@article{HaringLengRobinsonetal.2013, author = {Haring, Bernhard and Leng, Xiaoyan and Robinson, Jennifer and Johnson, Karen C. and Jackson, Rebecca D. and Beyth, Rebecca and Wactawski-Wende, Jean and Wyler von Ballmoos, Moritz and Goveas, Joseph S. and Kuller, Lewis H. and Wassertheil-Smoller, Sylvia}, title = {Cardiovascular Disease and Cognitive Decline in Postmenopausal Women: Results From the Women's Health Initiative Memory Study}, doi = {10.1161/JAHA.113.000369)}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-111376}, year = {2013}, abstract = {Background Data on cardiovascular diseases (CVD) and cognitive decline are conflicting. Our objective was to investigate if CVD is associated with an increased risk for cognitive decline and to examine whether hypertension, diabetes, or adiposity modify the effect of CVD on cognitive functioning. Methods and Results: Prospective follow-up of 6455 cognitively intact, postmenopausal women aged 65 to 79 years old enrolled in the Women's Health Initiative Memory Study (WHIMS). CVD was determined by self-report. For cognitive decline, we assessed the incidence of mild cognitive impairment (MCI) or probable dementia (PD) via modified mini-mental state examination (3 MS) score, neurocognitive, and neuropsychiatric examinations. The median follow-up was 8.4 years. Women with CVD tended to be at increased risk for cognitive decline compared with those free of CVD (hazard ratio [HR], 1.29; 95\% CI: 1.00, 1.67). Women with myocardial infarction or other vascular disease were at highest risk (HR, 2.10; 95\% CI: 1.40, 3.15 or HR, 1.97; 95\% CI: 1.34, 2.87). Angina pectoris was moderately associated with cognitive decline (HR 1.45; 95\% CI: 1.05, 2.01) whereas no significant relationships were found for atrial fibrillation or heart failure. Hypertension and diabetes increased the risk for cognitive decline in women without CVD. Diabetes tended to elevate the risk for MCI/PD in women with CVD. No significant trend was seen for adiposity. Conclusions: CVD is associated with cognitive decline in elderly postmenopausal women. Hypertension and diabetes, but not adiposity, are associated with a higher risk for cognitive decline. More research is warranted on the potential of CVD prevention for preserving cognitive functioning.}, language = {en} } @article{HaringLengRobinsonetal.2013, author = {Haring, Bernhard and Leng, Xiaoyan and Robinson, Jennifer and Johnson, Karen C. and Jackson, Rebecca D. and Beyth, Rebecca and Wactawski-Wende, Jean and Wyler von Ballmoos, Moritz and Goveas, Joseph S. and Kuller, Lewis H. and Wassertheil-Smoller, Sylvia}, title = {Cardiovascular Disease and Cognitive Decline in Postmenopausal Women: Results From the Women's Health Initiative Memory Study}, series = {Journal of the American Heart Association}, volume = {2}, journal = {Journal of the American Heart Association}, number = {e000369}, doi = {10.1161/JAHA.113.000369}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-129487}, year = {2013}, abstract = {Background-—Data on cardiovascular diseases (CVD) and cognitive decline are conflicting. Our objective was to investigate if CVD is associated with an increased risk for cognitive decline and to examine whether hypertension, diabetes, or adiposity modify the effect of CVD on cognitive functioning. Methods and Results-—Prospective follow-up of 6455 cognitively intact, postmenopausal women aged 65 to 79 years old enrolled in the Women's Health Initiative Memory Study (WHIMS). CVD was determined by self-report. For cognitive decline, we assessed the incidence of mild cognitive impairment (MCI) or probable dementia (PD) via modified mini-mental state examination (3 MS) score, neurocognitive, and neuropsychiatric examinations. The median follow-up was 8.4 years. Women with CVD tended to be at increased risk for cognitive decline compared with those free of CVD (hazard ratio [HR], 1.29; 95\% CI: 1.00, 1.67). Women with myocardial infarction or other vascular disease were at highest risk (HR, 2.10; 95\% CI: 1.40, 3.15 or HR, 1.97; 95\% CI: 1.34, 2.87). Angina pectoris was moderately associated with cognitive decline (HR 1.45; 95\% CI: 1.05, 2.01) whereas no significant relationships were found for atrial fibrillation or heart failure. Hypertension and diabetes increased the risk for cognitive decline in women without CVD. Diabetes tended to elevate the risk for MCI/PD in women with CVD. No significant trend was seen for adiposity. Conclusions-—CVD is associated with cognitive decline in elderly postmenopausal women. Hypertension and diabetes, but not adiposity, are associated with a higher risk for cognitive decline. More research is warranted on the potential of CVD prevention for preserving cognitive functioning.}, language = {en} } @article{DrechslerRitzTomaschitzetal.2013, author = {Drechsler, Christiane and Ritz, Eberhard and Tomaschitz, Andreas and Pilz, Stefan and Sch{\"o}nfeld, Stephan and Blouin, Katja and Bidlingmaier, Martin and Hammer, Fabian and Krane, Vera and M{\"a}rz, Winfried and Allolio, Bruno and Fassnacht, Martin and Wanner, Christoph}, title = {Aldosterone and cortisol affect the risk of sudden cardiac death in haemodialysis patients}, series = {European Heart Journal}, volume = {34}, journal = {European Heart Journal}, doi = {10.1093/eurheartj/ehs361}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-132562}, pages = {578-585}, year = {2013}, abstract = {Background: Sudden cardiac death is common and accounts largely for the excess mortality of patients on maintenance dialysis. It is unknown whether aldosterone and cortisol increase the incidence of sudden cardiac death in dialysis patients. Methods and results: We analysed data from 1255 diabetic haemodialysis patients participating in the German Diabetes and Dialysis Study (4D Study). Categories of aldosterone and cortisol were determined at baseline and patients were followed for a median of 4 years. By Cox regression analyses, hazard ratios (HRs) were determined for the effect of aldosterone, cortisol, and their combination on sudden death and other adjudicated cardiovascular outcomes. The mean age of the patients was 66 ± 8 years (54\% male). Median aldosterone was <15 pg/mL (detection limit) and cortisol 16.8 µg/dL. Patients with aldosterone levels >200 pg/mL had a significantly higher risk of sudden death (HR: 1.69; 95\% CI: 1.06-2.69) compared with those with an aldosterone <15 pg/mL. The combined presence of high aldosterone (>200 pg/mL) and high cortisol (>21.1 µg/dL) levels increased the risk of sudden death in striking contrast to patients with low aldosterone (<15 pg/mL) and low cortisol (<13.2 µg/dL) levels (HR: 2.86, 95\% CI: 1.32-6.21). Furthermore, all-cause mortality was significantly increased in the patients with high levels of both hormones (HR: 1.62, 95\% CI: 1.01-2.62). Conclusions: The joint presence of high aldosterone and high cortisol levels is strongly associated with sudden cardiac death as well as all-cause mortality in haemodialysed type 2 diabetic patients. Whether a blockade of the mineralocorticoid receptor decreases the risk of sudden death in these patients must be examined in future trials.}, language = {en} } @phdthesis{Schoenfeld2013, author = {Sch{\"o}nfeld, Stephan}, title = {Aldosteron und Cortisol bei Dialysepatienten - Effekt auf kardiale und vaskul{\"a}re Ereignisse}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-96156}, school = {Universit{\"a}t W{\"u}rzburg}, year = {2013}, abstract = {Dialysepatienten weisen eine hohe Anzahl kardiovaskul{\"a}rer Ereignisse auf. Betrachtet man die h{\"a}ufigsten Todesursachen von Dialysepatienten, so f{\"a}llt ein großer Teil in den kardiovaskul{\"a}ren Bereich. In dieser Arbeit wurde der Einfluss von Aldosteron und Cortisol auf kardiale und vaskul{\"a}re Ereignisse bei Dialysepatienten mit Diabetes mellitus untersucht. Dazu wurden Daten von 1255 Dialysepatienten mit Diabetes mellitus aus der Deutschen Diabetes Dialyse Studie analysiert. In der vorliegenden Arbeit konnte gezeigt werden, dass mit erh{\"o}hten Aldosteronkonzentrationen ein signifikanter Anstieg des Risikos f{\"u}r pl{\"o}tzlichen Herztod (HR: 1.69; 95\% CI: 1.06-2.69) einhergeht. Das Risiko an pl{\"o}tzlichem Herztod zu versterben war bei hohen Konzentrationen von Aldosteron und gleichzeitig vorliegenden hohen Konzentrationen von Cortisol noch deutlicher erh{\"o}ht (HR: 2.86, 95\% CI: 1.32-6.21). Ebenso war die Gesamtsterblichkeit signifikant erh{\"o}ht bei Patienten, die hohe Aldosteron- und Cortisolkonzentrationen aufwiesen im Vergleich zu Patienten mit niedrigen Spiegeln beider Hormone (HR: 1.62, 95\% CI: 1.01-2.62). In dieser Arbeit konnte somit ein deutlicher Zusammenhang hoher Aldosteron- und Cortisolkonzentrationen mit pl{\"o}tzlichem Herztod und Gesamtsterblichkeit gezeigt werden.}, subject = {Aldosteron}, language = {de} } @article{QuinklerBeuschleinHahneretal.2013, author = {Quinkler, Marcus and Beuschlein, Felix and Hahner, Stefanie and Meyer, Gesine and Sch{\"o}fl, Christof and Stalla, G{\"u}nter K.}, title = {Adrenal Cortical Insufficiency-a Life Threatening Illness With Multiple Etiologies}, series = {Deutsches {\"A}rzteblatt International}, volume = {110}, journal = {Deutsches {\"A}rzteblatt International}, doi = {10.3238/arztebl.2013.0882}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-131662}, pages = {51-52}, year = {2013}, abstract = {Background: The clinical signs of adrenal cortical insufficiency (incidence, ca. 25 per million per year; prevalence, ca. 400 per million) are nonspecific, and misdiagnoses are therefore common. Glucocorticoid substitution therapy has been in use for 50 years but is not a wholly adequate treatment. Our understanding of this disease remains incomplete in many ways. Methods: We selectively searched the Medline database for publications on adrenal cortical insufficiency, with particular attention to studies from the year 2000 onward (search terms: "adrenal insufficiency" or "Addison's disease" or "hypopituitarism"). Results: Hydrocortisone substitution therapy is often given in doses of 10-25 mg/day, timed according to the circadian rhythm. Gastrointestinal and other, febrile infections account for 30-50\% of life-threatening adrenocortical crises. Such crises affect 8 of 100 persons with adrenal cortical insufficiency per year and must be treated by the immediate administration of glucocorticoids and fluids. When persons with adrenal cortical insufficiency are acutely ill or are otherwise under unusual stress, they may need additional amounts of hydrocortisone, often in the range of 5-10 mg but occasionally as high as 200 mg. The sustained administration of excessive amounts of steroid can shorten patients' lives by several years. Inappropriate substitution therapy can cause other major medical conditions, such as metabolic syndrome and osteoporosis. Conclusion: Important measures for the prevention of adrenocortical crises include improved care by treating physicians, education of patients and their families, the provision of emergency identifying documents, and the prescription of glucocorticoid emergency kits.}, language = {en} } @article{BloemerPachelHofmannetal.2013, author = {Bl{\"o}mer, Nadja and Pachel, Christina and Hofmann, Urlich and Nordbeck, Peter and Bauer, Wolfgang and Mathes, Denise and Frey, Anna and Bayer, Barbara and Vogel, Benjamin and Ertl, Georg}, title = {5-Lipoxygenase facilitates healing after myocardial infarction}, series = {Basic Research in Cardiology}, volume = {108}, journal = {Basic Research in Cardiology}, number = {4}, doi = {10.1007/s00395-013-0367-8}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-132602}, year = {2013}, abstract = {Early healing after myocardial infarction (MI) is characterized by a strong inflammatory reaction. Most leukotrienes are pro-inflammatory and are therefore potential mediators of healing and remodeling after myocardial ischemia. The enzyme 5-lipoxygenase (5-LOX) has a key role in the transformation of arachidonic acid in leukotrienes. Thus, we tested the effect of 5-LOX on healing after MI. After chronic coronary artery ligation, early mortality was significantly increased in 5-LOX\(^{-/-}\) when compared to matching wildtype (WT) mice due to left ventricular rupture. This effect could be reproduced in mice treated with the 5-LOX inhibitor Zileuton. A perfusion mismatch due to the vasoactive potential of leukotrienes is not responsible for left ventricular rupture since local blood flow assessed by magnetic resonance perfusion measurements was not different. However, after MI, there was an accentuation of the inflammatory reaction with an increase of pro-inflammatory macrophages. Yet, mortality was not changed in chimeric mice (WT vs. 5-LOX\(^{-/-}\) bone marrow in 5-LOX\(^{-/-}\) animals), indicating that an altered function of 5-LOX\(^{-/-}\) inflammatory cells is not responsible for the phenotype. Collagen production and accumulation of fibroblasts were significantly reduced in 5-LOX\(^{-/-}\) mice in vivo after MI. This might be due to an impaired migration of 5-LOX\(^{-/-}\) fibroblasts, as shown in vitro to serum. In conclusion, a lack or inhibition of 5-LOX increases mortality after MI because of healing defects. This is not mediated by a change in local blood flow, but through an altered inflammation and/or fibroblast function.}, language = {en} }