SEPTEMBER – OCTOBER 2024 VOL 35 NO 3 • Associat ion between CHA2DS2-VASc score and aort ic valve sclerosis • Modi f ied David V re- implantat ion for valve-spar ing aort ic root replacement • Effect of insul in resistance on lef t ventr icular remodel l ing in hypertensives • Impact of COVID-19 on cardiology fel lowship training in sub-Saharan Afr ica • Transradial approach and decreased acute kidney injury fol lowing PCI • Esmarch bandage in giant saphenous vein closure wi th endovenous glue ablat ion • Effect of lactate levels on extubat ion t ime in CABG surgery • Dispar i t ies in pat ients’ understanding of cardiovascular disease management 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 3, SEPTEMBER – OCTOBER 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 133 FROM THE EDITOR’S DESK PA Brink CARDIOVASCULAR TOPICS 134 The association between CHA2DS2-VASc score and aortic valve sclerosis F Başyiğit • HT Gürsoy • ÖÖ Çelebi • KG Balcı • ÖU Elalmış • K Özbek • ÖÇ Karaaslan • M İleri • T Keleş • S Aydoğdu 140 Long-term experience of the modified David V re-implantation technique for valvesparing aortic root replacement S Sarikaya • K Kirali 147 Effect of insulin resistance on left ventricular remodelling in essential hypertensives: a cross-sectional study BK Phanzu • AN Natuhoyila • EK Vita • B Longo-Mbenza • J-R M’Buyamba Kabangu 155 Impact of the COVID-19 pandemic on cardiology fellowship training in a sub-Saharan African training centre: an African perspective E Amendezo • M Ngunga • AH Ahmed • MH Varwani • B Karau • R Kimeu • M Jeilan 160 Is the transradial approach associated with decreased acute kidney injury following percutaneous coronary intervention in patients not complicated by major bleeding and haemodynamic disturbance? T Dasli • B Turan 166 Evaluation of clinical results of esmarch bandage application in giant saphenous vein closure during endovenous glue ablation O Karahan • O Akkaya • E Aydogan 172 Effect of lactate levels on extubation time in coronary artery bypass grafting surgery S Öztürk
CONTENTS Vol 35, No 3, SEPTEMBER – OCTOBER 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. REVIEW ARTICLE 178 Disparities in patients’ understanding of cardiovascular disease management R Ayob • M Vally • R Khan • A Orchard CASE REPORTS 185 Delayed diagnosis of cardiac amyloidosis in a West African octogenarian D Ahadzi • A-S Yakubu • A Doku • F Agyekum • C Ofori • H Ayetey 189 Successful surgical treatment of left ventricular free wall rupture H Kara PUBLISHED ONLINE (Available on www.cvja.co.za and in PubMed)
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 AFRICA 133 From the Editor’s Desk In this issue of the journal, there are some interesting questions addressed. I highlight some below. Ayob and colleagues (page 178) ask pertinent questions about our ‘clients’, our patients and the public, and their grasp of the entities we are managing them for and our advice given. They tracked down studies from Cameroon, Kuwait, Tanzania, South Africa, USA, Malaysia, Australia, Ghana and Uganda, which is a wide spectrum. The conclusion was that there is generally little grasp of what cardiovascular disease is about: poor riskfactor awareness, not buying into lifestyle modification and not appreciating the need for monitoring and for medication compliance. Phanzu and co-workers (page 147) took an unconventional approach and reasoned that the left ventricular mass, calculated by echocardiography according to Devereux’s formula, has different contributing components. They asked to what extent insulin resistance and/or hyperinsulinaemia are associated with average left ventricular mass or with components of Devereux’s formula, and also separately analysed parameters of left ventricular diastolic function. The article makes interesting reading as it presents sophisticated work incorporating lateral thinking. Similarly, the association between CHA2DS2-VASc score, a score used to calculate the chance of stroke in persons with atrial fibrillation, and aortic valve sclerosis are not conditions that we normally associate with each other. The article by Başyiğit et al. (page 134) outlines some interesting reasoning on how the formula for risk in atrial fibrillation and aortic valve sclerosis can be co-evaluated, and they come to some interesting conclusions. Amendezo and co-workers (page 155) describe how the COVID-19 crisis led to fewer training episodes for budding cardiologists, and limited the fellows from achieving the necessary amount of skills base, often in highly technical areas, by the end of their training. They also suggest how it could be rectified. In an interesting case report, Ahadzi and colleagues (page 185) take us through the long-term follow up of an individual who was initially treated presumptively for heart failure with preserved ejection fraction from hypertensive disease, based on his clinical presentation and echocardiographic findings from three years earlier. By adopting a stepwise approach to the evaluation and revisiting the history, together with multimodality cardiac imaging, the diagnosis of cardiac amyloidosis was made. Several interesting fillers are also found at the end of some of the articles, such as how overweight as a child, with excess kilos in the teen years, can double the later risk of stroke; the cardiovascular benefits from weight-loss drugs, including semaglutide; experts challenge ‘one-size-fits-all’ aspirin guidelines; and frequent cannabis use bumps up heart attack risk. PA Brink Acting Editor-in-Chief Paul Brink
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 134 AFRICA Cardiovascular Topics The association between CHA2DS2-VASc score and aortic valve sclerosis Funda Başyiğit, Havva Tuğba Gürsoy, Özlem Özcan Çelebi, Kevser Gülcihan Balcı, Özgül Uçar Elalmış, Kerem Özbek, Özge Çakmak Karaaslan, Mehmet İleri, Telat Keleş, Sinan Aydoğdu Abstract Background: Antithrombotic therapy in atrial fibrillation is generally managed with the CHA2DS2-VASc score. Aortic valve sclerosis (AVS) is a focal thickening of the aortic valve without a restriction of motion. AVS is related to several cardiovascular risk factors. Our study was performed to evaluate whether the presence of AVS was associated with the CHA2DS2-VASc score. Methods: This cross-sectional, observational study comprised 411 patients with AVS grades 1–3 [AVS (+)] and 102 patients with AVS grade 0 [AVS (–)]. We compared CHA2DS2-VASc scores between the AVS (+) and AVS (–) groups. Results: We determined that the AVS (+) group had a higher CHA2DS2-VASc score than the AVS (–) group [3 (0–8) vs 1 (0–4), p < 0.001)]. Conclusion: In our study, the CHA2DS2-VASc score was found to be higher in patients with AVS than in those without AVS. AVS may predict cardiovascular risk in the general population. Keywords: aortic valve, atherosclerosis, coronary artery disease, inflammation Submitted 17/2/22; accepted 12/4/23 Published online 26/7/23 Cardiovasc J Afr 2024; 35: 134–139 www.cvja.co.za DOI: 10.5830/CVJA-2023-022 The CHADS2 and CHA2DS2-VASc scores are widely used to estimate stroke risk and guide antithrombotic therapy in patients with atrial fibrillation (AF).1 Recent studies have shown that CHADS2 and CHA2DS2-VASc scores, incorporating several cardiovascular (CV) risk factors, can also be helpful in different clinical situations besides AF. These scores have been demonstrated to have predictive values in terms of death in patients with stable coronary artery disease (CAD) and acute coronary syndromes.2,3 CHA2DS2-VASc, the updated version of CHADS2, contains seven clinical variables, several of which are also CV risk factors, including congestive heart failure (CHF), hypertension (HT), age ≥ 75 years, diabetes mellitus (DM), stroke/transient ischaemic event, vascular disease, age 65 to 74 years and gender category (female). Kim et al. indicated in their study that higher CHA2DS2-VASc scores had worse CV outcomes in acute myocardial infarction patients.3 Also recently, Shang et al. reported a correlation between the CHA2DS2-VASc score and the prevalence of carotid plaques.4 Aortic valve sclerosis (AVS) can be described by focal areas of thickening of the leaflets without a restriction of motion, with a peak velocity of less than 2.0 m/s.5 It can easily be detected by transthoracic echocardiography (TTE), a safe, inexpensive and widely used imaging method. In the past, it was believed that AVS was a degenerative disease associated with aging. However, the absence of AVS in approximately 50% of individuals above the age of 80 years suggested that different mechanisms play a role in its aetiology.6 Today it is clear that AVS is not only simply a degenerative process but it also represents a complex process involving lipoprotein deposition, chronic inflammation and activation of the calcification cascade, similar to atherosclerosis. Several studies have shown a relationship between atherosclerosis and AVS.6-9 Although a direct connection has not been established, available data suggest that most components of the CHA2DS2-VASc score are also potential risk factors for atherosclerosis.10 Therefore, a hypothesis that the CHA 2DS2VASc score may be associated with AVS seems plausible. The correlation between the overall CHA2DS2-VASc score and AVS has not yet been studied. Based on this knowledge, we sought to design a cross-sectional study to search the relationship between the overall CHA2DS2-VASc score and AVS in patients without AF. Methods This was a single-centre, cross-sectional and observational study designed with patients aged > 18 and ≤ 75 years. We included 513 patients consecutively who had undergone TTE due to various clinical indications in the Ankara City Hospital cardiology clinic between March and December 2021. Department of Cardiology, Ankara City Hospital, Ankara, Turkey Funda Başyiğit, MD, ftuna02@yahoo.com Havva Tuğba Gürsoy, MD Özlem Özcan Çelebi, MD Kevser Gülcihan Balcı, MD Özgül Uçar Elalmış, MD Kerem Özbek, MD Özge Çakmak Karaaslan, MD Mehmet İleri, MD Telat Keleş, MD Sinan Aydoğdu, MD
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 AFRICA 135 AVS was defined as calcification and thickening of a threeleaflet aortic valve with an aortic velocity of < 2 m/s. Patients with AF, aortic velocity ≥ 2 m/s, severe valvular heart disease, bicuspid aortic valve, estimated glomerular filtration rate (eGFR) ≤ 15 ml/ min, history of acute rheumatic fever, connective tissue disease and cancer were excluded. We analysed 411 patients with AVS grades 1–3 [AVS (+)] and 102 patients without AVS [AVS grade 0 AVS (–)]. The study protocol adhered to the ethical guidelines of the 2013 Declaration of Helsinki. This study was approved by the Ankara City Hospital Ethics Committee of the Ministry of Health Provincial Health Directorate (approval number E1-211638). We collected detailed information on gender, age, medical history, co-morbidities, results of routine blood laboratory test parameters and electrocardiographic data from the electronic medical reports of our hospital. The eGFR values were calculated by the modification of diet in renal disease (MDRD) equations. The CHA2DS2-VASc scores and diagnosis of all mentioned diseases of this score (CHF, HT, DM, stroke, vascular disease) were evaluated for each patient according to the current AF guideline of the European Society of Cardiology, published in 2020.11 All patients underwent TTE, performed by two experienced cardiologists who were unaware of the clinical status of the patients, using the Philips Affinity50 echocardiography device. The left ventricular posterior wall thickness (PWT), interventricular septal thickness (IVST), left ventricular end-diastolic diameter (LVEDD), left atrial diameter (LAD) and ascending aortic diameter were measured on the parasternal long-axis view. The left ventricular ejection fractions (LVEF) of the patients were calculated using Simpson’s biplane method. We evaluated left ventricular diastolic dysfunction (LVDD) according to the update published by the American Society of Echocardiography and the European Association of CV Imaging.12 We assessed AVS from the parasternal long, parasternal short and apical five-chamber views. The presence of AVS was confirmed without using tissue harmonic imaging to avoid high gain settings.13 We defined AVS as focal areas of increased echogenicity and thickening of the leaflets without a restriction of motion, and peak velocity of less than 2.0 m/s. We graded the severity of AVS on a scale of 0 to 3: 0 = normal (no involvement), 1 = mild (minor involvement of one leaflet), 2 = moderate (minor involvement of two leaflets or extensive involvement of one leaflet) and 3 = severe (extensive involvement of two leaflets or involvement of all three leaflets) (Fig. 1).9 We defined AVS grade 0 as AVS (–) and AVS grades 1, 2 and 3 as AVS (+). Statistical analysis All data were analysed using the SPSS version 22.0 software (SPSS Inc, Chicago, IL). Continuous parametric data are Fig. 1. Echocardiographic images of AVS grades showing (A) normal, (B) mild, (C) moderate, (D) severe grades. A C B D
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 136 AFRICA summarised as means ± standard deviation (SD) and were compared by t-test analysis. We used the Pearson chi-squared test to compare categorical data and the Mann–Whitney U-test for non-parametric analysis. Univariate and multivariate logistic regression was also used to assess the association between AVS and CHA2DS2-VASc scores. Fasting blood glucose (FBG), eGFR, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) levels; white blood cell (WBC) and neutrophil counts; PWT, IVST, LVEDD, LVDD, LAD, ascending aortic diameter, LVEF, insulin and statin therapies were adjusted in the multivariate logistic regression analysis. We used the area under the receiver operating characteristic (ROC) curve to determine the cut-off points of different CHA2DS2VASc scores in AVS patients. All tests were two-tailed and a p-value < 0.05 was considered statistically significant. Median CHA2DS2-VASc scores of AVS grades were compared with the Kruskal–Wallis H-test. The Spearman correlation test was used for the correlation of AVS grade and CHA2DS2-VASc score. Results We analysed 513 patients who underwent TTE because of different clinical indications [AVS grade 0, 102 (19.9%); AVS grade 1, 100 (19.5%); AVS grade 2, 134 (26.1%); AVS grade 3, 177 (34,5%)]. We divided patients into two groups according to detection of AVS (AVS grade 1–3) or not (AVS grade 0) (n = 411, 38.2% female, age 63.52 ± 7.24 years vs n = 102, 38.2% female; age 62.03 ± 5.26 years). The demographic and clinical data of participants are presented in Table 1. CHA2DS2-VASc scores of the study population and groups are shown in Fig. 2. We determined that the AVS (+) group had a higher prevalence of CAD, stroke and peripheral artery disease (PAD) than the AVS (–) group (54.3 vs 13.7%; 11.9 vs 0%; 22.9 vs 2.9%, respectively, all p values < 0.001). We also determined that the patients in the AVS (+) group were older and had higher CHA2DS2-VASc scores (63.52 ± 7.24 vs 62.03 ± 5.26 years, p = 0.012; 3 (0–8) vs 1 (0–4), p < 0.001, respectively). When we analysed TTE findings, we found that the AVS (+) group patients had lower LVEF and higher IVST, LAD and ascending aorta measurements when compared to the AVS (–) group (52.64 ± 10.76 vs 59.96 ± 4.55; 1.13 ± 0.14 vs 1.06 ± 0.11; 3.87 ± 0.45 vs 3.64 ± 0.3; 3.68 ± 1.73 vs 3.46 ± 0.29, respectively, all p-values < 0.001). LVDD was more common in the AVS (+) group than in the AVS (–) group (40.2 vs 70.3%, p < 0.001). We determined that oral antidiabetic (OAD) use, insulin and statin treatment rates were higher in the AVS (+) group than in the AVS (–) group (29.7 vs 11.7%, p = 0.001; 48.9 vs 19.6%, p < 0.001; 48.9 vs 19.6%, p < 0.001, respectively). A cut-off value of ≥ 2 for the CHA2DS2-VASc score was estimated to evaluate AVS, which had a sensitivity of 81.2% and Table 1. Demographic and clinical data according to AVS Demographics AVS (–), n = 102 AVS (+), n = 411 p-value Age, year 62.03 ± 5.26 63.52 ± 7.24 0.012 Gender, female, n (%) 39 (38.2) 157 (38.2) 0.995 Co-morbidities, n (%) DM 15 (14.7) 181 (44) < 0.001 HT 54 (52.9) 382 (92.9) < 0.001 CAD 14 (13.7) 223 (54.3) < 0.001 CHF 1 (1) 97 (23.6) < 0.001 Laboratory findings FBG, mg/dl (mmol/l) 101.69 ± 27.82 5.64 ± 1.54 119.65 ± 55.97 6.64 ± 3.11 0.024 Creatinine, mg/dl 0.82 ± 0.16 0.94 ± 0.31 0.001 TC, mg/l (mmol/l) 194.04 ± 44 5.03 ± 1.14 184.37 ± 45.84 4.78 ± 1.19 0.038 TG, mg/l (mmol/l) 162.86 ± 73.67 1.84 ± 0.83 174.18 ± 107.23 1.97 ± 1.21 0.646 HDL-C, mg/l (mmol/l) 47.28 ± 13 1.22 ± 0.34 43.23 ± 12.24 1.12 ± 0.32 0.012 LDL-C, mg/l (mmol/l) 114.1 ± 37.54 2.96 ± 0.97 107.3 ± 37.49 2.78 ± 0.97 0.043 WBC, × 103 cells/µl 6.98 ± 1.38 7.51 ± 1.79 0.035 Hb, g/dl 14.21 ± 1.47 13.71 ± 1.7 0.011 Plt, × 103 cells/µl 253.29 ± 59.07 267.44 ± 76.01 0.141 Echocardiographic findings LVEDD, cm 4.64 ± 0.36 4.80 ± 0.54 0.032 LVEF, % 59.96 ± 4.55 52.64 ± 10.76 < 0.001 PWT, cm 1.02 ± 0.1 1.08 ± 0.15 < 0.001 Aortic velocity, m/s 1.2 (1.0–1.9) 1.3 (1.0–1.9) 0.478 Ascending aorta diameter 3.46 ± 0.29 3.68 ± 1.73 < 0.001 LVDD, n (%) 41 (40.2) 289 (70.3) < 0.001 CHA2DS2VASc score 1 (0–4) 3 (0–8) < 0.001 CHA2DS2VASc ≥ 2 47 (46.0) 377 (91.7) < 0.001 Drugs, n (%) ASA 34 (33.3) 251 (61.0) < 0.001 Beta-blocker 25 (24.5) 269 (65.4) < 0.001 ACE inhibitor 22 (21.5) 154 (37.4) 0.002 Statin 20 (19.6) 201 (48.9) < 0.001 OAD 12 (11.7) 115 (27.9) 0.001 Insulin 1 (0.9) 53 (12.8) < 0.001 ACE: angiotensin converting enzyme, ASA: acetylsalicylic acid, AVS: aortic valve sclerosis, CAD: coronary artery disease, CHF: congestive heart failure, DM: diabetes mellitus, FBG: fasting blood glucose, Hb: haemoglobin, HDL-C: high-density lipoprotein cholesterol, HT: hypertension, LDL-C: low-density lipoprotein cholesterol, LVDD: left ventricular diastolic dysfunction, LVEDD: left ventricular end-diastolic diameter, LVEF: left ventricular ejection fraction, OAD: oral antidiabetic, Plt: platelets, PWT: posterior wall thickness, TC: total cholesterol, TG: triglyceride, WBC: white blood cells. 0 1 2 3 4 5 6 Frequency 120 100 80 60 40 20 0 CHA2DS2-VASc score 0 1 2 3 4 Frequency 40 30 20 10 0 CHA2DS2-VASc score 0 1 2 3 4 5 6 Frequency 120 100 80 60 40 20 0 CHA2DS2-VASc score Fig. 2. CHA2DS2-VASc scores (A) in the study population, (B) in the AVS (–) group and (C) in the AVS (+) group. A B C
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 AFRICA 137 specificity of 65.7%, area under the curve (AUC) of 0.833 with 95% CI (0.792–0.874) (Fig. 3). Patients with CHA2DS2-VASc score ≥ 2 were 7.366-fold (95% CI: 3.452–15.722) more likely to develop AVS compared with those who had a CHA2DS2-VASc score < 2 (Table 2). In the univariate logistic regression analysis, CHA2DS2-VASc score ≥ 2, FBG, HDL-C, LVEF, LVEDD, PWT, IVST, LAD, ascending aortic diameter, eGFR, WBC, neutrophil, insulin and statin therapies were found to be predictors of AVS. Moreover, we determined that CHA2DS2-VASc score ≥ 2, LVEF and ascending aortic diameter were independent predictors of AVS (Table 2). Median CHA2DS2-VASc scores among the AVS grades are shown in Fig. 4. We determined that median CHA2DS2-VASc scores showed a significant difference according to AVS grade [grade 0, n = 102, 1 (0–4); grade 1, n = 100, 3 (0–7); grade 2, n = 134, 3 (0–7); grade 3, n = 177, 4 (1–8), H (3) = 160,935, p < 0.001), respectively]. Median CHA2DS2-VASc scores of grades 0 and 1 and grades 2 and 3 were significantly different. On the other hand, median CHA2DS2-VASc scores of grades 1 and 2 were similar [1 (0–4) vs 3 (0–7), p = 0.001; 3 (0–7) vs 4 (1–8), p = 0.001, 3 (0–7) vs 3 (0–7), p = 0.26, respectively]. Also, to investigate whether AVS grade correlated with CHA2DS2-VASc score, Spearman correlation analysis was performed. A positive correlation was determined between AVS grade and CHA2DS2VASc score (r = 0.548, p < 0.001). Discussion The results of our study indicate three main findings: first, CHA2DS2-VASc ≥ 2 score was independently associated with AVS; second, the cut-off point of the CHA2DS2-VASc score to predict AVS was ≥ 2; finally, there was a positive correlation between the grade of AVS and the CHA2DS2-VASc score. The CHA2DS2-VASc score was initially designed for predicting embolic events and adjusting antithrombotic therapy in AF patients. This score drew attention because it included many CV risk factors together, and several studies encompassed it in different clinical settings. The CHA2DS2-VASc score was found to have predictive value both in acute and chronic coronary syndromes.2,3 Recently, Shang et al. detected a correlation between the CHA2DS2-VASc score and carotid plaques, known as a marker of subclinical atherosclerosis. Similarly, we determined an association between CHA2DS2-VASc score and AVS, a H(3) = 160.935, p < 0.001 n = 102 1 (0–4) n = 100 3 (0–7) n = 134 3 (0–7) n = 177 4 (1–8) CHA2DS2–VASc score Aortic valve sclerosis grade 0 1 2 3 8 6 4 2 0 Fig. 4. Median CHA2DS2-VASc scores according to AVS grades. Median CHA2DS2-VASc scores of AVS grades were compared with the Kruskal–Wallis H-test. Sensitivity AUC: 0.833; 95% CI: 0.792–0.874 Sensitivity: 81.2%; Specifity: 65.7% 0.0 0.2 0.4 0.6 0.8 1.0 1.0 0.8 0.6 0.4 0.2 0.0 1 – Specificity Fig. 3. ROC curves for CHA2DS2VASc score in order to evaluate AVS. The area under the ROC curve was utilised to figure out cut-off points of different CHA2DS2-VASc scores in AVS patients. Table 2. Odds ratio and 95% CI between the CHA2DS2VASc score and prevalence of AVS Univariate Multivariate Variables Odds ratio (95% Cl) p-value Odds ratio (95% CI) p-value CHA2DS2VASc ≥ 2 12.976 (7.684– 21.916) < 0.001 7.366 (3.452–15.722) < 0.001 FBG 1.011 (1.004–1.018) 0.004 0.995 (0.987–1.003) 0.251 TC 0.995 (0.99–1) 0.042 0.996 (0.977–1.017) 0.729 TG 1.001 (0.999–1.004) 0.294 HDL-C 0.976 (0.959–0.994) 0.008 1.012 (0.983–1.042) 0.414 LDL-C 0.994 (0.988–1) 0.039 1.003 (0.981–1.026) 0.763 LVEF 0.846 (0.8–0.893) 0.000 0.873 (0.816–0.934) < 0.001 LVEDD 2.196 (1.265–3.814) 0.005 0.493 (0.186–1.309) 0.156 IVST 74.842 (14.038–399.011) < 0.001 3.515 (0.121–102.031) 0.465 PWT 23.448 (4.783–114.954) < 0.001 7.209 (0.419–124.018) 0.174 LVDD 3.524 (2.250–5.521) < 0.001 0.943 (0.491–1.814) 0.861 LAD 5.488 (2.807–10.73) < 0.001 1.162 (0.408–3.308) 0.779 Asc. aorta dia. 3.798 (1.904–7.575) < 0.001 4.697 (1.758–12.549) 0.002 eGFR 0.97 (0.955–0.985) < 0.001 1.006 (0.985–1.027) 0.563 WBC 1.199 (1.044–1.378) 0.010 0.784 (0.525–1.171) 0.234 Neutrophils 1.432 (1.179–1.738) < 0.001 1.682 (0.993–2.85) 0.053 Insulin therapy 14.846 (2.028–108.688) 0.008 12.926 (1.246–134.103) 0.032 Statin therapy 3.952 (2.334–6.691) < 0.001 1.814 (0.918–3.582) 0.087 Asc. aorta dia: ascending aorta diameter, FBG: fasting blood glucose, eGFR: estimated glomerular filtration rate, HDL-C: high-density lipoprotein cholesterol, LAD: left atrial diameter, LDL-C: low-density lipoprotein cholesterol, LVDD: left ventricular diastolic dysfunction, LVEDD: left ventricular enddiastolic diameter, LVEF: left ventricular ejection fraction, IVST: interventricular septal thickness, OR: odds ratio, PWT: posterior wall thickness, TC: total cholesterol, TG: triglyceride, WBC: white blood cells.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 138 AFRICA marker of subclinical atherosclerosis. These results suggest that CHA2DS2-VASc score may be associated not only with clinical atherosclerosis but also with subclinical atherosclerosis. Shang et al. reported that CHA2DS2-VASc scores ≥ 2 in males and ≥ 3 in females were associated with carotid plaques. They also showed that male patients with a CHA2DS2-VASc score ≥ 2 had a 2.3-fold increased risk of developing carotid plaques.4 On the other hand, in our study, patients with CHA2DS2-VASc score ≥ 2 had a 7.4-fold increased risk of developing AVS than those with a CHA2DS2-VASc score < 2. Previous studies have shown the relationship between AVS and CV risk factors and morbidity and mortality.14,15 On the other hand, Rosa et al. reported that AVS was not associated with a higher risk of death and cardiac death.16 However, a meta-analysis by Pradelli et al. showed that increased absolute event rate in subjects with AVS reduced when the other known CV risks were taken into account. Therefore we believe that the negative association between AVS and cardiac death might be due to the higher baseline CV risks of the patient subgroups included in the study by Rosa et al.17 On the contrary, there are studies showing the association of AVS and CVmortality and morbidity in high-risk populations.18,19 Our results showing the association between AVS and CHA2DS2VASc score may contribute more information to this argument. Nevertheless, the results of our study do not allow us to support the correlation between CV prognosis and CHA2DS2-VASc score in AVS. Further studies should be designed to ascertain this issue. Our study determined that LVEF was lower in patients with AVS than in those without AVS. In our multivariate analysis, LVEF was also found to be an independent predictor of AVS. This may be explained by increased atherosclerotic burden leading to a decrease in LVEF in patients with AVS. Also, clinical studies show that low wall shear stress plays a significant role in the initiation of atherosclerosis within the coronary arterial wall and the progression of calcium deposition on the leaflets. In the same way, the non-coronary cusp was found to be affected initially, probably due to the low shear stress on the endothelium in diastole, given the absence of diastolic coronary flow in this cusp.6 Likewise, as LVEF decreased, shear stress through the aortic valve might decrease. Reduced shear stress might lead to repetitive injury and inflammation, progressive thickening and calcification of the aortic valve leaflets. LVEDD, PWT, IVST,LADandascendingaortameasurements by TTE were statistically higher in patients with AVS compared to patients without AVS in our study. This can be explained by the higher prevalence of HT in AVS, as was also observed in our study. We also detected LVDD more often in the AVS (+) than in the AVS (–) group. Both AVS and LVDD have been reported to be related to many CV risk factors, especially HT and DM and this may explain the relationship we found between them.20,21 DM, FBG level, as well as OAD and insulin therapies were statistically higher in the AVS (+) group in our study. Although hyperlipidaemia is a risk factor for AVS, TC and LDL-C levels were lower in the AVS (+) group. It might be because of the high prevalence of patients with hyperlipidaemia in the AVS (+) group using statins. Inflammation plays a critical role in both the pathophysiology of AVS and atherosclerosis.9 We also determined that WBC and neutrophil counts were higher in patients with AVS than in those without AVS. Additionally, we detected a correlation between AVS grade and CHA2DS2-VASc score. Our study is the first to report the relationship between AVS and CHA2DS2-VASc score and show a progressive rise in CHA2DS2-VASc score along with the grade of AVS. It seems logical to control risk factors for AVS as one would for CAD. There are several limitations in our study. First, it was a single-centre, cross-sectional and observational study having the limits inherent in its design. Second, data of the study population were obtained from the electronic medical report of our hospital, which had a selective bias. Third, unfortunately, we could not find a universally accepted AVS definition in the literature. A prospective cohort study to more accurately determine the prognostic value of the CHA2DS2-VASc score is necessary. Conclusion CHA2DS2-VASc score was higher in patients with AVS compared to those without AVS. Furthermore, the CHA2DS2-VASc score increased as the AVS grade increased. The pathophysiology of AVS is thought to have an inflammatory component besides a degenerative process, which is related to CV diseases. TTE, commonly used clinically, can easily detect AVS. A diagnosis of AVS might change the treatment goals of patients to decrease CV risk in the population. References 1. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2014; 64(21): e1–76. 2. Funabashi N, Uehara M, Takaoka H, Kobayashi Y. The CHA2DS2VASc score predicts 320-slice CT-based coronary artery plaques and >50% stenosis in subjects with chronic and paroxysmal atrial fibrillation. Int J Cardiol 2014; 172(1): e234–237. 3. Kim KH, Kim W, Hwang SH, Kang WY, Cho SC, et al. The CHA2DS2VASc score can be used to stratify the prognosis of acute myocardial infarction patients irrespective of presence of atrial fibrillation. J Cardiol 2015; 65(2): 121–127. 4. Shang L, Zhao Y, Shao M, Sun H, Feng M, et al. The association of CHA2DS2-VASc score and carotid plaque in patients with non-valvular atrial fibrillation. PLoS One 2019; 14(2): e0210945. 5. Bonow RO, Carabello BA, Kanu C, de Leon AC, Jr., Faxon DP, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 guidelines for the management of patients with valvular heart disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. Circulation 2006; 114(5):e84–231. 6. Branch KR, O’Brien KD, Otto CM. Aortic valve sclerosis as a marker of active atherosclerosis. Curr Cardiol Rep 2002; 4(2): 111–11 7. 7. Prasad Y, Bhalodkar NC. Aortic sclerosis – a marker of coronary atherosclerosis. Clin Cardiol 2004; 27(12): 671–673. 8. Di Minno MND, Di Minno A, Ambrosino P, Songia P, Pepi M, et al. Cardiovascular morbidity and mortality in patients with aortic valve sclerosis: A systematic review and meta-analysis. Int J Cardiol 2018;
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 AFRICA 139 260: 138–144. 9. Chandra HR, Goldstein JA, Choudhary N, O’’Neill CS, George PB, et al. Adverse outcome in aortic sclerosis is associated with coronary artery disease and inflammation. J Am Coll Cardiol 2004; 43(2): 169–175. 10. Uysal OK, Turkoglu C, Duran M, Pred Kaya MG, Sahin DY, et al. Predictive value of newly defined CHA2DS2-VASc-HSF score for severity of coronary artery disease in ST segment elevation myocardial infarction. Kardiol Po. 2016; 74(9): 954–960. 11. Hindricks G, Potpara T, Dagres N, Arbelo E, Bax JJ, et al. 2020 ESC guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for CardioThoracic Surgery (EACTS). Eur Heart J 2021; 42(5): 373–498. 12. Nagueh SF, Smiseth OA, Appleton CP, Byrd BF, 3rd, Dokainish H, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2016; 29(4): 277–314. 13. Gharacholou SM, Karon BL, Shub C, Pellikka PA. Aortic valve sclerosis and clinical outcomes: moving toward a definition. Am J Med 2011; 124(2): 103–110. 14. Völzke H, Haring R, Lorbeer R, Wallaschofski H, Reffelmann T, et al. Heart valve sclerosis predicts all-cause and cardiovascular mortality. Atherosclerosis 2010; 209(2): 606–610. 15. Stewart BF, Siscovick D, Lind BK, Gardin JM, Gottdiener JS, et al. Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. J Am Coll Cardiol 1997; 29(3): 630–634. 16. Da Rosa EM, Sant’anna JR, Oppermann LP, Castro I. Prognosis of aortic valve sclerosis in cardiovascular mortality of patients seen at the cardiology institute of Rio Grande do Sul. Arq Bras Cardiol 2007; 88(2): 234–239. 17. Coffey S, Cox B, Williams MJ. The prevalence, incidence, progression, and risks of aortic valve sclerosis: a systematic review and meta-analysis. J Am Coll Cardiol 2014; 63(25 Pt A): 2852–2861. 18. Otto CM, Lind BK, Kitzman DW, Gersh BJ, Siscovick DS. Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl J Med 1999; 341(3): 142–147. 19. Barasch E, Gottdiener JS, Marino Larsen EK, MChaves PH, Newman AB. Cardiovascular morbidity and mortality in community-dwelling elderly individuals with calcification of the fibrous skeleton of the base of the heart and aortosclerosis (the Cardiovascular Health Study). Am J Cardiol 2006; 97(9): 1281–1286. 20. Yadava SK, Dolma N, Lamichhane G, Poudel N, Barakoti M, et al. Prevalence of diastolic dysfunction in type 2 diabetes mellitus. Kathmandu Univ Med J 2017; 15(59): 212–216. 21. Nadruz W, Shah AM, Solomon SD. Diastolic dysfunction and hypertension. Med Clin North Am 2017; 101(1): 7–17. Excess kilos in teen years can double later stroke risk: Finnish study Women who were overweight or obese as teenagers or young adults had more than a two-fold increased risk for stroke before 55 years, suggest researchers, even if that excess weight was temporary. An analysis of more than 50 years of health data on 10 000 adults revealed that close to 5% experienced a stroke during the follow-up period, with the risk for ischaemic stroke being more than twice as high in women who were obese when they were teens or young adults. The risk was even higher for haemorrhagic stroke in both men and women with a history of obesity in youth, reports Medscape. ‘Our findings suggest that being overweight may have longterm health effects, even if the excess weight is temporary,’ said lead author Ursula Mikkola, BM, an investigator in the Research Unit of Population Health at the University of Oulu, Finland. She said healthcare professionals should pay attention to obesity in young people and work with them to develop healthier eating patterns and physical activity. ‘Such conversations about weight, however, should be approached in a non-judgemental and non-stigmatising manner,” she added. The study was published online in Stroke. Gender differences Childhood obesity has been associated with a heightened risk for cerebrovascular disease later in life, but most studies have focused on body mass index (BMI) at a single timepoint without considering its fluctuations throughout life, the investigators noted. For the study, investigators used data from the Northern Finland Birth Cohort 1966, a prospective, general populationbased birth cohort that followed 10 491 individuals (5 185 women) until 2020 or the first stroke, death, or moving abroad, whichever came first. Mean (SD) follow up for each participant was 39 years from age 14 years onward and 23 from age 31 years onward. The analysis was conducted between 1980 and 2020. BMI data were collected from participants at the age of 14 and 31 years. Age 14 covariates included smoking, parental socio-economic status, and age at menarche (for girls). Age 31 covariates included smoking and participants’ educational level. During the follow-up period, 4.7% of participants experienced stroke. Of these events, 31% were ischaemic strokes and 40% were transient ischaemic attacks. The remainder were haemorrhagic or other cerebrovascular events. continued on page 159…
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 140 AFRICA Long-term experience of the modified David V re-implantation technique for valve-sparing aortic root replacement Sabit Sarikaya, Kaan Kirali Abstract Objective: The modified David V technique is one of the valve-sparing aortic root replacement (V-SARR) techniques, which is an alternative to traditional composite valve graft root replacement techniques. We aimed to analyse our longterm experience with the modified David V re-implantation technique for the treatment of aortic root aneurysm and significant aortic valve insufficiency. Methods: From March 2009 to November 2021 the modified David V re-implantation technique, one of the V-SARR techniques, was performed on 48 patients in our centre. The results were analysed retrospectively. Two different-sized grafts were used in all patients. The grafts used in the proximal position were larger than the distal grafts. We performed both intra-operative and post-procedural transoesophageal echocardiography on each patient. All patients were followed by means of transthoracic echocardiography. The mean follow-up period was 5.7 ± 3.1 years. Results: The mean age of this cohort was 56.3 ± 14.3 years (24–79) and the majority were men (75%). The mean aortic root diameter was 5.1 ± 0.6 cm. The mean diameter for the assending aorta was 5.4 ± 2.1 cm. The in-hospital mortality rate was 4.2% (n = 2). One patient needed aortic valve replacement in the early postoperative period. Two (4.2%) patients died in the early postoperative period and four (8.3%) died in the late postoperative period. Overall survival was 91 ± 4 and 86 ± 5% at one and five years, respectively. Aortic valve insufficiancy was at moderate levels postoperatively. Freedom from moderate to severe residual aortic insufficiency was 89.6% at 10 years. None of the patients needed late re-operation of the aortic valve postoperatively. Freedom from valve re-operation was 100% at the end of the follow up. Conclusions: Our study shows that the David V technique is associated with excellent long-term durability, a remarkably low rate of valve-related complications, and it protects the re-implanted native aortic valve from a second operation. Additionally this technique could be safely implemented in patients with a bicuspid aortic valve and acute type A aortic dissection without leaflet deformity. Keywords: aortic valve-sparing root replacement, David procedure, re-implantation Submitted 5/4/23; accepted 12/4/23 Published online 31/5/23 Cardiovasc J Afr 2024; 35: 140–146 www.cvja.co.za DOI: 10.5830/CVJA-2023-018 In aortic root aneurysm surgery, if the aortic valve integrity is intact and in a good condition, valve-sparing aortic root replacement (V-SARR) is an alternative technique that is more attractive than other techniques and offers a good quality of life. However, the Bentall de Bono technique, which was first defined 50 years ago, is still the gold-standard technique.1-3 Possible problems related to a mechanical or bioprosthetic valve in the composite graft encouraged pioneers to search for alternative methods.4-6 Therefore, different techniques and modified forms have been described in the literature to protect the aortic valve. V-SARR techniques, defined in the literature over the years, are remodelling (Yacoup procedure, David III) and re-implantation techniques (David IV and David V).5-8 Recently, the David V re-implantation technique has become one of the most preferred V-SARR techniques. The same-size grafts are used in the proximal and distal positions. In the David V, a pseudo-sinus is created by narrowing the proximal graft both at the top and the bottom. In addition, a Stanford modification was described in the David V re-implantation technique. In the Stanford modification (a modified David V), a larger size graft (10–12 mm) is used in the proximal position rather than in the distal site. It is intended to create a neo-sinus by using two grafts with different sizes to mimic a natural aortic root and sinus of Valsalva.8 The neo-sinus ensures long-term durability of the transferred aortic valves.8,9 V-SARR techniques are technically challenging to perform, therefore, they require a cardiac centre and an operator with a high amount of experience with the procedure. This may be the reason why the use of the technique has remained limited.7 In our opinion, aortic root repair could be performed as commonly as mitral valve repairs, especially for modified V-SARR techniques. For this reason, we publish this case series on patients undergoing the modified David V procedure, and share our long-term experience with the procedure. Methods This retrospective cohort study with unidentified patient data was approved by the review ethics board of our hospital and a waiver of consent was obtained (approval no: 2023.02.655). Our hospital database was analysed retrospectively for patients who underwent the modified David V procedure between 2009 and 2021. Forty-eight patients were included in our study and they were operated on with only the modified David V technique. Department of Cardiovascular Surgery, Kosuyolu Heart Training and Research Hospital, Istanbul, Turkey Sabit Sarikaya, MD, sabitsarikaya@yahoo.com Department of Cardiovascular Surgery, Kosuyolu Heart Training and Research Hospital, Istanbul, Turkey Kaan Kirali, MD
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 AFRICA 141 Other V-SARR techniques were excluded. In our centre, all of these operations were performed by a single surgical team. Operations by other surgical teams were excluded from the study. Indications for the modifiedDavidV technique included aortic root aneurysm with or without significant aortic regurgitation (AR), as recommended by the guidelines,10,11 dystrophic AR with annulo-ectasia or acute aortic dissection. Two different-sized grafts were used in all patients. The grafts used in the proximal position were larger than the distal grafts. Electrocardiogram, echocardiogram and BT angiography screening were performed for all patients pre-operatively. If there was a discrepancy in the aortic measurements between the BT angiogram and echocardiography, the BT angiogram measurement was used. A transoesophageal echocardiography (TEE) was performed on all patients at the beginning of the surgery and after the cardiopulmonary bypass (CPB) was ended. Aortic insufficiency (AI) characteristics and aortic dimensions were obtained from intra-operative TEE. For elective operations, detailed pre-operative screening was performed for any underlying chronic diseases. Five patients (10.5%) were operated on urgently due to acute type A aortic dissection (ATAAD). The data obtained from the medical history were included in the data. Intubations lasting more than 24 hours postoperatively or re-entubations were defined as respiratory failure. Acute neurological pathologies, diagnosed with central nervous system imaging, were defined as cerebrovascular events. A concomitant surgical ablation was performed for the patients who had pre-operative atrial fibrillation. In the post-operative period, atrioventricular (A-V) block events requiring only pacemaker implantation were defined as a rhythm disorder. In order to evaluate bleeding complications, the need for massive blood transfusions and mediastinal exploratory surgery was investigated. Early mortality was defined as any death occurring during hospital stay or during the first 30 days after the operation, while any other death was considered as late mortality.12 We used standard straight grafts to reconstruct the root for all patients. Our re-implantation technique was performed with CPB, moderate hypothermia and intermittent antegrade and retrograde cold-blood cardioplegia. In one arch case, antegrade cerebral perfusion was used throughout the period of hypothermic systemic circulatory arrest and deep hypothermia was performed. After starting the CPB, a part of the external aortic root was carefully dissected with electrocautery. An aortic cross-clamp was inserted and cardioplegic arrest of the heart was achieved. A horizontal aortotomy 1 cm above the sinotubular junction (STJ) was performed and the valve was carefully examined. Once the other part of the external aortic root dissection was completed, the aortic sinuses were excised, leaving an average of a 5-mm suture rim and the coronary buttons were prepared. At the end of all three commissures, 4-0 pledgeted prolene sutures were placed to determine the angular position and the height of the commissures. The aortic graft was sized similarly to principles described by Khachatryan et al.13 We used the aortic biological valve-sizer instrument to determine the proximal graft size. The pledgeted commissural sutures were lifted in the vertical position and abutted against the outer surface of the biological valve sizer (Fig. 1). This region corresponds to the imaginary circular STJ. This allows the measurements to be made with the help of the biological valve sizer. We added 4–7 mm to the measured value and this corresponded to the proximal graft size (Fig. 2). This method gave us the advantage of observing the coaptations of the aortic cusps from the circular cavity of the biological valve sizer. The proximal part of the graft was implanted at the ventriculoaortic junction (VAJ) with 10–12 mattress sutures with/without pledgetes and the proximal graft was narrowed in this plane. Subsequently, the aortic cusps were continuously sutured with 5-0 prolene to the inner part of the stretched graft in a vertical position. Coronary buttons were anastomosed to the graft with 6-0 prolene. A graft that was smaller than the proximal graft was chosen as the distal graft. The two grafts were then anastomosed to each other with 4-0 prolene. The proximal graft was also narrowed in this plane. Hence, the pseudo-sinus was created (Fig. 3). Fig. 1. A: Sizing of the sinotubular junction diameter that will result in optimal aortic valve cusp coaptation. B: The diameter of the imagined circle at the level of the synotubular junction is measured and added to this value by 4 to 7 mm for the modified David V procedure. A B
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 142 AFRICA In TEE after CPB, a prerequisite for a successful repair is a coaptation length of at least 5 mm in the middle of the free border and an effective height of 8–10 mm. The presence of residual moderate AR or mild eccentric AR was an indication for re-exploration of the aortic valve.14,15 Transthoracic echocardiography (TTE) was performed on all patients in the early postoperative stage and after discharge, during follow up. Aortic valve insufficiency was evaluated using recent literature and international guidelines. Aortic valve insufficiency was categorised as: trace or trivial (0); mild (1); moderate (2); moderate–severe (3); or severe (4+). When the regurgitant volume was used to grade AI, 0 indicated no regurgitation; 1+ was a regurgitant volume < 30 ml; 2+ was a regurgitant volume of 30–44 ml; 3+ was a regurgitant volume of 45–60 ml; and 4+ was a regurgitant volume > 60 ml. Postoperative length-of-stay calculations excluded patients who had died in hospital. Two (4.2%) of the patients died within the first 30 days postoperatively and were included as early mortalities. Therefore, data from these two patients were excluded when calculating the median postoperative length of stay. Intra-operative conversion to a valve-replacing procedure because of severe valve dysfunction was considered repair failure.16 One patient had severe AI at postoperative day one and we had to perform an aortic valve replacement (AVR). The clinical follow up extended from 2.5 months to 9.8 years with a mean of 5.7 ± 3.1 years. The follow up was ended on 31 April 2022. The contact information of 45 live patients was obtained. These patients were contacted at six-month intervals and the data obtained were recorded. All of the patients were followed up every year as out-patients. Results were evaluated in terms of overall survival, incidence of re-operation, degree of residual aortic valve insufficiency and incidence of postoperative complications. Statistical analyses Statistical analyses were performed utilising SPSS version 23 software (SPSS, Inc, Chicago, IL, USA). The conformity of variables to a normal distribution was examined via visual (histogram and probability graphics) and analytical methods (Kolmogorov–Smirnov or Shapiro–Wilk tests). The definitive analysis was obtained using frequency tables for categorical variables and mean and standard deviation for normally distributed variables. Intensive care unit stay and discharge time were not normally distributed. They are given as median and interquartile range. Survival and freedom from re-intervention on aortic valve data were obtained from life table analyses and are presented with standard error. Fig. 3. The completed modified David V procedure is shown. Two different-sized grafts are used in this technique. The graft used in proximal position is always larger than the distal graft. Fig. 2. A. Measuring position of the diameter of the STJ for optimum valve coaptation. B. The modified David V intra-operative proximal graft sizing; in this case, the imaginary STJ is approximately 25 mm. Adding 5 mm to this value, the total value is the proximal graft size. A B
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