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Background: Despite advances in managing hypertension, hypertensive emergencies remain a common indication for emergency room visits. Our study aimed to determine the clinical profile of patients referred with hypertensive emergencies., Methods: We conducted an observational study involving patients aged ≥18 years referred with hypertensive crisis. A diagnosis of hypertensive emergencies was based on a systolic blood pressure (BP) ≥180 mmHg and/or a diastolic BP ≥110 mmHg, with acute hypertension-mediated organ damage (aHMOD). Patients without evidence of aHMOD were considered hypertensive urgencies. Hypertensive disorders of pregnancy and unconscious patients were excluded from the study., Results: Eighty-two patients were included, comprising 66 (80.5%) with hypertensive emergencies and 16 (19.5%) with hypertensive urgencies. The mean age of patients with hypertensive emergencies was 47.9 (13.2) years, and 66.7% were males. Age, systolic BP, and duration of hypertension were similar in the hypertensive crisis cohort. Most patients with hypertensive emergencies reported nonadherence to medication (78%) or presented de novo without a prior diagnosis of hypertension (36%). Cardiac aHMOD (acute pulmonary edema and myocardial infarction) occurred in 66%, while neurological emergencies (intracranial hemorrhage, ischemic stroke, and hypertensive encephalopathy) occurred in 33.3%. Lactate dehydrogenase (LDH) (P < 0.001), NT-proBNP (P=0.024), and cardiac troponin (P<0.001) were higher in hypertensive emergencies compared to urgencies. LDH did not differ in the subtypes of hypertensive emergencies., Conclusion: Cardiovascular and neurological emergencies are the most common hypertensive emergencies. Most patients reported nonadherence to medication or presented de novo without a prior diagnosis of hypertension., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: The diagnosis of infective endocarditis (IE) is based on the modified Duke/European Society of Cardiology (ESC) 2015 clinical criteria. The sensitivity of the criteria is unknown in South Africa, but high rates of blood culture negative endocarditis (BCNIE), coupled with a change in the clinical features of IE, may limit the sensitivity., Methods: The Tygerberg Endocarditis Cohort study prospectively enrolled patients with IE between November 2019 and June 2021. A standardised protocol for organism detection, with management of patients by an Endocarditis Team, was employed. Patients with definite IE by pathological criteria were analysed to determine the sensitivity of the current clinical criteria., Results: Eighty consecutive patients with IE were included of which 45 (56.3%) had definite IE by pathological criteria. In patients with definite IE by pathological criteria, 26/45 (57.8%) of patients were classified as definite IE by clinical criteria. BCNIE was present in 25/45 (55.6%) of patients and less than three minor clinical criteria were present in 32/45 (75.6%) of patients. The elevation of Bartonella serology to a major microbiological criterion of the modified Duke/ESC 2015 clinical criteria would increase the sensitivity (57.8% vs 77.8%; p=0.07)., Conclusion: The sensitivity of the modified Duke/ESC 2015 clinical criteria is lower than expected in patients with IE in South Africa, primarily due to the high rates of Bartonella -associated BCNIE. The elevation of Bartonella serology to a major microbiological criterion, similar to the status of Coxiella burnetii in the current criteria, would increase the sensitivity. The majority of patients with definite IE by pathological criteria had less than three minor criteria present., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Blood culture negative infective endocarditis (BCNIE) poses both a diagnostic and therapeutic challenge. High rates of BCNIE reported in South Africa have been attributed to antibiotic use prior to blood culture sampling., Objectives: To assess the impact of a systematic approach to organism detection and identify the causes of infective endocarditis (IE), in particular causes of BCNIE., Design: Prospective cohort study., Methods: The Tygerberg Endocarditis Cohort study prospectively enrolled patients with IE between November 2019 and February 2021. A set protocol for organism detection with management of patients by an endocarditis team was employed. This prospective cohort was compared with a retrospective cohort of patients with IE admitted between January 2017 and December 2018., Results: One hundred and forty patients with IE were included, with 75 and 65 patients in the retrospective and prospective cohorts, respectively. Baseline demographic characteristics were similar with a mean age of 39.6 years and male predominance (male sex=67.1%). The rate of BCNIE was lower in the prospective group (28/65 or 43.1%) compared with the retrospective group (47/75 or 62.7%; p=0.039). The BCNIE in-hospital mortality rate in the retrospective cohort was 23.4% compared with 14.2% in the prospective cohort (p=0.35). A cause was identified (including non-culture techniques) in 86.2% of patients in the prospective cohort, with Staphylococcus aureus (26.2%), Bartonella species (20%) and the viridans streptococci (15.3%) being most common., Conclusion: The introduction of a set protocol for organism detection, managed by an endocarditis team, has identified Staphylococcusaureus as the most common cause of IE and identified non-culturable organisms, in particular Bartonella quintana , as an important cause of BCNIE. A reduction in in-hospital mortality in patients with BCNIE was observed, but did not reach statistical significance., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Objectives: To determine the outcome of subclinical lupus myocarditis (LM) over twelve months with regards to: mortality; incidence of clinical LM and change in imaging parameters (echocardiography and cardiac magnetic resonance [CMR]). To evaluate the impact of immunosuppression on CMR evidence of myocardial tissue injury., Methods: SLE patients with and without CMR evidence of myocardial injury (as per 2009 Lake Louise criteria [LLC]) were included. Analysis at baseline and follow-up included: clinical evaluation, laboratory and imaging analyses (echocardiography and CMR). Clinical LM was defined as clinical features of LM supported by echocardiographic and/or biochemical evidence of myocardial dysfunction. Subclinical LM was defined as CMR myocardial injury without clinical LM., Results: Forty-nine SLE patients were included with follow-up analyses (after 12 months) available in 36 patients. Twenty-five patients (51%) received intensified immunosuppressive therapy during follow-up for indications related to SLE. Disease activity (SLEDAI-2K) improved (p < 0.001) from 13 (median;IQR:9-20) to 7 (3-11). One patient without initial CMR evidence of myocardial injury developed clinical LM. Mortality (n = 10) and SLE clinical features were similar between patients with and without initial CMR myocardial injury. Echocardiographic left ventricular ejection fraction (LVEF) (p = 0.014), right ventricular function (p = 0.001) and wall motion abnormalities (p = 0.056) improved significantly but not strain analyses nor the left LV internal diameter index. CMR mass index (p = 0.011) and LVEF (p < 0.001) improved with follow-up but not parameters identifying myocardial tissue injury (LLC). A trend towards a reduction in the presence of CMR criteria was counterbalanced by persistence (n = 7) /development of new criteria (n = 11) in patients. Change in CMR mass index correlated with change in T2-weighted signal (myocardial oedema) (r = 386;p = 0.024). Intensified immunosuppressive therapy had no significant effect on CMR parameters., Conclusion: CMR evidence of subclinical LM persisted despite improved SLEDAI-2K, serological markers, cardiac function and CMR mass index. Subclinical LM did not progress to clinical LM and had no significant prognostic implications over 12 months. Immunosuppressive therapy did not have any significant effect on the presence of CMR evidence of myocardial tissue injury. Improvement in CMR mass index correlated with reduction in myocardial oedema and may be used to monitor SLE myocardial injury.

Objective: The World Heart Federation (WHF) criteria incorporate a Doppler-based system to differentiate between 'physiological' and 'pathological' mitral regurgitation (MR)-a sole criterion sufficient for the diagnosis of WHF 'borderline' rheumatic heart disease (RHD). We have identified that interscallop separations (ISS) of the posterior mitral valve (MV) leaflet, can give rise to pathological MR in an otherwise-normal MV. We aimed to establish and compare the prevalence of ISS-related MR among South African children at high and low risk for RHD., Methods: A prospective cross-sectional echocardiographic study of 759 school children (aged 13-18) was performed. Cases with MR≥1.5 cm underwent a second comprehensive study to determine the prevalence of RHD according to the WHF guideline and establish the underlying mechanism of MR., Results: Of 400 high-risk children, two met criteria for 'definite RHD' (5 per 1000 (95% CI 1.4 to 18.0); p=0.5) and 11 for 'borderline RHD' (27.5 per 1000 (95% CI 15.4 to 48.6)). Of 359 low-risk children, 14 met criteria for borderline RHD (39 per 1000 (95% CI 23.4 to 64.4)). Comprehensive echocardiography identified an underlying ISS as the mechanism of isolated pathological MR in 10 (83.3%) high-risk children and 11 low-risk children (78.5%; p>0.99)., Conclusions: ISS are a ubiquitous finding among South African schoolchildren from all risk profiles and are regularly identified as the underlying mechanism of WHF pathological MR in borderline RHD cases. A detailed MV assessment with an emphasis on ascertaining the underlying mechanism of dysfunction could reduce the reported numbers of screened cases misclassified as borderline RHD., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: African American ethnicity is independently associated with lupus myocarditis compared with other ethnic groups. In the mixed racial population of the Western Cape, South Africa, no data exists on the clinical features/outcome of lupus myocarditis., Objectives: The objective of this study was to give a comprehensive description of the clinical features and outcome of acute lupus myocarditis in a mixed racial population., Methods: Clinical records (between 2008 and 2014) of adult systemic lupus erythematosus (SLE) patients at a tertiary referral centre were retrospectively screened for a clinical and echocardiographic diagnosis of lupus myocarditis. Clinical features, laboratory results, management and outcome were described. Echocardiographic images stored in a digital archive were reanalysed including global and regional left ventricular function. A poor outcome was defined as lupus myocarditis related mortality or final left ventricular ejection fraction (LVEF) <40%., Results: Twenty-eight of 457 lupus patients (6.1%) met inclusion criteria: 92.9% were female and 89.3% were of mixed racial origin. Fifty-three per cent of patients presented within three months after being diagnosed with SLE. Seventy-five per cent had severely active disease (SLE disease activity index ≥ 12) and 67.9% of patients had concomitant lupus nephritis. Laboratory results included: lymphopenia (69%) and an increased aRNP (61.5%). Treatment included corticosteroids (96%) and cyclophosphamide (75%); 14% of patients required additional immunosuppression including rituximab. Diastolic dysfunction and regional wall motion abnormalities occurred in > 90% of patients. LVEF improved from 35% to 47% (p = 0.023) and wall motion score from 1.88 to 1.5 (p = 0.017) following treatment. Overall mortality was high (12/28): five patients (17.9%) died due to lupus myocarditis (bimodal pattern). Patients who died of lupus myocarditis had a longer duration of SLE (p = 0.045) and a lower absolute lymphocyte count (p = 0.041) at diagnosis. LVEF at diagnosis was lower in patients who died of lupus myocarditis (p = 0.099) and in those with a persistent LVEF < 40% (n = 5; p = 0.046)., Conclusions: This is the largest reported series on lupus myocarditis. The mixed racial population had a similar prevalence, but higher mortality compared with other ethnic groups (internationally published literature). Patients typically presented with high SLE disease activity and the majority had concomitant lupus nephritis. Lymphopenia and low LVEF at presentation were of prognostic significance, associated with lupus myocarditis related mortality or a persistent LVEF < 40%., (© The Author(s) 2016.)

Introduction: The minimum criterion for the diagnosis of hypertrophic cardiomyopathy (HCM) is thickening of the left ventricular wall, typically in an asymmetrical or focal fashion, and it requires no functional deficit. Using this criterion, we identified a family with four affected individuals and a single unrelated individual essentially with restrictive cardiomyopathy (RCM). Mutations in genes coding for the thin filaments of cardiac muscle have been described in RCM and HCM with 'restrictive features'. One such gene encodes for cardiac troponin I (TNNI3), a sub-unit of the troponin complex involved in the regulation of striated muscle contraction. We hypothesised that mutations in TNNI3 could underlie this particular phenotype, and we therefore screened TNNI3 for mutations in 115 HCM probands., Methods: Clinical investigation involved examination, echocardiography, chest X-ray and an electrocardiogram of both the index cases and close relatives. The study cohort consisted of 113 South African HCM probands, with and without known founder HCM mutations, and 100 ethnically matched control individuals. Mutation screening of TNNI3 for diseasecausing mutations were performed using high-resolution melt (HRM) analysis., Results: HRM analyses identified three previously described HCM-causing mutations (p.Pro82Ser, p.Arg162Gln, p.Arg170Gln) and a novel exonic variant (p.Leu144His). A previous study involving the same amino acid identified a p.Leu144Gln mutation in a patient presenting with RCM, with clinical features of HCM. We observed the novel p.Leu144His mutation in three siblings with clinical RCM and varying degrees of ventricular hypertrophy. The isolated index case with the de novo p.Arg170Gln mutation presented with a similar phenotype. Both mutations were absent in a healthy control group., Conclusion: We have identified a novel disease-causing p.Leu144His mutation and a de novo p.Arg170Gln mutation associated with RCM and focal ventricular hypertrophy, often below the typical diagnostic threshold for HCM. Our study provides information regarding TNNI3 mutations underlying RCM in contrast to other causes of a similar presentation, such as constrictive pericarditis or infiltration of cardiac muscle, all with marked right-sided cardiac manifestations. This study therefore highlights the need for extensive mutation screening of genes encoding for sarcomeric proteins, such as TNNI3 to identify the underlying cause of this particular phenotype.

Background: Guidelines advise early angiography in non-ST elevation myocardial infarction (NSTEMI) to ensure an optimal outcome. Resource limitations in secondary hospitals in the Western Cape dictate a local guideline to treat NSTEMIs medically with out-patient assessment for angiography, unless mandatory indications for early angiography occur., Methods: A retrospective cohort study assessed NSTEMIs at Tygerberg Hospital (TBH), Karl Bremer Hospital (KBH) and Worcester Hospital (WH) over one year. Two cohorts were analysed, secondary hospitals (KBH and WH; SH) and secondary service within a tertiary hospital (TBH). Where differences were found, sub-analysis compared WH and KBH., Results: TBH and SH were similar at baseline and in clinical presentation. Cases at TBH were more likely to receive in-patient angiography (94 vs 51%, p < 0.0001), and had a lower in-patient mortality rate (6 vs 23%, p = 0.0326). There was no difference between KBH and WH in sub-analysis., Conclusion: This study confirmed that the management and mortality of NSTEMIs in the public health sector in the Western Cape, South Africa is not influenced by geography, but rather by the level of service available in the hospital of first presentation.