Abstract Background Mitral regurgitation is a frequent valvular disease, with an increasing prevalence. We analyzed the short-term outcomes of mitral valve repair procedures conducted in our clinic using a new semirigid annuloplasty ring featuring a gradual saddle shape design. Methods We retrospectively analyzed mitral valve repair surgeries performed at our Institution between December 2019 and November 2021 with the MEMO 4D semirigid annuloplasty ring. Results In total, 53 patients were included in the study. Mean patient age was 63.6 ± 11.7 years. Most patients presented with degenerative mitral valve regurgitation ( N = 44; 83%). The grade of mitral regurgitation was equal or more than 3 + in 98.1% of the patients ( N = 52). The most used ring size was size 34 mm ( N = 30, 56.6%). There was no intraoperative or hospital mortality. No cases of stroke, bleeding, endocarditis or other major complications occurred. At discharge, most patients were in NYHA class I. Postoperative echocardiographic results showed no (90.6%) or 1+ (5.7%) mitral valve regurgitation. Only 1 patient (1.9%) presented with mitral valve regurgitation grade 2+. Mean postoperative transvalvular gradient was low (mean = 3.3 ± 1.2 mmHg). No cases of LVOT obstruction or systolic anterior motion occurred. Conclusions Our series showed excellent mitral valve competency and very satisfactory early clinical outcomes. The transesophageal echocardiographic follow-up, despite obtained in a limited number of patients, further confirmed the effectiveness of findings of this preliminary experience.
EDITOR: The use of thoracic epidural anaesthesia (TEA) in patients undergoing cardiac surgery, although increasing in popularity, remains controversial [1,2]. Moreover, while relatively large series of patients undergoing coronary revascularization under TEA have been studied, a small number of cases has been reported in which TEA has been used in valvular cardiac surgery [3]. We report the successful use of TEA in a challenging case of mitral surgery, in a patient with severe co-morbidities and allergies contra-indicating the administration of non-steroidal anti-inflammatory drugs (NSAIDs) and opioids. The patient was previously rejected by other cardiosurgical centres. A 49-yr-old (157 cm, 59 kg) female with severe mitral regurgitation was scheduled for valve replacement. Co-morbidities included hypertension, a history of congestive heart failure and transient acute renal failure, pectus excavatum with severe respiratory deficit, multiple allergies (including various antibiotics, paracetamol and NSAIDs), previous transfusion reaction, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, post-thyroidectomy hypothyroidism and hypoparathyroidism. The patient was receiving amlodipine, clonidine, spironolactone, budesonide, calcium fumarate, salbutamol, beclomethasone, oxygen, l-thyroxine and calcium carbonate. She complained of fatigue and dyspnoea on minimum exertion and was orthopnoeic, with reduced chest expansion, reduced dipharagmatic mobility and abnormal sounds in the inferior pulmonary fields. Electrocardiography showed sinus rhythm and signs of left ventricular hypertrophy. Chest X-ray was consistent with the patient's cardiac and pulmonary diagnosis. Transthoracic echocardiography revealed moderate-to-severe mitral regurgitation caused by functional tethering and fibrosis of the posterior leaflet, moderate concentric left ventricular hypertrophy, hypokinetic cardiopathy with no geometric remodelling and left ventricular ejection fraction of 40%. It also showed increased pulmonary artery pressure (50 mmHg systolic), with moderate tricuspid regurgitation and mild right ventricular failure. No preoperative transoesophageal examination was performed because the patient did not tolerate the procedure. Spirometry confirmed the severe obstructive-restrictive pattern with forced expiratory volume in 1 s (FEV1) 31% and forced vital capacity (FVC) 43% of predicted. Partial pressure of O2 (PaO2) and CO2 (PaCO2) were 69 and 40 mmHg, respectively, with saturation of O2 (SaO2) 92% at arterial blood gases analysis on room air. Other biochemical and haematological parameters were within normal limits. In view of her preoperative status, it was believed that the patient would benefit from TEA. The risks and benefits were explained to her and she gave written informed consent. Epidural catheterization was performed on the day prior to surgery. Her pre-operative platelet count (390 × 109 mL−1) and coagulation (international normalized ratio (INR) 0.87, partial thromboplastin time (PTT) ratio 0.87) were within the normal range. Catheter placement was accomplished by an experienced anaesthesiologist in a high-dependency area. Monitoring included electrocardiogram, non-invasive blood pressure and pulse oximetry. The patient was positioned sitting upright and an 18-G epidural catheter was inserted at T5-T6, using the loss-of-resistance technique and a midline approach, in a single attempt. The catheter was advanced 6 cm cephalic into the epidural space. No bleeding was noted and a test dose of 2 mL of 2% lidocaine was injected. On the day of operation, the patient received her usual medication, followed by lorazepam 3 mg by mouth. Standard monitoring plus pulmonary artery catheter were applied. General anaesthesia consisted of fentanyl, midazolam, propofol, rocuronium and sevoflurane. After induction, a bolus dose of 5 mL of 1% lidocaine and fentanyl 5 μg mL−1 was administered by epidural catheter, with supplemental boluses of 3-5 mL of the same mixture throughout the operation (20 mL total amount) according to arterial pressure stability. A mitral valve replacement with mechanical prosthetic valve using moderately hypothermia (32°C) and cardiopulmonary bypass was performed. The patient was given 300 UI kg−1 of heparin and intermittent bolus doses to maintain the activated coagulation time (ACT) >480 s. At termination of bypass, normal coagulation was restored using protamine sulphate in the ratio of 1 mg kg−1 for every mg of heparin administered according to the ACT. Surgery was uneventful and no difficulties in haemostasis were noted. Weaning required inotropic support with epinephrine 0.05 μg −1kg min−1 and an enoximone 30 mg bolus plus 3 μg kg−1 min−1 continuous infusion. After the completion of the procedure, the patient was transferred to the intensive care unit. An epidural infusion of 0.2% ropivacaine and fentanyl 0.4 μg mL−1, at a rate of 4-7 mL h−1, was given as postoperative analgesia for the first 72 h. Inotropic support was progressively reduced and stopped on the first postoperative day. Also tracheal extubation was performed on the same day with good post-extubation gas exchanges in comparison with preoperative values. Good analgesia was obtained, with a pain score of 1 at rest and 3 during coughing. No parenteral opioids were required postoperatively. Neither paresthesiae nor heaviness were reported, nor any motor weakness was detected. Low-molecular-weight heparin (LMWH) 100 UI kg−1 twice daily was started on the second postoperative day as anticoagulation therapy. No oral anticoagulants were administered. The patient experienced a transient episode of atrial fibrillation that regressed after a 300 mg bolus dose of amiodarone on the third postoperative day. A pyrexia developed on the second and third days despite antibiotic prophylaxis with cefazoline. We removed the epidural catheter 12 h after a dose of LMWH and discharged the patient from ICU on the fourth postoperative day when starting oral anticoagulants. The risk-benefit ratio of applying TEA to patients undergoing cardiac surgery is a lively debated topic [1]. Many potential clinical benefits have been suggested and investigated, but effects on clinical outcomes remain to be determined and compared with the risk of epidural haematoma [1,4,5]. The only clear benefit of using TEA in cardiac surgical patients is enhanced postoperative analgesia [6]. Respiratory therapy and aggressive control of postoperative pain were considered key components in the management of this high-risk patient, and TEA played an important role in view of the long list of patient co-morbidietes. A cautious application of TEA [7] provided excellent postoperative analgesia without parenteral opioids and NSAIDs, and allowed a rapid recovery of consciousness, a reduced time to tracheal extubation and an early active respiratory physiotherapy and mobilization, thus simplifying postoperative management in this complex patient. Acknowledgements The study was conducted exclusively with departmental sources. There is no conflict of interest by any of the authors. We thank Giardina Giuseppe, RN and Castelnuovo Lara, RN for the care provided to this patient and for revising the manuscript. G. Crescenzi R. D. Covello G. Landoni M. De Luca G. Fracasso M. Melone S. M. Serini E. Bignami C. Rosica A. Zangrillo 1Department of Cardiothoracic and Vascular Anesthesia Istituto Scientifico San Raffaele Università Vita-Salute San Raffaele Milano, Italy
Abstract This study aimed to assess the predictors of acute kidney injury (AKI) during colistin therapy in a cohort of patients with bloodstream infections (BSI) due to colistin-susceptible Gram-negative bacteria, focusing on the role of serum albumin levels. The study consisted of two parts: (1) a multicentre retrospective clinical study to assess the predictors of AKI during colistin therapy, defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria; and (2) bioinformatic and biochemical characterization of the possible interaction between human serum albumin and colistin. Among the 170 patients included in the study, 71 (42%), 35 (21%), and 11 (6%) developed KDIGO stage 1 (K1-AKI), KDIGO stage 2 (K2-AKI), and KDIGO stage 3 (K3-AKI), respectively. In multivariable analyses, serum albumin <2.5 g/dL was independently associated with K1-AKI (subdistribution hazard ratio [sHR] 1.85, 95% confidence interval [CI] 1.17–2.93, p = 0.009) and K2-AKI (sHR 2.37, 95% CI 1.15–4.87, p = 0.019). Bioinformatic and biochemical analyses provided additional information nurturing the discussion on how hypoalbuminemia favors development of AKI during colistin therapy. In conclusion, severe hypoalbuminemia independently predicted AKI during colistin therapy in a large cohort of patients with BSI due to colistin-susceptible Gram-negative bacteria. Further study is needed to clarify the underlying causal pathways.
Abstract A 77-year-old female, known hypertensive and dyslipidemic on treatment presented with three episodes of syncope in the last two months. On examination; there was grade 4/6 harsh systolic murmur on the lateral sternal border. Transthoracic echocardiography was difficult because of mesocardia and abnormal rotation of the heart due to enlarged right sided chambers. There is mild left ventricular hypertrophy with normal ejection fraction, no left sided valvular disease. The right ventricle was hypertrophied and dilated with normal RV function. The pulmonary valve was thickened with significant systolic flow aliasing through the valve with significant regurgitation and huge main pulmonary trunk aneurysm (59 mm at its wideset diameter) (Figure 1). Transthoracic approach did not allow a correct alignment of the Doppler CW and the correct estimate of pulmonary valvulopathy; TEE was performed with a correct visualization of the valve in deep transgastric projection at 90 degrees. The valve was thickened, fibrotic, degenerated with systolic doming of leaflets (Figure 2) and peak systolic gradient ∼ 70 mmHg (Figure 3). 3D reconstruction of the valve showed a tricuspid valve (Figure 4) with a valve area ∼ 0.9 cm2 using planimetry in MPR (Figure 5). CT scan was performed which confirmed the main pulmonary trunk aneurysm ∼ 60 mm (Figure 6). Therefore, in light of the clinical and instrumental picture, the patient was referred to heart team discussion for the plan of surgical intervention. Discussion According to the ESC guidelines for grown up congenital heart disease in 2010, this pulmonary valve should be intervened upon as it is severe symptomatic PS (1), but there are 2 problems with this case; the first is significant associated PR, so no place for balloon dilatation here, the second problem is the pulmonary artery aneurysm (PAA). The dilemma of management of pulmonary PAA is that all the available data are about aortic aneurysms. Indications for intervention for PAA include: Absolute PAA diameter ≥ 5.5 cm, Increase in the diameter of the aneurysm of ≥ 0.5 cm in 6 mo, Compression of adjacent structures, Thrombus formation in the aneurysm sack, Evidence of valvular pathologies or shunt flow Verification of PAH, Signs of rupture or dissection (2). Surgery could include: Aneurysmorrhaphy only decreases the diameter of the vessel (3). Aneurysmectomy and repair or replacement of the right ventricular outflow tract is commonly used technique recently and mostly suits connective tissue disorders (6). Also, Replacement of the PA and the pulmonary trunk with a conduit (Gore-Tex or Dacron tubes, homografts, or xenografts) starting in the right ventricular outflow tract with replacement of the pulmonary valve (4). Conclusion PAA management is currently challenging because there are no clear guidelines on its optimal treatment. The presence of significant pulmonary valve dysfunction could affect the decision making of the associated PAA management. Abstract P180 Figure.
