PubMed · 14781512
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J GARCIA-BLANCO, J VINA. 1950. [Codeine hypotension].. https://pubmed.ncbi.nlm.nih.gov/14781512/
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BACKGROUND: VEGF seems to have a protective role on cardiac microcirculation, but no data are available on its action on cardiac function and morphology in diabetic patients. We sought to test the hypothesis that circulating VEGF levels could influence the cardiac performance in type 2 diabetic hypertensive patients. METHODS: We studied 30 patients with type 2 diabetes and hypertension, without severe cardiac, retinal, renal and peripheral vascular damage. Ten non-diabetic hypertensive patients represented the control group. VEGF plasma levels (ELISA) and echocardiographic parameters were evaluated. RESULTS: Diabetic patients had VEGF plasma levels higher than hypertensive non-diabetic subjects [median 82 (IQR 12-190) vs 50.5 (IQR 28-77) pg/mL, p=0.05]. Simple linear regression analysis showed that VEGF levels are related to relative wall thickness (RWT) and both endocardial and midwall systolic parameters in the diabetic patients. Multiple linear regression analysis showed that RWT and ejection fraction (EF) were the only independent correlates of VEGF (r2=0.274, p=0.03, p=0.05; respectively). CONCLUSIONS: Our data showed that high VEGF plasma levels are associated to a better systolic function in diabetic hypertensive patients with cardiac remodeling. VEGF may play a role in the improvement of cardiac performance in diabetes.
OBJECTIVES: To focus attention of the clinician on the anatomy and (patho)physiology of the vertebral venous system, so as to offer a tool to better understand and anticipate (potential) complications that are related to the application of percutaneous vertebroplasty and kyphoplasty. BACKGROUND: Percutaneous vertebroplasty and kyphoplasty are newly developed, minimally invasive techniques for the relief of pain and for the strengthening of bone in vertebral body lesions. With the clinical implementation of these techniques, a number of serious neurologic and cardiopulmonary complications have been reported in the international medical literature. Most complications appear to be related to the extrusion of bone cement into the vertebral venous system. METHODS: The literature about complications of percutaneous vertebroplasty and kyphoplasty is reviewed, and the anatomic and (patho)physiologic characteristics of the vertebral venous system are reported. Based on what is currently known from the anatomy and physiology of the vertebral venous system, the procedures of percutaneous vertebroplasty and kyphoplasty are analyzed, and suggestions are made to improve the safety of these techniques. CONCLUSIONS: Thorough knowledge of the anatomic and (patho)physiologic characteristics of the vertebral venous system is mandatory for all physicians that participate in percutaneous vertebroplasty and kyphoplasty. To reduce the risk of cement extrusion into the vertebral venous system during injection, vertebral venous pressure should be increased during surgery. This can be achieved by operating the patient in the prone position and by raising intrathoracic venous pressure with the aid of the anesthesiologist during intravertebral instrumentation and cement injection. Intensive theoretical and practical training, critical patient selection, and careful monitoring of the procedures, also taking into account patient positioning and intrathoracic and intra-abdominal pressures, will help to facilitate low morbidity outcomes in these very promising minimally invasive techniques.
The objective of this study was to assess heritability and identify chromosomal regions showing evidence of linkage to pulse pressure (PP), a simple indicator of proximal conduit vessel stiffness. Blood pressure data were analyzed for 8478 members of the National Heart, Lung and Blood Institute's (NHLBI) Framingham Heart Study. Long-term PP was defined using 2-stage analysis. First, the difference between systolic and diastolic blood pressure was averaged over all qualifying clinic examinations. In the second stage, mean PP was adjusted for mean age, time period of examination, and body mass index by regression analysis. PP values were available for 6421 individuals in 1593 families for heritability estimation and for 2492 individuals in 330 families for linkage analysis. Microsatellite markers covering the genome at 10 cM intervals were typed by the NHLBI Mammalian Genotyping Service; genome scan data were available on 1585 individuals with PP data. Heritability estimates of long-term PP accounting for hypertension treatment and for ignoring treatment were 0.52 and 0.51, respectively. Variance component linkage analysis identified several locations with suggestive evidence of linkage: chromosome 15 at 122 cM (logarithm of odds [LOD]=2.94), chromosome 7 at 71 cM (LOD=2.42), chromosome 5 at 53 cM (LOD=2.03), and chromosome 10 at 81 cM (LOD=1.83) for PP accounting for treatment. LOD scores were slightly lower when ignoring treatment, with the exception of a peak on chromosome 10 at 81 cM (LOD=2.58). In conclusion, we have demonstrated a substantial genetic component to PP and have identified 4 chromosomal regions that may harbor genes influencing vascular stiffness.