Previous Mitral Valve Repair Research Articles

WHEN CLINICAL FINDINGS TAKE YOU DOWN THE WRONG PATH: PERSISTENT FEVER IN A PATIENT WITH PREVIOUS CARDIAC SURGERY

Abstract Introduction In a patient who underwent previous cardiac surgery, persistent fever may be related to endocarditis. Symptoms and cardiovascular imaging, such as echocardiogram and PET/CT, may guide clinicians and surgeons to the correct diagnosis. Discussion A 43–years–old man came to our attention because of persistent fever (lasting several months) associated with cough and asthenia. When he was 5 years old, he underwent cardiac surgery for partial atrioventricular canal defect (atrial septal defect was about 4 cm) and mitral valve cleft. 14 years ago he undertook chemotherapy due to Hodgkin‘s lymphoma. Recently a cerebral artery aneurysm, radiologically defined as mycotic but proved to be fusiform, was diagnosed and treated with neurosurgery. During a recent hospitalization, blood culture positive for Streptococcus Mitis and brachial rash were reported and antibiotic therapy was started. Suspecting endocarditis, he was referred to our department. Echocardiogram revealed anterior mitral leaflet fissure, resulting in severe mitral regurgitation. Moreover a periannular cavity of doubtful interpretation (seemingly an abscess) was described. Subsequent 18FDG–PET/CT did not detect any abnormal cardiac metabolic activity. Due to severe valve regurgitation, cardiac surgery was performed: myxomatous degenerative mitral valve leaflets, failure of mitral valve cleft closure and anomalous coronary sinus communication to the left atrium (mimicking echocardiogram findings of suspected empty abscess cavity) were observed. Thus mitral valve replacement using a biological valve prosthesis was performed. Macroscopically there was no evidence of endocarditis, confirming PET/CT scan results. During the post–surgery period, third–degree atrioventricular block episodes were noted. Therefore a bicameral pacemaker was implanted. Conclusions This case report demonstrates the importance of not stopping at the first impression, as failure of previous mitral valve repair in a patient presented with persistent fever can mimic endocarditis. Therefore, the results of diagnostic tests should be compared to patients’ medical history and their clinical presentation.

Reoperation after failure of mitral valve repair for degenerative disease: A single surgeon experience

BackgroundWith an increasing number of patients undergoing mitral valve repair, more patients are presenting for reoperation. This study aimed to evaluate factors influencing mortality and survival of patients undergoing reoperation for mitral valve surgery after previous mitral valve repair under a single surgeon. MethodsWe retrospectively collected data from 117 patients who underwent reoperation after previous mitral valve repair between 2010 and 2022. We aimed to identify preoperative, operative, and postoperative factors affecting outcomes. The primary outcome was overall survival, and the secondary outcomes included prolonged hospital stay and in-hospital mortality. The mean follow-up was 9.13 ± 10.36 years (median, 6.50 years). ResultsOut of 117 patients, 85 underwent mitral valve replacement (MVR) and 32 underwent mitral valve repair (MVr). The mean age was 64.7 ± 12.7 years (65.5 ± 12.2 years in the MVR group and 62.7 ± 14.0 years in the MVr group), and 66 (56.4%) were men. On a standard multivariate analysis of the overall factors influencing mortality, advanced age was associated with a higher risk of overall mortality (hazard ratio [HR], 1.07; 95% confidence interval [CI], f1.03-1.12; P = .001). The urgency of surgical intervention also played a role, with a higher risk of in-hospital mortality in patients undergoing emergency reoperation (HR, 1.55; 95% CI, 1.60-149.05; P = .02). Furthermore, the presence of mixed lesions, encompassing both mitral regurgitation and stenosis, was strongly linked to increased overall mortality (HR, 17.09; 95% CI, 4.06-71.94; P < .001) and in-hospital mortality (HR, 1.75; 95% CI, 15.83-1925.61; P < .001). Infective endocarditis emerged as a prominent risk factor for overall mortality (HR, 992.08; 95% CI, 85.74-11,479.08; P < .001) and in-hospital mortality (HR, 5.83; 95% CI, 514.81-65,932.99; P < .001). Additionally, chronic obstructive pulmonary disease was associated with a significantly increased risk of overall mortality (HR, 4.3; 95% CI, 1.24-14.97; P = .02) ConclusionsOur single surgeon experience demonstrates that mitral valve reoperation after a previous repair is associated with good outcomes and survival.

Giant left atrium in previous mitral valve repair

Giant left atrium in previous mitral valve repair

P47 MITRAL VALVE RE–REPAIR THROUGH A RIGHT MINITHORACOTOMY

Abstract Objective Recurrent mitral valve regurgitation after prior repair is usually treated with re–repair or replacement through a median sternotomy. We report our small initial experience with mitral valve re–repair through a repeated minimally invasive approach. Methods From July 2018 to November 2021, 10 patients (median age 52 years IQR 49–68; male 90%) underwent isolated mitral valve re–repair with a right mini–thoracotomy approach with peripheral arterial and venous cannulation. Median Euroscore II was 2.05 (IQR 2.03–2.54). Results The median time from the original operation to redo surgery was 4.7 (3.5–8.1) years. Median cardiopulmonary bypass and cross–clamp times were 128 (IQR 109–134) and 99.5 (IQR 81–112) minutes, respectively. Failure of previous mitral valve repair was mainly due to Gore–Tex chordal rupture (3 patients), annular detachment (3 patients), native chordal rupture (2 patients), and posterior leaflet prolapse (2 patients). Concerning the surgical terchnique, a complete mitral valve ring Corcym Memo 3D or 4D was used in 8 patients while additional repair techniques were needed 5 patients (PTFE neochords implantation, cleft or commissure closure). No conversion to full sternotomy and no reoperation for bleeding was necessary. Median ICU and hospital stay were 2.0 (IQR 2.0–2.0) and 7.5 (7.0–9.0) days respectively. Median follow up time was 3.5 (2.8–3.9) years. Neither deaths nor major postoperative complications occurred in the follow–up period. Conclusions In our experience, mitral valve re–repair can be an attractive option for patients with failure of previous mitral valve surgery and can be safely performed through a minimally invasive approach with good outcomes. Main advantages seem to be the avoidance of extensive surgical dissection, optimal valve exposure, and low risk of surgical complications.

Clinical outcomes after implantation of a sutureless aortic bioprosthesis with concomitant mitral valve surgery: the SURE-AVR registry

BackgroundEarly treatment of aortic valve stenosis is recommended in eligible symptomatic patients with severe aortic valve stenosis who would otherwise have a poor prognosis. The sutureless aortic valve bioprosthesis offers an alternative to standard aortic valve replacement with a sutured valve, but limited data are available in patients who have undergone multiple valve procedures involving the new, sutureless technology. We sought to investigate outcomes in high operative risk patients with previous or concomitant valve surgery who were implanted with a sutureless valve.MethodsSURE-AVR is an ongoing, prospective, multinational registry of patients undergoing aortic valve replacement. In-hospital and post-discharge outcomes up to 5 years were collected.ResultsThe study population comprised 78 patients (mean ± SD: age 73.6 ± 7.6 years, logistic EuroSCORE 18.0 ± 17.5) enrolled at 13 sites who presented for concomitant or previous mitral valve repair (n = 45) or replacement (n = 33), with or without additional concomitant procedures, and were implanted with a sutureless valve. Mean ± SD overall aortic cross-clamp time was 109 ± 41 min and cardiopulmonary bypass time was 152 ± 49 min. Mean ± SD aortic pressure gradients decreased from 37.6 ± 17.7 mmHg preoperatively to 13.0 ± 5.7 mmHg at hospital discharge, and peak aortic pressure gradient from 61.5 ± 28.7 to 23.4 ± 10.6 mmHg. Early events included 1 death, 1 transient ischaemic attack, and 1 bleed (all 1.3%); a permanent pacemaker implantation was required in 6 patients (7.7%), and 2 reoperations (not valve related) (2.6%) took place. Over a median follow-up of 55.5 months (Q1 13.4, Q3 68.6), 12 patients died (6 cardiovascular and 6 non-cardiovascular, both 2.1% per patient-year). Five-year survival was 81.3%. Late paravalvular leak occurred in 2 patients (0.7% per patient-year) and permanent pacemaker implantation was required in 3 patients (0.1% per patient-year). There was no apparent rise in mean or peak aortic pressure gradient over the study.ConclusionsThese results suggest that the sutureless implant is a technically feasible procedure during mitral surgery and is associated with good clinical outcomes.

P1705 Is mitral stenosis per se worthy of anticoagulation therapy?

Abstract We present the case of a 76-year-old man with hypertension and previous mitral valve repair (MVR) due to severe mitral valve regurgitation. He had never experienced atrial fibrillation (AF), and therefore he was not anticoagulated. He had been asymptomatic for 15 years, however, recently he reported the onset of dyspnoea and a transthoracic echocardiogram showed moderate to severe mitral valve stenosis (MVS) in the context of previous MVR. A transesophageal echocardiogram was then requested and it confirmed the degree of MVS (panel A Color flow on mitral valve, panel B CW Doppler), but, astonishingly, it also showed the presence of a giant thrombus in the roof of the left atrium (Panel C,D,F 2D TOE, Panel E 3D TOE). The maximal dimensions of the mass were 3.3 to 4.5 centimetres and, surprisingly, no thrombus was found in the left appendage, which nevertheless had low-flow. MVS is very often associated with severe left atrial dilation and with the onset of atrial fibrillation. However, when a patient has at least moderate MVS and he is in sinus rhythm, there is no robust evidence supporting the initiation of anticoagulants. Though, this case underlines the tight correlation between MVS and thrombus formation regardless of the detectable presence of AF. Moreover, in contrast to usual AF patients, in this particular case left appendage was not involved and the huge mass occupied most of the left atrium, showing that MVS provokes significant low-flow in the atrium too. Abstract P1705 Figure.

Anomalous left coronary artery from the pulmonary artery (ALCAPA) diagnosed in adulthood: Varied clinical presentation, therapeutic approach and outcome

IntroductionThe diagnosis of ALCAPA syndrome is sporadic in adulthood, of the limited cases in the literature most are incidental or without symptoms. There is a broad spectrum of clinical manifestations of ALCAPA syndrome however, including sudden cardiac death. CasesWe present herewith a series of 12 consecutive patients with ALCAPA, all diagnosed in adulthood (between 18 and 73 years of age). Five patients developed symptoms (breathlessness) after the fourth decade of life, 3 were undiagnosed despite a history of previous mitral valve repair, one presented with heart failure, one with resuscitated cardiac arrest, whereas two patients were asymptomatic. We review in this paper, the clinical history, diagnostic approach and therapeutic choices of ALCAPA syndrome. ConclusionALCAPA syndrome is not confined to childhood, late diagnosis in adulthood has a varied clinical presentation. ALCAPA syndrome should be particularly considered as a potential, albeit uncommon cause of mitral regurgitation and/or dilated cardiomyopathy.

Minimally Invasive Port Access Approach for Reoperations on the Mitral Valve

In patients requiring a second-time or more operation on the mitral valve (MV), we assessed whether the outcomes of the minimally invasive port access approach (port access group) were equivalent to those of the traditional redo sternotomy approach (redo sternotomy group). In a retrospective review (1998-2011), 409 patients had previous MV operations requiring a second-time or more MV reintervention. Of those, 67 patients had the port access approach, and 342 had the redo sternotomy approach. Of the latter, 220 met the inclusion criteria because emergencies, patients with endocarditis, and those requiring concomitant procedures involving aortic valve and aorta were excluded. New York Heart Association class 2 or above, age, atrial fibrillation, and surgical indications were similar in both groups. The port access group had more patients with previous MV repair (78% [n = 52] vs 41% [n = 90], p < 0.01) than with MV replacement (19% [n = 13) vs 53% [n = 116], p < 0.01). Concomitant procedures were similar (20% [n = 14] vs 27% [n = 59], p = 0.4). The MV re-repair rates were similar (19% [n = 10] vs 22% [n = 20], p = 1). The cardiopulmonary bypass times (153 ± 42 minutes vs 172 ± 83 minutes, p = 0.07) and aortic cross-clamping times (104 ± 38 minutes versus 130 ± 71 minutes, p < 0.01) were lower in the port access group. Mortality was lower in the port access group, although not significantly (3.0% [n = 2] vs 6.0% [n = 13], p = 0.5). The rates of postoperative stroke were similar (3.0% [n = 2] vs 3.2% [n = 7], p = 1). On postoperative echocardiography, freedom from mitral regurgitation >2+ was 100% in the port access group and 99% in the redo sternotomy group. The mean hospital length of stay was 11 ± 15 days versus 14 ± 12 days (p = 0.07). The port access approach can be safely adopted for reoperations on the MV without compromising postoperative mortality or MV function.

Case 5/2014 - 41-Year-Old Woman with Rheumatic Disease and Previous Mitral Valve Repair with Pulmonary Embolism and Cardiogenic and Septic Shock.

A 41-year-old female sought medical care due to severe dyspnea. The patient had had acute rheumatic disease in childhood. During evolution, she developed mitral stenosis. The symptoms became incapacitating and she underwent mitral commissurotomy at 36 years. She progressed well for a few years until dyspnea recurred and she was once again submitted to surgery, at 41 years, when she underwent mitral valve plasty (03/16/2005). After the last surgery, she had dyspnea on great exertion for about three months, when it progressed and started to be triggered by middle, and finally by mild exertion, and at three days before hospitalization (10/10/2005), it had become present even at rest. The patient attributed the recent worsening to current medication discontinuation: captopril 25 mg, furosemide 80 mg, 0.25 mg digoxin and warfarin 2.5 mg daily. Physical examination (10/10/2005) showed the patient was in good general health, dyspneic, with a marked increase in jugular venous pressure, pulse rate of 92 bpm, blood pressure of 100/60 mmHg. Lung examination was normal. Cardiac auscultation showed irregular rhythm without additional heart sounds. Systolic murmur +/4+ was diagnosed in the mitral valve area. There were no alterations at the abdominal examination, but slight edema of the lower limbs. Laboratory tests (10/10/2005) showed hemoglobin 11.7 g/dL, hematocrit 35%, WBC, 3,900/ mm3, platelets, 12.9000 /mm3, creatinine 1.3 mg / dL, urea 31 mg / dL, sodium 135 mEq/L, potassium 3.6 mEq/L, INR 1.19 and activated partial thromboplastin time (patient / control) 1.09. The electrocardiogram (10/10/2005) showed frequency of 90 bpm, atrial fibrillation, low voltage QRS complex, undetermined QRS axis in the frontal plane and presence of intraventricular stimulus conduction disturbance, of the right branch type and decreased left ventricular potential, suggesting right ventricular overload (Figure 1). Figure 1 Atrial Fibrillation, low voltage QRS complexes, right bundle branch block, low voltage of left QRS complexes, right ventricle hypertrophy The patient was admitted for treatment. She remained in the emergency unit for five days and was admitted (on October 15, 2005). She received furosemide 120 mg intravenously, 40 mg of enalapril, 0.25 mg of digoxin, 50 mg of hydrochlorothiazide and 120 mg of enoxaparin daily by subcutaneous route, as well as dobutamine 10 µg/kg.min intravenously. At hospitalization she had hypotension, increased edema and creatinine elevation (Table 1). After three days, the patient developed anuria, anasarca and finally shock with hypotension with 60 mmHg despite the use of 15 µg/kg.min of dobutamine. Table 1 Laboratory assessment The laboratory tests (10/20/2005) showed creatinine 3.2 mg/dL and then 5.9 mg / dL, Urea 75 mg / dL and, during evolution, 115 mg / dL (Table 1). At physical examination (10/20/2005) the patient was in poor general condition, with blood pressure of 80/50 mmHg, heart rate 90 bpm, crackles in both lungs, arrhythmic heart sounds (atrial fibrillation), systolic murmur + / 4 + in the mitral area, ascites and edema ++++ / 4+. The electrocardiogram (20/10/2005) showed atrial fibrillation, heart rate of 100 bpm, low QRS voltage, intraventricular conduction disturbance of the right bundle branch block type stimulus, decreased left ventricular strength (Figure 2). Figure 2 Atrial Fibrillation, low voltage QRS complexes, right bundle branch block, low voltage of left QRS complexes in horizontal plane, right ventricle hypertrophy. The echocardiogram (on October 21) showed normal left ventricle, dilated and hypokinetic right ventricle, mitral valve calcification, commissural fusion, moderate stenosis and moderate tricuspid regurgitation (Table 2). Transesophageal echocardiogram (on October 21) showed pulmonary artery dilation with a large thrombus image (10 × 5.0 cm) extending to its left branch and the presence of autocontrast in the left atrium. Table 2 Echocardiograms The diagnosis of pulmonary thromboembolism was made and 100 mg of r-TPA was administered intravenously in two hours. The patient went into shock, which required vasoactive drugs. Intravenous norepinephrine was administered, associated with ceftriaxone and metronidazole, as well as vancomycin for empiric treatment of the systemic infection. Mechanical ventilation was initiated with tracheal intubation for ventilatory support. Pulmonary arteriography (on October 24) showed pulmonary artery pressures of 30/15/22 (systolic/diastolic/mean) mmHg. No images suggestive of pulmonary thromboembolism were identified. The patient had an abundant epistaxis episode, which required transfusion of fresh plasma. CT scan of the skull (on October 24) showed a hypoattenuating nodular area in the caudate nucleus head to the left, with no other alterations. Blood cultures (10/25/2005) showed the presence of A. baumannii (sensitive only to imipenem). Hemodialysis (on October 26) was not tolerated by the patient, due to hypotension, and could not be performed. The patient developed shock and died (10/26/2005).

The haemodynamic cascade

The haemodynamic cascade

Emergent cardiopulmonary bypass during pectus excavatum repair

Pectus excavatum is a chest wall deformity that produces significant cardiopulmonary disability and is typically seen in younger patients. Minimally invasive repair of pectus excavatum or Nuss procedure has become a widely accepted technique for adult and pediatric patients. Although it is carried out through a thoracoscopic approach, the procedure is associated with a number of potential intraoperative and post-operative complications. We present a case of cardiac perforation requiring emergent cardiopulmonary bypass in a 29-year-old male with Marfan syndrome and previous mitral valve repair undergoing a Nuss procedure for pectus excavatum. This case illustrates the importance of vigilance and preparation by the surgeons, anesthesia providers as well as the institution to be prepared with resources to handle the possible complications. This includes available cardiac surgical backup, perfusionist support and adequate blood product availability.

Mitral Re-Repair and Right Coronary Fistula Closure Advantage of Minimally Invasive Approach

A 51-year-old man developed severe mitral regurgitation 10 years after previous mitral valve repair; the echocardiographic images showed a remarkable eccentric jet toward posterior wall of left atrium associated with a high degree of pulmonary vein retrograde flow. The coronary arteriography pointed out no pathologic lesions but a coronary fistula from the proximal right coronary to the right atrium. The standard approach was avoided, and a right anterolateral minithoracotomy was chosen, providing an excellent view. Under cardiopulmonary bypass and mild hypothermia, the mitral valve was re-repaired, and a new ring was implanted. After aortic cross-clamp release, the right coronary fistula was closed through the right atrium. The postoperative course was uneventful, and the patient was discharged on the fourth postoperative day. In such a high-risk reintervention and concomitant procedure, we think that this different approach may represent a feasible and reliable alternative.

Late posterior failure after mitral valve repair in degenerative disease

Little is known regarding the mechanisms, the feasibility and the long-term results of re-repair in 'posterior failure' of a previous mitral valve repair performed for severe degenerative mitral regurgitation. We report our 16-year experience in redo surgery for late posterior failure of mitral valve repair in degenerative disease. From 1991 to 2004, 13 consecutive patients (10 males; median age: 65 years) were reoperated for late posterior failure of mitral valve repair. All patients had grade > or =3+ mitral regurgitation. Repair was mainly performed using Carpentier's techniques. Repair failure was due to posterior leaflet prolapse, leaflet retraction or leaflet dehiscence in eight (62%), three (23%) and two (15%) patients, respectively. Repair was performed in nine patients (69%). There was no perioperative death. During follow-up (median: 105 months; range: 40-170 months) one late death occurred in the mitral valve replacement group. One (11%) patient underwent mechanical mitral valve replacement 125 months after re-repair. Congestive heart failure occurred in one patient in each group. At the latest follow-up, all but one patient in the mitral valve repair group were in NYHA functional class I or II and all were in sinus rhythm. Doppler echocardiographic studies of the re-repaired valves (n=8) showed no or trivial, grade 1+ and grade 2+ residual mitral regurgitation in 6 (75%), 1 and 1 patients, respectively. Mean transmitral gradient was 3 mmHg (2-8 mmHg) and left ventricular ejection fraction was 59% (43-77%). In case of late posterior failure of mitral valve repair for severe degenerative, re-repair is feasible in about 70% of the patients with encouraging results at 10 years.

Redo mitral valve surgery: morphological features

Mitral valve (MV) repair is the surgery of choice in patients with mitral regurgitation. This study reviews the histological features of excised mitral leaflets and annuloplasty rings of patients who had previous MV repair or attempted repair. This study examines the morphological findings of 54 excised MV leaflets and 39 annuloplasty rings, excised over 15 years at one institution. Patients were separated into groups based on the time interval between surgeries: attempted repair, <30 days, 30-365 days, and >1 year. The fifty-four patients had a mean age of 55.7+/-17.9 years at the time of surgery after failed repair or attempted repair, of the MV. Index surgery for all patients had been performed between 1973 and 2005. The interval between index surgery and readmission (n=49, 91%, excluding those with MV replacement following attempted repair) was 6.61+/-7.12 years. Myxomatous change and infective endocarditis (IE) were found in valves with failed attempted MV repair. Nonleaflet (ischemic, chordal rupture, and flow abnormalities) and acquired changes, degenerative, myxomatous, and IE were found in valves repaired in patients at <30 days postoperatively. Degenerative changes (myxomatous and RF) were the main underlying pathology found in valves repaired between 31 and 365 days previously. At over 1 year after original surgery, repairs were found to have congenital, degenerative (myxomatous, rheumatic valvular disease, and IE) and nonleaflet (ischemic and chordal rupture) changes. Although MV repair is the preferred treatment for mitral regurgitation, failure of repair may occur in patients at the time of surgery or over varying periods after surgery. The pathological findings following repair include IE, fibrosis, calcification, and nodular thickening at and around the operative site, thickening and stiffening of the synthetic chordae tendinae due to tissue overgrowth, rupture of chordae tendinae, and progression of acquired degenerative disease.

Pulmonary Mucormycosis

A 56-year-old nondiabetic male presented for evaluation of fever and cough shortly after 6 cycles of chemotherapy for treatment of non-Hodgkins lymphoma. Over the subsequent few days, the patient developed hemoptysis, sepsis, hypotension, and severe immunocompromise (total white blood cell count = 100/mm3) and thrombocytopenia (platelet count = 41,000/mm3). Chest x-ray (normal one month prior) demonstrated a prominent cavitary lung lesion involving the left upper lobe (Fig 1 ; sternal wires are from a previous mitral valve repair procedure). Computed tomography of the chest provided additional anatomic detail (Fig 2 ). Because of the patient's rapid clinical deterioration, platelet transfusion and subsequent surgery were performed.Fig 2View Large Image Figure ViewerDownload (PPT) Exploration of the left hemithorax was conducted through a standard posterolateral thoracotomy. A large-diameter (11-cm) necrotic abscess was discovered, requiring anatomic left upper lobectomy. An intercostal muscle flap was used to cover the bronchial stump. After completion of the surgical procedure, the specimen was further examined (Fig 3 ). When the abscess was incised, a prominent rush of air was appreciated as the cavity decompressed and partially collapsed (Fig 4 ). The specimen was sent for histologic and microbiologic evaluation. Postoperatively, aggressive resuscitation was continued in the intensive care unit. Identification of Mucor species (Fig 5 , hematoxylin & eosin, ×400) allowed for treatment with amphotericin B. Unfortunately, the patient died 8 days after surgery following complications of septic shock, renal failure, suspected disseminated intravascular coagulation, and upper extremity ischemia.Fig 4View Large Image Figure ViewerDownload (PPT)Fig 5View Large Image Figure ViewerDownload (PPT)