JANUARY–APRIL 2023 VOL 34 NO 1 • Changing face of pulmonary embol ism with COVID-19 • Aortic regurgitation: multimodal assessment of quantification and impact • Dai ly troponin I and D-dimer levels and mortal ity in COVID-19 patients • Pre-morbid cardiometabol ic risks in informal settlements in South Africa • Association between SYNTAX score and anxiety–depressive disorders • SA Heart consensus statement on closure of patent foramen ovale 2021 • Resurgence of Shoshin beriberi during the COVID-19 pandemic • Aneurysmal degeneration in the Omniflow II biosynthetic vascular graft 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 34, No 1, JANUARY–APRIL 2023 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 3 FROM THE EDITOR’S DESK P Commerford CARDIOVASCULAR TOPICS 4 Changing face of pulmonary embolism with COVID-19 B Bagır tan • E Altuntas • S Yasar • KO Karabay 9 Aortic regurgitation: multimodal assessment of quantification and impact M-PB N’Cho-Mottoh • O Huttin • C Selton-Suty • S Scadi • L Filippetti • P-Y Marie 16 The impact of daily troponin I and D-dimer serum levels on mortality in COVID-19 pneumonia patients B Stavileci • E Ereren • E Özdemir • B Özdemir • M Cengiz • R Enar 23 Pre-morbid cardiometabolic risks among South Africans living in informal settlements K Mokwena • P Modjadji 30 The non-negligible association between SYNTAX score and anxiety–depressive disorders L Cerit • Z Cerit • H Duygu REVIEW ARTICLE 35 SA Heart consensus statement on closure of patent foramen ovale 2021 J Hitzeroth • P van der Bijl • F Michel • R Meel • BJ Cupido • E Klug
CONTENTS Vol 34, No 1, JANUARY–APRIL 2023 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. CASE REPORTS 40 Resurgence of Shoshin beriberi during the COVID-19 pandemic K Govind • GL Gaskin • DP Naidoo 44 The optimal diagnosis and treatment of intravenous leimyomatosis HY Liu • J-G Xu • C-X Zhang 48 Aneurysmal degeneration in the Omniflow II biosynthetic vascular graft I Selçuk • BB Güven 51 An unusually large left ventricular thrombus complicating anterior myocardial infarction: the value of multimodality imaging L Dhlamini • R Meel • M Nethononda 55 Left thoracotomy approach for aortic root surgery R Komarov • A Ismailbaev • A Simonyan • I Ermetov • Ivan Ivashov 59 Mycotic abdominal aortic aneurysm: two cases caused by Salmonella enterica Nehir Tandogar • M Şeyda Velioğlu Öcalmaz LETTER TO THE EDITOR 63 Alternative treatment of tricuspid valve vegetations S Lentini PASCAR NEWS 64 Netcare Umhlanga cardio-oncology unit centre of excellence PUBLISHED ONLINE (Available on www.cvja.co.za and in PubMed)
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 AFRICA 3 From the Editor’s Desk When the Covid-19 pandemic erupted, many of us older clinicians were barred from our hospitals and could only look on from the sidelines as our younger colleagues continued to look after patients under very difficult circumstances. I for one was pleased to be spared the trauma of working under the very difficult circumstances that prevailed but also somehow resented missing out on managing a new and challenging illness. The involvement of the cardiovascular system was unexpected in the early days and publications on pathophysiology and outcomes of those affected remain confusing. This issue of the Journal offers four articles addressing some of those issues. In a retrospective, single-centre study, Bagirtan and colleagues (page 4), report that traditional clinical predictive scores for pulmonary embolism had little discriminatory power in patients with COVID-19 and pulmonary embolism, demonstrated by computed tomography pulmonary angiography. These authors suggest that a higher D-dimer cut-off value should be considered to better screen such patients for pulmonary embolism. In another retrospective study Stavileci and others (page 16) identified several clinical markers of in-hospital mortality. Not unexpectedly troponin I and D-dimer follow-up values in the serum were more effective than other inflammatory markers in predicting mortality and the need for intensive care. Two unusual cases expand the literature about Covid-19. Govind and co-authors (page 40) describe two patients who presented with severe type B lactic acidosis and shock, initially thought to be due to bowel ischaemia/myocardial infarction and pulmonary sepsis, respectively. This led to a delay in the diagnosis of thiamine deficiency. In both cases there was a dramatic response to intravenous thiamine, confirming the diagnosis of Shoshin beriberi. Both patients admitted to drinking home-brewed alcohol during the time of COVID19 restrictions on alcohol consumption. The authors are to be congratulated on their clinical acumen in considering this all-too-often missed diagnosis. The report is also a sobering reminder of the unintended consequences of well-intentioned legislation such as the ban on all legal alcohol sale, which was imposed in South Africa during the pandemic. The SA Heart consensus statement on closure of patent foramen ovale 2021 (page 35) from Hitzeroth and co-authors provides some helpful guidelines on management of a condition that is common, being present in up to 25% of the general population. Percutaneous closure is readily available. The question remains as to when closure is indicated. The guidelines offer some useful answers. Pat Commerford Editor-in-Chief Professor PJ Commerford
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 4 AFRICA Cardiovascular Topics Changing face of pulmonary embolism with COVID-19 Bayram Bagırtan, Emine Altuntas, Servan Yasar, Kanber Ocal Karabay Abstract Aim: This study aimed to describe the baseline characteristics of coronavirus disease 2019 (COVID-19) patients with pulmonary embolism, and to examine the Geneva score, pulmonary embolism severity index (PESI), radiological and biochemical findings. Methods: From March 2020 to June 2021, the files of 41 COVID-19 patients with pulmonary embolism were accessed. Results: Mean D-dimer value was 6.04 mg/dl and 61% of the patients received at least one dose of anticoagulant treatment. In patients receiving deep venous thrombosis prophlaxis, an optimal D-dimer cut-off point was calculated as 5.69 mg/dl. The area under the curve was 0.753 (p = 0.007; sensivity 64%; specificity 62.5%). The mean Geneva score was 4.31, mean PESI was 72.48 and mean Qanadli score was 11.29. Conclusions: According to this study, traditional clinical predictive scores had little discriminatory power in these patients, and a higher D-dimer cut-off value should be considered to better diagnose patients for pulmonary embolism. Keywords: COVID-19, thrombosis, pulmonary embolism, D-dimer, anticoagulant therapy Submitted 12/10/21, accepted 9/2/22 Published online 4/3/22 Cardiovasc J Afr 2023; 34: 4–8 www.cvja.co.za DOI: 10.5830/CVJA-2022-011 With the emergence of coronavirus disease 2019 (COVID-19) in December 2019, a new pandemic page has been opened in the history of the world. The disease, which was initially thought to be a highly contagious viral infection, later evolved into a multisystem inflammatory and thrombotic disease due to the involvement of cardiovascular and pulmonary structures.1 A clinic of patients infected with COVID-19 ranges from completely asymptomatic to rapidly devastating courses with acute respiratory distress syndrome associated with high fatality rates. Pulmonary embolism (PE), deep-vein thrombosis, ischaemic stroke and myocardial infarction are examples of complications of the disease.1 Excessive inflammation, hypoxia, immobilisation, platelet activation and endothelial dysfunction are contributors to the prothrombotic state.2,3 COVID-19 infection affects not only the pulmonary parenchyma but also the pulmonary vascular bed. Autopsy studies have demonstrated the presence of thrombi in the pulmonary arteries and alveolar capillaries of individuals deceased from COVID-19.4,5 Recent studies have revealed that patients with COVID-19 had higher PE prevalence than usually encountered in non-infected critically ill patients. 6-9 Several prognostic indicators of mortality, such as admission clinical properties and laboratory parameters have been defined in PE. PE severity index (PESI) is a powerful predictor of a worse prognosis, and clinical use of PESI is recommended by the European Society of Cardiology. Also, the Geneva score is a clinical prediction rule to assess PE pre-test probability.10-13 This study aimed to describe the baseline characteristics of COVID19 patients with PE, and assess the Geneva score and PESI. Methods The study was retrospective and single centred. From March 2020 to June 2021, the files of all patients admitted to hospital with a diagnosis of PE were accessed. Among them, patients who had simultaneous COVID-19 infection were included in the study. The exclusion criteria were pregnancy and those younger than 18 years. According to World Health Organisation criteria, COVID-19 infectionwas determined by positive results from real-time reverse transcription polymerase chain reaction of nasopharyngeal swabs or by typical imaging characteristics on chest computed tomography. Patients without computed tomography pulmonary angiography (CTPA) to diagnose PE were excluded. The study protocol was approved by the local ethics committee. From the hospital record system, baseline information including demographic characteristics and co-existing medical conditions were obtained. Clinical parameters and biological findings at the diagnosis of PE were recorded for calculation of PESI andGeneva scores. Laboratory data such as complete blood count, albumin, D-dimer, C-reactive protein (CRP), ferritin, fibrinogen, fasting glucose and high-sensitivity (hs) troponin T levels, and kidney and liver function tests were collected on the day of diagnosis of PE. Data on pharmacological therapies, respiratory complications, morbidity and mortality were also gathered during the hospitalisation. CTPA examinations with 16-section (Cannon Aquilion Lightning, Canon Medical Systems Europe BV, Zoerterme Cardiology Department , Sancaktepe Sehit Prof Dr Ilhan Varank Education and Training Hospital, Istanbul, Turkey Bayram Bagırtan, MD Emine Altuntas, MD, emine_altuntas@hotmail.com Kanber Ocal Karabay, MD Radiology Department, Sancaktepe Sehit Prof Dr Ilhan Varank Education and Training Hospital, Istanbul, Turkey Servan Yasar, MD
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 AFRICA 5 the Netherlands) and 128-section (D Revolution Evo Gen 3, GE Healthcare, Waukesha, WI, USA) multislice CT devices were carried out. The CTPA protocol was performed using a multidetector scanner after intravenous injection of 50–75 ml of high-concentration iodinated contrast agent at a flow rate of 3–4 ml/s, which was triggered on the main pulmonary artery. The Qanadli score or CT obstruction index is calculated by regarding the arterial tree of each lung as having 10 segmental arteries (three to the upper lobes, two to the middle lobe and lingula, and five to the lower lobes). Embolus in a segmental artery = one point; embolus in the most proximal arterial level = a value equal to the number of segmental arteries arising distally. Weighting factor (for residual perfusion) = the degree of vascular obstruction (no thrombus = zero; partially occlusive thrombus = one; total occlusion = two). The maximal CT obstruction index = 40 for each patient (10 × maximum weighting of 2 = 20 for each side). Isolated subsegmental embolus is considered equal to a partially occluded segmental artery.14 In addition, a CT severity score of one to five was given using ground-glass opacities and consolidations and the extent of COVID-19 lung lesions and the percentage of lung volume affected.15 The CTPA results of COVID-19 and the presence of PE were analysed by an experienced radiologist. Statistical analysis In this study, the Statistical Package for Social Sciences (SPSS) 20.0 for Windows (USA, Armonk, New York) program was used for statistical analysis. Distribution of continuous data was assessed with the Kolmogorov–Smirnov test. Normally distributed variables are expressed as mean ± standard deviation, whereas non-normally distributed variables are given as median and interquartile range. Categorical variables are reported as numbers and percentages. Categorical variables were compared with the chi-squared test or Fisher’s exact test, where appropriate. Correlation analysis was used to examine the relationships between PESI score, Geneva score, CHA2DS2-VASc score, CRP, procalcitonin, fibrinogen, hs-troponin T, D-dimer and glucose. Receiver operating characteristic (ROC) curve analysis was performed and the Youden index was calculated to determine the optimal D-dimer threshold to predict in patients with COVID-19 and PE receiving thromboprophylaxis. Results Between March 2020 and June 2021, 581 patients were diagnosed with PE. After the exclusion of ineligible tests and a reduction for duplicate tests, a total of 41 cases were included in the study. The mean age was 53.92 years and 73.2% were male. Hypertension (10, 24.4%), ischaemic heart disease (five, 12.2%) and diabetes (seven, 17.7%) were the most common co-morbidities. Five patients were admitted to the intensive care unit (ICU), and the length of stay in ICU was nine days (IQR 9). The mean time from the nasopharyngeal swab test to pulmonary BTA was 13.28 days. Twenty-five of the patients needed oxygen. Twenty-five patients (61%) received thromboprophylaxis with enoxaparin by the time of admission. Four of the PE patients (9.8%) were diagnosed with deep venous thrombosis. The mean Geneva score was 4.31, and 92.7% of the patients fell into the low- to intermediate-risk group. The mean PESI was 72.48, and 65.9% of the patients were in Class I to II. The anthropometric and clinical characteristics are described in Tables 1 and 2. D-dimer levels were extremely high, while hs-troponin T levels were slightly elevated. Laboratory tests and radiological findings are presented in Table 1. The patients were also evaluated according to the severity of pneumonia and PE. Patients were classified according to the severity of lung involvement. Stage 3 to 5 involvement was observed in 29 (70.8%) of the patients. It was determined that 10 (34.5%) of them did not receive thromboprophylaxis (Table 3). The mean Qanadli score was 11.29. Bivariate analysis showed significant correlations between CHA2DS2-VASc and PESI scores (rho = 0.484, p = 0.001). Furthermore the Geneva score was positively correlated with the Qanadli score. In addition, a positive correlation was observed between the Qanadli score and the right/left ventricular (RV/LV) ratio. Correlation analysis results are given in Table 4. A ROC curve was performed to determine the optimal threshold for D-dimer to predict PE occurrence on CTPA in patients with COVID-19 receiving thromboprophylaxis. The area under the curve (AUC) was 0.753 (p = 0.007) (Fig. 1). Discussion The main findings of this study are that the Geneva score and PESI were not high in patients with COVID-19 and PE. Besides, most of the patients developed PE despite anticoagulant therapy. Table 1. Descriptive, radiological and biochemical parameters of the patients Variables Mean ± SD or n (%) Age (years) 53.92 ± 16.88 Gender, males 30 (73.2) Smoking 3 (7.3) Diabetes mellitus 7 (17.1) Hypertension 10 (24.4) Cerebrovascular event 2 (4.9) Congestive heart failure 0 Ischaemic heart disease 5 (12.2) Malignancy 3 (7.3) D-dimer (mg/dl) 6.04 (9.06) hs-troponin T (µg/ml) 0.0085 (0.01) Fibrinogen (mg/dl) 518 (226.5) Glucose (mg/dl) 113.7 (32.63) Creatinin (mg/dl) 0,79 (0.27) Procalcitonine (ng/ml) 0.1 (0.11) C-reactive protein (mg/dl) 69.01 (92.9) WBC (103/µl) 9154 ± 3771 Neutrophils (103/µl) 6865 ± 3573 Lymphocytes (103/µl) 1540 ± 686 Platelets (103/µl) 286 ± 126 Haemoglobin (g/l) 13.1 (1.88) Severity of COVID-19 pneumonia Stage 1 6 (14.6) Stage 2 6 (14.6) Stage 3 10 (24.4) Stage 4 11 (19.5) Stage 5 8 (19.5) Qanadli score 11.29 ± 8.63 RV/LV ratio 0.68 (0.13) WBC: white blood cells; LV: left ventricle; RV: right ventricle.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 6 AFRICA Our study shows that a higher D-dimer threshold (5.69 mg/dl) gives a better sensitivity and specificity to predict PE in patients with COVID-19 who need oxygen support. The main features of COVID-19 patients with PE have been described in several studies.16-18 The patient characteristics reported in this study confirmed that male gender and longer delay from onset of symptoms to hospitalisation were associated with an increased risk of PE. Also, the patients were younger. The traditional risk factors of PE, as previously described, were not associated with the occurrence of PE in our study. There is no consensus in the world on the D-dimer cut-off point to suspect PE in COVID-19 patients. The International Society of Thrombosis and Hemostasis considered that a three- to four-fold increase in D-dimer concentration may be significant in terms of guidance for recognition and management of coagulopathy in COVID-19.19 This cut-off value differs slightly between studies. In the study of Mouhat et al., workers found that a D-dimer concentration greater than 2 590 ng/ml conferred a 17-fold increase in the risk of PE in 162 hospitalised patients with COVID-19 pneumonitis, with a resultant sensitivity of 83.3% and specificity of 83.8%.20 Ventura-Diaz et al. placed this threshold at 2 903 ng/ml (resultant sensitivity 81%) in their retrospective cohort of 242 hospitalised patients with COVID19, with a PE prevalence of 30%.21 In another study a total of 193 patients underwent CTPA Sensitivity 1.0 0.8 0.6 0.4 0.2 0.0 0.0 0.2 0.4 0.6 0.8 1.0 1 – Specificity Fig. 1. ROC curve to determine the optimal threshold for D-dimer to predict PE occurrence on CTPA in patients with COVID-19 receiving thromboprophylaxis (AUC: 0.753; p = 0.007; 95% CI: 0.593–0.912; 64% sensitivity; 62.5% specificity; D-dimer = 5.69 mg/dl). Table 2. Clinical characteristics of the patients Characteristics Mean ± SD or n (%) Intensive care unit admission 5 (12.2) Length of stay in intensive care unit (days) 9 (12.5) Length of stay hospital (days) 9 (6.5) Mortality in hospital 0 Duration between CT and swab (days) 13.28 ± 7.69 Rhythm SR 40 (97.6) AF 1 (2.4) Need for oxygen support 25 (61) Systolic blood pressure (mmHg) 124.75 ± 17.66 Diastolic blood pressure (mmHg) 76.04 ± 10.95 Haemoptysis 2 (4.9) CHA2DS2-VASc 1.3 ± 1.5 Geneva score 4.31 ± 1.58 Class of Geneva score Low 13 (31.7) Intermediate 25 (61) High 3 (7.3) PESI score 72.48 ± 24.62 Class of PESI score Class I 18 (43.9) Class II 9 (22) Class III 11 (26.8) Class IV 2 (4.6) Class V 1 (2.4) Under anticoagulant therapy 25 (61) No thromboprophlaxis 16 (39) DVT thromboprophylaxis dose 14 (34.1) Modified thromboprophylaxis dose 2 (4.9) Full thromboprphylaxis dose 9 (22) Deep venous thrombosis 4 (9.8) AF: atrial fibrillation; CT: computed tomography; DVT: deep venous thrombosis; PESI: pulmonary embolism severity index; SR: sinus rhythm; AF: atrial fibrillation; CHA2DS2-VASc: congestive heart failure, hypertension, age > 75 years, diabetes mellitus, stroke, vascular disease, age 65–75 years, sex category. Table 3. Anticoagulant dosage according to severity of COVID-19 pneumonia in patients Anticoagulant dosage Severity of pneumonia Stage 1–2 Stage 3–5 No thromboprophlaxy 6 (50) 10 (34.5) DVT thromboprophylaxis dose 2 (16.7) 12 (41.4) Modified thromboprophylaxis dose 0 (0) 2 (6.9) Full thromboprphylaxis dose 4 (33.3) 5 ( 17.2) DVT: deep venous thrombosis. Table 4. Correlation analysis between D-dimer and some laboratory parameters and clinical scores Parameters 1 2 3 4 5 6 7 CHA2DS2-VASc R p 1 . PESI score R 0.484 1 p 0.001 Geneva score R 0.078 0.273 1 p 0.628 0.084 Qanadli score R 0.078 0.091 0.327 1 p 0.628 0.570 0.037 RV/LV ratio R 0.203 0.015 0.199 0.427 1 p 0.204 0.924 0.213 0.005 C-reactive protein R p 0.098 0.546 0.180 0.266 0.082 0.616 0.029 0.857 0.045 0.784 1 D-dimer R 0.200 0.259 0.108 0.067 0.084 0.197 1 p 0.211 0.102 0.500 0.677 0.600 0.222 CHA2DS2-VASc: congestive heart failure, hypertension, age > 75 years, diabetes mellitus, stroke, vascular disease, age 65–75 years, sex category; LV: left ventricle; RV: right ventricle.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 AFRICA 7 imaging and were classified into PE-positive (n = 33) and -negative groups. Physiological, radiological and biochemical parameters were compared and ROC curve analysis was conducted to determine a predictive D-dimer threshold. They proposed that in the absence of other clinical signs, a D-dimer threshold of 2 495 ng/ml could be used with high sensitivity and specificity to predict PE in hospitalised patients with COVID-19 (with 100% sensitivity and 90.6% specificity).22 In our study, the mean D-dimer value of all patients was 6.04 (IQR 9.06) and the cut-off point was 5.69 in patients who recieved thromboprophylaxis. Because of the prothrombotic state highlighted in COVID19, previous studies have reported that thrombus described by CTPA was in the majority of cases segmental or subsegmental during COVID-19-related PE. Some authors have suggested that a localised immunothrombosis process could contribute to the development of a thrombus within the lung inflammation area.23,24 For diagnostic accuracy and assessment of disease severity, in our study, the thrombus load was calculated from CTPA data using the Qanadli score.25 The mean Qanadli score was 11.29, which means that the distribution of thrombus localisation was mostly segmental and subsegmental. A study of 61 patients investigated the correlation between radiological and clinical–biochemical features in a cohort of hospitalised COVID-19 patients. PE was detected in only 14 patients and deep-vein thrombosis in five. The Qanadli score, RV/LV ratio, revised Geneva score and PESI were calculated in this patient group. It was found that the Qanadli score had a significant correlation with PESI, D-dimer, serum hs-troponin, serum albumin, arterial pressure of oxygen-to-inspired fraction of oxygen ratio (pO2/FiO2) and length of hospital stay. 26 In our study, there was a positive correlation between only the Qanadli and Geneva scores. Silva et al. evaluated the accuracy of the Wells and Geneva scores to predict PE in patients with SARS-CoV-2 infection in their study. There was no statically significant difference between the average Wells score in patients with and without PE (1.04 and 0.89, respectively, p = 0.733) and the AUC demonstrated that the Wells score had no discriminatory power (AUC = 0.5). The Geneva score of the groups was also similiar (4.20 vs 3.93, respectively, p = 0.420), with the AUC being 0.54.27 In our cohort, patients who developed PE had a pretest probability in the intermediate to low range, as confirmed by the Geneva score. The spectrum of mortality risk assessed by the PESI score ranged from Class I to III, but no patients died in our study. In the study of Wu et al., the median of the PESI was 88.1 (34–130).26 In our study, the mean of the PESI was 72.48 ± 24.62. This difference may have been due to the fact that our patients were younger. Although most of the hospitalised patients with COVID19 were on anticoagulant therapy, the incidence of PE was high. SARS-CoV-2 infection promotes endothelial dysfunction, prothrombotic events and pulmonary microthrombi, and the inflammatory host response leading to PE has been proven in autopsy studies.28 Poissy et al. showed that patients with COVID19 infection had a higher frequency of PE than patients infected with other infections.8 COVID-19 is now considered a pro-thrombotic disease with systemic inflammation. Post-mortem studies showed widespread alveolar damage and inflammation in patients. In the light of these data, it was determined that the pathogenic mechanism of PE was pulmonary intravascular coagulopathy.28,29 Despite prophylactic anticoagulation in patients with COVID-19, they can still develop thrombotic events. In a case series of 22 patients followed up in the ICU due to COVID-19 infection, PE was found in 20 patients, although all patients had received thromboprophylaxis.8 Similar results have been supported by other studies.30,31 In our study, 61% of the patients received at least one dose of anticoagulant treatment. There are several limitations to our study. It was a retrospective analysis of patients admitted with COVID-19 who underwent a CTPA, therefore, there may have been selection bias. In other words, the patients selected for CTPA were suspected of having a high pretest probability of PE. The sample size was small. There was a restriction on accessing different diagnostic tests and complex logistics to confirm PE, such as transthoracic echocardiography. Conclusion PE is seen frequently in patients with COVID-19 infection despite thromboprophylaxis. According to our results, traditional clinical prediction scores such as the PESI and Geneva score have little discriminatory power. A high D-dimer cut-off value should be considered a better measure to determine patients with PE. References 1. Grasselli G, Zangrillo A, Zanella A, Antonelli M, Cabrini L, Castelli A, et al. Baseline characteristics and outcomes of 1591 patients infected with SARS-CoV-2 admitted to ICUs of the Lombardy region, Italy. COVID-19 Lombardy ICU Network. J Am Med Assoc 2020; 323(16): 1574–1581. 2. Klok FA, Kruip MJHA, van der Meer NJM, Arbous MS, Gommers DAMPJ, Kant KM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19.Thromb Res 2020; 191(1): 145–147. 3. Goeijenbier M, van Wissen M, van de Weg C, Jong E, Gerdes VE, Meijers JC, et al. Viral infections and mechanisms of thrombosis and bleeding. J Med Virol 2012; 84(10): 1680–1696. 4. Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in Covid-19. N Engl J Med 2020; 383(2): 120–128. 5. Edler C, Schröder AS, Aepfelbacher M, Fitzek A, Heinemann A, Heinrich F, et al. Dying with SARS-CoV-2 infection – an autopsy study of the first consecutive 80 cases in Hamburg, Germany. Int J Legal Med 2020; 134(5): 1275–1284. 6. Leonard-Lorant I, Delabranche X, Severac F, Helms J, Pauzet C, Collange O, et al. Acute pulmonary embolism in COVID-19 patients on CT angiography and relationship to D-dimer levels. Radiology 2020; 296(3): E189–E191. 7. Klok FA, Kruip MJHA, van der Meer NJM, Arbous MS, Gommers DAMPJ, Kant KM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020; 191: 145–147. 8. Poissy J, Goutay J, Caplan M, Parmentier E, Duburcq T, Lassalle F, et al. Pulmonary embolism in COVID-19 patients: awareness of an increased prevalence. Circulation 2020; 142(2): 184–186. 9. Danzi GB, Loffi M, Galeazzi G, Gherbesi E. Acute pulmonary embolism and COVID-19 pneumonia: a random association? Eur Heart J 2020; 41(19): 1858.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 8 AFRICA 10. Konstantinides SV, Torbicki A, Agnelli G, Danchin N, Fitzmaurice D, Galie N, et al. ESC Committee for Practice Guidelines (CPG). Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J 2014; 35(43): 3033–3069. 11. Aujesky D, Obrosky DS, Stone RA, Auble TE, Perrier A, Cornuz J, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med 2005; 172(8): 1041–146. 12. Agnelli G, Becattini C. Acute pulmonary embolism. N Engl J Med 2010; 363(3): 266–274. 13. Chan CM, Woods C, Shorr AF. The validation and reproducibility of the pulmonary embolism severity index. J Thromb Haemost 2010; 8(7): 1509–1514. 14. Qanadli SD, El Hajjam M, Vieillard-Baron A, Joseph T, Mesurolle B, Oliva VL. New CT index to quantify arterial obstruction in pulmonary embolism: comparison with angiographic index and echocardiography. Am J Roentgenol 2001; 176(6): 1415–1420. 15. Yang R, Li X, Liu H, Zhen Y, Zhang X, Xiong Q, et al. Chest CT severity score: an imaging tool for assessing severe COVID-19. Radiology 2020; 2(2): e200047. 16. Fauvel C, Weizman O, Trimaille A, Mika D, Pommier T, Pace N, et al. Pulmonary embolism in COVID-19 patients: A French multicentre cohort study. Eur Heart J 2020; 41(32): 3058–3068. 17. Klok FA, Kruip M, van der Meer N, Arbous MS, Gommers DM, Kant KM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020; 191: 145–147. 18. Trimaille A, Curtiaud A, Marchandot B, Matsushita K, Sato C, Leonard-Lorant I, et al. Venous thromboembolism in non-critically ill patients with COVID-19 infection. Thromb Res 2020; 193: 166–169. 19. Thachil J, Tang N, Gando S, Falanga A, Cattaneo M, Levi M, et al. ISTH interim guidance on recognition and management of coagulopathy in COVID-19. J Thromb Haemost 2020; 18(5): 1023–1026. 20. Mouhat B, Besutti M, Bouiller K, Grillet F, Monnin C, et al. Elevated D-dimers and lack of anticoagulation predict PE in severe COVID-19 patients. Eur Respir J 2020; 4: 2001811. 21. Ventura-Diaz S, Quintana-Perez JV, Gil-Boronat A, Herrero-Huertas M, Gorospe-Sarasúa L, Montilla J, et al. A higher D-dimer threshold for predicting pulmonary embolism in patients with COVID-19: a retrospective study. Emerg Radiol 2020; 27(6): 679–689. 22. Nadeem I, Anwar A, Jordon L, Mahdi N, Rasool MU, Dakin J, et al. Relationship of D-dimer and prediction of pulmonary embolism in hospitalized COVID-19 patients: a multicenter study. Future Microbiol 2021; 16: 863–870. 23. Van Dam LF, Kroft LJM, van der Wal LI, Cannegieter SC, Eikenboom J, de Jonge E, et al. Clinical and computed tomography characteristics of COVID-19 associated acute pulmonary embolism: A different phenotype of thrombotic disease? Thromb Res 2020; 193: 86–89. 24. Middeldorp S, Coppens M, van Haaps TF, Foppen M, Vlaar AP, Müller MCA, et al. Incidence of venous thromboembolism in hospitalized patients with COVID-19. J Thromb Haemost 2020; 18: 1995–2002. 25. Grillet F, Behr J, Calame P, Aubry S, Delabrousse E. Acute pulmonary embolism associated with COVID-19 pneumonia detected by pulmonary CT angiography. Radiology 2020; 296(3): E186–E188. 26. Wu MA, Colombo R, Arquati M, Ippolito S, Taino A, Ruggiero D, et al. Clinical-radiological correlations in COVID-19-related venous thromboembolism: Preliminary results from a multidisciplinary study. Int J Clin Pract 2021; 75(9): e14370. 27. BV Silva, C Jorge, J Rigueira, T Rodrigues, P Silverio Antonio, P Morais, et al. Wells and Geneva decision rules to predict pulmonary embolism: can we use them in Covid-19 patients? Eur Heart J Cardiovasc Imag 2021; 22(Suppl 3). 28. Calabrese F, Pezzuto F, Fortarezza F, Hofman P, Kern I, Panizo A, et al. Pulmonary pathology and COVID-19: Lessons from autopsy. The experience of European pulmonary pathologists. Virchows Archiv 2020; 477: 359–372. 29. Carsana L, Sonzogni A, Nasr A, Rossi RS, Pellegrinelli A, Zerbi P, et al. Pulmonary post-mortem findings in a series of COVID-19 cases from northern Italy: a two-centre descriptive study. Lancet Infect Dis 2020; 20(10): 1135–1140. 30. Llitjos JF, Leclerc M, Chochois C, Monsallier JM, Ramakers M, Auvray M, et al. High incidence of venous thromboembolic events in anticoagulated severe COVID-19 patients. J Thromb Haemost 2020; 18: 1743–1746. 31. Trimaille A, Curtiaud A, Matsushita K, Marchandot B, Von Hunolstein JJ, Sato C, et al. Acute pulmonary embolism in patients with and without COVID-19. J Clin Med 2021; 10(10): 2045.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 AFRICA 9 Aortic regurgitation: multimodal assessment of quantification and impact Marie-Paule Bernadette N’Cho-Mottoh, Olivier Huttin, Christine Selton-Suty, Soukaina Scadi, Laura Filippetti, Pierre-Yves Marie Abstract Background: The assessment of severity of aortic regurgitation (AR) by transthoracic echocardiography (TTE) remains challenging in routine practice. Contemporary guidelines recommend cardiovascular magnetic resonance imaging (CMR) in patients with significant disease and suboptimal TTE images. The objective of this study was to assess the role of CMR in the evaluation of severity of AR and to compare both modalities in the quantification of regurgitation and left ventricular volumes. Methods: Fifty consecutive patients who had isolated chronic AR and who underwent TTE and CMR within an interval of less than three months between May 2009 and June 2020 were included. The main indication for CMR was difficulties in quantifying AR, either because of lack of multiparametric analysis (only one method possible) or because of discrepancies in the different methods by TTE. Results: In 25 patients, precise grading of AR was not possible by echocardiography. Among them, CMR finally detected seven patients with mild AR, 11 with moderate AR and seven with severe AR. For the 25 patients who had AR quantification by TTE, there was concordance between TTE and CMR in only seven patients (28%), and the AR was re-graded by CMR in 18 patients, including eight patients with severe AR by TTE and moderate AR by CMR. The concordance between TTE and CMR was weakly significant (intraclass correlation coefficient = 0.39, 95% confidence interval: 0.003– 0.67, p = 0.02). There was a moderate correlation between left ventricular volumes measured by TTE and by CMR (left ventricular end-diastolic volume: r = 0.57; p = 0.01; left ventricular end-systolic volume: r = 0.47, p = 0.01) but regurgitant volumes were not correlated (r = 0.04; p = 0.8). No TTE parameter of quantification was correlated with regurgitant volume measured by CMR. Conclusion: The concordance of AR quantification by CMR and TTE was weak. CMR re-graded some patients with severe AR by TTE into moderate AR. This should motivate practitioners to systematically assess all significant AR by CMR in order to improve quantification and optimise clinical management. Keywords: aortic regurgitation, quantification, multimodality, cardiac magnetic resonance Submitted 10/2/21, accepted 24/2/22 Published online 8/3/22 Cardiovasc J Afr 2023; 34: 9–15 www.cvja.co.za DOI: 10.5830/CVJA-2022-013 Reliable assessment of severity of valvular regurgitation is crucial in the prognosis and clinical management of patients with aortic regurgitation (AR).1 Transthoracic echocardiography (TTE) is the primary clinical imaging modality to assess severity of AR, but AR quantification remains challenging in routine practice.2 The current recommended echocardiographic assessment of AR uses both quantitative and semi-quantitative criteria. The proximal isovelocity surface area (PISA) method, using two-dimensional (2D) colour Doppler echocardiography is the most widely used approach to estimate the regurgitant volume (RVol) and effective regurgitant orifice area (EROA).3-5 However, this method has several limitations: difficulty in correctly identifying the flow convergence zone, confined flow convergence zones (patients with cusp perforation or commissural leaks), and obtuse flow convergence angles such as those with aneurysmal dilation of the ascending aorta.3 Contemporary guidelines2,6 recommend cardiovascular magnetic resonance imaging (CMR) in patients with significant disease and suboptimal TTE images, which acknowledges CMR’s superior capacity to quantify AR volume and regurgitant fraction by direct measurement of aortic blood flow and to accurately compare right ventricular (RV) and left ventricular (LV) stroke volumes.7,8 The objective of this study was to assess the role of CMR in the evaluation of severity of AR in current practice and to compare both modalities in the quantification of regurgitation and LV volumes. Methods This study was performed in the Cardiology Department of Nancy University Hospital Centre (Brabois Hospital). Three analysis and archiving databases were used: DxCare for clinical data, Echopac version R3 for echocardiographic data and Syngovia for CMR data. All consecutive patients who had isolated chronic AR and who underwent TTE and CMR within an interval of less than three months, from May 2009 to June 2020, were included (Fig. 1). Patients with primary cardiomyopathy and those with other significant valvular disease and atrial fibrillation were excluded. Echocardiographic examinations were performed using commercially available scanners (Vivid 7, Vivid 9 or Vivid 95, Department of Cardiology, Institut Lorrain du Cœur et des Vaisseaux, Nancy University Hospital, Vandoeuvre les Nancy, France Marie-Paule Bernadette N’Cho-Mottoh, MD, nchomottoh@yahoo.fr Olivier Huttin, MD, MSc Christine Selton-Suty, MD Soukaina Scadi, MD Laura Filippetti, MD Pierre-Yves Marie, MD, PhD Institut de Cardiologie d’Abidjan, Abidjan, Ivory Coast Marie-Paule Bernadette N’Cho-Mottoh, MD
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 10 AFRICA General Electric-Vingmed, Horten, Norway) using a 2.5-MHz phased-array cardiac probe with subjects in the left lateral recumbent position. An experienced sonographer acquired a complete 2D standard echocardiography, including apical four- and two-chamber LV views. All images were acquired at a frame rate of 50 to 70 frames/s for 2D views. Before each acquisition, images were optimised for endocardial visualisation. LV diameters were measured in time–motion mode or in 2D mode when the time–motion line was not perpendicular to the LV longitudinal axis. The left ventricle was considered severely dilated by TTE for a left ventricular end-diastolic diameter (LVEDDTTE) > 70 mm. LV volumes were calculated from apical four- and two-chamber views according to Simpson’s biplane method.9 AR severity was assessed by an integrated approach using four quantification methods: vena contracta width, PISA, diastolic flow reversal velocity in the descending aorta, and pression half-time (PHT). The vena contracta width was obtained from the parasternal long-axis view. A narrow colour sector scan coupled with the zoom mode was used to improve measurement accuracy. Using a Nyquist limit of 50–60 cm/s, a vena contracta width < 3 mm correlates with mild AR, whereas a width > 6 mm indicates severe AR. Depending on the orientation of the jet, PISA was measured in the apical five-chamber or parasternal long-axis view with the lower Nyquist limit set at 30 cm/s. Peak AR jet velocity and integral velocity time were determined using continuous-wave Doppler across the aortic valve. The PISA radius was measured from a stop frame as the distance between the regurgitant orifice and the first aliasing in early diastole (closest to the peak of regurgitant velocity) (Fig. 2). Grading of the severity of AR classified regurgitation as mild when EROA was < 10 mm² or RVol was < 30 ml, and moderate or severe when EROA was ≥ 30 mm² or RVol was ≥ 60 ml. End-diastolic velocity flow reversal in the descending aorta (EDVDA) was measured in the upper descending aorta at the aortic isthmus level using a suprasternal view with pulsed Doppler. The sample volume was placed at the origin of the left subclavican artery and it was aligned as much as possible along the major axis of the aorta. The Doppler filter was decreased to its lowest setting to allow detection of low velocities (< 10 cm/s). End-diastolic velocity measured at peak R wave exceeding 20 cm/s indicated severe AR.3 PHT was obtained from the AR flow curve obtained for an apical five-chamber view.3 A PHT of < 200 ms indicated severe AR, whereas a value of > 500 ms was in favour of mild AR. CMR imaging was performed on a 3T system (General Electric Signa HDxt) with an eight-phased-array cardiac coil, electrocardiogram triggered and breath-holding in expiration. After a series of scouting images to determine the position and orientation of the left ventricle within the thorax, Ciné Fiesta sequences for cardiac morphology and function were performed with a steady-state free precession technique in 10 to 15 parallel short-axis views. Each slice (slice thickness: 8 mm, gap: 0 mm) was obtained during one breath-hold of 10 to 15 seconds. CMR and TTE left ventricular ejection fractions (LVEF) were based on endocardial tracing of the LV chamber from the images on different axis views. On each image, end-diastole was defined as the frame in the cardiac cycle in which the cardiac volume was largest. End-systole was defined just before the opening of the mitral valve leaflet or the frame in the cardiac Five patients with AF Twelve patients with significant other valvular disease or cardiomyopathy TTE available within three months of CMR 229 patients with a main diagnosis of aortic regurgitation 198 patients 50 patients Fig. 1. Flow chart of the population. Fig. 2. Regurgitant volume by the PISA method.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 AFRICA 11 cycle in which the cardiac volume was smallest. Papillary muscles were included in the cavity for the tracing. Quantitative determination of LVEF was calculated using left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) estimates as follows: LVEF = LVEDV – LVESV ______________ LVEDV according to the guidelines.10,11 Both Simpson’s method and the area–length method were applied on CMR. On short-axis view (Fig. 3), the outline of the endocardial border of the left ventricle was traced manually on all slices of each phase by one experienced cardiologist or one radiologist using standard software (Mass Research software, version V2013-EXP, Leiden University Medical Center). Volumes were computed by Simpson’s method of disk summation where the sum of the cross-sectional areas was multiplied by the slice thickness. On CMR, the left ventricle was considered dilated for a LVEDVCMR > 246 ml. Phase-contrast cardiac magnetic resonance (PC-CMR) images were also acquired in order to compute the stroke volume. On PC images, the lumen of the ascending aorta was segmented automatically and corrected manually throughout the cardiac cycle (Fig. 4). Blood flow within the vessel has been computed by summing the regions of interest.12 The average flow velocity (cm/s) was multiplied by the area of the vessel (cm²) to obtain flow (ml/s) at each point. Stroke volume (ml) was obtained by dividing cardiac output (l/min) by heart rate (bpm).13 AR grading was defined as follows: mild, AR volumes < 30 ml (regurgitation fraction < 30%); moderate, AR volumes 30–59 ml (regurgitation fraction 30–49%); severe, AR volumes ≥ 60 ml (regurgitation fraction ≥ 50 %).6 Statistical analysis The statistical analysis was performed using SPSS for Windows (SPSS version 17, Chicago, Illinois). Continuous variables are expressed as means ± standard deviations. Categorical variables are expressed as percentages. Differences between CMR and TTE were compared using the Student’s t-test. Pearson’s correlation coefficients were calculated by linear regression for continuous variables. A p-value < 0.05 was considered significant. The intraclass correlation coefficient (ICC) for a two-way random-effects model with absolute agreement was calculated to assess the concordance between TTE andCMR for quantification of AR severity. ICCs were categorised as excellent (ICC ≥ 0.75), good (ICC 0.6–0.74), fair (ICC 0.4–0.59) or poor (ICC < 0.4).14,15 Results From May 2009 to June 2020, 198 patients had both a CMR and TTE showing AR. After checking the delay between both examinations (< 3 months) and after exclusion of patients with AF and those with other significant valvular disease and primary cardiomyopathy, AR was the sole and main diagnosis in 50 (25.2%) patients, who constituted our population. The clinical data are summarised in Table 1. Out of the 50 patients, 13 (26%) had bicuspid aortic valve and eight (16%) had aortic valvular prosthesis. The mean time between TTE and CMR was 44.2 ± 19.5 days. Regarding echocardiography, the PISA method was possible in 19 patients (38%). According to this method, seven patients (14%) had mild AR, eight (16%) had moderate AR and four (8%) had severe AR. The EDVDA measurement was used in 12 patients (24%) and severe AR was detected in eight patients (16%). The vena contracta was measured in 28 patients (56%) and we classified 10 patients (20%) with severe AR, two (4%) with mild AR and 16 (36%) with moderate AR. PHT was measured in 21 patients (42%) and nine (18%) had mild AR, none had severe AR and 12 (24%) had moderate AR. Fig. 3. Basal and mid-ventricular short-axis view with diastolic and systolic contours. Fig. 4. Phase-contrast ciné CMR in the transverse plane at the level of the pulmonary artery bifurcation. A: magnitude and phase images. B: flow curve in the ascending aorta with holodiastolic retrograde flow. A B
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 12 AFRICA Table 2 shows the distribution of patients by number of TTE quantification methods. Only one method of quantification had been possible in 20 (40%) patients. Among the 30 patients who had more than one method of quantification, five (10%) had discrepancies in results. Therefore, for 25 (50%) cases, the operator had difficulty in assessing AR severity and considered TTE as inconclusive for the quantification of AR. Finally, with TTE, AR was considered mild in eight (16 %) patients, moderate in seven (14%), severe in 10 (20%) and inconclusive in 25 (50%) patients. The main indication for use of CMR was difficulties in quantifying AR, either because of lack of multiparametric analysis (only one method possible) or because of discrepancies in the different methods by TTE. The indication for use of CMR was inconclusive TTE in 25 (50%) patients, aortic bicuspid valve in 13 (26%), valvular aortic prosthesis in eight (16%) and ascending aortic assessment in 17 (34%) patients. Among the 25 patients (50%) with non-conclusive TTE results, CMR was also indicated in six patients (12%) for aortic bicuspid valve, three (6%) for aortic prosthesis and four patients (8%) for ascending aortic assessment. Among all patients, AR quantification by CMR was as follows: 14 patients (28%) had mild AR, 26 (52%) had moderate AR and 10 had (20%) severe AR. Among the 25 patients (50%) with inconclusive TTE, CMR finally detected 14% with mild AR (seven patients), 22% with moderate AR (11 patients) and 14% with severe AR (seven patients). Among the 25 patients (50%) who had AR graded by TTE, quantification of AR was concordant with both methods in seven patients (14%). Compared to CMR, AR was underestimated in six (12%) patients (five considered mild by TTE and moderate by CMR, and one considered moderate by TTE and severe by CMR). AR was overestimated in 12 (24%) patients (eight considered severe by TTE and moderate by CMR, and four considered moderate by TTE and mild by CMR) (Table 3). Therefore, AR was re-graded by CMR in 18 (36%) patients. The concordance between the two AR quantification modalities (TTE and CMR) was weakly significant (ICC = 0.39, 95% CI: 0.003–0.67, p = 0.02). Among all patients, six (12%) had a LVEDDTTE > 70 mm. Out of these six patients, AR grade using TTE was determined as follows: severe in three (6%) patients, inconclusive in two (4%) and mild in one patient (2%). The three patients who had severe AR using TTE were classified as severe by CMR in two patients and moderate in one. The two with inconclusive AR were classified as moderate in one patient and severe in the other using CMR. Lastly, the only patient with mild AR on TTE was classified as moderate on CMR. Twenty-five patients (50%) had inconclusiveARquantification on TTE. Among them, seven had severe AR on CMR and five had subsequent aortic valvular replacement. Two patients with severe AR on CMR had medical therapy and close follow up. All patients with possible AR quantification using TTE, and severe AR on CMR, had aortic valve replacement (Fig. 5). Among the six patients with LVEDDTTE > 70 mm, three had aortic valvular replacement (two patients with severe AR on TTE and CMR, and one with inconclusive AR on TTE and severe AR on CMR). LV volume measurements were performed on all patients, both by TTE and CMR (Table 2). LV volumes were lower with TTE than with CMR: LVEDVTTE vs LVEDVCMR (95.9 ± 27.4 vs 133.3 ± 38.1 ml/m², p < 0.01) and LVESVTTE vs LVESVCMR (65.0 ± 25.5 vs 41.1 ± 21.1 ml/m², p < 0.01). On the other hand, LVEFTTE was higher than LVEFCMR (54.1 ± 10.5 vs 51.8 ± 8.6%, p = 0.03). Table 1. Clinical data Patient characteristics Number (%) or mean ± SD Age (years) 52.1 ± 16.1 Gender (male) 38 (76) Systolic blood pressure (mmHg) 135.1 ± 20.1 Diastolic blood pressure (mmHg) 72.2 ± 10.4 Heart rate (bpm) 69.8 ± 13.0 Body surface area (m²) 1.9 ± 0.2 Body mass index (kg/m²) 25.7 ± 4.6 Hypertension 27 (54) Diabetes mellitus 2 (4) Dyslipidaemia 6 (12) Coronary artery disease 5 (10) NYHA class I 38 (76) II 6 (12) III 5 (10) IV 1 (2) NYHA, New York Heart Association. Table 2. TTE and CMR data TTE and CMR data Number (%) or mean ± SD LVEDVTTE (ml/m²) 95.9 ± 27.4 LVESVTTE (ml/m²) 41.1 ± 21.1 LVEDDTTE (mm) 61.4 ± 7.8 LVESDTTE (mm) 43.2 ± 9.1 LVEFTTE (%) 54.1 ± 10.5 RVolTTE (ml) 53.3 ± 21.6 EDVDA (cm/s) 18.1 ± 6.4 PHT (ms) 460.6 ± 153.1 Vena contracta (mm) 5.3 ± 2.4 Inconclusive quantification by TTE 25 (50) Number of quantification methods by TTE One method 20 (40) Two methods 14 (28) Three methods 8 (16) Four methods 8 (16) Disagreement between TTE methods 5 (10) LVEDVCMR (ml/m²) 133.3 ± 38.1 LVESVCMR (ml/m²) 65.1 ± 25.5 RFCMR (%) 35.5 ± 14.1 RVolCMR (ml) 29.7 ± 17.1 LVEFCMR (%) 51.8 ± 8.6 Late gadolinium enhancement 5 (10) TTE, transthoracic echocardiography; CMR, cardiovascular magnetic resonance imaging; LVEDV, left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; LVEDD, left ventricular end-diastolic dimension; LVESD, left ventricular end-systolic dimension; LVEF, left ventricular ejection fraction; RVol, regurgitant volume; EDVDA, end-diastolic velocity in the descending aorta; PHT, pressure half-time; RF, regurgitant fraction. Table 3. Comparison of AR severity on TTE and CMR AR severity, n (%) CMR Mild Moderate Severe TTE Mild 3 (6) 5 (10) 0 (0) Moderate 4 (8) 2 (4) 1 (2) Severe 0 (0) 8 (16) 2 (4) Inconclusive 7 (14) 11 (22) 7 (14) AR, aortic regurgitation; TTE, transthoracic echocardiography; CMR, cardiovascular magnetic resonance imaging
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