MARCH/APRIL 2022 VOL 33 NO 2 • Vacuum-assisted closure therapy in pat ients wi th infected venous leg ulcers • Prevalence, pat terns and predictors of dysl ipidaemia in Niger ia • Outcome of concomi tant lef t atr ial ablat ion dur ing valvular heart surgery • Inter leukin-6 and echocardiographic parameters in pregnancy • Fi rst Mal ian ser ies of surgery for rheumat ic valve disease • Immature platelet count and fract ion and transfusion need in CABG • Anaesthesia techniques in postoperat ive pain and hospi tal discharge • Restr ict ive cardiomyopathy of lef t ventr icle af ter 20 years of haemodialysis • Electrocardiogram mani festat ions of hyponatraemia CardioVascular Journal of Afr ica (off icial journal for PASCAR) www.cvja.co.za
PEARLOC 4 mg/5 mg, 4 mg/10 mg, 8 mg/ 5 mg, 8 mg/10 mg. Each tablet contains 4, 8 mg perindopril tert-butylamine respectively and 5, 10 mg amlodipine respectively. S3 A50/7.1.3/0230, 0231, 0232, 0233. For full prescribing information, refer to the professional information approved by SAHPRA, February 2021. *FDC – Fixed-dose combination. 1) Bahl VK, et al. Management of hypertension with fixed combination of perindopril and amlodipine in daily clinical practice. Results from the STRONG prospective, observational, multicentre study. American Journal of Cardiovascular Drugs 2009(3):135-142. 2) Bertrand ME. Perindopril / Amlodipine combination: an optimal synergy for cardiovascular protection. European Heart Journal supplements 2009;11(supplement E):E22-E25. 3) Data on file. PCA784/09/2021. For further product information contact PHARMA DYNAMICS P O Box 30958 Tokai Cape Town 7966 Fax +27 21 701 5898 Email info@pharmadynamics.co.za CUSTOMER CARE LINE 0860 PHARMA (742 762) / +27 21 707 7000 www.pharmadynamics.co.za NEW PERINDOPRIL TERT-BUTYLAMINE / AMLODIPINE 4 mg/5 mg 4 mg/10 mg 8 mg/5 mg 8 mg/10 mg INTRODUCING OUR Perindopril/Amlodipine, an optimal synergy for: • Significant BP reductions1 • Improved tolerability1 • Reduction of CV events2 Pearloc is: • Bioequivalent to the Originator (Perindopril Arginine/Amlodipine)3 • Cost-effective vs the Originator3 PERINDOPRIL TERT-BUTYLAMINE/ AMLODIPINE *FDC
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 33, No 2, MARCH/APRIL 2022 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 43 FROM THE EDITOR’S DESK P Commerford CARDIOVASCULAR TOPICS 44 The effectiveness of vacuum-assisted closure therapy in patients with infected venous leg ulcers EE Tekin • MA Yeşiltaş • A Uysal • İ Haberal 52 Prevalence, patterns and predictors of dyslipidaemia in Nigeria: a report from the REMAH study B Chori • B Danladi • P Nwakile • I Okoye • U Abdullahi • K Zawaya • I Essien • K Sada • M Nwegbu • J Ogedengbe • A Aje • G Isiguzo • A Odili 60 Outcome of concomitant left atrial ablation during valvular heart surgery: an African perspective D Nyamande • RF Chauke • SM Mazibuko • SP Ramoroko 65 Interleukin-6 and its correlations with maternal characteristics and echocardiographic parameters in pre-eclampsia, gestational hypertension and normotensive pregnancy D Gencheva • F Nikolov • E Uchikova • R Mihaylov • B Pencheva • M Vasileva 74 The role of immature platelet count and immature platelet fraction in determining the need for transfusion in patients undergoing CABG C Yücel • S Ketenciler • H Gemalmaz • N Kayalar 79 First Malian series of surgery for rheumatic valve disease: opening of the centre, clinical features and peri-operative realities M Coulibaly • SA Koita • M Doumbia • B Diallo • SI Traore • BI Diarra • B Coulibaly • S Daffe • A Maiga • M Toure • RA Zongo • G Fofana • SA Beye • B Diallo • MB Diarra • DM Diango • Y Coulibaly 84 The effect of different anaesthesia techniques on postoperative pain and hospital discharge in varicose vein surgery M Mutlu • S Turkmen
CONTENTS Vol 33, No 2, MARCH/APRIL 2022 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. CONGRESS REPORT 88 The joint 15th Pan-African Society of Cardiology and Kenya Cardiac Society congress proceedings, 2021 CASE REPORTS 95 Restrictive cardiomyopathy caused by diffuse calcification of the left ventricle after 20 years of haemodialysis C-C Yang • C-S Tsai • Y-T Tsai • C-Y Lin • J-L Chen • P-S Hsu 98 Electrocardiogram manifestations of hyponatraemia S Zou • Q Zhang • S Gao • M Luo • X Gan • K Liang PUBLISHED ONLINE (Available on www.cvja.co.za and in PubMed)
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 AFRICA 43 The optimal management of patients with atrial fibrillation undergoing heart valve repair or replacement remains unresolved. There have, over the years, been strongly voiced opinions about left atrial appendage amputation and the various modifications of the Cox procedure. There is still no consensus on the optimal strategy. Nyamande and colleagues (page 60) report a retrospective analysis of their experience and point out that their results are similar to reports from other parts of the world. However, a significant number of their patients reverted to atrial fibrillation. Whatever strategy is adopted there can be no way to escape the need for meticulous attention to anticoagulation after valve repair or replacement in all patients and particularly in those who have been in atrial fibrillation. The endpoint the authors measured was cardiac rhythm. The most important and relevant endpoint is cardioembolic events, the most clinically important of which is stroke. Clinicians recognise that stroke after major cardiac surgery remains a significant problem, particularly in the elderly. It is encouraging that cardiac surgeons, Tekin and colleagues (page 44), have examined whether surgical technique contributes to the risk of stroke. Many surgical techniques have not been subjected to scientific scrutiny but remain entrenched by firmly held opinion. The analysis is neutral and does not answer the question, but the authors should be commended for attempting to answer an important question. The prevalence of risk factors for cardiac diseases remains incompletely explored in African populations. This is particularly important as Africa is currently faced with a double burden of communicable and non-communicable diseases (NCDs). The latter, which was less common in past decades, is predicted to take the lead in the next decade. Knowledge of the prevalence of risk factors is important if Africa is to prepare to reduce the predicted rise in NCDs. There is not a great deal of information on risk factors for cardiovascular disease in African populations. Odili and co-authors (page 52) and all those involved in the ambitious REMAH study are to be congratulated on concluding a landmark study to close some of the gaps in our knowledge. It is clear that cardiological expertise to diagnose and cardiac surgical facilities to treat the victims of rheumatic heart disease in Africa are sorely lacking. The report from Coulibaly and co-workers (page 79) regarding the effort in Mali is a wonderful example of the generous assistance of donors from abroad to alleviate the sad situation in Africa. It shows what can be done with goodwill and funding. I look forward to the follow-up report from this and other groups doing similar work in Africa, which will detail not just patients treated but numbers of local staff trained and able to carry on the important work in their home country. The report of the 15th PASCAR and Kenya Cardiac Society congress (page 88) is a remarkable document. The very existence of these organisations, the many national bodies, and their close collaboration would have been almost unthinkable in the 1970s and 80s. The fact that they do exist and collaborate collegially is a tribute to all who have worked so hard for many years to unite all African societies seeking to improve cardiovascular health for Africans. PJ Commerford Editor-in-Chief From the Editor’s Desk
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 44 AFRICA Cardiovascular Topics The effectiveness of vacuum-assisted closure therapy in patients with infected venous leg ulcers Esra Ertürk Tekin, Mehmet Ali Yeşiltaş, Ayhan Uysal, İsmail Haberal Abstract Aim: In this study, we aimed to investigate the effect of vacuum-assisted closure therapy on venous stasis wound healing in patients with chronic venous leg ulcers. Methods: Vacuum-assisted closure therapy was applied on a total of 14 venous leg ulcers. All patients had post-thrombotic syndrome. Quantitative wound culture samples were obtained before the procedure and local wound assessments were performed. The primary outcome measures included wound healing as assessed by a local wound examination during each dressing change and the rate and velocity of ulcer reduction. Wound healing was defined as the complete closure of the ulcer, while rapid wound healing was defined as a ≥ 30% reduction in the ulcer size by week four. Results: No surgical debridement or surgical corrective procedure was applied in any patient. The mean length of hospital stay was 32.3 days. The mean number of vacuumassisted closure therapies for each case was 17.8 and the mean time to dressing change was 72.3 hours. Multidrugresistant Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus were detected in three and four patients, respectively. Wound culture results became negative after a mean duration of vacuum-assisted closure therapy of 12.1 days. None of the patients needed antibiotic therapy until the procedure was completed. Compared to baseline, the mean ulcer reduction rates were 46.4% for the first six applications and 72.8% for the subsequent applications. Conclusion: Our study results suggest that vacuum-assisted closure therapy promotes rapid wound healing in patients with severe post-thrombotic syndrome with venous stasis leg ulcers, and reduces the need for antibiotics by reducing the biological burden. Keywords: vacuum-assisted closure therapy, venous ulcer, postthrombotic syndrome, wound infection, rapid wound healing. Submitted 7/12/20; accepted 30/6/21 Published online 26/7/21 Cardiovasc J Afr 2022; 33: 44–50 www.cvja.co.za DOI: 10.5830/CVJA-2021-034 The primary aims of wound healing are to restore the tissue architecture and integrity of the skin, achieve aesthetically favourable and sustainable results, relieve pain, improve patient comfort and quality of life, and prevent undesirable complications in a cost-effective manner.1 Chronic leg ulcers affect nearly 1% of the adult population.2 The prevalence of active leg ulcers has been estimated to be 15%.3 Venous disease accounts for 80% of all chronic leg ulcers.1 Venous hypertension has been proposed to be the main underlying pathophysiological mechanism of reflux and/ or obstruction of the venous system.1 Standard treatment includes surgical debridement, wound dressing with topical antimicrobials, compression therapy, pharmacological treatment and corrective procedures. Venous ulcers are the most common ulcers of the lower limbs however, the rate of complete healing is very low despite the application of standard treatment.4 Post-thrombotic syndrome (PTS), an important chronic consequence of deep-vein thrombosis (DVT), is an important condition for which patients frequently seek medical advice. PTS occurs in 20 to 50% of patients with DVT. PTS may present with clinical manifestations ranging from mild clinical symptoms to more severe manifestations, such as chronic leg pain, persistent oedema, and leg ulcers that limit activity and the ability to work.5 In five to 10% of patients, DVT will progress to severe PTS, which can include venous leg ulcers. A multidisciplinary approach should be used for venous ulcer management, which includes compression therapy, skin care and topical dressings. When conservative therapy fails, surgical or endovascular procedures may be recommended to treat large reflux vessels in selected patients. However, ulcers may be resistant to all treatment and frequently recur. Chronic wounds never become sterile and are mostly colonised with micro-organisms of the normal flora of intact skin. Chronic wounds are commonplace for bacteria and these bacteria do not always cause infections per se. The level of bacterial burden can be described as one of the following four conditions: (1) contamination, (2) colonisation, (3) critical colonisation, and (4) infection.6 Department of Cardiovascular Surgery, Mersin City Training and Research Hospital, Mersin, Turkey Esra Ertürk Tekin, MD, dresraer@yahoo.com Department of Cardiovascular Surgery, Bakirkoy Dr Sadi Konuk Training and Research Hospital, Istanbul, Turkey Mehmet Ali Yeşiltaş, MD Cardiovascular Surgery Clinic, Firat University Medical Faculty, Elazığ, Turkey Ayhan Uysal, MD Department of Cardiovascular Surgery, Istanbul University, Cerrahpasa Institute of Cardiology, Istanbul, Turkey İsmail Haberal, MD
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 AFRICA 45 Bacterial colonisation is present in approximately 80 to 100% of leg ulcers.7,8 Several studies have demonstrated that increased bacterial bioburden prolongs the wound-healing process.8 Bacterial diversity and density are critical factors for prolonged healing processes.9,10 In the presence of infected ulcers, bacteria invade living dermal and subdermal tissues, and the clinical manifestations include worsening pain, warmth, swelling and erythema of the skin around the ulcer, which hamper wound healing. Wound infection prolongs the duration of response to chronic ulcers and delays collagen synthesis, slowing the epithelialisation process and secreting proteases.9 Wound culture is the mainstay of treatment for chronic wounds.11 The most common culprits of chronic leg ulcers are Staphylococcus aureus (S aureus), Pseudomonas aeruginosa (P aeruginosa), Escherichia coli (E coli), Proteus mirabilis (P mirabilis) and Enterobacter cloacae (E cloacae).12 In recent years, however, the spectrum of micro-organisms most frequently isolated has expanded. A few years ago, researchers paid particular interest to gram-positive micro-organisms such as S aureus. However, gram-negative bacteria are more frequently being isolated worldwide and have become more clinically significant.13 Although S aureus is the most common pathogen in leg ulcers, recent studies have demonstrated higher rates of anaerobic and gram-negative bacilli in clinically infected leg ulcers than in those without infection.14,15 The majority of bacteria are resistant to a variety of antibiotics, such as doxycycline and penicillin, and more than half of cases have multidrug resistance (MDR).16,17 Vacuum-assisted closure (VAC) therapy is used for chronic wounds to stimulate rapid wound healing. The therapy consists of an open-cell polyurethane sponge sealed by an adhesive drape 400 to 600 microns in size and 0.703 to 0.0228 kgf/cm3 compression with an open-cell structured network. An open-cell, soft connection port is placed, and the other end of the port is mounted on the device, producing negative pressure (Fig. 1). The VAC system provides sub-atmospheric pressure for physical contraction by removing toxins, excessive interstitial fluid and cell debris from the wound bed. Macrostrain is the visible change that occurs when negative pressure contracts the foam that is in direct contact with the wound bed, drawing the wound edges together (Fig. 2).18 Due to the macrostrain effect, wound edges are diminished, and exudate and infectious material are removed, leading to reduced bacterial bioburden and tissue oedema. The VAC drape is an adhesive layer, ensuring a closed, moist, wound-healing environment and preventing external contamination. In recent years, VAC therapy using local negative pressure has been used as a non-invasive adjunct in the field of plastic and reconstructive surgery. The clinical efficacy of VAC therapy has been shown in the treatment of venous leg ulcers.19 In our study on the healing of infected chronic venous stasis leg ulcers in patients with severe PTS after DVT, we aimed to investigate the effect of VAC treatment, to elucidate its mechanism of action and to determine whether it could be used for these patients with limited treatment options. Methods Patients with chronic venous stasis ulcers who were admitted to the cardiovascular surgery clinic between January 2016 and January 2019 and diagnosed with severe PTS were included in this study. PTS Villata–Prandoni severity rating scoring was performed for all patients. Twelve patients with a Villata– Prandoni score > 14 (mean age: 50.2 years; range 38–71 years) were considered to have severe PTS. VAC treatment was applied to the 12 patients with severe PTS and 14 venous stasis ulcers. Written informed consent was obtained from each patient. The inclusion criteria were as follows: previous diagnosis of DVT, severe PTS, chronic venous insufficiency, a venous ulcer that did not heal despite venous correction procedures, and clinical signs and symptoms of infection with microorganism growth in the pre-procedural wound culture. The exclusion criteria were as follows: acute DVT, peripheral arterial insufficiency [ankle–brachial index (ABI) < 0.8], anti-aggregant and anticoagulant therapy, visible vascular structures, untreated osteomyelitis, necrotic wounds with severe scarring, and decision to undergo venous correction and compression therapy first for ulcer healing. The study protocol was approved by the ethics committee of the Republic of Turkey, Ministry of Health, Turkish Medicines and Medical Devices Agency, Research & Development Department (65355327-604.01.02-E.134, Decree No. 26). The study was conducted in accordance with the principles of the Declaration of Helsinki. Fig. 1. VAC system. 1 shows the collection reservoir; 2 shows pressure and mode control device; 3 shows polyurethane sponge and drape; 4 shows the connection port. Fig. 2. Macrostrain effect of VAC system. 1 2 3 4
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 46 AFRICA Demographic and clinical characteristics of the patients were recorded. Before the procedure, quantitative woundculture samples were collected from all ulcers, and systemic antibiotic therapy was initiated according to the isolated strains. The wounds were washed with isotonic saline before the placement of the VAC sponge and necrotic tissue was removed. No local antiseptic agents were used for dressing changes. A VAC device (Smith & Nephew RENASYS EZ MAX NPWT device, Switzerland AG, Baar, Switzerland) was utilised at 125 mmHg continuous negative pressure for the first six consecutive applications and at 80 to 125 mmHg (mean: 100 mmHg) intermittent negative pressure for the subsequent applications.19 The wound was examined for signs of infection during every dressing change. The length and width of the wound were measured by the classical method and the results were recorded in cm.20 Wound healing, formation of granulation tissue and epithelialisation were evaluated and captured by photography. No surgical debridement or surgical corrective procedure was applied in any patient. None of the patients received venotonic agents during the hospitalisation period. Wound healing was defined as the complete closure of the ulcer, while rapid wound healing was defined as a ≥ 30% reduction in the ulcer size by week four.21 Primary outcome measures included wound healing as assessed by local wound examination at every dressing change,22 and the rate and velocity of ulcer reduction. Statistical analysis Statistical data were evaluated using Windows-compatible Statistical Package for Social Sciences 13.0 (SPSS 13.0) (SPSS Inc, Chicago, IL). Descriptive data are expressed as medians (interquartile ranges) or as numbers and frequencies. Significant differences between mean values were analysed using the Mann–Whitney U-test, the Wilcoxon signed ranks test and the Kruskal–Wallis test, and subgroups with significant differences from each other were analysed using the Bonferroni corrected Mann–Whitney U-test. The chi-squared test was used to evaluate the relationships between categorical variables. In all analyses, p < 0.05 was considered significant. Results The mean number of VAC therapies for each case was 17.8 (range 12.4–26.8) and the mean time between dressing changes was 72.3 hours (range 61.1–83.4). The mean length of hospital stay was 32.3 days (range 24.2–38.6). The wound surfaces of all ulcers were measured before VAC therapy, and the mean length and width were found to be 9.2 cm (range 6.1–12.6) and 8.1 cm (range 3–14.2), respectively. The mean pre-procedural wound surface area was 68.2 cm2 (range 22.5–154.6). Pre-procedural local wound and infection examination results and wound surface area measurements are summarised in Table 1. Compared to baseline, the mean reduction rates of ulcers were 46.4% for the first six applications and 72.8% for the subsequent applications (Fig 3). In addition, all ulcers were colonised by a variety of bacteria at baseline (Figs 4–7). MDR P aeruginosa and methicillin-resistant S aureus (MRSA) were detected in three and four patients, respectively (Table 1). Before VAC therapy, the mean dosage of antibiotic therapy was three times daily (range 1–8) for each patient. Quantitative wound culture results became negative after a mean duration of Table 1. Pre-procedural wound assessments and wound surface measurements (n = 14) No. Location Size and decollation (cm2) Bacterial spp. Wound edges/surroundings Wound bed/ surface Exudate/drainage Pain 1 Right medial malleolus 90.92 MSSA Regular/indurated Fibrinous Fibrinous/moderate Transient 2 Right lateral malleolus 45.15 Pseudomonas aeruginosa Regular/erythematous Fibrinous Purulent/moderate Persistent 3 Mid-anterior of right leg 78.98 Pseudomonas aeruginosa Regular/erythematous Fibrinous Purulent/severe Persistent 4 Left medial malleolus 49.51 MRSA Irregular/indurated Fibrinous Serous/moderate Transient 5 Right lateral leg 53.05 Beta-haemolytic streptococci Irregular/indurated Fibrinous Fibrinous/severe Transient 6 Medial malleolus 83.62 MRSA Regular/indurated Fibrinous Serous/moderate Transient 7 Anterior leg, inferior 55.81 Actinomyces israelii Irregular/increase temperature Fibrinous Purulent/moderate Persistent 8 Anterior leg, middle 29.63 Eubacterium rectale Irregular/erythematous Fibrinous Purulent/severe Persistent 9 Anterior leg, middle 22.52 MRSA Irregular/erythematous Fibrinous Fibrinous/moderate Transient 10 Lateral leg, inferior 37.96 Escherichia coli Regular/indurated Fibrinous Serous/moderate Transient 11 Medial malleolus 66.04 Escherichia coli Regular/macerated Fibrinous Serous/moderate Transient 12 Anterior and posterior leg 154.56 Pseudomonas aeruginosa Irregular/increase temperature Fibrinous Purulent/moderate Persistent 13 Medial, middle 145.88 MRSA Irregular/erythematous Fibrinous Fibrinous/moderate Persistent 14 Medial, inferior 41.17 Propionibacterium acnes Regular/erythematous Fibrinous Purulent/moderate Persistent MRSA: methicillin-resistant Staphylococcus aureus; MSSA: methicillin-sensitive Staphylococcus aureus. Treatment duration Baseline Week 2 Week 4 Week 6 Week 8 Wound surface area (cm2) (width × length) 80 70 60 50 40 30 20 10 0 Fig 3. Ulcer reduction rate according to treatment weeks
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 AFRICA 47 Fig. 5. Pre-procedural image of venous leg ulcer and granulation formation and epithelialisation after VAC therapy. Fig. 6. Granulation tissue and epithelialisation phase after VAC therapy. Fig. 7. Pre-procedural image of venous leg ulcer on medial malleolus and complete wound healing after VAC therapy. Fig. 4. Infected venous leg ulcer and complete wound healing after VAC therapy.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 48 AFRICA VAC of 12.1 days (range 5–21) (mean number of VAC sessions 4.2). None of the patients needed antibiotic therapy until the VAC therapy was completed. The mean duration of leg ulcers was 7.2 months. Of all the ulcers, recurrence was observed in one case twice and in another three times. Five of the ulcers were newly diagnosed. Discussion In this study, we examined the effect of VAC therapy on venous stasis wound healing in patients with chronic venous leg ulcers. Our study results showed that VAC therapy was an effective and rapid method of treating venous leg ulcers and had an accelerated wound-healing effect. Negative pressure was first used for wound healing in 1993 by Fleischmann et al.23 Approximately 70% of chronic leg ulcers are caused by venous diseases. The underlying aetiology of venous insufficiency is venous hypertension.24 However, its pathogenesis, ranging from valve regurgitation to ulceration, remains unclear. Clinical symptoms of venous insufficiency include oedema, lipodermatosclerosis, hyperpigmentation, hyperkeratosis and atrophie blanche (white atrophy).25 At a microvascular level, microlymphangiopathy, dilatations of the larger lymph vessels, dilatation and extension of capillaries, occlusion of the capillaries by microthrombi or white cells, decline in the number of functional capillaries, increase in the capillary passage, leakage of plasma proteins and red blood cells into the interstitium and accumulation of iron into the interstitium and siderophages, accumulation of fibrins, and inward growth of the fibroblasts along the fibrin fibres can occur.24 Most studies consider that haemodynamic alterations occurring at the microvascular level explicitly indicate venous ulceration.26,27 In our study, chronic venous insufficiency was the main aetiology of all ulcers. Clinical studies have reported low rates of wound healing with standard treatment of venous leg ulcers.27 General medical management is the cornerstone of standard treatment. This is followed by clinical examination and the maintenance of adequate oxygenation and perfusion. An intervention is planned, if required. For the underlying pathology, venous surgery, endovenous laser ablation, radiofrequency ablation, sclerotherapy, or subfascial endoscopic perforator surgery may be applied. In certain cases, compression therapy is useful with local wound care. In a retrospective, multicentre study, 68 patients with venous leg ulcers were treated with serial debridement, and complete wound closure was achieved in 32 (47%) patients by week 12.28 In the remaining centres, 298 patients were treated and complete healing was achieved in 88 (30%) patients by week 12. In our study, none of the patients received surgical debridement. The mean reduction rate of ulcers was 46.4% by week four, indicating a greater reduction in a shorter time compared to the data in the literature. The most frequently isolated micro-organisms in infected venous leg ulcers are P aeruginosa, S aureus and haemolytic streptococci.9 Surgical debridement followed by wound dressing with topical antibiotics and antimicrobials is recommended for the management of bacterial bioburden. In a Cochrane Review of 25 published studies, there was a statistically significant result in favour of cadexomer iodine compared to standard care in the frequency of complete healing at six weeks.29 In addition, there was some evidence to show a reduction in the bacterial bioburden in patients with infected venous leg ulcers. In another study, increased blood flow reduced interstitial tissue oedema and eliminated harmful bacterial enzymes, promoting the wound-healing process and quality.30 In our study, all ulcers were infected at baseline. Consistent with the literature, MDR P aeruginosa and MRSA were isolated in three and four patients, respectively. In addition, current consensus guidelines recommend antibiotic treatment for a minimum of two weeks unless persistent evidence of wound infection is present.31 In our study, the mean duration of antibiotic therapy was 4.5 days (mean: three to 12 days) for the first six applications. Quantitative wound culture results became negative after a mean VAC duration of 12.1 days and none of the patients needed antibiotic therapy until the end of the VAC therapy. The wound culture became negative five days after the initiation of VAC therapy (two sessions) in three patients. In our study population, antibiotics reduced the bacterial colonisation and bioburden in the wound site and removed the need for surgical debridement. Additionally, no local antiseptic agents were used for dressing changes. During the third dressing change with a sterile adhesive bandage, the new formation of granulation tissue and surroundings was evident. No bacterial growth was detected in subsequent VAC applications until the end of the therapy. Our application seems to be consistent with the literature, suggesting the use of antibiotics for a minimum of two weeks. Although the wounds were closed with dressings, VAC therapy was completed without the need for surgical debridement and further antibiotic therapy in all cases. In a study analysing 679 swabs of 285 patients with venous leg ulcers, 76.1% gram-positive and 58.2% gram-negative bacteria were isolated.12 In our study, gram-negative bacteria were found to be associated with more pain and were isolated in eight ulcers. These patients reported a higher pain severity, consistent with the literature. High-pressure (30–40 mmHg) compression stockings are recommended for venous leg ulcers. In a Cochrane Review of 19 databases and two randomised, controlled trials, the authors investigated the effect of compression stockings in preventing the recurrence of venous ulcers.32 Half of the patients were unable to wear compression stockings on their own, with a 30 to 65% non-compliance rate. In addition, compression therapy was found to be more effective than no compression therapy, high-pressure compression stockings were more effective than low-pressure stockings, and multi-layer compression bandages were more effective than single-layer bandages. In over 400 patients with ulcer healing, the continuous use of compression stockings reduced the recurrence rate after three to five years of follow up. In a randomised, controlled study, the healing and recurrence rates after treatment with compression with or without surgery were evaluated in patients with leg ulcers.33 Venous duplex imaging of ulcerated or recently healed legs in 500 patients from three centres was performed, and the recurrence rate was found to be significantly lower at four years in the combinationtherapy group than in the compression-alone group (24 vs 52%, respectively). However, up to 20% of leg ulcers showed no healing by 50 weeks after compression therapy.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 AFRICA 49 In another study, the likelihoods of wound healing were only 22% for large ulcers and 71% for smaller ulcers with long-term compression therapy.34 In our study, none of the patients was instructed to wear compression stockings during VAC therapy. However, given that compression therapy reduces the ulcer recurrence rate, all patients in our institute were recommended to wear high-pressure (30–40 mmHg) compression stockings continuously throughout the day at the end of the treatment. Previous studies have demonstrated that venous leg ulcers affect 0.76% of males and 1.42% of females in adults aged between 65 and 95 years.4 In our study, all patients were males. Furthermore, possible risk factors for venous leg ulcers include advanced age, female gender, familial history of leg ulcers, white race, obesity, history of DVT or phlebitis, previous severe traumatic leg injury, chronic lower-limb oedema, sedentary lifestyle, and a job requiring prolonged standing.35 Although venous leg ulcers more frequently affect elderly individuals, the first diagnosis was made at the age of 40 years in 22% and at the age of 30 years in 13% of patients.21 In their study, Taylor et al.36 found advanced age and male gender to be significant predictors of poor outcomes. Similarly, in our study, the oldest case was 79 years old, in whom diabetic foot and venous leg ulcers had recurred three times within the previous 18 months. In another study, bacterial colonisation was associated with delayed wound healing in patients with venous leg ulcers, and beta-haemolytic streptococci and anaerobic bacteria were the main culprits of delayed healing.8 Consistent with these findings, beta-haemolytic streptococci were isolated in one of our patients with the longest healing time. This case was also the oldest patient, with diabetic foot ulcer. He received 21 sessions of VAC and antibiotic therapy twice daily for 15 days. Nonetheless, we consider that the aetiology of delayed wound healing is multifactorial in venous leg ulcers. A previous history of leg trauma is considered a poor prognostic factor for leg ulcers.36 In our study, one patient had a history of leg trauma and the ulceration did not respond to previous standard treatment, with the longest ulceration time (12 months). In addition, arterial pathologies were detected in 25% of venous leg ulcers.37,38 In our study, one patient with peripheral arterial insufficiency (ABI < 0.8) was excluded, to obtain more reliable results. VAC therapy is associated with an increased risk for thromboembolism and is contra-indicated in such patients.39 In our study, we also excluded two patients with a history of DVT and one patient with acute DVT. Documentation of the characteristics of the wound bed and the wound site is of utmost importance to evaluate the healing process and the treatment response. Wound assessment requires an accurate and reproducible measurement.20 It is also critical for evaluation of the response rates. In their study, Kantor et al.40 examined the relationship between planimetric wound area and simple wound measurements and found that the correlation between simple values and planimetric area was significantly decreased for wounds > 40 cm2. In our study, we used simple measurements, and the baseline ulcer area was found to be 68.2 cm2 (mean baseline length 9.2 cm, mean baseline width 8.1 cm). Additionally, wounds with < 30% healing within the four-week treatment period were classified as hard-to-heal wounds by week 12; such patients should be re-examined for accurate diagnosis and treatment.41 In our study, the mean wound surface area was measured as 29.4 cm2 at the end of the six VAC applications by week three, indicating a 42.7% reduction. The reduction velocity was the highest within the first two weeks of VAC therapy, which can be attributed to the necrotic tissue-reducing and tissue oedemareducing effects of VAC. Until week four, the mean time to reduction was slower, however, formation of the granulation tissue increased due to the new tissue formation in the wound bed induced by VAC during this period. The epithelialisation phase covering the wound surface continued in week four. In a similar study showing the efficacy of VAC therapy, a total of 60 patients with chronic leg ulcers were equally randomised to either VAC therapy or conventional wound care.42 Among the patients receiving VAC therapy, split-thickness skin grafting was performed for wound-bed preparation. In these patients, the median preparation time was reduced by 58%, and the overall complete healing time was reduced by 35.6%, compared to the conventional wound-care group. In addition, VAC therapy reduced the treatment-related cost by 28.8% and the total nursing time by 39.9%. In our study, we achieved a 42.7% reduction in ulcer size at three weeks with VAC therapy, indicating rapid wound healing. Themain limitationof this study is the use of a classical woundmeasurement technique, which might have underestimated the accurate length and width over time, depending on the change in the wound shape. Therefore, further studies should use maximum vertical length and diameter (diameter and tissue measurement) measurements for the wound surface.43 Additionally, although it is not feasible in daily clinical practice, three-dimensional images can be obtained using sophisticated systems such as stereophotogrammetry.44 Conclusion VAC therapy is an effective and safe option for the treatment of complicated and hard-to-heal wounds and venous leg ulcers. In our study, VAC therapy enhanced wound healing, reduced the bacterial bioburden and the need for antibiotic therapy, and promoted the regression of infection. Based on these study findings, we suggest that VAC therapy is an effective and suitable tool for the treatment of venous leg ulcers. References 1. Mekkes JR, Loots MAM, van der Wal AC, Bos JD. Causes, investigation and treatment of leg ulceration. Br J Dermatology 2003; 148(3): 388–401. 2. Margolis DJ, Bilker W, Santanna J, Baumgarten M. Venous leg ulcer: Incidence and prevalence in the elderly. J Am Acad Dermatology 2002; 46: 381–386. 3. Callam MJ, Harper DR, Dale JJ, Brown D, Gibson BB, Prescott RJ. Lothian and for the Valley leg ulcer healing trial, Part 1: elastic versus nonelastic bandaging in the treatment of chronic leg ulceration. Phlebology 1992; 7(4): 136–141. 4. Falanga V, Margolis D, Alvarez O, Auletta M, Maggiacomo F, Altman M, et al. Rapid healing of venous ulcers and lack of clinical rejection with an allogeneic cultured human skin equivalent. Human Skin Investigators Group. Arch of Dermatol 1998; 134: 293–300. 5. Kahn SR, ComerotaAJ, CushmanM, et al.; AmericanHeart Association Council on Peripheral Vascular Disease, Council on Clinical Cardiology, and Council on Cardiovascular and Stroke Nursing. The postthrom-
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 50 AFRICA botic syndrome: evidence-based prevention, diagnosis, and treatment strategies: a scientific statement from the American Heart Association. Circulation 2014; 130(18): 1636–1661. 6. Bates-Jensen BM, Schultz G, Ovington LG. Management of exudate, biofilms, and infection. In: Sussman C, Bates-Jensen B, eds. Wound care: a Collaborative Practice Manual for Health Professionals. Lippincott Williams & Wilkins, 2012: 457–476. 7. Brook I, Frazier EH. Aerobic and anaerobic microbiology of chronic venous leg ulcers. Int J Dermatol 1998; 37: 426–428. 8. Halbert AR, Stacey MC, Rohr JB, Jopp-McKay A. The effect of bacterial colonization on venous ulcer healing. Aust J Dermatol 1992; 33: 75–80. 9. Bowler PG. The 105 bacterial growth guideline: reassessing its clinical relevance in wound healing. Ostomy Wound Manage 2003; 49(1): 44–53. 10. Davies CE, Hill KE, Newcombe RG, Stephen P, Wilson MJ, Harding KG. A prospective study of the microbiology of chronic venous leg ulcers to re-evaluate the clincial predictive value of tissue biopsies and swabs. Wound Repair Regen 2007; 15(1): 17–22. 11. Reich-Schupke S, Altmeyer P, Stücker M. Actual procedures of diagnostics and treatments of crural venous ulcer in specialized German praxis and clinics. Phlebologie 2009; 38: 77–82. 12. Engelberg WL, Dörler M, Stücker M, Reich-Schupke S. Impact of gram-negative bacteria on the treatment of venous leg ulcers. Int Wound J 2018; 15(6): 958–965. 13. Ho J, Tambyah PA, Paterson DL. Multiresistant gram-negative infections: a global perspective. Curr Opin Infect Dis 2010; 23(6): 546–553. 14. Bowler PG, Davies BJ. The microbiology of infected and noninfected leg ulcers. Int J Dermatol 1999; 38: 573–578. 15. Hansson C, Hoborn J, Moller A, Swanbeck G. The microbial flora in venous leg ulcers without clinical signs of infection. Acta Dermatol Venereol (Stockh) 1995; 75: 24–30. 16. Sancak B. Staphylococcus aureus ve antibiyotik direnci. Mikrobiyol Bul 2011; 45(3): 565–576. 17. Aktaş Z, Satana D, Kayacan Ç, Can B, Gönüllü N, Ömer Küçükbasmaci Ö. Pseudomonas aeruginosa suşlarinda antibiyotik duyarlilik oranlari ve beta-laktam direnç mekanizmalarinin tiplendirilmesi. Mikrobiyol Bul 2012; 46(3): 386–397. 18. Saxena V, Hwang CW, Huang S, Eichbaum Q, Ingber D, Orgill DP. Vacuum-assisted closure: microdeformations of wounds and cell proliferation. Plastic Reconstruct Surg 2004; 114(5): 1086–1096. 19. Lantis JC, Gendics C. VAC therapy appears to facilitate STSG take when applied to venous leg ulcers. 2nd World Union of Wound Healing Societies Meeting; 2004 July 8–13; Paris 2004, Vol. 87. 20. Öien RF, Hakansson MD, Hansen BU, Bjellerup MD. Measuring the size of ulcers by planimetry: a useful method in the clinical setting. J Wound Care 2002; 11(5): 165–168. 21. Alavi A, Sibbald RG, Phillips TJ, Miller OF, Margolis DJ, Marston W, et al. What’s new: management of venous leg ulcers. Approach to venous leg ulcers. J Am Acad Dermatol 2016; 74(4), 627–640; quiz 641–642. 22. Worcestershire Health and Care NHS Trust, Wound Assessment and Management guidelines, 2015. 23. Fleischmann W, Strecker W, Bombelli M, Kinzl L. Vacuum sealing as treatment of soft. Unfallchirurg 1993; 96(9): 488–490. 24. Peus D, Heit JA, Pittelkow MR. Activated protein C resistance caused by factor V gene mutation: common coagulation defect in chronic venous leg ulcers? J Am Acad Dermatol 1997; 36: 616–620. 25. Köksal C, Alsalehi S, Kocamaz Ö, Sunar H. Kronik venöz yetmezlik tedavisi. Koşuyolu Heart J 2010; 13(2): 28–33. 26. Falanga V, Eaglstein W. The trap hypothesis of venous ulceration. Lancet 1993; 341: 1006–1008. 27. Robson MC, Hanfnt J, Garner W, Jenson J, Serena T, Wyatt G, et al. The healing of chronic venous ulcers is not enhanced by the addition of topical repifermin (KGF-2) to standardized care. J Appl Res 2004; 4: 302–311. 28. Cardinal M, Eisenbud DE, Armstrong DG, Zelen C, Driver V, Attinger C, et al. Serial surgical debridement: a retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Rep Reg 2009; 17: 306–311. 29. O’Meara S, Al-Kurdi D, Ologun Y, Ovington LG, Martyn-St James M, Richardson R. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database Syst Rev 2010; 1: CD003557. 30. Morykwas MJ, Argenta LC, Shelton-Brown EI, McGuirt W. Vacuumassisted closure: a new method for wound control and treatment: animal studies and basic foundation. Ann Plast Surg 1997; 38(6): 553–562. 31. Pugliese DJ. Infection in venous leg ulcers: considerations for optimal management in the elderly. Drugs Aging 2016; 33(2): 87–96. 32. Nelson EA, Bell-Syer SE, Cullum NA. Compression for preventing recurrence of venous ulcers. Cochrane Database Sys Rev 2000; 4: CD002303. 33. Barwell JR, Davies CE, Deacon J, Harvey K, Minor J, Sassano A, et al. Comparison of surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): randomised controlled trial. Lancet 2004; 363(9424): 1854–1859. 34. Margolis DJ, Allen-Taylor L, Hoffstad O, Berlin JA. The accuracy of venous leg ulcer prognostic models in a wound care system. Wound Repair Regen 2004; 12(2): 163–168. 35. Carpentier PH, Marico HR, Biro C, Poncot-Makinen CO, Franco A. Prevalence, risk factors, and clinical patterns of chronic venous disorders of lower limbs: a population-based study in France. J Vasc Surg 2004; 40: 650–659. 36. Taylor RJ, Taylor AD, Smyth JV. Using an artificial neural network to predict healing times and risk factors for venous leg ulcers. J Wound Care 2002; 11(3): 101–105. 37. O’Donnell Jr TF, Passman MA, Marston WA, Ennis WJ, Dalsing M, Kistner RL, et al. Management of venous leg ulcers: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vasc Surg 2014; 60 (suppl 2): 3–59. 38. Andersson E, Hansson C, Swanbeck G. Leg and foot ulcer prevalence and investigation of the peripheral arterial and venous circulation in a randomised elderly population. An epidemiological survey and clinical investigation. Acta Derm Venereol 1993; 73: 57–61. 39. Leijnen M, Steenvoorde P, van Doorn L, Zeillemaker AM, da Costa SA, Oskam J. Does VAC increase the risk of venous thromboembolism? J Wound Care 2007; 16: 211–212. 40. Kantor J, Margolis DJ. Efficacy and prognosis value of simple wound measurements. Arch Dermatol 1998; 134: 1571–1574. 41. Han G, Ceilley R. Chronic wound healing: a review of current management and treatments. Adv Ther 2017; 34(3): 599–610. 42. Vuerstaek JDD, Vainas T, Wuite J, Nelemans P, Neumann MHA, Veraart JCJM. State-of-the-art treatment of chronic leg ulcers: a randomized controlled trial comparing vacuum-assisted-closure (VAC) with modern wound dressings. J Vasc Surg 2006; 44(5): 1029–1038. 43. Flanagan M. Wound measurement: can it help us to monitor progression to healing? J Wound Care 2003; 12(5): 189–194. 44. Palmer RM, Ring EJF, Ledgard LA. Digital video technique for radiographs and monitoring ulcers. J Photogr Sci 1989; 37: 65–67.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 AFRICA 51 CALSAR 5/80 mg, 5/160 mg, 10/160 mg. Each tablet contains amlodipine/valsartan 5/80 mg, 5/160 mg, 10/160 mg respectively. S3 A51/7.1.3/1106, 1107, 1108. For full prescribing information, refer to the professional information approved by SAHPRA, March 2021. 1) Karpov Y, et. al. Amlodipine/valsartan single-pill combination: a prospective, observational evaluation of the real-life safety and effectiveness in the routine treatment of hypertension. Advanced Therapeutics 2012;29(2):134-147. 2) Fogari R, et. al. Effect of valsartan addition to amlodipine on ankle oedema and subcutaneous tissue pressure in hypertensive patients. Journal of Human Hypertension 2007;21:220-224. 3) Data on file. *FDC - Fixed-dose combination. CRA721/10/2021. For further product information contact PHARMA DYNAMICS P O Box 30958 Tokai Cape Town 7966 Fax +27 21 701 5898 Email info@pharmadynamics.co.za CUSTOMER CARE LINE 0860 PHARMA (742 762) / +27 21 707 7000 www.pharmadynamics.co.za AMLODIPINE / VALSARTAN *FDC : • E ectively lowers BP1 • Gets up to 8/10 patients to goal 1 • Works synergistically to reduce oedema2 CALSAR: • Is up to 50% LESS vs the Originator 3 • O ers a UNIQUE 5/80 mg dosage DILIGENT WORKERS NEW INTRODUCING OUR AMLODIPINE / VALSARTAN *FDC RANGE PACKED IN 30 TABLETS | | |
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 52 AFRICA Prevalence, patterns and predictors of dyslipidaemia in Nigeria: a report from the REMAH study Babangida Chori, Benjamin Danladi, Peter Nwakile, Innocent Okoye, Umar Abdullahi, Kefas Zawaya, Ime Essien, Kabiru Sada, Maxwell Nwegbu, John Ogedengbe, Akinyemi Aje, Godsent Isiguzo, Augustine Odili Abstract Aim: The aim of this study was to determine the prevalence and predictors of dyslipidaemia in adults in Nigeria. Methods: Using the WHO criteria, we determined dyslipidaemia using serum lipid levels of 3 211 adult Nigerians, aged at least 18 years, obtained between March 2017 and February 2018 from two communities (rural and urban) in a state from each of the six geopolitical zones of Nigeria. Results: The overall prevalence of low high-density lipoprotein cholesterol (l-HDL), elevated low-density lipoprotein cholesterol (e-LDL), hypertriglyceridaemia (h-TG) and hypercholesterolaemia (h-CHL) were 72.5,13.6, 21.4 and 7.5%, respectively. The adjusted odds of h-CHL [odds ratio (95% confidence interval) 1.47 (1.10–1.95)], h-TG [1.89 (1.48–2.41)] and e-LDL [1.51 (1.03–2.15)] increased with obesity. Being a rural dweller increased the odds of h-TG [1.55 (1.29–1.85)], e-LDL [1.38 (1.10–1.73)] and l-HDL [1.34 (1.14–1.58)]. The odds of h-CHL [2.16 (1.59–2.95)], h-TG [1.21 (1.01–1.47)], e-LDL [1.42 (1.13–1.80)] and l-HDL [0.78 (0.65–0.93)] increased with hypertension. Diabetes mellitus doubled only the odds of h-TG [2.04(1.36–3.03)]. Conclusion: The prevalence of dyslipidaemia, particularly low HDL-C, is high among adult Nigerians. Keywords: dyslipidaemia, elevated LDL cholesterol, low HDL cholesterol, hypercholesterolaemia, hypertriglyceridaemia, subSaharan Africa Submitted 16/4/21, accepted 12/7/21 Published online 15/11/21 Cardiovasc J Afr 2022; 33: 52–59 www.cvja.co.za DOI: 10.5830/CVJA-2021-037 Africa is currently faced with a double burden of communicable and non-communicable diseases (NCDs). The latter, which was less common in past decades, is predicted to take the lead in the next decade.1 The sudden rise in the burden of NCDs, which is fuelled partially by the adoption of urbanised and unhealthy lifestyles, is understood to be the repercussion of increasing prevalence of cardiovascular diseases (CVD) risk factors, including high blood pressure, obesity, dyslipidaemia and diabetes mellitus. Dyslipidaemia is a major driver of atherosclerosis,2 from which various CVD are known to originate.3,4 Dyslipidaemia, together with smoking, obesity, hypertension and diabetes mellitus, account for over 80% of the CVD burden across the globe.5,6 Lack of reliable data remains a major challenge to assessing the burden of dyslipidaemia in Africa and this is responsible for the misconception that dyslipidaemia rarely occurs. A recent review of dyslipidaemia among Africans living in Africa indicates that countrywide, data are scarce and the burden of dyslipidaemia is high.7 Nigeria possesses a fast-growing economy and population, which is expected to contribute hugely to the burden of dyslipidaemia in Africa. As in many other African nations, the Circulatory Health Research Laboratory, College of Health Sciences, University of Abuja, Abuja, Nigeria Babangida Chori, BSc Benjamin Danladi, BSc Department of Community Health, University of Uyo Teaching Hospital, Uyo, Akwa Ibom, Nigeria Peter Nwakile, MB BS, MWACP Department of Medicine, Chukwuemeka Odumegwu University, Awka, Anambra, Nigeria Innocent Okoye, MB BS, FWACP Department of Medicine, Federal Medical Centre, Gusau, Zamfara, Nigeria Umar Abdullahi, MB BS, FMCP Kabiru Sada, MB BS, FMCP Department of Medicine, Federal Teaching Hospital Gombe, Gombe, Nigeria Kefas Zawaya, MB BS, FMCP Department of Medicine, University of Uyo, Akwa Ibom, Nigeria Ime Essien, MB BS, FM Department of Chemical Pathology, Faculty of Basic Clinical Sciences, University of Abuja, Abuja, Nigeria Maxwell Nwegbu, MB BS, FWACP Department of Human Physiology, Faculty of Basic Medical Sciences, University of Abuja, Abuja, Nigeria John Ogedengbe, MB BS, PhD Department of Medicine, University College Hospital, Ibadan, Oyo, Nigeria Akinyemi Aje, MB BS, FMCP Department of Medicine, Federal University Teaching Hospital, Abakaliki, Ebonyi, Nigeria Godsent Isiguzo, MB BS, WACP Circulatory Health Research Laboratory, College of Health Sciences, University of Abuja; Beside School of Nursing, University of Abuja Teaching Hospital, Gwagwalada, Abuja, Nigeria Augustine Odili, MB BS, PhD, augustine.odili@uniabuja.edu.ng
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