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Ischemická choroba srdeční (ICHS) je nejčastější příčinou předčasné invalidizace a úmrtí ve většině civilizovaných zemí. V celosvětovém měřítku závažnost tohoto onemocnění stoupá. Ve vyspělých zemí je incidence ICHS 5-10 nových případů na 1000 obyvatel za 1 rok.¹ V České republice je každý druhý muž a každá třetí žena ve věku nad 40 let ohrožena ICHS. V roce 2001 bylo onemocnění srdce a cév příčinou 53% všech úmrtí a 51% všech hospitalizací.²
The aim of this study was to examine the internal thoracic artery (ITA) in human foetuses. The research material consisted of 32 human foetuses (18 female, 14 male) from the 21st to 24th week of intrauterine life. After intravascular injection with white latex LBS 3060, the foetuses were fixed in 10% neutral formalin solution. The whole course of the ITA was prepared. Photographic documentation was performed with a Nikon Coolpix 4500 digital camera, and source pictures of arteries were rendered in a Digital Computer System Analysis. The ITA was evaluated with regard to its origin, length, distance from the edge of the sternum to two intercostal spaces (2nd, 5th) and division into terminal branches. The right ITA (RITA) arose from the ascending (68.7%), arcuate (21.9%) and descending (3.2%) parts of the subclavian artery. In other cases (6.2%) it was a branch of the thyrocervical trunk. The left ITA (LITA) was a branch of the ascending (78.1%) and arcuate (21.9%) parts of the subclavian artery. The ITA was longer in male foetuses. Regardless of sex, the LITA was longer than the RITA. Coefficient correlation between the RITA and LITA was 0.92 (p < 0.001). The distance of the ITA from the edge of sternum in the 2nd and 5th intercostal spaces on both sides was greater in females. It appeared most frequently in the 6th space (43.7% right-sided and 56.3% left-sided). Typical bifurcation of the ITA into the superior epigastric artery and the musculophrenic artery was observed in 78.1% of cases on the right side and in 81.25% of cases on the left side.
Background. Shift work may affect the occurrence and severity of hypertension, ischemic heart disease and dyslipidemia. The aim of the study was to assess the prevalence of ischemic heart disease, hypertension and dyslipidemia in shift workers. Material and methods. The study was carried out in the Bogdanka mine in Łęczna, Poland. The questionnaire, which was designed by the author of this work, was conducted among 700 shift workers who worked underground in the mine. Statistical analysis was performed using STATISTICA v. 7.1 (StatSoft, Poland) software. Results. Participants who believed that shift work may lead to deterioration of their health also believed that it may affect the occurrence of ischemic heart disease and hypertension. Almost one in four respondents had blood pressure values of > 139/89 mmHg. Almost one in ten respondents was receiving treatment for hypertension. A small number of respondents reported abnormal total cholesterol, HDL cholesterol and triglyceride levels. Conclusions. In the opinion of respondents, shift work can exacerbate hypertension and ischemic heart disease. Abnormal values of total cholesterol and its LDL and HDL fractions increased with age and length of work, while abnormal triglyceride values were reported most frequently by supervisors. It seems necessary to introduce training for shift workers, aimed at presenting them with the principles of prevention of cardiovascular diseases; for example, how to deal with stress, change eating habits, stop smoking and reduce coffee intake, and how to encourage physical activity and good sleep hygiene.
Heart disease and depression are highly co-morbid. Clinical and experimental research over the past 70 years has led to several neurohumoral hypotheses of causative factors present under the conditions of either heart failure or of psychological depression. Some of these hypothesized factors are common to both disorders and are therefore attractive candidates to account for the high incidence of co-occurrence of depression and heart disease. One experimental approach to study the co-morbidity of heart failure and depression has been to study the behavioral, biochemical and physiological changes in a chronic mild stress model of depression and in heart failure induced by experimental myocardial infarction. Our studies have led us to focus on the pro-inflammatory cytokines, in particular tumor necrosis factor (TNF)-alpha, and the renin-angiotensin-aldosterone system. Both of these families of humoral factors are elevated in human heart failure and in depression and the two experimental models we have studied. The demonstrated validity of each of these models will be of great value in elucidating the nature of the actions and interactions of these humoral agents as they contribute to the co-morbid conditions of heart failure and depression.
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