Clinical supervisors’ perceptions regarding the factors that promote or inhibit nursing students’ skills transfer from the skills laboratory to the clinical practice environment

Magister Curationis - MCurBackground: Nursing as a profession is based on firm knowledge, values, clinical skills and attitudes. In the current dynamic healthcare system nursing students are challenged to be insightful and have clinical reasoning and psychomotor skills in order to apply theory to practice. Clinical teaching is therefore considered an essential part of the undergraduate nursing curriculum, as it provides the opportunity for students to apply theory to practice in the skills laboratory and then to transfer it into real life situations. Nursing students spend time in the clinical practice environment learning the skills and values of the nursing profession, with the goal of achieving the clinical learning outcomes, as prescribed by their nursing education institution and the South African Nursing Council. During this time nursing students depend on the support of clinical supervisors and nursing staff in the clinical practice environment to meet their learning outcomes. Clinical supervisors for the undergraduate nursing programme, at the university included in the study, are tasked with clinical teaching in the skills laboratory, supervision of nursing students in clinical practice and assessment of learning. Nonetheless, there are challenges ascertained by the clinical supervisors, which inhibits students from achieving their learning outcomes. Purpose of the study: The purpose of the study was to explore and describe the clinical supervisor’s perception of students’ skills transfer from skills laboratory to the clinical environment

Renal denervation restores autonomic imbalance and prevents atrial fibrillation in patients with hypertensive heart disease : a pilot study

Thesis (PhD)--Stellenbosch University, 2020.ENGLISH ABSTRACT: Background: Atrial fibrillation (AF) is associated with increased cardiovascular morbidity and mortality, but it is uncertain if catheter-based renal denervation (RD) can reduce AF in patients with hypertensive heart disease (HHD). Methods: Patients who were ≥ 55 years old, in sinus rhythm, taking ≥ 3 anti-hypertensive drugs including a diuretic, with echocardiogram-confirmed HHD and suspected coronary artery disease, were randomised to undergo RD or sham procedure. Patients with renal impairment, significant valvular heart disease and untreated thyroid disease were excluded. The primary endpoint, the first episode of subclinical AF (SAF) lasting ≥ 6 minutes, was detected using an implantable loop recorder which was scanned every six months. Six-month follow-up (6MFU) office systolic blood pressure (SBP), cardiovascular mortality and restoration of autonomic imbalance were secondary endpoints. Results: Eighty patients were randomised: 42 underwent RD and 38 a sham procedure. After an average follow-up of three years, fewer RD patients experienced SAF: 6 of 42 patients (14.3%) vs 15 of 38 (39.5%) sham patients (odds ratio (OR), 0.26; 95% CI, 0.1 to 0.71, p = 0.01). Fast AF (ventricular rate ≥ 100 bpm) occurred in 10 sham patients (26.3%) vs 1 RD patient (2.4%): OR, 14.64; 95% CI, 1.77 to 120.91; p = 0.002). The incidence of cardiovascular death was higher in the sham than RD group (6 of 38 (15.8%) vs 1 of 42 (2.4%): OR, 7.69; 95% CI, 0.88 to 67.12; p = 0.049). Non-ST elevation myocardial infarction (NSTEMI) incidence was lower in the RD than sham group (2.3% vs 18.4%: OR, 0.108; 95% CI, 0.01–0.92; p = 0.02). The 6MFU between-group SBP difference was not significant (−3.8 mmHg; p = 0.49). Resting and one-minute recovery heart rate did not differ between groups at 6MFU. Conclusion: In patients with HHD, RD reduces subclinical and fast AF, NSTEMI and cardiovascular death independent of lowering blood pressure. RD was not associated with improvement of surrogate markers of autonomic imbalance.Doctora

Percutaneous left atrial appendage occlusion: A South African experience

Background. Atrial fibrillation (AF) is associated with all-cause mortality, heart failure and non-fatal stroke, and thromboprophylaxis is traditionally provided with oral anticoagulants (OACs). Percutaneous left atrial appendage occlusion (LAAO) with a dedicated device is an alternative approach to thromboprophylaxis in patients with AF who are: (i) intolerant to OACs (e.g. life-threatening haemorrhage); (ii) non-adherent to OACs; or (iii) at a high bleeding risk with OACs. Non-inferiority of LAAO compared with OACs was demonstrated in e.g. the WATCHMAN Left Atrial Appendage System for Embolic Protection in Patients With Atrial Fibrillation (PROTECT AF) trial. Only very limited data are available on percutaneous LAAO in South Africa (SA), and no local outcome data have been reported.Objectives. To compare the safety and efficacy outcomes of an SA percutaneous LAAO programme with larger international series. Methods. All patients undergoing percutaneous LAAO from 2013 to 2020 at a single centre (SAEndovascular, Kuils River Netcare Hospital, SA) were included from an ongoing registry. Survival analysis was performed with the Kaplan-Meier method.Results. Of 101 LAAO recipients (mean (standard deviation) age 77 (10) years, 64% male) analysed, 90 (90%) had permanent AF, 1 (1%) persistent AF and 9 (9%) paroxysmal AF. The most common indication for LAAO was previous severe bleeding (n=23; 23%). The mean device size was 23 (3) mm and the procedural success rate was 98%. After a median (interquartile range) follow-up of 21 (5 - 41) months, 6 patients (6%) experienced stroke or all-cause mortality. Four patients (4%) had a life-threatening procedural complication (tamponade n=2 (2%) and device embolisation n=2 (2%)). These outcomes are comparable to large international series, e.g. PROTECT AF.Conclusions. The safety and efficacy outcomes of an SA percutaneous LAAO programme were comparable to large international series. A successful percutaneous LAAO programme is feasible in a southern African contex

Genetic variation in angiotensin II type 2 receptor gene influences extent of left ventricular hypertrophy in hypertrophic cardiomyopathy independent of blood pressure

Introduction. Hypertrophic cardiomyopathy (HCM), an inherited primary cardiac disorder mostly caused by defective sarcomeric proteins, serves as a model to investigate left ventricular hypertrophy (LVH). HCM manifests extreme variability in the degree and distribution of LVH, even in patients with the same causal mutation. Genes coding for renin—angiotensin—aldosterone system components have been studied as hypertrophy modifiers in HCM, with emphasis on the angiotensin (Ang) II type 1 receptor (AT1R). However, Ang II binding to Ang II type 2 receptors (AT2R) also has hypertrophy-modulating effects. Methods. We investigated the effect of the functional +1675 G/A polymorphism (rs1403543) and additional single nucleotide polymorphisms in the 3' untranslated region of the AT2R gene ( AGTR2) on a heritable composite hypertrophy score in an HCM family cohort in which HCM founder mutations segregate. Results. We find significant association between rs1403543 and hypertrophy, with each A allele decreasing the average wall thickness by ~0.5 mm, independent of the effects of the primary HCM causal mutation, blood pressure and other hypertrophy covariates ( p = 0.020). Conclusion. This study therefore confirms a hypertrophy-modulating effect for AT2R also in HCM and implies that +1675 G/A could potentially be used in a panel of markers that profile a genetic predisposition to LVH in HCM

Long-term follow-up of R403W MYH7 and R92W TNNT2 HCM families : mutations determine left ventricular dimensions but not wall thickness during disease progression

The original publication is available at http://www.cvja.co.za/CVJA holds the copyrightThe clinical profile and prognosis of patients with hypertrophic cardiomyopathy, a primary cardiac muscle disease caused mostly by mutations in sarcomeric protein-encoding genes, have been linked to particular disease-causing mutations in the past. However, such associations are often based on cross-sectional observations, as longitudinal studies of the progression of the disease in genotypically defined patients are sparse. Most importantly, the relative contribution of age, gender and genetic cause to disease profile and progression has not yet been reported, and the question remains whether one or more of these factors could mask the effect of the other(s). Methods: We previously described cross-sectional family studies of two hypertrophic cardiomyopathy (HCM)-causing mutations, R92WTNNT2 and R403WMYH7, both associated with minimal hypertrophy, but with widely different life expectancies. We re-investigated 22 and 26 R92WTNNT2 and R403WMYH7 mutation carriers in these and additional South African R92WTNNT2 families after a mean 11.08 ± 2.79 years, and compared the influence of the two mutations, in the context of age and gender, on disease progression. Results: We demonstrated a positive correlation between age and interventricular septal thickness for both mutations, with more than a third of all mutation carriers developing clinically recognised hypertrophy only after the age of 35 years. This period of hypertrophically silent HCM also coincided with the years in which most sudden cardiac deaths occurred, particularly in male R92WTNNT2 carriers. Statistical analyses indicated that the particular mutation was the strongest determinant of left ventricular remodelling; particularly, LVESD increased and EF reduction was noted in the majority of R403WMYH7 carriers, which may require clinical follow-up over the longer term. Conclusions: Statistical modelling of follow-up data suggests that an interplay between unidentified, possibly genderassociated factors, and the causal mutation are the determinants of eventual cardiac function and survival, but not of the extent of hypertrophy, and emphasises the need for long-term follow-up even in individuals with apparently mild disease.Publishers' Versio

Diagnostic performance of dobutamine stress echocardiography: A South African experience

Background. Dobutamine stress echocardiography (DSE) is a well-established modality for the diagnosis of coronary artery disease, but there are no reported diagnostic data in southern Africa. Objectives. To compare the safety, sensitivity and specificity of a South African (SA) DSE programme with larger, international series. Methods. All patients undergoing DSE from 2019 to 2021 at a single SA centre were included. A new wall motion abnormality (≥2 segments) signified inducible ischaemia. Results. A total of 106 patients (mean (standard deviation) age 61 (11) years, 68% male) were analysed. Six patients (6%) experienced chest pain during DSE and 4 (4%) developed an atrial arrhythmia. The sensitivity and specificity for epicardial coronary stenosis were 77% and 74%, respectively, changing to 82% and 72% when excluding those who had previous coronary artery bypass surgery. Conclusion. The sensitivity, specificity and safety of an SA DSE programme were comparable to international series. A DSE programme is feasible in a resource-constrained environment

Genetic Modifiers for the Long-QT Syndrome

Background— Long-QT syndrome is an inherited cardiac channelopathy characterized by delayed repolarization, risk of life-threatening arrhythmia, and significant clinical variability even within families. Three single-nucleotide polymorphisms (SNPs) in the 3′ untranslated region of KCNQ1 were recently suggested to be associated with suppressed gene expression and hence decreased disease severity when located on the same haplotype with a disease-causing KCNQ1 mutation. We sought to replicate this finding in a larger and a genetically more homogeneous population of KCNQ1 mutation carriers. Methods and Results— The 3 SNPs (rs2519184, rs8234, and rs10798) were genotyped in a total of 747 KCNQ1 mutation carriers with A341V, G589D, or IVS7-2A>G mutation. The SNP haplotypes were assigned based on family trees. The SNP allele frequencies and clinical severity differed between the 3 mutation groups. The different SNP haplotypes were neither associated with heart rate–corrected QT interval duration (QTc) nor cardiac events in any of the 3 mutation groups. When the mutation groups were combined, the derived SNP haplotype of rs8234 and rs10798 located on the same haplotype with the mutation was associated with a shorter QTc interval ( P <0.05) and a reduced occurrence of cardiac events ( P <0.01), consistent with the previous finding. However, when the population-specific mutation was controlled for, both associations were no longer evident. Conclusions— 3′ Untranslated region SNPs are not acting as genetic modifiers in a large group of LQT1 patients. The confounding effect of merging a genetically and clinically heterogeneous group of patients needs to be taken into account when studying disease modifiers

Genetic variation in angiotensin-converting enzyme 2 gene is associated with extent of left ventricular hypertrophy in hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy, a common, inherited cardiac muscle disease, is primarily caused by mutations in sarcomeric protein-encoding genes and is characterized by overgrowth of ventricular muscle that is highly variable in extent and location. This variability has been partially attributed to locus and allelic heterogeneity of the disease-causing gene, but other factors, including unknown genetic factors, also modulate the extent of hypertrophy that develops in response to the defective sarcomeric functioning. Components of the renin-angiotensin-aldosterone system are plausible candidate hypertrophy modifiers because of their role in controlling blood pressure and biological effects on cardiomyocyte hypertrophy