No description available.

No description available.

Global assessment of myocardial function is widely performed by estimating ejection fraction (EF), but many common cardiac diseases initially affect the myocardium on a regional, rather than global, basis. Computed tomography (CT), most commonly applied to assess the coronary arteries, is a prime candidate for such regional analysis. This doctoral thesis makes steps towards regional CT functional analysis with two clinical and two technical contributions. The first clinical contribution focuses on evaluating the feasibility and utility of functional analysis with currently available CT technology. Our study found that CT strain analysis could identify regional wall motion abnormalities in cardiomyopathy that are not otherwise detected using conventional metrics of myocardial function such as EF. In order for cine CT of the heart to become routine clinical practice, improvements need to be made to the image acquisition protocol. The second clinical contribution focus on making these improvements with results pointing to the possibility of one millisievert range cine CT images with high (>50 milliseconds) temporal resolutions. Moving to technical considerations, a key concern has been how to better characterise the myocardium in CT. To address this, the first technical contribution examines the use of feature-based attribute vectors, which were found to improve image registration towards deriving more reliable motion estimations. The second technical contribution focus on developing a pipeline tailored towards CT strain analysis. Noting that CT naturally provides information in 3D, a 3D hyperelastic biomechanical model fitting method was evaluated. Analysis of an infarction model demonstrated that regional myocardial strain can be estimated in the 3D space and areas of infarction can be detected. By considering both technical and clinical perspectives, these advances will contribute to the the field of regional cardiac functional analysis towards improving patient care.

No description available.

No description available.

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

The tenn Acute Coronary Syndrome (ACS) encompasses a spectrum of patients who present with chest discomfort or other symptoms caused by myocardial ischemia or infarction. Since critical or acute care nurses care for such patients, they should have a thorough knowledge of ACS pathophysiology and current treatments for ACS The purpose of this research study is to explore and describe the knowledge level that the critical care nurses in a state hospital in East Texas feel they have regarding ACS. This study was quantitative, descriptive and contextual in design, in which a sample survey was performed, using a questionnaire based on a literature study. The response of most ofthe critical care nurses tested was that they felt they had insufficient knowledge. An in-service training session has been proposed to help improve the nurses' knowledge and expertise on ACS. / Health Studies / M.A. (Nursing Science)

Submitted in fulfillment of the Degree of Masters in Technology: Clinical Technology, Durban University of Technology, 2011. / Background: Idiopathic dilated cardiomyopathy (IDC) is a primary myocardial disease of unknown cause characterized by left ventricular or biventricular dilatation and impaired myocardial contractility. Idiopathic dilated cardiomyopathy (IDC) is the second commonest cause of heart failure in Africa. Some patients with idiopathic dilated cardiomyopathy present with significant pulmonary hypertension (PHT) which maybe out of keeping with the usual degree of PHT seen in patients with this disorder. Methods and Material: This is a prospective and longitudinal follow-up study of 66 patients with IDC who were evaluated after satisfying the inclusion and exclusion criteria of this study. The clinical evaluation of each patient included a complete medical history, physical examination, 12 lead electrocardiogram, 2D-echocardiography, continuous wave (CW), pulsed wave (PW), and tissue Doppler imaging (TDI). Results: The mean age of all patients was 48.5 ± 12.8, with 39/66 (59.1%) patients being male. The prevalence of pulmonary arterial hypertension (PAH) was documented in 47 patients (71.2%, 95% CI: 59 - 83%). Mean left ventricular ejection fraction (LVEF) was 25.3 ± 8.8%, and mean left atrial volume index (LA volume) was 44.5±19.8 ml/m2. Mitral regurgitation (MR) occurred in 56/66 (84.8%) of patients with moderate or severe MR detected in 60.6% of all cases of IDC. The presence of a tricuspid regurgitant jet was found in 56/66 (84.9%), with (95% CI: 75 -93%). Right ventricular dilatation was found in 65/66 (98.5%), with (95% CI: 95 - 101%). ii Age, LA volume, LVEF and MR were included into a multivariate logistic regression model to predict PAH. Only MR presence was independently associated with PAH adjusted (OR 6.02, 95% CI: 1.15- 31.47) (p= 0.03). Conclusion: The study has shown that there is a significant prevalence of pulmonary arterial hypertension (PAH), right heart involvement and tricuspid regurgitant jet in IDC patients. The present study also showed that in patients with dilated cardiomyopathy, the degree of mitral regurgitation was a good predictor of PAH.

Thesis (MSc)--Stellenbosch University, 2001. / ENGLISH ABSTRACT: Introduction: It is well documented that insulin offers cardioprotection under ischaemic stress. In the past it was believed that the protective effects of insulin, such as the (a) recruitment of glucose transporters to enhance glucose entry into the cell, (b) stimulation of glycolysis, (c) enhancement of glycogen synthesis, (d) improved protein synthesis, and (e) positive inotropic and chronotropic properties, were metabolic of origin, but lately the emphasis has shifted towards the diverse signal transduction pathways elicited by insulin. Although these beneficial effects of insulin on ischaemia/reperfusion induced injury have been studied for many years, the exact protective mechanism is still not resolved. Aim: To investigate the influence of insulin on the signaling pathways as a possible protective mechanism against ischaemia/reperfusion and therefore to investigate the possible roles and cross signaling of cyclic adenosine monophosphate (cAMP), protein kinase B (PKB) and p38 mitogen activated protein kinase (p38 MAPK) in the cardioprotection offered by insulin to the reperfused, ischaemic myocardium. Materials and methods: Isolated rat hearts were perfused retrogradely in accordance with the Langendorff technique (95%02, 5% C02). After 30 min of stabilization, hearts were subjected to 30 min global low flow ischaemia (0,2 ml/min), followed by 30 min of reperfusion. Hearts perfused with standard Krebs Henseleit solution containing 5 mM glucose were compared to hearts perfused with a perfusion solution containing 5 mM glucose and 0,3 IlIU/ml insulin. Wortmannin was added during either ischaemia or reperfusion. Left ventricular developed pressure (LVDP), rate pressure product (RPP), tissue cAMP and PKB and p38 MAPK activation were measured. Results: Insulin treated hearts showed improved functional recovery (P<0.05) during reperfusion after ischaemia vs. non-insulin treated hearts (85.5±4.6% vs. 44.8±4.9%). However, the addition of wortmannin (a Pl3-kinase inhibitor) to the perfusion solution during either ischaemia or reperfusion abolished the improved recovery. At the end of ischaemia, cAMP levels of the insulin treated hearts were elevated significantly, while the cAMP content in the non-insulin treated hearts returned to control levels. Addition of wortmannin during ischaemia abolished this rise in cAMP. Wortmannin added during reperfusion only did not alter the levels of cAMP at the end of reperfusion. Activation of p38 MAPK was transient during ischaemia for both insulin and non-insulin treated hearts. Addition of wortmannin during ischaemia did not alter p38 MAPK levels at the end of ischaemia. P38 MAPK was activated significantly (P<0.001) in the non-insulin treated hearts vs. insulin treated hearts during reperfusion. Wortmannin, added at the onset of reperfusion, could partially abolish the effects of insulin to suppress p38 MAPK activation after 30 min of reperfusion. Activation of PKB in insulin treated hearts was significantly higher than non-insulin treated hearts during stabilization and early ischaemia. This activity was depressed by 30 min of ischaemia in both presence and absence of insulin. Wortmannin, when added before induction of ischaemia did not further lower this. The presence of insulin resulted in occurrence of strong PKB activation during reperfusion, peaking at 15 minutes and diminishing at 30 minutes. Wortmannin, added at the onset of reperfusion, abolished PKB activity measured at the end of reperfusion. Conclusion: Insulin exerted a positive inotropic effect and delayed the onset to ischaemic contracture. Inhibition of Pl3-kinase by wortmannin abolished the protective effects of insulin, arguing for an insulin stimulated PKB involvement in cardiac protection. Insulin also increased cAMP production and attenuated activation of p38 MAPK, both associated with improved recovery. This evidence suggested possible cross signaling between different signaling pathways. / AFRIKAANSE OPSOMMING: Agtergrond: Insulin beskerm harte wat aan isgemiese stres blootgestel word. Alhoewel hierdie voordelige effekte van insulien reeds vir verskeie jare bestudeer is, is die presiese meganisme waarmee insulien die hart beskerm steeds nie duidelik nie. Navorsers het die beskermende effekte van insulien aan metaboliese gevolge soos: (a) verhoogde glukose transport d.m.v. inspanning van meer glukose transporters (b), stimulering van glikolise, (c) vebeterde glikogeensintese, (d) verhoogde proteiensintese, en (e) die positiewe inotropiese en chronotropiese eienskappe van insulien toegeskryf. Onlangs het die fokus verskuif na ander diverse seintransduksiepaaie. Doel: Die doel van hierdie studie was dus om die moontlike betrokkenheid van hierdie sientransduksiepaaie asook die interaksie tussen sikliese adenomonofosfaat (cAMP), proteïn kinase B (PKB) en p38 MAPK in die beskerming wat insulien aan die isgemiese, gereperfuseerde miokardium bied, te bestudeer. Materiale en Metodes: Geïsoleerde rotharte is geperfuseer in ooreenstemming met die Langendorff metode. Na 30 min van stabilisasie is harte blootgestel aan 30 min. globale lae vloei isgemie (0,2 ml/min), en daarna is harte vir 30 min. geherperfuseer. Harte wat geperfuseer is met 'n perfusaat wat 5mM glukose bevat is vergelyk met harte wat geperfuseer is met 'n perfusaat wat 5mM glukose en 0,3 ~IU/ml insulien bevat. Sommige harte is geperfuseer met 'n perfusie oplossing waar wortmannin bygevoeg is tydens óf isgemie óf tydens herperfusie. Linker ventrikulêre ontwikkelde druk (LVDP), tempo-druk produk (RPP), weefsel cAMP-vlakke asook PKB en p38 MAPK aktiwiteit is gemeet. Resultate: Insulien-behandelde harte het funksioneel beduidend beter herstel tydens herperfusie na isgemie as harte wat nie met insulien behandel is nie (85.5±4.6% vs. 44.8±4.9%). Byvoeging van wortmannin by die perfusie oplossing tydens óf isgemie óf reperfusie, het die toename in herstel wat gesien is in die insulien-behandelde harte, opgehef. Die cAMP vlakke in die insulienbehandelde harte het aan die einde van isgemie beduidend gestyg (P<0.001), terwyl vlakke in harte wat nie met insulien behandel is nie, na kontrole vlakke teruggekeer het. Die teenwoordigheid van wortmannin in die perfusie oplossing tydens isgemie, het die styging in cAMP voorkom , terwyl die byvoeging van wortmannin tydens herperfusie. nie die cAMP vlakke beïnvloed het nie. Die aktivering van p38 MAPK tydens isgemie was van verbygaande aard in beide die insulien-behandelde harte en harte wat nie met insulien behandel is nie. Die byvoeging van wortmannin tydens isgemie het nie die p38 MAPK aktivering beïnvloed nie. P38 MAPK is beduidend geaktiveer tydens herperfusie in harte wat nie met insulien behandel is nie vergeleke met die insulien-behandelde harte. Die byvoeging van wortmannin tydens reperfusie kon die effek van insulien om p38 MAPK aktivering te onderdruk, gedeeltelik ophef. PKB aktivering tydens die stabilisasie fase en vroeë isgemie was beduidend hoër in die insulien-behandelde harte vs. die harte wat nie met isulien behandel is nie. Die aktiwiteit is onderdruk deur 30 min isgemie ongeag die teenwoordigheid van insulien. Die byvoeging van wortmannin tydens isgemie het PKB aktivering nie verder verlaag nie. Die teenwoordigheid van insulien het 'n sterk aktivering van PKB tydens herperfusie veroorsaak met 'n piek na 15 min en 'n verlaging na 30 min. Wortmannin bygevoeg aan die begin van herperfusie, het PKB aktiwiteit opgehef aan die einde van reperfusie. Opsomming: Insulien het 'n positiewe inotropiese invloed gehad, en het die begin van isgemiese kontraksie vertraag. Die inhibisie van Pl3-kinase deur wortmannin het die beskermende effekte van insulin opgehef, wat 'n insulin gestimuleerde PKB betrokkenheid aandui. Insulien het ook verhoogte cAMP produksie en verlaagde p38 MAPK aktivering tot gevolg gehad, en beide is geassosieer met verbeterde herstel. Hierdie resultate dui dus op moontlike interaksie tussen die verskillende seintransduksiepaaie.