Thesis (Ph.D.). / Written for the Dept. of Epidemiology and Biostatistics. Title from title page of PDF (viewed 2008/05/08). Includes bibliographical references.

Thesis (doctoral)--Rijksuniversiteit te Utrecht, 1981. / English, summary and foreword in Dutch. Includes bibliographies.

Lau Siu Wai Maggie. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 236-245). / List of Figures --- p.i / List of Tables --- p.viii / List of Abbreviations --- p.x / Abstract --- p.xii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Postulated Pathophysiology of Essential Hypertension --- p.1 / Chapter 1.2 --- Measurement of Cardiac Output (CO) by Transthoracic Electrical Bioimpedance (TEB) and Other Methodologies --- p.6 / Chapter 1.3 --- Measurement of Blood Pressure --- p.10 / Chapter 1.4 --- Use of Antihypertensive Agents in Essential Hypertension --- p.12 / Chapter Chapter 2. --- The Method of Transthoracic Electrical Bioimpedance --- p.15 / Chapter 2.1 --- Introduction --- p.15 / Chapter 2.2 --- Development of Theory --- p.18 / Chapter 2.3 --- Measurements of Haemodynamic Parameters --- p.24 / Chapter 2.4 --- Literature Review - Validity of the Technique --- p.30 / Chapter Chapter 3 --- A Study on Reproducibility of Thoracic Electrical Bioimpedance in Healthy Subjects --- p.39 / Chapter 3.1 --- Objectives --- p.39 / Chapter 3.2 --- Methodology --- p.39 / Chapter 3.2.1 --- Subjects --- p.39 / Chapter 3.2.2 --- Study design --- p.41 / Chapter 3.2.3 --- Non-invasive haemodynamic monitoring --- p.41 / Chapter 3.2.4 --- Blood Pressure Measurement --- p.43 / Chapter 3.2.5 --- Isometric Exercise --- p.43 / Chapter 3.2.6 --- Data analysis --- p.44 / Chapter 3.2.7 --- Statistical analysis --- p.46 / Chapter 3.3 --- Results --- p.50 / Chapter 3.3.1 --- Systolic blood pressure --- p.50 / Chapter 3.3.2 --- Diastolic blood pressure --- p.52 / Chapter 3.3.3 --- Mean arterial pressure --- p.54 / Chapter 3.3.4 --- Heart rate --- p.55 / Chapter 3.3.5 --- Thoracic fluid index --- p.58 / Chapter 3.3.6 --- Stroke index --- p.60 / Chapter 3.3.7 --- Cardiac index --- p.62 / Chapter 3.3.8 --- Systemic vascular resistance index --- p.65 / Chapter 3.4 --- Discussion --- p.70 / Chapter Chapter 4 --- Literature Review --- p.73 / Chapter 4.1 --- Atenolol: Beta-adrenoceptor antagonists with β1-selectivity --- p.73 / Chapter 4.2 --- Pindolol: Beta-adrenoceptor antagonists with ISA --- p.78 / Chapter 4.3 --- Alpha1-adrenoceptor antagonists --- p.81 / Chapter 4.4 --- Angiotensin Converting Enzyme Inhibitors --- p.84 / Chapter 4.5 --- Calcium Channel Blockers --- p.87 / Chapter 4.6 --- Central Alpha Agonist --- p.91 / Chapter 4.7 --- Thiazide Diuretics --- p.94 / Chapter Chapter 5 --- The Integrated Hypertension Study --- p.97 / Chapter 5.1 --- Objectives --- p.97 / Chapter 5.2 --- Methodology --- p.97 / Chapter 5.2.1 --- Subjects --- p.97 / Chapter 5.2.2 --- Study design --- p.109 / Chapter 5.2.3 --- Non-invasive haemodynamic monitoring --- p.110 / Chapter 5.2 4 --- Blood Pressure Measurement --- p.111 / Chapter 5.2.5 --- Isometric Exercise --- p.111 / Chapter 5.2.6 --- Data analysis --- p.111 / Chapter 5.2.7 --- Statistical analysis --- p.112 / Chapter 5.2.8 --- Limitations of the study --- p.113 / Chapter 5.3 --- Results --- p.117 / Chapter 5.3.1 --- Atenolol --- p.117 / Chapter 5.3.2 --- Pindolol --- p.125 / Chapter 5.3.3 --- Doxazosin --- p.132 / Chapter 5.3.4 --- Enalapril --- p.138 / Chapter 5.3.5 --- Nifedipine Retard --- p.145 / Chapter 5.3.6 --- Methyldopa --- p.152 / Chapter 5.3.7 --- Cyclopenthiazide --- p.160 / Chapter 5.4 --- Comparisons of the anti-hypertensive drugs studied --- p.167 / Chapter 5.4.1 --- Baseline values --- p.167 / Chapter 5.4.2 --- Percentage changes after active treatment --- p.170 / Chapter 5.5 --- Discussion --- p.196 / Chapter 5.5.1 --- Atenolol --- p.196 / Chapter 5.5.2 --- Pindolol --- p.199 / Chapter 5.5.3 --- Doxazosin --- p.200 / Chapter 5.5.4 --- Enalapril --- p.202 / Chapter 5.5.5 --- Nifedipine Retard --- p.203 / Chapter 5.5.6 --- Methyldopa --- p.204 / Chapter 5.5.7 --- Cyclopenthiazide --- p.205 / Chapter 5.5.8 --- Comparison of the anti-hypertensive drugs studied --- p.206 / Chapter Chapter 6 --- Acute haemodynamic effects of Atenolol and Pindolol --- p.208 / Chapter 6.1 --- Objectives --- p.208 / Chapter 6.2 --- Methodology --- p.208 / Chapter 6.2.1 --- Subjects --- p.208 / Chapter 6.2.2 --- Study Design --- p.209 / Chapter 6.2.3 --- Statistical analysis --- p.209 / Chapter 6.3 --- Results --- p.211 / Chapter 6.3.1 --- Acute haemodynamic changes of atenolol --- p.211 / Chapter 6.3.2 --- Acute and short-term haemodynamic changes of atenolol --- p.219 / Chapter 6.3.3 --- Acute haemodymmic changes of pindolol --- p.221 / Chapter 6.3.4 --- Acute and short-term haemodymmic changes of pindolol --- p.222 / Chapter 6.3.5 --- Comparison of the acute haemodymmic effects of atenolol and pindolol --- p.226 / Chapter 6.4 --- Discussion --- p.230 / Chapter Chapter 7 --- Conclusion --- p.232 / References --- p.236 / Acknowledgements

Thesis (Ph. D.)--University of Washington, 1999. / Vita. Includes bibliographical references (leaves 52-56).

Introduction: High-stress situations, such as military deployments, may be a risk factor for hypertension. The relationship between the stress triggered by combat deployment and hypertension is unknown. Acute stress from combat conditions can cause a temporary rise in blood pressure, which decreases within hours or days. Cross-sectional studies have shown no association between hypertension and deployment to the 1991 Gulf War or to Vietnam. Self-reported hypertension often is used as an outcome in large population studies. Fair to substantial agreement has been observed between self-reported hypertension and various sources of administrative data, medical records, and blood pressure measurements. The goal of this dissertation was to determine whether recent deployment to Iraq and Afghanistan was associated with new-onset hypertension.Methods: Baseline Millennium Cohort Study questionnaires (July 2001 to June 2003) were completed by 77,047 individuals. Follow-up questionnaires (June 2004 to February 2006) were completed by 55,021 responders. The relationship between new-onset hypertension and history of a recent military deployment was assessed through multivariable logistic regression (N=37,075). Baseline data were analyzed cross-sectionally to assess factors associated with prevalent hypertension (N=70,100). Kappa statistics were used to compare self-reported hypertension with provider diagnosed hypertension and prescription antihypertensive medication dispensed (N=41,129).Results: The 3-year incidence of hypertension was 6.9%. After adjusting for demographic and lifestyle characteristics, deployers without combat exposure were less likely to develop new-onset hypertension compared to nondeployers (odds ratio [OR]=0.74; 95% confidence interval [CI]: 0.64, 0.85). There was no association between deployment with combat exposure and hypertension compared to nondeployers (OR=0.94; 95% CI: 0.82, 1.07). Among deployers reporting combat exposures, the risk for incident hypertension was 1.31 (95% CI: 1.07, 1.61) compared to deployers not reporting combat exposures. The prevalence of self-reported hypertension at baseline among Cohort members was 10.4%. There was moderate agreement between self-reported hypertension and provider-diagnosed hypertension, as well as antihypertensive medications dispensed.Conclusion: Military service members are adversely affected by hypertension. Although deployers had lower incidence of hypertension compared to nondeployers, individuals reporting combat exposures were more likely to report new-onset hypertension. Self-reported hypertension had moderate reliability compared with provider-diagnosed hypertension and dispensed antihypertensive medication.

Title: Analysis of pharmacotherapy and drug related problems in patients with arterial hypertension in Greece Student: Zisis Papadopoulos Tutor: Jiri Vlcek Department of Social and Clinical Pharmacy, Charles University in Prague, Faculty of Pharmacy in Hradec Kralove Background: Arterial hypertension or high blood pressure is a chronic medical condition which is characterized by elevated blood pressure in the arteries and is an important risk factor for future development of cardiovascular disease. Also belongs to asymptomatic diseases because it usually does not cause symptoms for years until a vital organ is damaged. Moreover is a major cause of morbidity and mortality, due to its association with some other serious diseases like coronary heart disease, cerebrovascular disease, atherosclerosis, renal disease, dyslipidemia, diabetes, obesity and metabolic syndrome. Arterial hypertension for adults, who don't suffer from any other kind of diseases, is defined by an elevation of blood pressure to 140 / 90 mm Hg or to higher values. Aim: In the theoretical part the main aim is to analyze information regarding etiopathogenesis, diagnostic methods and treatment strategies of arterial hypertension, as well as classification and causes of drug-related-problems to antihypertensive agents. In the...

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2002. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 4 uppsatser.

Made available in DSpace on 2014-06-11T19:28:02Z (GMT). No. of bitstreams: 0 Previous issue date: 2004-02-16Bitstream added on 2014-06-13T19:15:55Z : No. of bitstreams: 1 correa_fob_me_arafo.pdf: 2398179 bytes, checksum: 762e3a720233fd398699c82e570416b6 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / O diltiazem é um bloqueador dos canais de cálcio indicado para o tratamento da hipertensão e diversos tipos de angina. Esse medicamento pode provocar aumento gengival, embora apresente baixa prevalência. O objetivo deste trabalho foi avaliar a influência da dosagem e do período de administração do diltiazem na indução ou não de aumento gengival em ratos. Quarenta ratos machos jovens foram distribuídos aleatoriamente em oito grupos de acordo com a dosagem e o período de aplicação. Os animais receberam 0 (controle), 5, 20 e 50 mg/kg de peso corporal/dia do diltiazem e foram sacrificados após 20 e 40 dias. Posteriormente, foram realizadas análises macroscópica, histológica e histométrica do tecido gengival. Macro e microscopicamente o tecido gengival de todos os animais dos grupos controle e experimentais apresentou características de normalidade. A análise histométrica da gengiva livre vestibular do primeiro molar inferior demonstrou que não houve influência da dosagem para cada período de aplicação, sendo que somente o grupo de 20 mg/kg mantido 40 dias apresentou uma redução significativa de área de tecido epitelial (teste de Kruskall-Wallis, p=0,010) em relação ao grupo controle/40 dias. Ao analisar a influência do período, por meio do teste de Mann-Whitney, foi verificado que somente o grupo de 20mg/kg apresentou redução significativa tanto de área de tecido conjuntivo (p=0,0367) quanto de tecido epitelial (p=0,0122) comparando-se o período de 20 e 40 dias. Os autores concluíram que o diltiazem não induziu aumento gengival em ratos. Estudos posteriores são necessários para avaliar a influência da dosagem de 20 mg/kg e de dosagens superiores às empregadas neste estudo. / Diltiazem is a calcium channel blocker for treatment of hypertension and various types of angina. It may also, however, provoke gingival overgrowth although this is not frequent. This study evaluated the influence of dosage and duration of diltiazem administration on inducing gingival overgrowth in rats. Forty young male rats were separated into eight groups according to the dosage and duration of administration. The animals received 0 (control), 5, 20 or 50 mg of diltiazem daily per kilogram of bodyweight. They were sacrificed after 20 or 40 day periods for macroscopic, histologic and histometric analysis of the gingiva. Macro and microscopic characteristics of the gingival tissue of all animals studied were found to be normal. Histometric analyses of the free buccal gingiva of the first lower molars showed that regarding the dosage for each period only the group of 20 mg/kg administered for 40 days presented a significant reduction in the area of the epithelial tissue in relation to the control group (p=0,010). Analyses of the time periods indicated that only the 20mg/kg group presented a significant reduction in both the connective (p=0.0367) and epithelial tissues (p=0.0122) when the 20 and 40 day durations were compared. The authors concluded that diltiazem did not induce gingival overgrowth in rats or influence their weight gain. Studies are now necessary to evaluate the influence of the 20 mg/kg and of the larger dosages administered in this study.

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