mechanical AVR.41 In highly selected patients without aortic root dilation, a Ross procedure using a pulmonary homograft may be considered. It should be emphasised that performance of a Ross procedures requires intense postoperative follow-up and blood pressure control and therefore may be a poor choice in patients with complicated psychosocial issues.

Perioperative considerations

Prompt surgery is critically important as acute AR is often poorly tolerated. The desire for ‘preoperative optimisation’ must be balanced against the need for urgent/emergent intervention in the rapidly deteriorating patient in cardiogenic shock. With teamwork, there typically is enough time to complete an appropriate preoperative work-up and counsel the patient and family accordingly without excessive delays in intervention.

Acute AR makes the myocardium more vulnerable to the operative ischaemic period due to the reduced diastolic coronary perfusion pressure and increased myocardial oxygen demands. Myocardial protection in the operating room can be challenging. Administering ‘antegrade’ cardioplegia in the aortic root is ineffective and therefore retrograde cardioplegia delivery (via coronary sinus) and direct ostial antegrade are typically given.42 43

Perioperative TOE assessment is critical to evaluate the repair immediately after the procedure and before closing the chest in the operating room. Typically, postrepair AR is ≤1+ (mild) is considered acceptable as AR ≥2+ is associated with subsequent development of significant (≥3+) AR.44 It is also important to assess postrepair aortic valve systolic gradients to avoid patient–prosthetic mismatch with a prosthetic valve or excessive annular reduction with a reconstruction procedure. Long-term periodic echocardiographic imaging is especially important following aortic valve repair to assess for late failure given the limited experience with these approaches. An effective heart valve team ensures coordination of surgical care and long-term patient follow-up.

Prognosis and long-term outcomes

Patients who present with acute AR are a heterogenous population due to the diverse causes of acute AR. Published data typically looks at the aetiological group as a whole, such as aortic dissection or endocarditis, and outcomes are rarely stratified by variables such as acute AR. Some data can be extrapolated from the results but must be interpreted cautiously.

In the large, multicentre, multinational International Registry of Acute Aortic Dissection, >25% of patients with a type-A dissection had hypotension and 15% presented with shock. These groups had a higher in-hospital mortality, with an OR of 1.95 for hypotension and 2.69 for shock. In-hospital mortality for surgical management was 18% and for medical management was 57%. Of the surgical patients who survived to discharge, there were 96% and 90.5% 1-year and 3 year survival, respectively.45

The International Collaboration on Endocarditis and European Infective Endocarditis registries note aortic valve involvement in 32% of endocarditis cases and heart failure in 15%–32% of patients. Heart failure and pulmonary oedema were associated with an increased risk of mortality with odds-ratios of 2.09 and 1.79, respectively, while surgery was associated with a decreased risk. In-hospital mortality for all-comers was 17%.46 47 No long-term data were reported.

Conclusion

Acute native AR is a life-threatening condition, most commonly resulting from aortic dissection or endocarditis. Rapid clinical diagnosis is an essential part of the treatment pathway and should considered in any patient with signs and symptoms of unexplained cardiogenic shock or elevated LVEDP. TTE is the preferred diagnostic modality, although TOE and CT can be complementary in certain scenarios. The definitive management for acute AR is surgery. Surgical repair, rather than replacement, is first-line and can be achieved in secondary AR and in primary AR without extensive leaflet/perivalvular destruction. In non-repairable valves, replacement with bioprosthetic/mechanical valve or homograft can be performed.

Key messages

  • There are a multitude of aetiologies that can lead to acute aortic regurgitation, although endocarditis and type A aortic dissection are the most common.

  • Acute aortic regurgitation is an important cause of acute cardiorespiratory decompensation. It is characterised by a reduced cardiac output and elevated left ventricle end-diastolic filling pressures. This results in cardiogenic shock and respiratory insufficiency.

  • Diagnosis of acute aortic regurgitation is multimodal. It typically involves the use of transthoracic echocardiography and identification of a broad regurgitant jet with a steep regurgitant slope on Doppler and diastolic flow reversal in the descending aorta. CT imaging is particularly helpful in cases of dissection due to its ability to characterise the extent of dissection and point of propagation.

  • Intensive care unit care can help to stabilise patients with acute aortic regurgitation, but definitive management is surgical.

  • Surgical repair is preferred over valve replacement and is typically performed for secondary aortic regurgitation resulting from type A aortic dissection.

  • Valve replacement is frequently required in cases of primary aortic regurgitation such as endocarditis due to significant leaflet destruction.

  • A multidisciplinary team composed of both cardiologists and CT surgeons is critical in management of acute aortic regurgitation.

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Footnotes

  • Twitter @chrisryanburke

  • Contributors All authors contributed to manuscript inception, drafting, and final revisions.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

  • Author note References which include a * are considered to be key references.