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排序方式: 共有10000条查询结果,搜索用时 15 毫秒
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Noël M Dewailly E Chateau-Degat ML Counil É Laouan-Sidi EA Lonn E 《Atherosclerosis》2012,221(2):558-564
ObjectiveTo evaluate subclinical atherosclerosis in Nunavik Inuit and its correlation to traditional cardiovascular disease risk factor.MethodThe intima–media thickness (IMT) of 12 segments of the carotid arteries (IMT12_seg) free of plaque were assessed in randomly selected 40 years old and older Inuit from. Clinical assessment was performed which included fasting plasma glucose, fasting insulin, systemic blood pressure, body mass index, smoking, circulating blood lipids and oral glucose tolerance test. In addition, documented presence of ischemic heart disease (IHD), stroke, diabetes mellitus, hypertension and dyslipidemia were determined from medical files.ResultsThe average age of the 287 participants was 51.2 ± 0.6 years (56.8% women). Mean IMT12_seg was 0.80 ± 0.17 mm (range: 0.55–1.47 mm). Compared with disease free Inuit, individuals with history of stroke showed greater carotid internal IMT (0.68 ± 0.01 mm vs. 0.96 ± 0.15 mm respectively; p < 0.005) but no difference was observed for IHD. Hypertensive and dyslipidemic Inuit had higher IMT12_seg compared to risk factor free individuals but no difference was observed in diabetics. None of the clinical assessments were associated with IMT12_seg. In a multivariate backward elimination model, only age, gender, and medically documented history of hypertension were found to be predictors of IMT12_seg (adjusted r-square of 0.54; p < 0.0001).ConclusionCompared with disease free Nunavik Inuit, subclinical signs of atherosclerosis determined by IMT was higher in individual diagnosed with stroke. Independent predictors of IMT12_seg in our group were age, gender and history of hypertension. No other traditional risk factors imparted IMT. 相似文献
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Fraysse B Weinberger F Bardswell SC Cuello F Vignier N Geertz B Starbatty J Krämer E Coirault C Eschenhagen T Kentish JC Avkiran M Carrier L 《Journal of molecular and cellular cardiology》2012,52(6):1299-1307
Hypertrophic cardiomyopathy (HCM) is frequently caused by mutations in MYBPC3 encoding cardiac myosin-binding protein C (cMyBP-C). The mechanisms leading from gene mutations to the HCM phenotype remain incompletely understood, partially because current mouse models of HCM do not faithfully reflect the human situation and early hypertrophy confounds the interpretation of functional alterations. The goal of this study was to evaluate whether myofilament Ca(2+) sensitization and diastolic dysfunction are associated or precede the development of left ventricular hypertrophy (LVH) in HCM. We evaluated the function of skinned and intact cardiac myocytes, as well as the intact heart in a recently developed Mybpc3-targeted knock-in mouse model carrying a point mutation frequently associated with HCM. Compared to wild-type, 10-week old homozygous knock-in mice exhibited i) higher myofilament Ca(2+) sensitivity in skinned ventricular trabeculae, ii) lower diastolic sarcomere length, and faster Ca(2+) transient decay in intact myocytes, and iii) LVH, reduced fractional shortening, lower E/A and E'/A', and higher E/E' ratios by echocardiography and Doppler analysis, suggesting systolic and diastolic dysfunction. In contrast, heterozygous knock-in mice, which mimic the human HCM situation, did not exhibit LVH or systolic dysfunction, but exhibited higher myofilament Ca(2+) sensitivity, faster Ca(2+) transient decay, and diastolic dysfunction. These data demonstrate that myofilament Ca(2+) sensitization and diastolic dysfunction are early phenotypic consequences of Mybpc3 mutations independent of LVH. The accelerated Ca(2+) transients point to compensatory mechanisms directed towards normalization of relaxation. We propose that HCM is a model for diastolic heart failure and this mouse model could be valuable in studying mechanisms and treatment modalities. 相似文献
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Pillai SK Abdel-Mohsen M Guatelli J Skasko M Monto A Fujimoto K Yukl S Greene WC Kovari H Rauch A Fellay J Battegay M Hirschel B Witteck A Bernasconi E Ledergerber B Günthard HF Wong JK;Swiss HIV Cohort Study 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(8):3035-3040