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Mini-invasive Surg 2020;4:53. 10.20517/2574-1225.2020.41 © The Author(s) 2020.
Open Access Review

Percutaneous mitral valve repair in acute mitral regurgitation: case report and review of the literature

1Non-invasive Cardiology Unit, Cardio Center, Humanitas Clinical and Research Center - IRCCS, Rozzano-Milan 20089, Italy.

2Department of Biomedical Sciences, Humanitas University, Pieve Emanuele-Milan 20090, Italy.

3Interventional Cardiology Unit, Cardio Center, Humanitas Clinical and Research Center - IRCCS, Rozzano-Milan 20089, Italy.

4Coronary Care Unit, Cardio Center, Humanitas Clinical and Research Center - IRCCS, Rozzano-Milan 20089, Italy.

Correspondence Address: Dr. Damiano Regazzoli, Interventional Cardiology Unit, Cardio Center, Humanitas Research Hospital, Rozzano-Milano 20089, Italy. E-mail: damiano.regazzolilancini@humanitas.it

    This article belongs to the Special Issue Percutaneous Mitral Valve Repair
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    © The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.


    Acute mitral regurgitation is a heterogeneous and life-threatening pathology, with severe hemodynamic consequences and extremely adverse outcomes. Traditionally, the definitive treatment is prompt surgical intervention after hemodynamic stabilization. Nowadays, however, percutaneous repair of mitral valve with MitraClip device has emerged as a safe and effective therapeutic option. Evidences in this field are still scarce. Hereby, we report the case of an 82-year-old woman with lateral ST-elevation myocardial infarction determining severe acute mitral regurgitation (MR) with an asymmetric leaflet tethering mechanism. Due to prohibitive operative risk and unstable hemodynamic status, the patient underwent a successful urgent MitraClip procedure with optimal reduction of MR and immediate hemodynamic improvement. Moreover, we provide a review of the available literature regarding the echocardiographic assessment of acute MR, results of published cases and possible management of this complex pathology.


    Percutaneous repair of mitral regurgitation (MR) with the MitraClip device (Abbott Vascular, Abbott Park, Illinois, USA) is an established therapeutic option for patients with prohibitive surgical risk and anatomically suitable mitral valve (MV)[1]. Implanted in over 100,000 patients worldwide, MitraClip procedure is safe and boasts a highly favourable risk-benefit ratio. While the impact of percutaneous MV repair on outcomes in chronic severe symptomatic MR has been evaluated for years in detail, data regarding the use of percutaneous edge-to-edge procedure in patients with severe acute MR are scarce and limited to case reports or small-size registries. Acute MR is a complex and heterogeneous pathology, with severe hemodynamic consequences and extremely adverse outcomes[2]. Traditionally, in most cases, after hemodynamic stabilization, the definitive treatment is surgical intervention. Nowadays, the MitraClip device is proving to be a valuable therapeutic option in high-risk patients.

    Hereby, we present a case of acute severe ischemic mitral regurgitation successfully treated with MitraClip procedure.

    Case description

    We report the case of an 82-year-old female patient, who presented to emergency department for chest pain lasting for 72 h. The EKG revealed a latecomer lateral ST-elevation myocardial infarction, with ST-depression in V1-V4, ST-elevation and q waves in V7-V9. She had a history of arterial hypertension, rheumatoid arthritis, thalassemia minor, and radiotherapy-treated tongue cancer.

    A bedside echocardiogram showed a left ventricular ejection fraction (LVEF) of 40% due to akinesia of posterior and lateral walls, normal left ventricular and atrial dimensions, mild MR, normal right ventricular function and size. Urgent coronary angiography was performed and showed a flow-limiting stenosis in the proximal tract of a dominant circumflex coronary artery. The coronary lesion was treated with balloon angioplasty and implantation of two drug-eluting stents. A severe no-reflow followed and prompted the use of intraortic balloon pump (IABP) for hemodynamic stabilization and the intracoronary injection of nitroprusside and adrenaline. The patient was transferred to Coronary Care Unit and remained hemodynamically stable for the subsequent 24 h.

    Then, a sudden hemodynamic collapse occurred, with pulmonary congestion and hypotension requiring intubation and high-dose vasopressors. Trans-thoracic and trans-esophageal echocardiogram (TEE) showed acute severe MR with eccentric jet directed towards the posterior wall of left atrium, due to extreme tethering of the posterior leaflet with partial posteromedial papillary muscle rupture and pseudoprolapse of the anterior leaflet [Figure 1]. The patient was deemed inoperable due to prohibitive surgical risk (age, subacute myocardial infarction with no-reflow injury, upper thorax radiotherapy, dual antiplatelet therapy, hemodynamic instability; STS score - risk of mortality: 66.6%; Euroscore II: 43.52%) and despite the highly challenging morphology of valvular disease, a salvage MitraClip procedure was the only feasible path. The mechanism of MR was complex: a Carpentier type IIIC (asymmetric systolic restriction) with a main jet located at A3-P3 extended to the medial section of A2-P2, plus a partial posteromedial papillary muscle rupture implicating an additional risk of mechanical complications, a coaptation gap > 10 mm, a posterior leaflet of 9 mm, but without calcifications at the grasping zone and with a suitable MV area (> 4 cm²)[3].

    Figure 1. Baseline trans-esophageal echocardiogram showing partial postero-medial papillary muscle rupture (A, circle), extreme tethering of posterior leaflet with pseudoprolapse of anterior leaflet (B) and wide eccentric jet of severe mitral regurgitation mainly originating from A3-P3 (C, arrow) and extended to the medial section of A2-P2 (C, arrowhead)

    The patient underwent an urgent percutaneous edge-to-edge procedure under general anaesthesia, with IABP and vasopressor support, and using fluoroscopic and TEE guidance. An XTR Clip was first implanted in A3-P3 position with residual moderate MR and mean gradients of 3 mmHg [Figure 2], then an NTR Clip was used in A2-P2 position with a resulting minimal MR and mean gradients of 4 mmHg [Figure 3].

    Figure 2. Intraprocedural trans-esophageal echocardiogram of XTR clip implantation: A3-P3 grasping (A), residual moderate mitral regurgitation located laterally to the clip (B) and transmitral gradients (C)

    Figure 3. Intraprocedural trans-esophageal echocardiogram of NTR clip implantation: A2-P2 grasping (A), residual minimal mitral regurgitation (B) and transmitral gradients (C)

    The patient’s hemodynamics progressively improved, and she was successfully weaned off mechanical ventilation and pharmacological support. Her post-operative recovery was uncomplicated and the patient was discharged on the tenth post-procedural day with residual mild MR and mean gradients of 5 mmHg [Figure 4].

    Figure 4. Discharge trans-thoracic echocardiogram showing residual mild mitral regurgitation and mean gradient of 5 mmHg


    Acute MR is a medical and surgical emergency. Indeed, differently from chronic valvular diseases, acute MR occurs suddenly in normal sized hearts, without time for adaptative left atrial and ventricular enlargement. This results in a rapid increase of left atrial pressure with consequent pulmonary congestion and, despite initial hyperdynamic ventricular contraction, a risk of progressive reduction of cardiac output with hypotension and peripheral hypoperfusion[4]. Thus, patients with acute MR usually present with severe dyspnea, and slip towards cardiogenic shock.

    Timely diagnosis may be insidious, due to nonspecific clinical pattern and equalization of left ventricular and atrial pressures leading to a soft or absent murmur[2]. Even pulmonary edema can be atypical with unilateral involvement if the regurgitant jet is eccentrically directed into either the right or the left pulmonary veins[2]. Echocardiography is key to diagnosis and proper management of the different causes of this disease[5].

    Traditional management involves medical stabilization and surgical intervention, with a timing strictly related to the specific etiology of valve dysfunction[6]. MitraClip device has emerged as a new therapeutic alternative which is promising and potentially life-saving.

    In the following sections, the main aspects of acute MR will be analysed with a focus on the amenability and use of percutaneous edge-to-edge repair technique in this condition.


    Identifying the precise mechanism and cause of acute MV disease is fundamental to tailor the most appropriate therapeutic strategy for each patient. Acute MR counts few mechanisms and many possible causes, as detailed in Table 1. First of all, the distinction between structural damages and functional alterations is fundamental, because organic causes always require repair, whereas functional causes may improve after targeting the underlying myocardial infarction, ischemia, or systolic dysfunction[5].

    Table 1

    Classification of acute mitral regurgitation mechanisms and causes

    Organic/structural damage
        Carpentier type I (normal leaflet motion): perforationInfective endocarditis
        Carpentier type II (excessive leaflet motion): prolapse/flail (papillary muscle rupture, chordal rupture)Infective endocarditis
    Myocardial ischemia
    Myxomatous degeneration
    Fibroelastic deficiency
    Idiopathic chordal rupture
    Functional alteration
        Carpentier type III (restricted leaflet motion): symmetric/asymmetric systolic restrictionMyocardial ischemia
        Carpentier type IV: systolic anterior motion of the leafletsHypertrophic cardiomyopathy
    Takotsubo cardiomyopathy

    One major organic cause is chordal rupture which may occur in an otherwise totally normal valve or in a MV affected by Barlow’s disease or fibroelastic deficiency.

    Device-related MR is a rare yet possible complication of left ventricular mechanical support devices due to catheter impingement in the chordal apparatus or leaflet tissue[7]. Iatrogenic MR is also reported after percutaneous mitral valvotomy for rheumatic mitral stenosis, albeit unlikely if patients are adequately selected.

    Infective endocarditis can cause leaflet perforation and tears, papillary muscle and chordal rupture or may reduce systolic coaptation due to masses or abscesses interfering with leaflets’ apposition.

    Extremely rare etiologies include chest traumas, systemic inflammatory diseases or acute rheumatic fever which remains a serious concern in endemic areas[8,9].

    Ischemic papillary muscle rupture is another major cause of acute massive MR, with more frequent involvement of the posterior papillary muscle during inferior myocardial infarctions.

    Acute myocardial ischemia or infarction may cause acute functional MR with systolic symmetrical or asymmetrical leaflet tethering, due to global or regional ventricular systolic dysfunction.

    Another functional cause of MR is systolic anterior motion (SAM) of mitral leaflets in hypertrophic obstructive cardiomyopathy or Takotsubo cardiomyopathy[2].


    Diagnosis of acute MR

    Echocardiography is essential for diagnosis. As opposed to chronic MR, left atrial and ventricular sizes are usually normal in acute MR, except for preexisting conditions influencing chambers’ dimension, compliance and hemodynamic tolerance. For instance, patients with a history of chronic MR and preserved ventricular systolic function have enlarged cardiac volumes and tolerate the further volumetric increase better than patients with normal sized hearts or with preexisting reduced LVEF. Color Doppler may underestimate the severity of MR, owing either to rapid equalization of left atrial and ventricular pressures or to an eccentric direction of the regurgitant jet with “Coanda” effect. Consequently, the use of color Doppler-based quantitative measures such as regurgitant volume and effective regurgitant orifice area may be misleading and even challenging, due to severe acute congestive heart failure with tachycardia. Vena contracta width and continuous wave Doppler signal represent reliable semiquantitative tools to quickly evaluate the significance of MR. A triangular and dense continuous wave Doppler curve supports the diagnosis of acute MR. It mirrors the rapid decline in late systolic velocity as a consequence of the abrupt increase in left atrial pressure. Systolic pulmonary venous flow reversal in one or both pulmonary veins can be found but tachycardia or atrial fibrillation can mask these findings. Any measure or value should be interpreted in the clinical context, as patients with acute heart failure and acute MR may appear to have only moderate MR when assessed by semi-quantitative and quantitative methods. Indeed, an acute significant MR should be suspected in patients with a clinical pattern of acute heart failure, with evidence of hyperdynamic LV without systolic or diastolic dysfunction, and with anatomic imaging of MV lesions[10,11].

    Trans-thoracic echocardiography is the first-line examination in the assessment of acute dyspnea, feasible at bedside and sufficient to raise the clinical suspicion, but often inconclusive regarding the identification of the mechanism of MR, the evaluation of the MV anatomy and preoperative planning, which all require TEE. As such, three-dimensional (3D) echocardiography should always be adopted, as it provides anatomical details not detectable with two-dimensional (2D) imaging, enabling a dynamic and comprehensive assessment of MV tissue, and seizes dataset for off-line multiplanar reconstructions[12].

    Mechanism and cause of MR

    The first step of echocardiographic evaluation of MR mechanism is the distinction between organic/structural damage and functional alteration of MV [Table 1]. Close assessment of leaflet motion, anatomic lesions and finally the Color Doppler-based evaluation of convergence area and regurgitant jets are required.

    A structural lesion with normal leaflet motion is generally due to a leaflet perforation. In this case, TEE should evaluate the position, shape and dimensions of the perforation, detect any sign suggestive of endocarditis, such as masses, vegetations or abscesses and explore mitral-aortic junction, left ventricular outflow tract and the position of other intracardiac devices. Indeed, an ambitious combined percutaneous procedure of MitraClip plus occluder would be contraindicated in the presence of active endocarditis, and an accurate preoperative planning should take into account the risk of iatrogenic obstruction of ventricular outflow or interference with proximally-located prostheses[13].

    Leaflet flails and prolapse are categorised as Carpentier type II mechanism and occur through sudden rupture of chordae tendineae or papillary muscles due to many possible causes[11]. Myxoid degeneration or Barlow’s disease is a major cause of chordal rupture and remains extremely challenging for percutaneous repair due to altered anatomy, including extensive leaflet thickening, multi-segmental prolapse, elongated or fused chordae tendineae, diffuse calcifications and annular dilatation[14]. Beyond procedural challenges, the main issue is the balance between a relevant residual MR due to the highly mobile and redundant leaflets and a resultant iatrogenic mitral stenosis owing to extensive grasping with multiple clips. However, the introduction of MitraClip XTR device, with a wider reach and longer clip arms than NTR, has broadened the “graspable” MV anatomies, including Barlow’s disease, as documented by a few case series[15-17]. Nonetheless, myxoid degeneration appears early in life and patients are usually referred for surgery due to young age and low risk, on the contrary fibroelastic deficiency affects elderly people with significantly different operative risk. In fibroelastic deficiency MV is characterized by impaired production of connective tissue and shows thin leaflets, prolapse of single segments, and rupture of thin chordae with limited flail width[14]. MitraClip has been shown to be feasible and safe in this type of MV anatomy, even in octogenarians, but care should be taken in cases of fragile leaflet tissue due to the risk of grasping-related leaflet tears or lacerations[18].

    Papillary muscle rupture is a severe, albeit rare, mechanical complication of acute myocardial infarction. This anatomic lesion is challenging given the large flail width and flail gap with frequent commissural localization requiring an extensive grasping with a concomitant high risk of chordal entanglement[19]. As a papillary muscle head may mimic an endocarditic mass, clinical context should guide the differential diagnosis[20]. Moreover, infective endocarditis itself may be causative of chordal rupture and papillary muscle laceration, in the presence of typical echocardiographic criteria such as vegetations and abscesses[21].

    Among functional alterations of MV, the main cause of acute MR is myocardial ischemia. Indeed, in the very acute phase of myocardial infarction, even modest valve tenting due to regional and/or global left ventricular dysfunction may result in hemodynamically-significant MR[22]. Echocardiography should be performed to assess the presence of wall motion abnormalities and myocardial scarring, and the “symmetry” of mitral leaflets with respect to their point of coaptation. In cases of asymmetric tenting, it is generally the posterior leaflet that tethers while the anterior leaflet shows a ‘‘pseudoprolapse’’ motion. The MR jet is eccentric and oriented against the posterior wall of left atrium. In cases of symmetric tethering, both leaflets are tented but the coaptation point is displaced apically at the leaflets’ tips, and the jet is typically central[23].

    An infrequent cause of acute MR is SAM of mitral leaflet, which represents a life-threatening condition and may result also in critical left ventricular outflow tract obstruction. Hypertrophic obstructive cardiomyopathy is the main pathology associated with SAM and is characterized by abnormalities of MV and subvalvular apparatus, such as malpositioned papillary muscles, elongated chordae and thickened leaflets[24]. These anatomic features may impact on transmitral gradients and residual MV area after MitraClip procedure[25]. SAM with left ventricular outflow obstruction may occur in several other conditions such as Takotsubo cardiomyopathy, hypertensive hypertrophic cardiopathy, hypovolemia, severe bleeding, sepsis, vasodilatation, sympathetic activation, pericardial tamponade, after aortic valve replacement, and after surgical mitral valve repair[25]. In these acute conditions a transcatheter edge-to-edge technique certainly sounds appealing to target both MR and hypotension.

    Finally, rheumatic heart disease is commonly regarded as a contraindication to MitraClip procedures, owing to high risk of mitral stenosis. However, a recently published case report has shown the feasibility of percutaneous MV repair in a rheumatic MV with baseline mean gradients inferior to 4 mmHg[26]. Accurate measurement of MV area through 3D-based multiplanar reconstruction, evaluation of trans-mitral mean gradients and exclusion of calcifications at the grasping area are essential to decision-making and preoperative planning.

    As outlined above, absolute anatomic limitations are very few. Hahn[27] listed the echocardiographic features associated with ideal and challenging anatomies and highlighted a few relative contraindications. The absolute contraindications include severe and extended calcifications of the grasping zone, short leaflet length (< 7 mm) and small baseline MV area (< 3.5 cm²)[15].

    Real-world evidences of MitraClip procedure in acute MR

    Real-world experience on percutaneous edge-to-edge repair of acute MR is uniquely derived from case reports and small-size registries, listed and synthetized in Table 2[19,28-43].

    Table 2

    Case reports and registries of MitraClip in patients with acute MR

    TitleRef.Cause and mechanism of acute MRPatientsHemodynamic settingProcedure and acute resultEarly outcomesDischargeFollow-up
    Case reports
      Percutaneous mitral valve repair using the MitraClip in acute cardiogenic shockZuern et al.[29]Acute cardiogenic shock and MOF in ischemic cardiomyopathy (2 previous anterior wall myocardial infarctions)51-year-old male
    LVEF = 15%
    LVESD = 58 mm
    LVEDD = 67 mm
    BNP = 2786 ng/L
    Cardiogenic shock and MOF
    IABP and inotropes
    LAP = 36 mmHg
    PAP = 75/44 mmHg
    CO = 3.0 L/min
    1 clip (A2-P2)
    MR grade = 1-2+
    PCWP = 29 mmHg
    PAP = 66/37 mmHg
    CO = 4.3 L/min
    Device successAlive (postop day 7)
    LVEF = 15%
    LVESD = 59 mm
    LVEDD = 68 mm
    sPAP = 32 mmHg
    BNP = 1,210 ng/L
    MR grade = 1-2+
    LVEF = 20%
    LVESD = 54 mm
    LVEDD = 63 mm
    sPAP = 34 mmHg
    BNP = 681 ng/L
      Successful Percutaneous Mitral Valve Repair with the MitraClip System of Acute Mitral Regurgitation due to Papillary Muscle Rupture as Complication of Acute Myocardial InfarctionBilge et al.[30]Posterolateral STEMI, successful primary PCI of proximal circumflex artery with loss of marginal branch
    Complete rupture of the anterolateral papillary muscle with A1-P1 flail and lateral jet
    60-year-old female
    LVEF = 45%
    Pulmonary edema and cardiogenic shock
    sPAP = 65 mmHg
    7 days after admission
    1 clip (A1-P1)
    MR grade = 0
    Minor hemorrhagic stroke 2 days after MitraClipAlive (postop day 9)30-day
    MR grade = 1+
      MitraClip for Papillary Muscle Rupture in Patient With Cardiogenic ShockWolff et al.[31]Latecomer lateral STEMI, with occlusion of large first obtuse marginal artery
    Complete rupture of anterolateral papillary muscle with flail of A2
    68-year-old male
    LVEF = 25%
    Mild to moderate right ventricular dysfunction
    STS score = 64% EuroSCORE II = 75%
    Cardiogenic shock and ventricular arrhythmias
    IABP and intropes
    Mean LAP = 37 mmHg
    v-waves = 55 mmHg
    2 clips (A2-P2)
    MR grade = 2+
    v-wave = 30 mmHg
    Device successMR grade = 1-2+
    LVEF = 30%
    LVEDD = 51 mm
    LVESD = 46 mm
    RV function = normal
    MR grade = 1-2+
    LVEF = 38%
    LVEDD = 62 mm
    LVESD = 50 mm
      MitraClip Implantation After Acute Ischemic Papillary Muscle Rupture in a Patient With Prolonged Cardiogenic ShockBahlmann et al.[32]Lateral NSTEMI
    Complete rupture of the posterior papillary muscle
    77-year-old male
    Log Euroscore = 78%
    Cardiogenic shock and pulmonary edema
    IABP and inotropes
    Mean LAP = 21 mmHg
    Mean PAP = 24 mmHg
    Stroke volume index = 21 mL/m2
    CO = 4.6 L/min
    CI = 2.2 L/min/m2
    3 clips
    MR grade = 0
    Mean LAP = 22 mmHg
    Mean PAP = 26 mmHg
    Stroke volume index = 38 mL/m2
    CO = 6.8 L/min
    CI = 3.2 L/min/m2
    Device successAlive (postop day 16)-
      Percutaneous Mitral Valve Repair With Mitraclip System in a Patient With Acute Mitral Regurgitation After Myocardial InfarctionRodríguez-Santamarta et al.[33]Inferolateral STEMI, successful primary PCI of proximal circumflex artery
    Ischemic asymmetric posterior leaflet tethering
    A2-P2 and A3-P3
    76-year-old male
    STS score = 6.7%
    Log Euroscore = 29.1%
    Pulmonary edema2 clips (A2-P2; lateral to the first one)
    MR grade = 1+
    MV MG < 5 mmHg
    MR grade (4th day) = 1+Alive
    NYHA I
    NYHA I
      Effective Percutaneous “Edge-to-Edge” Mitral Valve Repair With MitraClip in a Patient With Acute Post-MI Regurgitation Not Related to Papillary Muscle RuptureTarsia et al.[34]Inferior STEMI, successful primary PCI of right coronary artery and marginal branch, complete revascularization of left anterior descending artery after 48 hours
    Ischemic symmetric leaflet tethering with central jet (A2-P2)
    65-year-old female
    Log Euroscore = 42%
    Cardiogenic shock and pulmonary edema
    IABP and inotropes
    1 clip (A2-P2)
    MR grade = 0
    Device success
    No major complications
    Alive (postop day 7)6-month
    NYHA I
    MR grade = 0
      Acute Mitral Regurgitation Secondary to Papillary Muscle Tear Is Transcatheter Edge-to-Edge Mitral Valve Repair a New Paradigm?Valle et al.[35]Inferior STEMI, successful primary PCI of saphenous vein graft to right coronary artery
    Partial tear of the posteromedial papillary muscle with flail of A2-A3
    84-year-old male
    LVEF = mildly reduced
    Cardiogenic shock and MOF
    Mean LAP = 29 mmHg
    v-wave = 59 mmHg
    3 clips in a “zipper” approach
    MR grade = 1+
    MV MG = 5 mmHg
    Mean LAP = 14 mmHg
    v-wave = 20 mmHg.
    MR grade = 1-2+
      Use of MitraClip for Postmyocardial Infarction Mitral Regurgitation Secondary to Papillary Muscle DysfunctionYasin et al.[36]Inferior NSTEMI
    Partial rupture of posteromedial papillary muscle with flail of posterior leaflet
    68-year-old maleCardiogenic shock and pulmonary edema
    v-a ECMO
    5 day after admission
    2 clips (A2-P2, P1-P2)
    MR grade = 1+
    MR grade (3th day) = 1+
    Device success
    MR grade = 1+
      Edge-to-edge mitral valve repair for acute mitral valve regurgitation due to papillary muscle rupture: a case reportPapadopoulos et al.[19]Anterior STEMI, successful primary PCI of intermediate artery
    Partial rupture of the anterolateral papillary muscle with flail of A1-A2 and P1
    85-year-old female
    Log Euroscore = 43%
    STS score = 13%
    LVEF = 40%
    Cardiogenic shock and pulmonary edema
    IABP and inotropes
    2 clips (A2-P2, A1-P1) with a “zipping” of the lateral commissure
    MR grade = 1-2+
    MV area = 2.1 cm2
    MV MG = 6 mmHg
    Device successAlive (postop day 7)20-month
    MR grade = 2+
    MV MG = 6 mmHg
      One-stop-shop totally percutaneous approach for severe aortic and mitral regurgitation in cardiogenic shockPagnotta et al.[37]Latecomer anterior STEMI, successful primary PCI of proximal right coronary artery and left circumflex artery (proximal left anterior descending artery occluded)
    Retraction and calcification of posterior mitral leaflet and severe aortic regurgitation in a mediastinal radiotherapy-related valvular heart disease
    57-year-old male
    LVEF = 30%
    Log Euroscore = 17.7%
    Cardiogenic shock
    IABP and inotropes
    1 XTR clip
    MR grade = 1+
    MV MG = 5 mmHg
    MR grade = 1+
    MV MG = 5 mmHg
    LVEF = 35%
      Successful MitraClip XTR for Torrential Mitral Regurgitation Secondary to Papillary Muscle Rupture as a Complication of Acute Myocardial InfarctionVillablanca et al.[38]Lateral NSTEMI, successful primary PCI of proximal and mid-circumflex artery
    Complete rupture of posteromedial papillary muscle with flail of P2-P3
    70-year-old male
    LVEF = 60%
    STS score = 14.3%
    Cardiogenic shock and pulmonary edema
    Impella CP, then exchanged with IABP plus inotropes
    Mean LAP = 22 mmHg
    v-wave = 60 mmHg
    CO = 3.7 L/min
    CI = 1.8 L/min/m2
    1 XTR clip (A2-P2)
    MR grade = 1+
    MV MG = 1 mmHg
    Mean LAP = 10 mmHg
    v-wave = 12 mmHg,
    CO = 4.9 L/min
    CI = 2.8 L/min/m2
    -Alive (postop day 3)6-month
    NYHA I
    MR grade = 1+
      Transcatheter Mitral Valve Edge-to-Edge Repair with the New MitraClip XTR System for Acute Mitral Regurgitation Caused by Papillary Muscle RuptureKomatsu et al.[28]Inferior STEMI, successful primary PCI of culprit single-vessel disease
    Posteromedial papillary muscle rupture with anteriorly directed eccentric jet
    Coaptation gap = 1 cm
    MV area = 6.2 cm2
    MV MG = 3 mmHg
    55-year-old male
    LVEF = 55%
    Pulmonary edema, cardiogenic shock and acute kidney injury
    IABP and vasopressors
    V wave = 50 mmHg
    2 clip XTR (A2-P2)
    MR grade = 1-2+
    MV MG = 3 mmHg
    MV area = 2.94 cm2
    V wave = 17 mmHg
    MR grade = 2+ (eccentric)
    No HF symptoms
    Case series or registries
      Percutaneous Mitral Valve Repair for Acute Mitral Regurgitation After an Acute Myocardial InfarctionEstévez-Loureiro et al.[39]AMI without papillary muscle rupture:
    • 2 STEMI

    • 3 NSTEMI

    Days between MI and clip:
    • 8-12 days = 3 pts

    • 33-49 = 2 pts

    N of patients = 5
    Age = 51 – 76 years
    Median Euroscore = 29.1%
    5/187 MitraClip procedures (2.7%)
    Period: 10/2010-01/2015
    Cardiogenic shock = 3
    NYHA IV = 2
    IABP or inotropes = 4
    Median sPAP = 62 mmHg
    N of clips:
    • 1 clip = 1 (20%)

    • 2 clips = 3 (60%)

    • 3 clips = 1 (20%)

    MV area > 1.5 cm2 = 5 (100%)
    MV MG < 5 mmHg = 5 (100%)
    MR grade ≤ 2+ = 5 (100%)
    Device success = 5/5
    Median sPAP = 38 mmHg
    No major complications
    Deaths = 1 (20%) (due to MOF 1 week after MitraClip)Median follow-up = 317 days
    NYHA class
    • I = 1 (20%)

    • II = 3 (60%)

    MR grade
    • 2+ = 2 (40%)

    • 1+ = 2 (40%)

      Percutaneous edge-to-edge mitral valve repair for the treatment of acute mitral regurgitation complicating myocardial infarction: A single centre experienceAdamo et al.[40]AMI without papillary muscle rupture:
    • 3 STEMI

    • 2 NSTEMI

    N of patients = 5
    Age = 73 ± 6 years
    Males = 3
    Median Euroscore = 27.1 ± 13%
    Median STS score = 10.2 ± 6%
    5/79 MitraClip procedures (6.3%)
    Period: 10/2010-10/2015
    Cardiogenic shock = 4
    Pulmonary edema = 1
    IABP and inotropes = 4
    Inotropes = 1
    53 ± 33 days from admission
    N of clips:
    • 1 clip = 2

    • 2 clips = 3

    Device success = 5/5Deaths = 01 death due to non-cardiovascular causes 57 days after MitraClip
    1 left-ventricular assist device implantation 60 days after MitraClip
      Percutaneous edge-to-edge mitral valve repair may rescue select patients in cardiogenic shock: findings from a single center case seriesFlint et al.[41]Cardiogenic shock:
    • AMI = 3

    • acute papillary muscle rupture = 1

    • chordal rupture = 1

    • acute leaflet flail = 1

    • acute worsening of functional and degenerative MR = 1

    • acute worsening of functional MR = 1

    N of patients = 12
    Age = 71.7 ± 12.8 years
    Males = 9
    LVEF = 46 ± 12%
    STS score (MV repair) = 33.4 ± 22.3%
    STS score (MV replacement) = 23.9 ± 18.2%
    12/135 MitraClip procedures (9%)
    Period: 11/2013-10/2018
    Cardiogenic shock
    -IABP + inotropes = 3
    -IABP + nitroprusside = 1
    -inotropes + nitroprusside = 1
    -inotropes = 6
    -nitroprusside = 1
    -ECMO = 1
    Mean LAP = 27 ± 9
    Mean PAP = 38 ± 11
    Mean sPAP = 57 ± 17
    Mean RAP = 13 ± 5
    CI = 2.2 ± 0.5
    CO = 4.3 ± 1.2
    N of clips = 2.3 ± 0.7
    MR grade
    • 0 = 1

    • 1+ = 8

    • 2+ = 3

    MV MG = 5.0 ± 2.7 mmHg
    LVEDD = 5.4 ± 0.8 cm
    LVEF = 37 ± 15%
    -Death (6th day) = 1
    Resolution of shock = 10
    Inotrope-dependent = 1
    Deaths = 4 (26-282 days)
      Salvage MitraClip in severe secondary mitral regurgitation complicating acute myocardial infarction: data from a multicentre international studyHaberman et al.[42]AMI within 90 days:
    • 12 STEMI

    • 8 NSTEMI

    • 11 anterior

    • 9 inferior-posterior

    No evidence of structural valvular damage
    N of patients = 20
    Age = 68 ± 10 years
    Males = 6 (30%)
    LVEF = 35.9 ± 12.5%
    LVEF < 30% = 7
    Period: 01/2011-09/2018
    Cardiogenic shock = 8
    sPAP = 60 ± 12 mmHg
    v-wave = 31 ± 25 mmHg
    Days after MI = 32 (7-90)
    Clips = 1 – 3
    MR grade 1+ = 12
    MR grade 2+ = 7
    PAP = 40 ± 13 mmHg
    v-wave = 17 ± 5 mmHg
    Device success = 19/20
    In one patient, a posterior leaflet tear occurred after the second clip implantation and urgent MV replacement surgery was performed but the patient died.
    Death = 1Median follow-up = 15 months
    Death = 1 (3 weeks after discharge)
      Transcatheter mitral valve repair in patients with acute
    myocardial infarction: insights from the European Registry of
    MitraClip in Acute Mitral Regurgitation following an acute
    myocardial infarction (EREMMI)
    Estévez-Loureiro et al.[43]STEMI
    • anterior = 10 (22.7%)

    • inferior = 17 (38.6%)

    • lateral = 10 (22.7%)

    • undetermined = 2 (4.5%)

    Primary PCI = 30 (68.2%)
    MR grade
    • 3+ = 4 (10.3%)

    • 4+ = 35 (89.7%)

    MR jet location:
    • A1-P1 = 3 (7.5%)

    • A2-P2 = 36 (90%)

    • A3-P3 = 6 (15%)

    N of patients = 44
    Age = 70.0 ± 10.8 years
    Males = 63.6%
    Euroscore II = 15.1% (6.2-23.2)
    LVEF = 35% (26-44)
    LVEDD = 55.5 (48.2-59.5) mm
    44/883 MitraClip procedures (5%)
    Period: 01/2016-12/2018
    Mechanical support
    • ECMO = 2 (4.5%)

    • IABP = 14 (31.8%)

    Inotropes = 24 (54.5%)
    sPAP = 52.5 (25-77.5) mmHg
    TAPSE = 16.5 (16-20.3) mm
    Median n of clips = 2 (1-2)
    Median MV MG = 3 mmHg (2-4)
    Median time from MI = 18 days (13-36.8)
    Device success = 86.6%
    Median length of stay after
    procedure = 16 (8-27) days
    Death = 4 (9.1%)
    Cardiac surgery = 1 (2.3%)
    Death = 8 (18.2%)
    HF rehosp = 8 (18.2%)
    Cardiac surgery = 3 (6.8%)
    MR grade
    • 0/1+ = 31.1%

    • 2+ = 41.4%

    • 3+ = 17.2%

    • 4+ = 10.3%

    • I = 13.8%

    • II = 62.1%

    • III = 17.2%

    • IV = 6.9%

    The vast majority of cases occurred as complications of acute myocardial infarction, due to either ischemic leaflet tethering or papillary muscle ruptures (more often the posteromedial one). A primary PCI was always performed, except for late presentations due to the likely risk of reperfusion injury of already necrotic walls. The hemodynamic status was generally critical with evidence of cardiogenic shock and pulmonary edema requiring intubation, inotropes and mechanical support, mainly IABP and only in few cases veno-arterial extracorporeal membrane oxygenation. The Heart Team’s decision to proceed with MitraClip was primarily guided by the high surgical risk due to hemodynamic instability, acute/subacute ischemia, dual antiplatelet therapy, advanced age or comorbidities in a few cases, and the favourable risk-benefit balance of percutaneous edge-to-edge approach. Hemodynamic stabilization and likeliness of MR improvement with revascularization or medical therapy were the main determinants of the timing of procedure. One to three clips were deployed with an almost complete procedural success, due to significant reduction of MR, huge reduction of left atrial pressures and increase of cardiac output. Haberman et al.[42] reported one case of posterior leaflet tear during a second clip implantation, followed by urgent MV surgery and lastly by patient death. Early outcomes were promising, with high survival rates, sustained reduction of MR grade and improved functional class. These results are even more reassuring if compared with surgical ones; in a multicentre surgical registry of 279 patients treated with emergency surgery for acute severe MR, due to myocardial infarction, acute endocarditis or degenerative MV disease, the 30-day mortality was 22.5% with worse survival rates in case of acute myocardial infarction, endocarditis, shock, coronary artery disease and systolic dysfunction[44]. Despite the evidences seem extremely optimistic regarding outcomes of MitraClip in almost every acute setting, a publication bias has to be recognized, and the interventionalists’ and imagers’ experience should be considered during Heart Team decision-making. Certainly, MitraClip shows several advantages over surgery. Firstly, MitraClip is safe and does not preclude a delayed surgical procedure in case of failure, thus a “bridge” procedure may be always attempted without significant additional risks. Secondly, percutaneous procedures permit to avoid the cardiopulmonary bypass and the associated systemic inflammatory storm and myocardial oxidative stress. Furthermore, transcatheter procedures do not cause abnormal motion of the right ventricle or interventricular septum, which may impact on long-term LV performance[43].

    Decision-making and management

    We propose a flow-chart that may be helpful for acute MR decision-making and management [Figure 5].

    Figure 5. Proposed flow-chart for acute MR decision-making and management. “Carpentier type” refers to Carpentier classification of MR mechanisms, as exposed in Table 1. AE: acute endocarditis; C.t.: Carpentier type; MR: mitral regurgitation; MV: mitral valve; PCI: percutaneous coronary intervention; TEE: trans-esophageal echocardiography; TTE: trans-thoracic echocardiography

    Once acute MR is diagnosed, the initial goal is hemodynamic stabilization through inotropes/vasopressors and temporary mechanical circulatory supports (IABP, Impella and extracorporeal membrane oxygenation) in cases of cardiogenic shock, intravenous diuretic therapy and non-invasive/invasive ventilation for massive pulmonary edema with acute respiratory distress. Hypertensive or normotensive patients benefit from afterload reduction with intravenous vasodilator therapy, which reduces MR, diminishing pulmonary congestion and increases forward cardiac output[6].

    Then, an accurate trans-esophageal echocardiographic characterization of acute MR is needed to tailor the subsequent actions. The finding of a Carpentier type I lesion, as a leaflet perforation, should lead to exclude an active acute endocarditis, which represents a contraindication for MitraClip procedure and an indication for cardiac surgery[45]. Clinical context and laboratory tests are pivotal to distinguish active endocarditic processes from a treated state, for which percutaneous interventions are not contraindicated. Careful history taking is sufficient to exclude a device-related (transcatheter prosthetic aortic valves and intracardiac left ventricular assist devices) mechanism.

    A Carpentier type II mechanism (leaflet prolapse/flail, rupture of chordae or papillary muscle) warrants a wide differential diagnosis between multiple potential causes. As already reported for Carpentier type I, active endocarditic processes should be excluded, as well. Myocardial ischemia or infarction may cause partial or complete rupture of a papillary muscle and could be targeted with medical therapy or percutaneous myocardial revascularization, before treating the MV lesion. A case-by-case judgement is fundamental and should consider the presence of ongoing myocardial ischemia, the timing of onset of myocardial infarction, the extension of coronary artery disease, the type of MV lesion (partial versus complete rupture), and the differential burden between ischemic and valvular diseases. Primary percutaneous coronary intervention for an ST-elevation myocardial infarction is always indicated, except for delayed infarctions without evidence of ongoing ischemia, as they would not yield significant benefits from revascularization and yet be complicated by reperfusion injury[46,47]. Early surgical intervention is crucial for complete papillary muscle rupture, although partial rupture may benefit from percutaneous revascularization or a brief period of stabilization[48]. When acute MR is caused by chordal rupture in MV affected by fibroelastic deficiency or Barlow’s disease, anatomic evaluation has a central role to ensure the feasibility of an eventual MitraClip procedure, as already explained in previous paragraphs.

    The observation of a Carpentier type III mechanism is related to regional or global LV systolic dysfunction. Medical therapy and percutaneous coronary intervention can acutely reduce the degree of ischemic MR, and an earlier reperfusion time is associated with greater reduction in MR severity[49]. Thus, if hemodynamic conditions are stable after revascularization or medical therapy implementation, a “wait and see” strategy may be undertaken with close and constant monitoring.

    A Carpentier type IV mechanism, namely a SAM of mitral leaflets, observed in hypertrophic and Takotsubo cardiomyopathies, represents an insidious cause of acute MR. Echocardiographic diagnosis is exceedingly important, as vasodilators, inotropes or IABP worsen the clinical and hemodynamic status. Beta-blockers, volume expansion, inotrope discontinuation, afterload augmentation with vasopressors and lastly mechanical circulatory supports (Impella and extracorporeal membrane oxygenation) are the weapons to turn to[50,51].

    After the initial phases of echocardiographic diagnosis, hemodynamic stabilization, medical therapy implementation and eventually percutaneous coronary revascularization, it is time for Heart Team assessment. Interventionalists, cardiac surgeons, imagers, intensivists and heart failure specialists must meet to tailor the best therapeutic pathway, weighing all clinical and anatomical factors: age, comorbidities, hemodynamic status, response to medical therapy, MR mechanism, surgical risk, other surgical targets and single centre’s experience. In cases of low surgical risk, presence of an indication for concomitant cardiac surgery and organic MV disease, cardiac surgery is the first-choice treatment. Differently, in our opinion, MitraClip should be always attempted in a stepwise approach, as it is a safe procedure and does not preclude a delayed surgical intervention. Even in low-risk patients undergoing isolated MV surgery with a low probability of surgical repair, MitraClip may be attempted, above all in high-volume centers. Eligibility for percutaneous edge-to-edge procedure requires only three conditions: possibility to grasp and approximate the leaflets, low risk of MV stenosis, and good-quality TEE imaging[19].


    Acute MR is a life-threatening condition, traditionally treated as a medical and surgical emergency. Percutaneous edge-to-edge repair of MV is a safe and effective therapeutic option, does not preclude delayed cardiac surgery and is potentially able to solve almost any type of MV disease, with very few contraindications. Echocardiographic identification of the precise valvular lesion and Heart Team evaluation are pivotal to tailor the best therapeutic pathway for each patient. Literature confirms optimal results of MitraClip in acute MR, but further studies are warranted to shed light on feasibility and limitations of this powerful procedure.


    Authors’ contributions

    Involved in clinical care: Sanz-Sánchez J, Chiarito M, Briani M, Fazzari F, Corrada E, Bragato RM, Pagnotta PA, Regazzoli D

    Wrote the manuscript: Cannata F, Regazzoli D

    Supervised and coordinated all aspects of the research: Stefanini GG, Reimers B

    Contributed to critical revision of the manuscript and approved the final version of the manuscript: Cannata F, Sanz-Sánchez J, Chiarito M, Briani M, Fazzari F, Bertoldi LF, Ferrante G, Corrada E, Bragato RM, Stefanini GG, Pagnotta PA, Reimers B, Regazzoli D

    Availability of data and materials

    Not applicable.

    Financial support and sponsorship


    Conflicts of interest

    All authors declared that there are no conflicts of interest.

    Ethical approval and consent to participate

    Not applicable.

    Consent for publication

    A written informed consent for publication was obtained.


    © The Author(s) 2020.


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    Cite This Article

    Cannata F, Sanz-Sánchez J, Chiarito M, Briani M, Fazzari F, Bertoldi LF, Ferrante G, Corrada E, Bragato RM, Stefanini GG, Pagnotta PA, Reimers B, Regazzoli D. Percutaneous mitral valve repair in acute mitral regurgitation: case report and review of the literature. Mini-invasive Surg 2020;4:53. http://dx.doi.org/10.20517/2574-1225.2020.41




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