Esta pesquisa de abordagem quali-quantitativa objetivou compreender o significado atribuído pelas mulheres climatéricas à doença arterial coronariana (DAC), analisando a relação que elas estabelecem na vivência com tais episódios (climatério e DAC). O referencial teórico-metodológico utilizado na análise da pesquisa foi o interacionismo simbólico, respaldado no método de análise de conteúdo. Na fase quantitativa, utilizou- se como instrumento de coleta de dados a Escala de Avaliação da Menopausa (MRS) com quarenta (40) mulheres; dessas 40 mulheres participaram da fase qualitativa, a técnica de grupos focais, vinte e cinco (25) mulheres. A pesquisa foi realizada no Ambulatório de Cardiologia do Hospital Universitário da Universidade Federal do Maranhão. A idade média das mulheres foi de 58 anos, menopausa aos 45 anos; a maioria com baixa escolaridade, exercia atividades do lar; somente uma (01) fora usuária de terapia hormonal. Os sintomas mais frequentes relatados foram: ansiedade, mal estar no coração, irritabilidade, problemas musculares e nas articulações. Os sintomas mais intensos, entretanto, foram os problemas musculares e nas articulações, ansiedade, mal estar no coração, esgotamento físico e mental. Ao referirem o significado do climatério e menopausa, as mulheres não conseguiram definir claramente o climatério, pois associavam-no ao envelhecimento e às doenças. O significado da DAC é descrito como uma manifestação grave e incurável, de caráter multifatorial, com intensos sintomas, sentimentos e emoções como taquicardia, palpitação, cansaço, dor, incapacidade, dependência, inutilidade, impotência, tristeza, humilhação e medo, os quais provocavam modificações no cotidiano de suas vidas, levando à incapacidade física para executar atividades domésticas e do trabalho, o que as definia como sendo doentes. Na perspectiva das mulheres, o climatério é um importante marcador de mudança de estado de saúde, ou seja, um período permeado de mal-estar e de forte inclinação para se considerarem como enfermas (enfermidade). No entanto, somente a partir do diagnóstico da DAC, elas assumem o papel de doente / The purpose of this qualitative and quantitative research is to understand the meaning assigned by menopausal women with coronary artery disease (CAD) and analyze the relation that they establish in their experiences with such episodes (climacteric and CAD). The theoretical and methodological framework used in the analysis of the survey was the symbolic interactionism supported by the content analysis method. Quantitative phase was used as an instrument for data collection Menopause Rating Scale (MRS) to forty (40) women; of these 40 women participated in the qualitative phase, the focus groups technique, with twenty five (25) women. The research was conducted at the Cardiologic Clinic at the University Hospital of the Federal University of Maranhão. The average age of the patients was 58 years old, menopause at age 45, most with low education, used to do the household chores, of which only one was a user of hormone therapy. The most frequent reported symptoms were anxiety, malaise at heart, irritability, muscle and joint problems. However, the most intense symptoms found were muscle and joint problems, anxiety, malaise at heart, physical and mental exhaustion. When referring to climacteric and menopause, women could not clearly define the climacteric; associating these symptoms to aging and diseases. The significance of CAD is described as an incurable and severe manifestation, multifactorial with intense symptoms, feelings and emotions such as tachycardia, palpitations, fatigue, pain, disability, dependence, helplessness, powerlessness, sadness, humiliation and fear, which causes changes in their daily lives, leading to physical inability to work and to do the household chores, defining them as sick people. From the women perspective, menopause is an important change marker in health status, in other words, a permeate period of malaise and steeply sloping to consider themselves sick (illness), however, is based on the diagnosis of CAD that they assume the diseased condition

Lan Wei. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 260-301). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Photocopy. Ann Arbor, Mich. : UMI Dissertation Services, 2002. xx, 301 p. : ill. ; 22 cm. / Abstracts in English and Chinese.

Wan Din. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 155-175). / ABSTRACT --- p.1 / ACKNOWLEDGMENTS --- p.3 / LIST OF TABLES --- p.5 / LIST OF FIGURES --- p.7 / LIST OF ABBREVIATIONS --- p.8 / Chapter I. --- INTRODUCTION --- p.9 / Chapter I.A. --- Menopause --- p.9 / Chapter I.A.1. --- Definition of the Menopause --- p.9 / Chapter I.A.2. --- Pathophysiology of Ovarian Failure --- p.10 / Chapter I.B. --- Effects of the Menopause --- p.13 / Chapter I B.1. --- Acute Effects --- p.13 / Chapter I.B.2. --- Medium Term Effects --- p.14 / Chapter I.B.3. --- Chronic Effects --- p.15 / Chapter I.B.3.a. --- Osteoporosis --- p.15 / Chapter I.B.3.b. --- Coronary Artery Disease (CAD) --- p.17 / Chapter I.C. --- Management of the Menopause --- p.19 / Chapter I.C.1. --- Hormone Replacement Therapy --- p.21 / Chapter I.C.2. --- Oestrogens --- p.22 / Chapter I.C.2.a. --- Oral Oestrogens --- p.22 / Chapter I.C.3. --- Progestogens --- p.24 / Chapter I.C.3.a. --- Combined Oestrogen and Progestogen Therapy --- p.24 / Chapter I.C.4. --- Complications and Contraindications to Hormone Replacement Therapy --- p.26 / Chapter II. --- LITERATURE REVIEW --- p.34 / Chapter II.A. --- Atherosclerosis --- p.35 / Chapter II.B. --- Risk Factors for Coronary Artery Disease --- p.37 / Chapter II.B.1. --- Age and Sex --- p.38 / Chapter II.B.2. --- Age at Menopause --- p.38 / Chapter II.B.3. --- Family History --- p.38 / Chapter II.B.4. --- Serum Lipids --- p.39 / Chapter II.B.5. --- Blood Pressure --- p.39 / Chapter II.B.6. --- Smoking --- p.40 / Chapter II.B.7. --- Diabetes Mellitus --- p.40 / Chapter II.C. --- The Effect of the Menopause on Risk Factors for Coronary Heart Disease --- p.41 / Chapter II.C.1. --- The Effect of the Menopause on Lipids and Lipoproteins --- p.41 / Chapter II.C.2. --- The Effect of the Menopause on Glucose and Insulin Metabolism --- p.43 / Chapter II.C.3. --- The Effect of the Menopause on Coagulation --- p.44 / Chapter II.C.4. --- The Effect of the Menopause on the Arterial Wall --- p.45 / Chapter II.D. --- The Risk of Coronary Artery Disease After the Menopause --- p.46 / Chapter II.D.1. --- The Effect of the Menopause on Peripheral Vascular Disease (PVD) --- p.47 / Chapter II.E. --- The Effect of the Hormone Replacement Therapy on Coronary Artery Disease Risk --- p.49 / Chapter II.F. --- The Mechanism of Cardioprotection of Oestrogen --- p.63 / Chapter II.F.1. --- The Indirect Effect of the Hormone Replacement Therapy on the Cardiovascular System --- p.64 / Chapter II.F.1.a. --- The Effect on Lipids and Lipoproteins --- p.64 / Chapter II.F.1.b. --- The Effect on Coagulation and Fibrinolysis --- p.66 / Chapter II.F.1.c. --- The Effect on Insulin and Glucose Metabolism --- p.67 / Chapter II.F.2. --- The Direct Effects of the Hormone Replacement Therapy on the Cardiovascular System --- p.67 / Chapter II.F.2.a. --- The Effect of Oestrogen on Vascular Contractility --- p.68 / Chapter II.F.2.b. --- The Effect of Oestrogen on Endothelial Dysfunction --- p.69 / Chapter II.F.2.C. --- Other Possible Direct Actions of Oestrogen --- p.72 / Chapter II.G. --- The Effects of Oestrogen on Blood Flow --- p.73 / Chapter III. --- RESEARCH PLAN --- p.78 / Chapter III.A. --- Formation of Research Hypothesis --- p.78 / Chapter III B. --- Research Hypothesis --- p.80 / Chapter III.C. --- Plan of Studies --- p.81 / Chapter III.C.1. --- Pilot Study --- p.81 / Chapter III.C.2. --- Randomized Controlled Study --- p.81 / Chapter IV. --- METHODOLOGY --- p.84 / Chapter IV.A. --- Pilot Study --- p.84 / Chapter IV.B. --- Study Population --- p.87 / Chapter IV.B.1. --- Recruitment of Cases --- p.88 / Chapter IV.B.1.a. --- Patients' Consent --- p.88 / Chapter IV.B.1.b. --- Method of Recruitment --- p.88 / Chapter IV.B.1.e. --- Research Methodology --- p.89 / Chapter IV.C. --- Ethical Considerations --- p.90 / Chapter IV.D. --- Samples Size Calculation --- p.92 / Chapter IV.E. --- Statistical Analysis --- p.93 / Chapter IV.F. --- Physical Principles of the Measurement of Peripheral Resistance --- p.94 / Chapter IV.F.1. --- The Arterial Analogue Waveform --- p.97 / Chapter IV.F.2. --- Peak Systolic Velocity --- p.98 / Chapter IV.G. --- Measurement of Pulsatility Index --- p.100 / Chapter IV.G.1. --- Establishment of Methodologies Used to Measure Peripheral Blood Flow --- p.105 / Chapter IV.G.2. --- Training of the Investigator --- p.107 / Chapter IV.H. --- Assay for Serum Oestradiol --- p.108 / Chapter IV.H.1. --- Principles --- p.108 / Chapter IV.H.2. --- Reagents --- p.109 / Chapter IV.H.3. --- Sample Dilution --- p.111 / Chapter IV.H.4. --- Calibration --- p.112 / Chapter IV.H.5. --- Quality Control --- p.112 / Chapter IV.H.6. --- Assay Validation --- p.113 / Chapter V. --- RESULTS --- p.115 / Chapter V.A. --- Pilot Study --- p.115 / Chapter V.B. --- Study Population --- p.118 / Chapter V.B.1. --- Characteristics of the Patients at Recruitment --- p.120 / Chapter V.B.2. --- Doppler Measurements --- p.123 / Chapter V.B.3. --- Pulsatility Index and Serum Oestradiol --- p.135 / Chapter VI. --- DISCUSSION --- p.137 / Chapter VI.A. --- Overview --- p.132 / Chapter VI.A.1. --- The Pilot Study --- p.133 / Chapter VI.B. --- Study Population --- p.136 / Chapter VI.C. --- Doppler Ultrasound as a Measurement of Vascular Resistance and Blood Flow --- p.142 / Chapter VI.C.1. --- Reliability of Doppler Study --- p.143 / Chapter VI.D. --- Pulsatility Index and Hormone Replacement Therapy --- p.146 / Chapter VI.E. --- Effects of Oestrogen on Pulsatility Index --- p.150 / Chapter VI.F. --- Conclusions --- p.152 / Chapter VI.G. --- Future Directions --- p.153 / REFERENCES --- p.155 / APPENDIX1 --- p.176

INTRODUÇÃO: Uma alta prevalência de apnéia obstrutiva do sono (AOS) tem sido relatada em paciente com doença arterial coronária (DAC). Vários mecanismos relacionados à AOS, incluindo dessaturação da oxi-hemoglobina e aumento da demanda de oxigênio, aumento da atividade simpática bem como estado pro trombótico, podem ser perigosos nos pacientes com DAC. Entretanto, a AOS é pouco reconhecida e não é rotineiramente pesquisada nos pacientes admitidos em unidade de cuidados coronários (UCC) com DAC. O padrão ouro para o diagnóstico de AOS é a polissonografia noturna (PSG), método impraticável na UCC, pois implica no deslocamento do paciente para o laboratório de sono. OBJETIVOS: Construir e validar um monitor de oximetria para diagnóstico de AOS em pacientes admitidos na UCC com diagnóstico de DAC aguda. MÉTODOS: Foi inicialmente desenvolvido monitor de oximetria continua que registra os dados derivados dos monitores da UCC e permite a determinação do índice de dessaturação da oxi-hemoglobina (IDO) através de análise visual da curva de oximetria. O monitor foi então utilizado em pacientes consecutivos admitidos na UCC com diagnóstico de DAC aguda. Uma amostra desta população foi também estudada através de PSG, num período máximo de três meses após a alta. RESULTADOS: Trinta e sete pacientes foram estudados através de monitorização de oximetria durante a noite na UCC. PSG foi também realizada em vinte pacientes. AOS, diagnosticada pelo monitor de oximetria contínua (IDO > 5/hora), estava presente em 43% dos pacientes. AOS foi diagnosticada em 45% dos pacientes estudados com PSG (índice de apnéia e hipopnéia > 15 eventos por hora). Houve um bom nível de concordância entre o diagnóstico de AOS pelo monitor de oximetria na UCC e pela polissonografia - kappa = 0.898; p < 0.0001. O IDO determinado pelo monitor se correlacionou de forma significativa com o índice de apnéia e hipopnéia (r = 0.737; p < 0.0001). O diagnóstico de AOS através do monitor demonstrou sensibilidade de 88,9% e especificidade de 100%. CONCLUSÃO: O monitor desenvolvido no presente trabalho, que permite o registro da oximetria contínua a partir de dados que já são habitualmente coletados na UCC, é um método simples e preciso para o diagnóstico de AOS na UCC. / BACKGROND: A high prevalence of Obstructive sleep apnea (OSA) has been reported in patients with coronary artery disease (CAD). Several OSA related mechanisms, such as oxygen desaturation, high sympathetic activity, increased cardiac oxygen demand and a prothrombotic state, may be particularly dangerous in acute CAD patients. Nevertheless, OSA is frequently underdiagnosed and patients with CAD are not routinely screened for OSA when admitted to the Coronary Care Unit (CCU). OBJECTIVES: To build and validate a continuous overnight oximetry, by recording oximetry data derived from the CCU monitor, for the detection of OSA in acute CAD patients. DESIGN: We studied consecutive patients recruited on the basis of the presence of acute CAD requiring CCU, analyzed overnight continuous oximetry data and further compared it with full overnight polysomnography (PSG). RESULTS: Thirty-seven patients underwent overnight oxygen saturation monitoring in the CCU and 20 of these patients were submitted to PSG, performed within 3 months after hospital discharge. OSA was present in 43% and 45% of the patients studied by overnight oxygen saturation monitoring and PSG, respectively. The oxymetry derived oxygen desaturation index and the PSG derived apnea hypopnea index were strongly correlated (r = 0,737; p < 0,0001). There was a good level of agreement between abnormal oxymetric results and abnormal PSG results (kappa = 0.898; p < 0,0001). Overnight oximetry had a sensitivity of 88.9% and a specificity of 100% for OSA diagnosis. CONCLUSIONS: Continuous overnight oximetry derived from monitors that are already present in the CCU is a simple and accurate method for the diagnosis of OSA in the CCU.

In this thesis sleep, psychological symptoms and quality of life (Qol) in patients undergoing coronary artery bypass grafting (CABG) at the University Hospital in Linköping were evaluated. Interviews and 24-hour polysomnography were performed prior to surgery, immediately after surgery and again at one month, with a six-month-follow-up mailed questionnaire. Habitual sleep was evaluated using the Uppsala Sleep Inventory questionnaire and a diary the recorded mornings. The Spielberger State of Anxiety Scale and the Zung's Self-rating Depression Scale were used to measure anxiety and depression, respectively. Physical functional capacity was assessed according to the New York Heart Association's (NYHA) classes and Qol, with the Nottingham Health Profile instrument (NHP). A retrospective evaluation of nurse's documentation about sleep was also performed. In addition, the quality and quantity of sleep were assessed before surgery and in the immediate postoperative period in a pilot study, with a one-month follow-up interview. The results indicated disturbed sleep, and changes in behaviour and mental state after surgery due to fragmented sleep, pain and anxiety. Forty-four patients were examined prior to surgery. The results showed that almost two-fifths experienced too little sleep habitually and 50 % had a combination of at least two sleep problems. Poorer health, higher level of anxiety and increased difficulties maintaining sleep (DMS) were consistent with significantly longer sleep latency, increased fragmented sleep, and reduced stages 3 and 4 and RIM sleep measured by polysomnography. The level of Qol on the NBP was significantly associated with objectively measured sleep. In the immediate period following CABG there is a changed distribution of sleep, with a reduction of nocturnal sleep duration and an increase in daytime sleep, which had almost returned to preoperative values one month after surgery. Qol was significantly improved six months after surgery compared to before surgery. It was noted that patients with a more anxiety prone reactivity during six months following CABG had significantly more sleep disturbances, reduced energy and functional physical capacity, and lower quality of life, compared to those without such reactivity. Significantly more sleep disturbances, reduced energy and lower quality of life were more prominent among those with sadness/depression or cognitive/behavioural fatigue as reactions to sleep loss. A higher degree of cognitive/behavioural fatigue and dysphoria reactions were associated with a higher NYHA class. In conclusion, patients with coronary artery disease have poor quantity and quality of sleep. Increased psychological symptoms in patients with CAD prior to surgery were associated with greater symptoms six months after surgery. Physical functional capacity and quality of life were significantly improved six months after surgery. / 1999

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / "August 2000." Typescript. Vita. Includes bibliographical references (leaves 186-210). Also available on the Internet.

Source: Masters Abstracts International, Volume: 47-06, page: 3373. Advisers: Kelly Volcik; Sarah Baraniuk. Includes bibliographical references.

No description available.

Εισαγωγή: Τα επίπεδα της ενδοθηλίνης-1 (ΕΤ-1) στο περιφερικό πλάσμα αυξάνονται μετά από αγγειοπλαστική των στεφανιαίων αρτηριών με μπαλόνι (PTCA) λόγω μηχανικής βλάβης του ενδοθηλίου των στεφανιαίων αρτηριών κατά την επέμβαση. Η ΕΤ-1 έχει ανεβρεθεί σε ανθρώπινα ενδοκαρδιακά και μυοκαρδιακά κύτταρα. Δεν είναι γνωστό αν η ΕΤ-1 αυξάνεται μετά από θερμική βλάβη του μυοκαρδίου κατά τη διενέργεια κατάλυσης αρρυθμιών με ρεύμα ραδιοσυχνότητας. Μέθοδοι: Προσδιορίσαμε τα επίπεδα ΕΤ-1 στο περιφερικό πλάσμα πριν την εκτέλεση, αμέσως μετά και στις 2 και 6 ώρες μετά από PTCA (31 ασθενείς), και κατάλυση με ρεύμα ραδιοσυχνότητας (16 ασθενείς). Δεκαπέντε ασθενείς που υποβλήθηκαν σε διαγνωστικό καθετηριασμό και 13 ασθενείς που υποβλήθηκαν σε διαγνωστική ηλεκτροφυσιολογική μελέτη χρησιμοποιήθηκαν ως μάρτυρες. Αποτελέσματα: Τα επίπεδα ΕΤ-1 στο περιφερικό πλάσμα αυξήθηκαν σημαντικά αμέσως μετά την PTCA σε σχέση με τα επίπεδα πριν την επέμβαση (55.1±20.1 vs. 42.7±14.9 pg/ml, p<0.01) και στις 2 ώρες μετά την κατάλυση με ρεύμα ραδιοσυχνότητας σε σχέση με εκείνα πριν την επέμβαση (98.0±11.7 vs. 53.0±17.4 pg/ml, p<0.01). Στις 2 ώρες μετά την PTCA και στις 6 ώρες μετά την κατάλυση με ρεύμα ραδιοσυχνότητας τα επίπεδα ΕΤ-1 πλάσματος δεν διέφεραν στατιστικά από τα επίπεδα πριν την επέμβαση. Στις ομάδες ελέγχου (στεφανιογραφία και ηλεκτροφυσιολογική μελέτη) δεν παρατηρήθηκε αύξηση της ΕΤ-1. Η καμπύλη κινητικής της ΕΤ-1 κατέδειξε πολύ υψηλότερες τιμές ΕΤ-1 στους ασθενείς που υποβλήθηκαν σε κατάλυση με ρεύμα ραδιοσυχνότητας σε σχέση με αυτούς που υποβλήθηκαν σε PTCA (p<0.001). Τα επίπεδα ΕΤ-1 αμέσως μετά την PTCA συσχετίζονταν με το ολικό γινόμενο πίεσης-χρόνου διαστολής του μπαλονιού κατά την αγγειοπλαστική (r=0.56, p<0.01). Δεν υπήρχε συσχέτιση των επιπέδων ΕΤ-1 και του αριθμού των βλαβών που προκλήθηκαν κατά τη διενέργεια κατάλυσης με ρεύμα ραδιοσυχνότητας. Κανένας ασθενής στην ομάδα της PTCA δεν εμφάνισε οξεία ισχαιμία ή άλλη σοβαρή επιπλοκή μετά την επέμβαση. Κανένας ασθενής στην ομάδα της κατάλυσης με ρεύμα ραδιοσυχνότητας δεν εμφάνισε αρρυθμία ή άλλες ανεπιθύμητες επιπλοκές μετά την επέμβαση. Συμπεράσματα: Εκτός από τη μηχανική πίεση του ενδοθηλίου κατά τη διενέργεια PTCA, η βλάβη του ενδομυοκαρδίου από τη θερμική ενέργεια που χρησιμοποιείται κατά την κατάλυση με ρεύμα ραδιοσυχνότητας αντιπροσωπεύει άλλον έναν μηχανισμό αύξησης της ενδογενούς παραγωγής ενδοθηλίνης. Η πιθανή προέλευση αυτής της ΕΤ-1 είναι τα κύτταρα του ενδοκαρδίου ή/και μυοκαρδίου. Η αύξηση της ΕΤ-1 μετά την κατάλυση με ρεύμα ραδιοσυχνότητας είναι μεγαλύτερη και πιο καθυστερημένη σε σχέση με την αύξηση της ΕΤ-1 που παρατηρείται μετά PTCA. Παρόλαυτά δεν συνοδεύεται από ανεπιθύμητες κλινικές δράσεις στην άμεση περίοδο μετά την επέμβαση. / Background: Plasma levels of Endothelin-1 (ET-1) increase after coronary angioplasty (PTCA) due to endothelial injury during the procedure. ET-1 has been found in human endocardial and myocardial cells. It is not known whether ET-1 increases after thermal injury induced by radiofrequency ablation (RFA) lesions. Methods: We determined peripheral vein plasma ET-1 levels at baseline, immediately after, and at 2 and 6 hours post-procedure in 31 patients undergoing PTCA and 16 patients undergoing RFA. Patients subjected to diagnostic coronary angiography (n=15) and electrophysiologic study (n=13) served as controls. Results: ET-1 levels increased significantly from baseline immediately post-PTCA (55.1±20.1 vs. 42.7±14.9 pg/ml, p<0.01) and at 2 hours post-RFA (98.0±11.7 vs. 53.0±17.4 pg/ml, p<0.01) and returned to baseline at 2 hours post-PTCA and 6 hours post-RFA. There was no change in the control groups. ET-1 kinetics curve was significantly higher post-RFA compared to post-PTCA (p<0.001). ET-1 immediately post-PTCA correlated with total pressure-time product applied during the procedure (r=0.56, p<0.01). There was no correlation of ET-1 levels and the number of RFA applications. No patient developed ischemia post-PTCA. There were no complications or arrhythmia recurrence post-RFA. Conclusions: Endocardial thermal injury during RFA is another mechanism of endothelin increase apart from mechanical injury of the coronary endothelium during PTCA and represents further evidence for the existence of the peptide in the human endomyocardial cells. ET-1 increase is delayed and more pronounced post-RFA compared to post-PTCA. Despite that, it does not seem to have any clinical impact in the immediate post-RFA period.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 4 uppsatser.