MAY – AUGUST 2024 VOL 35 NO 2 • Effect of di fferent pr iming f luids in cardiopulmonary bypass surgery • Modi f ied David V re- implantat ion technique for valve-spar ing aort ic root replacement • Cross-sect ional study of adul t mi tral valve disease at Chr is Hani Baragwanath Hospi tal • Esmarch bandage appl icat ion in giant saphenous vein closure dur ing endovenous glue ablat ion • Empagl i f lozin signi f icant ly prevents QTc prolongat ion due to ami tr iptyl ine intoxicat ion • Changes in blood pressure af ter catheter-based renal denervat ion in South Afr ica • Effects of intravenous sodium thiosul fate on vascular calci f icat ion in dialysis pat ients • Coronary artery bypass graf t ing in a pat ient wi th si tus inversus total is CardioVascular Journal of Afr ica (off icial journal for PASCAR) www.cvja.co.za
Pharmaco Distribution (Pty) Ltd. 3 Sandown Valley Crescent, South Tower, 1st Floor Sandton, 2196. PO Box 786522, Sandton, 2146. South Africa Tel: +27 11 784 0077. Fax: +27 11 784 6994. www.pharmaco.co.za ISA _ 21 _ 01 References: 1. Ismo® South African SAHPRA aproved package insert. 2. Ismo 20 Product Monograph(2015). 3. Abshagen,U. 1992. Pharmacokinetics of isosorbide mononitrate. The American Journal of Cradiology, [online] 70 (17),pp.G61-G66 4. Thadani U, Maranda CR, Amsterdam E, et al. Lack of Pharmacological Tolerance and Rebound Angina Pectoris during Twice-daily Therapy with isosorbide-5-mononitrate. Annals of Internal Medicine. 1994.; 120: 353-359. ISMO®-20 R/7.1.4/136. Each Ismo®-20 Tablet contains Isosorbide-5-mononitrate 20mg. S3 For full prescribing information, please refer to the approved package insert R T S Q P R T S Q P P Long term prophylaxis and management of Angina Pectoris1 No first-pass metabolism. 100% bioavalability2,3 Twice-daily dosing regimen shown to avoid withdrawal and tolerance4 Trust the Original!
ISSN 1995-1892 (print) ISSN 1680-0745 (online) Cardiovascular Journal of Afr ica www.cvja.co.za CONTENTS INDEXED AT SCISEARCH (SCI), PUBMED, PUBMED CENTRAL AND SABINET Vol 35, No 2, MAY – AUGUST 2024 EDITORS Editor-in-Chief (South Africa) PROF PAT COMMERFORD Assistant Editor PROF JAMES KER (JUN) Regional Editor DR A DZUDIE Regional Editor (Kenya) DR F BUKACHI Regional Editor (South Africa) PROF R DELPORT EDITORIAL BOARD PROF PA BRINK Experimental & Laboratory Cardiology PROF R DELPORT Chemical Pathology PROF MR ESSOP Haemodynamics, Heart Failure & Valvular Heart Disease DR OB FAMILONI Clinical Cardiology DR V GRIGOROV Invasive Cardiology & Heart Failure PROF J KER (SEN) Hypertension, Cardiomyopathy, Cardiovascular Physiology DR J LAWRENSON Paediatric Heart Disease PROF A LOCHNER Biochemistry/Laboratory Science DR MT MPE Cardiomyopathy PROF DP NAIDOO Echocardiography PROF B RAYNER Hypertension/Society PROF MM SATHEKGE Nuclear Medicine/Society PROF YK SEEDAT Diabetes & Hypertension PROF H DU T THERON Invasive Cardiology INTERNATIONAL ADVISORY BOARD PROF DAVID CELEMAJER Australia (Clinical Cardiology) PROF KEITH COPELIN FERDINAND USA (General Cardiology) DR SAMUEL KINGUE Cameroon (General Cardiology) DR GEORGE A MENSAH USA (General Cardiology) PROF WILLIAM NELSON USA (Electrocardiology) DR ULRICH VON OPPEL Wales (Cardiovascular Surgery) PROF PETER SCHWARTZ Italy (Dysrhythmias) PROF ERNST VON SCHWARZ USA (Interventional Cardiology) SUBJECT EDITORS Nuclear Medicine and Imaging DR MM SATHEKGE Heart Failure DR G VISAGIE Paediatric DR S BROWN Paediatric Surgery DR DARSHAN REDDY Renal Hypertension DR BRIAN RAYNER Surgical DR F AZIZ Adult Surgery DR J ROSSOUW Epidemiology and Preventionist DR AP KENGNE Pregnancy-associated Heart Disease PROF K SLIWA-HAHNLE 69 FROM THE EDITOR’S DESK PA Brink CARDIOVASCULAR TOPICS 70 Effect of different priming fluids on extravascular lung water, cell integrity and oxidative stress in cardiopulmonary bypass surgery H Ulugöl • MG Can • U Aksu • K Vardar • M Ökten • F Toraman 75 Mid-term experience of the modified David V re-implantation technique for valve-sparing aortic root replacement S Sarikaya • K Kirali 82 Systemic immune–inflammation index, and neutrophil-to-lymphocyte and plateletto-lymphocyte ratios can predict clinical outcomes in patients with acute coronary syndrome FÖ Karadeniz • Y Karadeniz • E Altuntaş 89 A cross-sectional study of the spectrum, aetiology and clinical characteristics of adult mitral valve disease at Chris Hani Baragwanath Academic Hospital E Banderker • G Roozen • M Tsitsi • R Meel 96 Investigation of left ventricular changes according to valve type in patients with surgical replacement due to isolated aortic stenosis A Güner • M Işık • Ö Tanyeli • S Yıldırım • E Ege • VB Taban 102 Evaluation of clinical results of esmarch bandage application in giant saphenous vein closure during endovenous glue ablation O Karahan • O Akkaya • E Aydogan 106 Empagliflozin significantly prevents QTc prolongation due to amitriptyline intoxication VŐ Barış • E Gedikli • AB Dinçsoy • A Erdem
CONTENTS Vol 35, No 2, MAY – AUGUST 2024 FINANCIAL & PRODUCTION CO-ORDINATOR ELSABÉ BURMEISTER Tel: 021 976 8129 Fax: 086 664 4202 Cell: 082 775 6808 e-mail: elsabe@clinicscardive.com PRODUCTION EDITOR SHAUNA GERMISHUIZEN Tel: 021 785 7178 Cell: 083 460 8535 e-mail: shauna@clinicscardive.com CONTENT MANAGER MICHAEL MEADON (Design Connection) Tel: 021 976 8129 Fax: 0866 557 149 e-mail: michael@clinicscardive.com The Cardiovascular Journal of Africa, incorporating the Cardiovascular Journal of South Africa, is published 10 times a year, the publication date being the third week of the designated month. COPYRIGHT: Clinics Cardive Publishing (Pty) Ltd. LAYOUT: Jeanine Fourie – TextWrap PRINTER: Tandym Print/Castle Graphics ONLINE PUBLISHING & CODING SERVICES: Design Connection & Active-XML.com All submissions to CVJA are to be made online via www.cvja.co.za Electronic submission by means of an e-mail attachment may be considered under exceptional circumstances. Postal address: PO Box 1013, Durbanville, RSA, 7551 Tel: 021 976 8129 Fax: 0866 644 202 Int.: +27 21 976 8129 e-mail: info@clinicscardive.com Electronic abstracts available on Pubmed Audited circulation Full text articles available on: www.cvja. co.za or via www.sabinet.co.za; for access codes contact elsabe@clinicscardive.com Subscription: To subscribe to the online PDF version of the journal, e-mail elsabe@clinicscardive.com • R500 per issue (excl VAT) • R2 500 for 1-year subscription (excl VAT) The views and opinions expressed in the articles and reviews published are those of the authors and do not necessarily reflect those of the editors of the Journal or its sponsors. In all clinical instances, medical practitioners are referred to the product insert documentation as approved by the relevant control authorities. 111 Changes in blood pressure after catheter-based renal denervation in South Africa IO Ebrahim • M Ntsekhe • B Rayner • M Fahy • G Mancia • M Böhm; on behalf of the Global SYMPLICITY Registry investigators SYSTEMATIC REVIEW 115 Effects of intravenous sodium thiosulfate on vascular calcification in dialysis patients with end-stage renal disease: a systematic review and meta-analysis Y-H Song • A Ning • N Guo • Y Yang • F Tang • N Zhao • J Hu • H Wu • T Peng • Y-F Xiao • G-Y Cai CASE REPORTS 124 Identification and treatment of asymptomatic central venous catheter thrombosis after TAVI X Huang 127 Coronary artery bypass grafting in a patient with situs inversus totalis T Okan • C Topaloglu • O Kucuk • S Bayraktaroglu • N Ceylan PUBLISHED ONLINE (Available on www.cvja.co.za and in PubMed)
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 AFRICA 69 From the Editor’s Desk Professor Patrick Commerford has been Editor-in-Chief of the journal since 2014. After 10 years of holding the fort at the journal, he has retired. It has been an honour to have had a person of his stature heading the journal. We wish him and his family strength in the coming years. In the interim period between the passing of the journal’s founder, Professor AJ Brink in 2012, and Professor Commerford’s appointment, I took on the editorial responsibilities. I will be stepping in once again, temporarily, during this transition period. This is also perhaps a time to reflect. As Bob Dylan sang in 1964, The Times They Are A-Changin’ – time does not stand still and the environment changes constantly. Until recently, the belief was that the publishing team should be on hand for meetings, and so it was until the Covid-19 epidemic and lock-down from March 2020 to April 2022. Civil liberties were curtailed and during this time we had no physical meetings. Yet, the journal prevailed. So, with modern communication, is there a real need for a physical office with everybody on hand? The answer is no! This is somewhat reminiscent of the current debate in South Africa about the phasing out of printed newspapers. An old blackand-white photo is circulating of a night office preparing the newspaper to be printed overnight. The journalists around a round table have cigarettes in hand, smoke is swirling to the roof, and ashtrays abound – nostalgia! Yes, we do need an anchor, the go-to for articles, congress abstracts and programmes. But an editor-in-chief does not have to have an office and be close by. So, the next editor could be anywhere in Africa. As with PASCAR, face-to-face meetings can be achieved electronically. For strategic reasons, we need to think long term. Institutions have a longer life than individuals. We have to think about the future. Today, our operations are anchored by a dedicated team without a physical office: • Elsabe Burmeister manages the peer-review process, finances and journal production. • Michael Meadon and his team handle online services, including website management, PubMed Central deposits and other electronic services. • Shauna Germishuizen manages copy-editing and journal production. We have had offers from well-known commercial companies to manage the process. Editing may be in one country and creating PDFs in another. But this is costly! Additionally, the CVJA has transitioned to a new peer-review and editorial system, Open Journal Systems (OJS), hosted by SABINET. This change is part of our strategy to ensure the journal’s long-term sustainability and adaptability. The current selection of articles in this issue includes two from South Africa and the rest from Turkey and other countries. Ebrahim Banderker and colleagues from Chris Hani Baragwanath Academic Hospital discuss adult mitral valve disease (MVD). In contrast to the developed world countries, rheumatic MVD is most prevalent in South Africa. The largest group tended to be older African females with co-morbidities with predominant rheumatic mitral regurgitation. Iftikhar O Ebrahim and co-workers are from Groote Schuur and the University of Cape Town. They discuss the South African experience with blood pressure effects after catheter-based renal denervation. This forms part of the Global SYMPLICITY Registry. An interesting systematic review from China addresses the issue of vascular calcification in end-stage renal disease and how sodium thiosulfate, in contrast to statins, warfarin and others, may be a solution. There are also some interesting fillers from other sources. These are short and make for interesting reading. One is about a new ‘more reliable’ NHLS LDL cholesterol calculation method. Reported is also a study from the US that current risk formulae may be overstating the need for statins to prevent heart disease in some people. On atrial fibrillation (AF) there are two: (1) a call to re-assess the growing burden of AF and its consequences, and (2) a study suggesting that AF is rising among younger people. PA Brink Acting Editor-in-Chief Paul Brink
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 70 AFRICA Cardiovascular Topics Effect of different priming fluids on extravascular lung water, cell integrity and oxidative stress in cardiopulmonary bypass surgery Halim Ulugöl, Meltem Güner Can, Uğur Aksu, Kubra Vardar, Murat Ökten, Fevzi Toraman Abstract Background: Discussions continue on the ideal priming fluid in adult cardiac surgery. The purpose of this prospective study was to evaluate the effects of different types of priming fluids on extravascular lung water, cell integrity and oxidative stress status. Methods: Thirty elective coronary artery bypass surgery patients were randomised prospectively into two groups. The first group received colloid priming fluid, while the second group received crystalloid priming fluid. Extravascular lung water index, advanced oxidative protein products, total thiol, free haemoglobin, ischaemic modified albumin and sialic acid levels were measured. Moreover, intra-operative and postoperative outcomes were reviewed. Results: There were no significant differences between the groups with regard to extravascular lung water index, oxidative stress parameters or cell integrity (p > 0.05). Similarly, no significant differences were observed between the patients with regard to intra-operative and postoperative outcomes (p > 0.05). Conclusions: The presumed superiority of colloidal priming for cardiopulmonary bypass could not be confirmed in our study. Keywords: priming fluid, extravascular lung water index, oxidative stress, cell integrity Submitted 19/11/22, accepted 8/2/23 Published online 6/3/23 Cardiovasc J Afr 2024; 35: 70–74 www.cvja.co.za DOI: 10.5830/CVJA-2023-006 Coronary artery bypass grafting (CABG) causes an acute inflammatory response, which results in systemic inflammatory response syndrome (SIRS), leading to organ damage.1-3 In cardiopulmonary bypass (CPB) circuits, non-physiological environmental factors such as foreign surfaces, haemodilution, non-pulsatile flow and temperature variations can induce an inflammatory response. Furthermore, the balance between pro- and anti-oxidant mediators is disturbed, resulting in excessive accumulation of reactive oxygen species.4 In turn, this redox imbalance, which is called oxidative stress, triggers the inflammatory response and initiates an oxidative vicious circle.2,5 Inflammatory processes accompanied by oxidative stress can affect the barrier function of the plasma membrane, leading to changes in intra- and extravascular volume status.6 Pulmonary oedema is a complication following CABG. Accumulation of extravascular lung water (EVLW), as a consequence of increased permeability or increased hydrostatic pressure in the pulmonary capillaries after CABG, is increased in the oedematous lungs and has been described in several studies.7-10 Transpulmonary thermodilution technique is used to monitor the cardiac preload volume through the global end-diastolic volume (GEDV) and estimates EVLW volume, which is considered a reliable estimate of interstitial lung oedema.11 Different types of priming fluids were used in CPB circuits to provide organ protection and perfusion.12-14 Crystalloid and colloid priming fluids are still in use, and, to date, no standard solution has gained general acceptance.15,16 Crystalloid-based priming fluids were found to reduce colloid oncotic pressure (COP) and cause CABG-related oedema.17 However, 6% hydroxyethyl starch 130/0.4 (6% HES) as a synthetic colloid can increase the COP.18 Despite all that is known, the effects of the composition of the priming fluid on the outcome parameters, such as EVLW, duration of extubation and intensive care unit (ICU)/hospital stay in CABG remain unclear.13,19,20 The primary aim of this study was to test the hypothesis that colloid priming fluid provides protective effects against oxidative stress and interstitial pulmonary oedema in CABG. As a secondary aim, we compared the short-term outcome parameters. Methods After the study protocol was approved by the ethics committee (ATADEK-723) and written informed consent was obtained from each patient, 30 consecutive patients scheduled for elective CABG were selected for the study. The patients were randomly Department of Anesthesiology and Reanimation, Acıbadem Mehmet Ali Aydınlar University, Altunizade Hospital, Istanbul, Turkey Halim Ulugöl, MD, halimulugol@yahoo.com.tr Meltem Güner Can, MD Fevzi Toraman, MD Department of Biology, Faculty of Science, University of Istanbul, İstanbul, Turkey Uğur Aksu, PhD Kubra Vardar, MSc Department of Cardiovascular Surgery, Acıbadem Mehmet Ali Aydınlar University, Altunizade Hospital, Istanbul, Turkey Murat Ökten, MD
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 AFRICA 71 allocated to two groups. The patients in group 1 (n = 15) were primed with a 6% HES (1 200 ml 6% HES, Voluven®; Fresenius Kabi, Germany), while the patients in group 2 were primed with a crystalloid solution (1 200 ml 0.9 % NaCl; n = 15, Polifleks®; Polifarma, Istanbul, Turkey). Exclusion criteria were assigned as the patient’s age not being between 18 and 65 years, left ventricular ejection fraction < 40%, emergent/urgent operations, additional valvular diseases, impaired renal function (estimated glomerular filtration rate > 60 ml/min) and co-morbid disease (except for hypertension). Anaesthetic and surgical management of the patients was performed by the same anaesthetist and surgical team. A standard monitoring regimen, including invasive arterial pressure, central venous pressure, peripheral oxygen saturation, five-lead electrocardiogram, regional cerebral oxygen saturation and end-tidal CO2 monitoring was performed. A 5-Fr femoral arterial thermistor-tipped catheter connected to the pulse index contour continuous cardiac output analysis monitor (PiCCO Technology, Pulsion Medical Systems, Germany) was inserted into each patient. The extravascular lung water index (ELWI), stroke volume index (SVI), systemic vascular resistance index (SVRI), cardiac index (CI) and global end-diastolic volume index (GEDI) were measured using the thermodilution and pulse contour analysis methods. The anaesthesia regimen was intravenously induced with fentanyl and propofol. Tracheal intubation was intravenously facilitated with rocuronium. Anaesthesia was maintained with sevoflurane at one minimum alveolar concentration in air/ oxygen and a maintenance dose of rocuronium and fentanyl. Ventilation of the patients was adjusted to maintain normoxia and normocapnia. Heparin (300 IU/kg) and additional heparin were given until the activated clotting time was > 400 seconds. As the CPB concluded, protamine sulphate was administered at the same dosage as the initially administered heparin dose to antagonise the heparin effect. Dopamine, dobutamine, norepinephrine, epinephrine, or combinations thereof were used as inotrope or vasopressors. The patients were transferred to the cardiac ICU after surgery. Standard CPB techniques were employed. The CPB circuit was primed according to each patient’s study group. During CPB, standard cannulation of the ascending aorta and right atrium was performed. Pump flows at 2.0–2.4 l/min/m2 of the body surface area, moderate systemic hypothermia (32°C) and intermittent anterograde blood cardioplegia was used. Homogenous cooling and rewarming were provided. Packed red blood cells were transfused to maintain haemoglobin levels between 6 and 8 g/dl during the pump period and between 8 and 10 g/dl after reperfusion. Fresh frozen plasma and platelet transfusions were used, according to the laboratory and clinical findings. Normal saline solution was administered to meet the volume loss by evaporation and through the urine. Inaddition toPiCCOandoxidative stress statusmeasurements, heart rate, mean arterial pressure, the partial pressure of carbon dioxide and oxygen (pCO2–pO2), and serum level of haematocrit, glucose and lactate were recorded. The duration of extubation and ICU/hospital stay were also determined. Haemodynamic variables [heart rate (beats/min), mean arterial pressure (mmHg)], blood gas analysis [pH, pCO2 (mmHg), pO2 (mmHg), lactate (mmol/l) and biochemical variables (glucose (mg/ dl), hematocrit (%)] were obtained at the following times: T0 (zero time point), T1 (after anaesthesia induction), T2 (five minutes after the initiation of CPB), T3 (after cross-clamping), T4 (after weaning from CPB), T5 (at admission to the ICU), T6 (third hour after ICU admission) and T7 (24th hour after ICU admission). Using the transpulmonary thermodilution and PiCCO methods, ELWI, SVI, SVRI, CI and GEDI were evaluated at the T1, T4, T5, T6 and T7 time points. In addition, blood samples were obtained to evaluate the oxidative stress status and cellular integrity. For this purpose, serum advanced oxidative protein products (AOPP), total thiol (T-SH), free haemoglobin (fHb), ischaemic modified albumin (IMA) and sialic acid (SA) levels were measured at the T0, T5 and T7 time points. The AOPP levels were measured to determine the protein oxidation using a modified method of Hanasand et al.21 The measurement of IMA levels was performed to show three-dimensional modification of plasma albumin using a modification of the Bar-Or et al. method.22 The measurement of T-SH determination was performed to thiol modification of protein, which is based on the method of Sedlak and Lindsay.23 The SA levels were determined by the method of Sydow.24 The level of fHb was determined to show the oxidant-mediated homolysis using the method by Harboe.25 Statistical analysis After the determination of distribution of data sets using the Kolmogorov–Smirnov and Shapiro–Wilk tests, all data are presented as mean ± SEM. Statistical analysis was performed using GraphPad Prism v5.0 (GraphPad Software, La Jolla, CA, USA). The sample size was estimated using G*Power software (version 3.1; Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany). To this, the study power was accepted as 80%, the type 1 alpha error was 0.05 and the effect size was accepted as 58% according to the ELWI change,26 as primary outcome. A comparative analysis of the two groups at the same time point was performed using the unpaired t-test and one-way ANOVA. The Bonferroni post hoc test was used for repeated measurements. Differences between values were considered statistically significant at p < 0.05. Results Table 1 shows haemodynamic, biochemical and arterial blood gas measurements at seven time points in the groups. There were similar results in both groups at all time points (p > 0.05). For the colloid group, the IMA levels (ABS units) were measured as 0.511 ± 0.047 at T1, 0.475 ± 0.059 at T5 and 0.457 ± 0.055 at T7. For the crystalloid group, the IMA levels (ABS units) were measured as 0.388 ± 0.074 at T1, 0.355 ± 0.063 at T5 and 0.424 ± 0.080 at T7. For the colloid group, the T-SH levels (μmol/g protein) were measured as 33.6 ± 2.1 at T1, 76.7 ± 10.4 at T5 and 77.7 ± 20.7 at T7. For the crystalloid group, the T-SH levels (μmol/g protein) were measured as 39.2 ± 4.1 at T1, 55.3 ± 5.8 at T5 and 64.1 ± 6.7 at T7. For the colloid group, the AOPP levels (mmol/g protein) were measured as 24.5 ± 2.2 at T1, 34.9 ± 3.4 at T5 and 30.6 ± 3.8 at T7. For the crystalloid group, the AOPP levels (mmol/g protein) were measured as 34.0 ± 3.8 at T1, 42.1 ± 6.0 at T5 and 37.4 ± 4.8 at T7.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 72 AFRICA For the colloid group, the fHb levels (g/l) were measured as 0.08 ± 0.02 at T0, 0.19 ± 0.04 at T5 and 0.06 ± 0.01 at T7. For the crystalloid group, the fHb levels (g/l) were measured as 0.14 ± 0.03 at T1, 0.24 ± 0.06 at T5 and 0.08 ± 0.04 at T7. For the colloid group, the SA levels (mg/g protein) were measured as 0.38 ± 0.03 at T1, 0.55 ± 0.06 at T5 and 0.66 ± 0.08 at T7. For the crystalloid group, the SA levels (mg/g protein) were measured as 0.48 ± 0.06 at T1, 0.56 ± 0.06 at T5 and 0.69 ± 0.09 at T7. No significant differences in oxidative stress and cellular injury parameters were found between the colloid and crystalloid group at any time (Table 2) (p > 0.05). The changes in all PiCCO parameters are presented in Table 3. There was no significant difference between the groups (p > 0.05). ELWI (ml/kg) was measured as 11.7 ± 1.6 (T1), 11.8 ± 1.3 (T4), 10.6 ± 1.2 (T5), 8.5 ± 0.7 (T6) and 9.4 ± 1.1 (T7) in group 1 and as 8.4 ± 0.7 (T1), 9.5 ± 1.2 (T4), 8.6 ± 0.7 (T5), 7.7 ± 1.0 (T6) and 7.3 ± 0.6 (T7) in group 2. No significant differences were found between the two groups (p > 0.05). The ELWI course at the different time points is presented in Fig. 1. Discussion In this study, we compared two different priming fluids for EVLW, oxidative stress, cell integrity and ICU/hospital length of stay during CABG. A minimal increase in EVLW that did not reach statistical significance was observed in the crystalloid priminge fluid compared to the colloid priming fluid at all time points. Colloid and crystalloid priming fluids were also similar in their effects on cell integrity and oxidative stress. Furthermore, there were no differences between the groups in terms of postoperative ventilation times and length of ICU or hospital stay. Performing coronary revascularisation using the CPB technique is an effective and safe technique, but fluidaccumulation in the extravascular space is a phenomenon associated with the CPB technique.27 Fluid extravasation leads to increased water content in the tissues, which results in cardiac and pulmonary dysfunction. The mechanisms contributing to this fluid shift are complex and attributed to a decrease in plasma oncotic pressure with the use of priming fluids during CPB, SIRS secondary to the exposure of blood to foreign surfaces, hypothermia or ischaemia–reperfusion injury. This study was undertaken primarily to investigate changes in EVLW and oxidative stress status when different types of priming fluids were used for CPB. It was hypothesised that the crystalloid priming group (group 2) would have higher levels of ELWI, which would have apparent clinical effects, while the colloid priming fluid was expected to have beneficial effects during the peri-operative period. It was previously believed that transcapillary fluid shift is determined solely by the balance between hydrostatic pressure and COP.28 However, the revised Starling equation, which has been accepted in recent years, has changed the view on fluid balance.29 According to this equation, fluid movement from the intravascular space to the tissue is less affected by COP. The most important factor determining transcapillary fluid movement is the endothelial glycocalyx layer and the COP in the Table 2. Time-dependent changes in oxidative stress and cellular injury parameters in the two groups Time Group IMA (ABS units) T-SH (umol/g protein) AOPP (mmol/g protein) fHb (g/l) SA (mg/g protein) T1 G1 G2 0.511 ± 0.047 0.388 ± 0.074 33.6 ± 2.1 39.2 ± 4.1 24.5 ± 2.2 34.0 ± 3.8 0.08 ± 0.02 0.14 ± 0.03 0.38 ± 0.03 0.48 ± 0.06 T5 G1 G2 0.475 ± 0.059 0.355 ± 0.063 76.7 ± 10.4 55.3 ± 5.8 34.9 ± 3.4 42.1 ± 6.0 0.19 ± 0.04 0.24 ± 0.06 0.55 ± 0.06 0.56 ± 0.06 T7 G1 G2 0.457 ± 0.055 0.424 ± 0.080 77.7 ± 20.7 64.1 ± 6.7 30.6 ± 3.8 37.4 ± 4.8 0.06 ± 0.01 0.08 ± 0.04 0.66 ± 0.08 0.69 ± 0.09 IMA, ischaemic modified albumin; T-SH, total thiol; AOPP, advanced oxidative protein products; fHb, free haemoglobin; SA, sialic acid. Table 3. Time-dependent parameters measured with PiCCO technology in the two groups Time Group PiCCO CI (l/min/m2) PiCCO SVI (ml/m2) PiCCO GEDI (ml/m2) PiCCO GEF (%) PiCCO ELWI (ml/kg) T1 G1 G2 2.3 ± 0.2 2.1 ± 0.1 33.3 ± 3.4 29.3 ± 2.8 642 ± 61 628 ± 33 20.0 ± 2.2 21.0 ± 1.4 11.7 ± 1.6 8.4 ± 0.7 T4 G1 G2 2.3 ± 0.3 2.4 ± 0.2 26.6 ± 1.7 31.2 ± 2.0 717 ± 84 614 ± 31 16.6 ± 2.1 23.2 ± 1.6 11.8 ± 1.3 9.5 ± 1.2 T5 G1 G2 2.4 ± 0.2 2.3 ± 0.1 27.5 ± 2.9 29.2 ± 1.0 749 ± 83 607 ± 90 17.6 ± 2.6 21.3 ± 0.8 10.6 ± 1.2 8.6 ± 0.7 T6 G1 G2 2.6 ± 0.2 2.5 ± 0.1 27.6 ± 2.8 26.0 ± 1.3 711 ± 81 639 ± 50 17.0 ± 2.6 19.4 ± 1.6 8.5 ± 0.7 7.7 ± 1.0 T7 G1 G2 3.0 ± 0.1 2.9 ± 0.2 33.9 ± 1.8 34.5 ± 2.2 848 ± 28 698 ± 48 18.5 ± 2.0 19.7 ± 0.9 9.4 ± 1.1 7.3 ± 0.6 PiCCO, pulse index contour continuous cardiac output; CI, cardiac index; SVI, stroke volume index; GEDI, global end-diastolic index; GEF, global ejection fraction; ELWI, extravascular lung water index. ELWI (ml/kg) Priming fluids t1 t4 t5 t6 t7 15 10 5 0 Crystaloid Colloid Fig. 1. Time-dependent changes in ELWI (ml/kg) in the two groups. ELWI, extravascular lung water index. Table 1. Haemodynamic, biochemical and arterial blood gas measurements in the two groups Time Grp HR (beats/min) MAP (mmHg) pCO2 (mmHg) pO2 (mmHg) Haematocrit (%) Glucose (mg/dl) Lactate (mmol/l) T1 G1 G2 62.2 ± 4.0 57.0 ± 3.0 74.1 ± 3.0 80.3 ± 4.0 36.0 ± 0.7 36.5 ± 1.3 159.4 ± 4.0 179.2 ± 10.2 36.1 ± 2.1 40.0 ± 1.5 129.4 ± 15.3 116.6 ± 6.8 1.2 ± 0.1 1.5 ± 0.2 T4 G1 G2 80.5 ± 4.0 74.7 ± 4.0 69.5 ± 2.0 67.0 ± 2 35.5 ± 0.9 36.2 ± 0.9 123.8 ± 12.9 113.7 ± 6.5 29.0 ± 1.8 27.1 ± 1.0 165.2 ± 18.6 139.7 ± 10.7 1.8 ± 0.3 1.8 ± 0.2 T5 G1 G2 85.5 ± 6.0 77.7 ± 2.0 88.8 ± 4.0 77.0 ± 5.0 33.4 ± 1.0 31.7 ± 1.1 135.2 ± 13.6 118.8 ± 10.1 31.7 ± 1.2 29.6 ± 1.1 166.5 ± 17.0 142.6 ± 12.0 1.7 ± 0.3 1.9 ± 0.2 T6 G1 G2 93.8 ± 4.0 94.9 ± 4.0 79.0 ± 3.0 76.4 ± 3.0 34.6 ± 1.1 34.3 ± 1.7 131.8 ± 8.5 149.7 ± 7.6 33.1 ± 1.3 31.8 ± 1.1 163.9 ± 10.5 144.9 ± 11.3 2.3 ± 0.3 2.3 ± 0.3 T7 G1 G2 87.5 ± 3.0 83.9 ± 4.0 83.1 ± 3.0 82.2 ± 3.0 36.4 ± 1.0 38.4 ± 0.9 96.0 ± 6.6 99.8 ± 6.7 29.9 ± 1.3 30.0 ± 1.0 175.0 ± 10.5 183.5 ± 7.0 2.0 ± 0.4 2.2 ± 0.3 HR, heart rate; MAP, mean arterial pressure; pCO2, partial pressure of carbon dioxide; pO2, partial pressure of oxygen.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 AFRICA 73 sub-glycocalyx. In our study, sialic acid, one of the glycocalyx damage markers, was found to be similar in both groups. As a result, EVLWI was similar in patients receiving colloid and crystalloid fluids. In a meta-analysis of 29 studies published in 2022, the strategies of crystalloid and colloid priming were compared.30 The authors emphasised that both priming fluids were similar in terms of COP. Various types of priming fluids have been researched, but no consensus has been reached on the ideal composition to prevent SIRS and fluid extravasation. The literature contains a few studies related to the effects of priming fluids on ELWI. In a previous study by Hoeft et al.,8 the researchers demonstrated that priming with a colloid fluid attenuated the increase in EVLW when compared to the effects of a pure crystalloid priming solution. Similarly, in a study investigating the effects of a hyperoncotic solution on EVLW and pulmonary function, the researchers found that post-CPB, EVLW was unchanged in the HES group, but elevated by 22% in the crystalloid group.19 They also indicated that the colloid solution prevented EVLW accumulation in the early post-pump period. Sade et al.31 designed a study to determine whether there were important differences in the clinical effects of HES, albumin and lactate Ringer’s solution (LRS) when used in priming fluid. They found greater somatic and pulmonary fluid accumulation in the LRS group and suggested that colloid was preferable to crystalloid priming fluids. However, no beneficial effects concerning the clinical parameters and patient outcomes could be demonstrated in the majority of the studies using colloid priming fluids. Our study differs from previous studies in that most prior studies of the effects of different priming fluids on clinical outcomes focused on the impairment of blood coagulation and renal function related to HES usage.32,33 In our study, we evaluated ELWI together with the oxidative stress status, which are the two main mechanisms that contribute to CPB-related organ damage. We have shown that two different priming fluids with similar results in terms of cell integrity and oxidative stress did not increase lung fluid content. Choi et al.34 studied the effects of HES in comparison with human albumin and found no difference in the inflammatory response. Similarly, Lioi et al.35 compared three different priming fluids (lactate Ringer’s solution, human albumin and 10% HES) and found no statistically significant differences between the groups with regard to inflammatory cytokines. In our study, the oxidative stress parameters were similar in both groups. Although there are numerous methods available for the assessment of oxidative stress, AOPP, IMA, fHb and T-SH levels have been proposed as possible markers of redox status. As an inflammatory marker, SA, which is known to have a significant correlation with other plasma acute-phase proteins, such as C-reactive protein and fibrinogen, was chosen.36,37 Neither of the priming fluids used in our study caused detrimental effects on the redox or inflammatory status. As a first limitation of our study, different processes of cellular damage such as apoptosis, inflammation and DNA damage may have taken place in our experimental set-up. However, in order not to spoil the perspective of the study, we only wanted to associate oxidative stress with lung water. The second limitation is that only male subjects should have been included in the study so that hormonal changes did not affect the study. However, to avoid difficulties while generalising the findings, our study was carried out with a mixed-gender population. Conclusion In our study, while the oxidative stress parameters were similar in both groups, mild increases in ELWI that did not reach statistical significance were observed in the crystalloid group. The colloid (6% HES) priming fluid was shown to be similar to the crystalloid fluid in terms of ELWI. Further studies on high-risk patients are warranted to explore the effects of different priming fluids on clinical parameters and patient outcomes. References 1. Levy JH, Tanaka KA. Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 2003; 75(2): S715–720. 2. Wan S, LeClerc JL, Vincent JL. Inflammatory response to cardiopulmonary bypass: mechanisms involved and possible therapeutic strategies. Chest 1997; 112(3): 676–692. 3. Chenoweth DE, Cooper SW, Hugli TE, Stewart RW, Blackstone EH, Kirklin JW. Complement activation during cardiopulmonary bypass: evidence for generation of C3a and C5a anaphylatoxins. N Engl J Med 1981; 304(9): 497–503. 4. Morita K, Ihnken K, Buckberg GD, Ignarro LJ. Oxidative insult associated with hyperoxic cardiopulmonary bypass in the infantile heart and lung. Jpn Circ J 1996; 60(6): 355–363. 5. Seghaye MC, Grabitz RG, Duchateau J, Busse S, Dabritz S, Koch D, et al. Inflammatory reaction and capillary leak syndrome related to cardiopulmonary bypass in neonates undergoing cardiac operations. J Thorac Cardiovasc Surg 1996; 112(3): 687–697. 6. Chignalia AZ, Yetimakman F, Christiaans SC, Unal S, Bayrakci B, Wagener BM, et al. The glycocalyx and trauma: a review. Shock 2016; 45(4): 338–348. 7. Hachenberg T, Tenling A, Rothen HU, Nystrom SO, Tyden H, Hedenstierna G. Thoracic intravascular and extravascular fluid volumes in cardiac surgical patients. Anesthesiology 1993; 79(5): 976–984. 8. Hoeft A, Korb H, Mehlhorn U, Stephan H, Sonntag H. Priming of cardiopulmonary bypass with human albumin or Ringer lactate: effect on colloid osmotic pressure and extravascular lung water. Br J Anaesth 1991; 66(1): 73–80. 9. Boldt J, Bormann BV, Kling D, Scheld H, Hempelmann G. Influence of acute normovolemic hemodilution on extravascular lung water in cardiac surgery. Crit Care Med 1988; 16(4): 336–339. 10. Jin X, Chen Z, Wang M, Lu W, Zhang W, Sun J. [Effects of hyperoncotic cardiopulmonary bypass prime on extravascular lung water and cardiopulmonary function in patients undergoing coronary artery bypass surgery]. Zhonghua Yi Xue Za Zhi 2014; 94(9): 646–650. 11. Monnet X, Teboul JL. Transpulmonary thermodilution: advantages and limits. Crit Care 2017; 21(1): 147. 12. Mehlhorn U, Allen SJ, Davis KL, Geissler HJ, Warters RD, Rainer de Vivie E. Increasing the colloid osmotic pressure of cardiopulmonary bypass prime and normothermic blood cardioplegia minimizes myocardial oedema and prevents cardiac dysfunction. Cardiovasc Surg 1998; 6(3): 274–281. 13. Jansen PG, te Velthuis H, Wildevuur WR, Huybregts MA, Bulder ER, van der Spoel HI, et al. Cardiopulmonary bypass with modified fluid gelatin and heparin-coated circuits. Br J Anaesth 1996; 76(1): 13–19. 14. Buhre W, Hoeft A, Schorn B, Weyland A, Scholz M, Sonntag H. Acute affect of mitral valve replacement on extravascular lung water in patients
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 74 AFRICA receiving colloid or crystalloid priming of cardiopulmonary bypass. Br J Anaesth 1997; 79(3): 311–316. 15. London MJ. Pro: colloids should be added to the pump prime. J Cardiothorac Anesth 1990; 4(3): 401–405. 16. D’Ambra MN, Philbin DM. Con: colloids should not be added to the pump prime. J Cardiothorac Anesth 1990; 4(3): 406–408. 17. Verheij J, van Lingen A, Beishuizen A, Christiaans HM, de Jong JR, Girbes AR, et al. Cardiac response is greater for colloid than saline fluid loading after cardiac or vascular surgery. Intensive Care Med 2006; 32(7): 1030–1038. 18. Zdolsek JH, Bergek C, Lindahl TL, Hahn RG. Colloid osmotic pressure and extravasation of plasma proteins following infusion of Ringer’s acetate and hydroxyethyl starch 130/0.4. Acta Anaesthesiol Scand 2015; 59(10): 1303–1310. 19. Eising GP, Niemeyer M, Gunther T, Tassani P, Pfauder M, Schad H, et al. Does a hyperoncotic cardiopulmonary bypass prime affect extravascular lung water and cardiopulmonary function in patients undergoing coronary artery bypass surgery? Eur J Cardiothorac Surg 2001; 20(2): 282–289. 20. Scott DA, Hore PJ, Cannata J, Masson K, Treagus B, Mullaly J. A comparison of albumin, polygeline and crystalloid priming solutions for cardiopulmonary bypass in patients having coronary artery bypass graft surgery. Perfusion 1995; 10(6): 415–424. 21. Hanasand M, Omdal R, Norheim KB, Goransson LG, Brede C, Jonsson G. Improved detection of advanced oxidation protein products in plasma. Clin Chim Acta 2012; 413(9–10): 901–906. 22. Bar-Or D, Rael LT, Bar-Or R, Slone DS, Mains CW, Rao NK, et al. The cobalt–albumin binding assay: insights into its mode of action. Clin Chim Acta 2008; 387(1–2): 120–127. 23. Sedlak J, Lindsay RH. Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissue with Ellman’s reagent. Anal Biochem 1968; 25(1): 192–205. 24. Sydow G. A simplified quick method for determination of sialic acid in serum. Biomed Biochim Acta 1985; 44(11–12): 1721–1723. 25. Harboe M. A method for determination of hemoglobin in plasma by nearultraviolet spectrophotometry. Scand J Clin Lab Invest 1959; 11: 66–70. 26. Lomivorotov VV, Fominskiy EV, Efremov SM, Nepomniashchikh VA, Lomivorotov VN, Chernyavskiy AM, et al. Hypertonic solution decreases extravascular lung water in cardiac patients undergoing cardiopulmonary bypass surgery. J Cardiothorac Vasc Anesth 2013; 27(2): 273–282. 27. Olthof CG, Jansen PG, de Vries JP, Kouw PM, Eijsman L, de Lange JJ, et al. Interstitial fluid volume during cardiac surgery measured by means of a non-invasive conductivity technique. Acta Anaesthesiol Scand 1995; 39(4): 508–512. 28. Starling EH. On the absorption of fluids from the connective tissue spaces. J Physiol 1896; 19(4): 312–326. 29. Levick JR. Revision of the Starling principle: new views of tissue fluid balance. J Physiol 2004; 557(Pt 3): 704. 30. Beukers AM, de Ruijter JAC, Loer SA, Vonk A, Bulte CSE. Effects of crystalloid and colloid priming strategies for cardiopulmonary bypass on colloid oncotic pressure and haemostasis: a meta-analysis. Interact Cardiovasc Thorac Surg 2022; 35(3). 31. Sade RM, Stroud MR, Crawford FA, Jr., Kratz JM, Dearing JP, Bartles DM. A prospective randomized study of hydroxyethyl starch, albumin, and lactated Ringer’s solution as priming fluid for cardiopulmonary bypass. J Thorac Cardiovasc Surg 1985; 89(5): 713–722. 32. Tiryakioglu O, Yildiz G, Vural H, Goncu T, Ozyazicioglu A, Yavuz S. Hydroxyethyl starch versus Ringer solution in cardiopulmonary bypass prime solutions (a randomized controlled trial). J Cardiothorac Surg 2008; 3: 45. 33. Gurbuz HA, Durukan AB, Salman N, Tavlasoglu M, Durukan E, Ucar HI, et al. Hydroxyethyl starch 6%, 130/0.4 vs. a balanced crystalloid solution in cardiopulmonary bypass priming: a randomized, prospective study. J Cardiothorac Surg 2013; 8: 71. 34. Choi YS, Shim JK, Hong SW, Kim JC, Kwak YL. Comparing the effects of 5% albumin and 6% hydroxyethyl starch 130/0.4 on coagulation and inflammatory response when used as priming solutions for cardiopulmonary bypass. Minerva Anestesiol 2010; 76(8): 584–591. 35. Liou HL, Shih CC, Chao YF, Lin NT, Lai ST, Wang SH, et al. Inflammatory response to colloids compared to crystalloid priming in cardiac surgery patients with cardiopulmonary bypass. Chin J Physiol 2012; 55(3): 210–218. 36. Tseke P, Grapsa E, Stamatelopoulos K, Samouilidou E, Rammos G, Papamichael C, et al. Correlations of sialic acid with markers of inflammation, atherosclerosis and cardiovascular events in hemodialysis patients. Blood Purif 2008; 26(3): 261–266. 37. Jinghua L, Tie Z, Ping W, Yongtong C. The relationship between serum sialic acid and high-sensitivity C-reactive protein with prehypertension. Med Sci Monit 2014; 20: 551–555. Fewer people may need statins to prevent heart disease: US study A new way of determining heart disease risk could slash the numbers of people who are prescribed statins, suggests a recent study, although doctors warn that more information is needed and patients shouldn’t stop taking their medications. Statins are used by millions of people as protection against high levels of low-density lipoprotein (LDL) cholesterol, one of the causes of cardiovascular disease. Doctors prescribe the daily pills based on 2013 guidelines from the American Heart Association (AHA) and the American College of Cardiology (ACC), which estimate risk based on age, diabetes, blood pressure and other factors, reports NBS News. In the latest study, Dr Tim Anderson, an assistant professor of medicine at the University of Pittsburgh, and colleagues analysed the potential impact of a new heart disease risk calculator dubbed PREVENT, released by the AHA last year, and compared estimates with older guidelines. The data were from 3 785 adults aged 40 to 75 years, all of whom were participants in the National Health and Nutrition Examination Survey (NHANES). The new calculator was developed to give a more accurate assessment of a person’s likelihood of developing heart disease by incorporating newly recognised risk factors such as kidney disease and obesity. The researchers found that among the participants, the 10-year risk of developing heart disease determined with the new tool was about half that estimated with the previous one, according to the report published in J Am Med Assoc Internal Medicine. Using PREVENT to calculate the 10-year risk for developing heart disease, the researchers determined that some 40% fewer people would have met the criteria for a statin prescription. continued on page 81…
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 AFRICA 75 Surgical experience in adults with Ebstein’s anomaly: long-term results Ozge Altas, Sabit Sarikaya Objective: The aim of this study was to review late results of the surgical treatment of Ebstein’s anomaly with reconstruction and replacement in adults. Methods: Medical records of 28 consecutive patients operated on between 1991 and 2014 were reviewed retrospectively. Surgical repair was performed in 19 (67.9%) patients (Hardy: two, Danielson: three, modified Danielson: six, Carpentier: three, Kay annuloplasty reinforced with ring: two), whereas tricuspid valve replacement was performed in nine patients (32.1%). Primary long-term outcomes consisted of right ventricular function, survival and freedom from re-operation. We evaluated the additional impacts of residual tricuspid insufficiency and type of surgery on survival. Results: In-hospital mortality rate was 7.1% (n = 2) due to low cardiac output status and sepsis. Patients showed a significant postoperative decrease in tricuspid regurgitation (p < 0.001), right atrial size (p < 0.001) and pulmonary hypertension (p = 0.002). The mean follow-up time was 140 ± 71.4 months, with a median of 126 months (105–192). Late mortality occurred in two patients and there was no significant difference in terms of survival based on residual tricuspid insufficiency (p = 0.57) and type of surgery (p = 0.094). Overall survival rates were 89.3, 85.4, 85.4 and 68.3% at five, 10, 15 and 20 years, respectively. Conclusion: Although complex leaflet reconstruction techniques have evolved to achieve a more physiological and durable repair, both approaches can be performed safely on specific patients and can be alternated, with acceptable rates of survival and re-operation. Keywords: tricuspid valve, Ebstein anomaly, congenital heart disease Submitted 29/1/23, accepted 16/2/23 Published online 23/3/23 Cardiovasc J Afr 2024; 35: 75–81 www.cvja.co.za DOI: 10.5830/CVJA-2023-008 Having accounted for 1% of congenital heart disease, Ebstein’s anomaly (EA) is associated with abnormalities of the tricuspid valve (TV) leaflets and right ventricle (RV), including atrialisation due to apical displacement of the tricuspid annulus. The surgical strategy for patients with EA is controversial and varies according to anatomical severity, however significant progress has been made since the early 1950s in understanding and managing the disease. Treatment was formerly directed towards valve repair rather than replacement due to unsatisfactory late results of prosthetic valves.1-3 Lately, leaflet reconstruction techniques, such as Carpentier and cone repairs, have become the firstchoice treatment when available, providing good anatomical and physiological results.4,5 Classic approaches emphasise monocuspid coaptation of the TV and cause off-centre diastolic flow, leading to late valvular regurgitation. On the other hand, the modern approach creates near-anatomical repair by re-attaching leaflets clockwise to the true annulus and induces central blood flow.5 However, these types of interventions cannot be offered to all patients. It is not feasible to perform in the presence of pulmonary hypertension (PHT), a severely enlarged RV or when there is lack of septal leaflet tissue. This report summarises our experience with the surgical management of EA using various techniques and assessing postoperative complications, long-term survival and freedom from re-operation. Methods Ethical approval was obtained from our institutional ethics committee. Informed patient consent was waived due to the retrospective nature of the study. FromMarch 1991 toDecember 2014, themedical records of 28 patients undergoing surgery for EA were examined and included in a retrospective study evaluating the long-term follow up of at least five years. Patients having significant tricuspid insufficiency (TI) with symptoms of dyspnoea or right-sided heart failure defined as New York Heart Association (NYHA) class III or IV, progressive cardiomegaly, rhythm disturbances and paradoxical embolism were indicated for surgery.6 Patients were excluded if the surgery was performed by the congenital heart surgery team or if they had congenitally corrected transposition of the great arteries or pulmonary atresia with intact ventricular septum and complex conotruncal abnormalities. Data of the demographic variables, intra-operative process and postoperative outcomes were collected retrospectively. Demographic and clinical data are presented in Table 1. Pulmonary embolism due to a right atrial thrombus was the first finding in one patient. Other patients mostly suffered from decreased exercise capacity, along with dyspnoea (82.1%) and oedema (39.2%). Cardiovascular risk factors were diabetes mellitus in one patient (3.6%), hyperlipidaemia in seven (25%), arterial hypertension in six (21.4%), and smoking was present in three patients (10.7%). Pre-operative cardiac assessment was done with transthoracic echocardiography to diagnose associated pathologies and the data are summarised in Table 2. Previous cardiac operations included partial biventricular repair for pulmonary atresia (n = 1), mitral valve replacement (MVR) and aortic valve replacement (AVR) (n = 1), and open mitral commissurotomy (n Koşuyolu High Specialisation Education and Research Hospital, Istanbul Provincial Health Directorate, Istanbul, Turkey Ozge Altas, MD, dr.ozgealtas@gmail.com Sabit Sarikaya, MD
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 2, May – August 2024 76 AFRICA = 1). The last follow up was performed by review of the results of any recent examinations at our institution in 2020. Early operative management in our centre typically includes the simpler and more familiar method, which is repair or replacement of the TV and plication of the atrialised RV, concomitant with correction of the associated anomaly. Tricuspid repair, which is the main goal of surgery, evolved through various modifications. The integrity of the anterior leaflet and the attachment location are the first steps to be checked for successful repair. Initially, correct physiological anatomy of the valve was achieved by bringing the hinge line of the septal and posterior leaflet parallel to the annulus, by transverse plication of the atrialised RV (Hunter–Lillehei–Hardy technique, n = 2). Subsequently, we carried out posterior free-wall plication of the RV and reduction of the right atrium (RA), causing a form of monocuspid valve with/ without anterior papillary muscle approximation to the septum, which was centred (classical/modified Danielson technique, n = 3/9). Later, the techniques targeted the leaflets instead of the ventricle for reconstruction of the valve. The plan was switched to re-attach the anterior leaflet to the true annulus by enforcing it with a ring. The posterior wall was longitudinally plicated to obtain sufficient coaptation (Carpentier technique, n = 3). Additionally, Kay annuloplasty, reinforcing with a flexible ring, was utilised in two patients. Valve repair without a ring was performed in patients with minimal annular dilation and less severe pulmonary hypertension. In cases of severe RV dysfunction and more severe PHT, ring annuloplasty was chosen to form annular stabilisation, avoiding inevitable redilatation with deterioration of valve repair. The repair was checked with a saline test, as well as intra-operative echocardiography. Unfulfilled leaflet coaptation can be repaired either by bicuspidisation or reshaping of the valve with a pericardial patch. Consequently, valve replacement (n = 9) with a tissue prosthesis at the level of the true tricuspid annulus was preferred when repair was not feasible. The valve tissue adjacent to the RV outflow tract was excised to avoid obstruction of the tract. A flow chart of interventions can be seen in Fig. 1. Surgical procedures are documented in Table 3. Since postoperative ventricular arrhythmias were common, we preferred to plicate or resect the thin, atrialised ventricle to maintain contractility. Precautions were typically taken on suture lines to avoid injury to the conduction system or right coronary artery. One patient underwent MVR due to severe regurgitation. Radiofrequency ablation was utilised in one patient (3.6%) with chronic atrial fibrillation (AF). Mean cardiopulmonary bypass time was 106.3 ± 30.7 minutes with a mean aortic cross-clamp time of 65.2 ± 19.5 minutes. Statistical analysis Descriptive statistics for categorical variables are given as frequency and percentage, and continuous variables as mean ± SD or median (min–max). Variables of pre- and post-operative echocardiographic evaluations were compared with either the paired samples t-test or Wilcoxon–rank sum test, as appropriate. Survival was estimated using the Kaplan–Meier method and age- and gender-matched groups were compared using the log-rank test. Analyses were performed with SPSS 15.0.1 for Windows (SPSS Inc, Chicago, IL, USA) and p < 0.05 was considered statistically significant. Results Follow up was available for 21 of the 23 survivors (91.3%) and confirmed by clinical evaluation, outside physician report or death notice. The mean age of patients was 33.7 ± 17.7 years (range: 13–54), of whom 15 (53.6%) were female. Most patients were in sinus rhythm pre-operatively. One patient was in chronic Table 1. Clinical characteristics of patients (n = 28) Patient characteristics Mean ± SD or number (%) Age (years) 33.7 ± 17.7 Gender (female) 15 (53.6) NYHA class: III 9 (32.1) IV 17 (60.7) Dyspnoea 23 (82.1) Oedema 11 (39.2) Cyanosis 5 (17.8) Palpitations 21 (75) NYHA: New York Heart Association. Table 2. Pre-operative echocardiographic evaluation of patients Parameters Number (%) or mean ± SD Echocardiographic data TR ≥ 3 PHT (mmHg) RAD (cm) RVESD (mm) RVEDD (mm) RVEF (%) Low LVEF (%) Carpentier classification A–B C–D 23 (82.1) 52.7 ± 12.6 6.1 ± 0.6 37.7 ± 11 52.4 ± 14.1 60.3 ± 5.8 2 (7.1) 23 (82.1) 5 (17.8) Associated cardiac anomalies ASD PFO VSD MR AR 10 (35.7) 1 (3.6) 2 (7.1) 4 (14.3) 3 (10.7) Arrhythmias Atrial fibrillation RBBB Supraventricular tachycardia 1 (3.6) 5 (17.8) 10 (35.7) Prior cardiac surgery MVR + TVR AVR + MVR AMK + tricuspid reconstruction 3 (10.7) 1 1 1 ASD: atrial septal defect; AR: aortic regurgitation; LVEF: left ventricular ejection fraction; MR: mitral regurgitation; PFO: patent foramen ovale; PHT: pulmonary hypertension; RAD: right atrial diameter; RV: right ventricle; RVEDD: right ventricular end-diastolic diameter; RVEF: right ventricular ejection fraction; RVESD: right ventricular end-systolic diameter; TR: tricuspid regurgitation; VSD: ventricular septal defect. Table 3. Operative data Operative data Number (%) Tricuspid valve repair Hardy Danielson/modified Danielson Carpentier Kay annuloplasty Tricuspid valve replacement ASD closure VSD closure MVR 19 (67.9) 2 (10.5) 3/9 (63.2) 3 (15.8) 2 (10.5) 9 (32.1) 11 (39.3) 2 (10.5) 1 (3.6) ASD: atrial septal defect; MVR: mitral valve replacement; VSD: ventricular septal defect.
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