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Maternal arrhythmias during pregnancy.
No full textINTRODUCTION: An increased incidence of maternal cardiac arrhythmias is observed during pregnancy and they can range from clinically irrelevant isolated premature beats to debilitating supraventricular and ventricular tachycardias.
DISCUSSION: Management of arrhythmias during pregnancy is similar to that in non-pregnant patients. However, the presence of the foetus and the risk of teratogenicity, the haemodynamic changes, the effect of therapy on labour, delivery and lactation must be evaluated. Antiarrhythmic drug selection depends on the specific arrhythmia being treated and the cardiac condition of the mother. Although no drug is completely safe, most are well tolerated and can be given with relatively low risk. Some antiarrhythmic agents, such as propranolol, metoprolol, digoxin and quinidine, have been extensively tested during pregnancy and have proved to be safe; they should therefore, whenever possible, be used as a first-line. For supraventricular tachycardia, intravenous adenosine may be used to terminate the arrhythmia if vagal manoeuvres fail. If possible, drug therapy should be avoided during the first trimester of pregnancy. When drug treatment fails or is not indicated because of the haemodynamic instability of the patient, direct current cardioversion can be used.
CONCLUSION: Most patients with arrhythmias during pregnancy can be treated with an excellent result
Effetti sul sistema cardiovascolare dei modulatori selettivi del recettore per gli estrogeni (SERMs).
No full textI modulatori selettivi del recettore degli estrogeni (SERMs) legano il recettore degli estrogeni con elevata affinità ed hanno effetti estrogenici o anti-estrogenici con una modalità tessuto specifica. Essi hanno numerosi effetti biologici sul sistema cardiovascolare. Sia il raloxifene che il tamoxifene diminuiscono il livello plasmatico del colesterolo LDL e non alterano il livello del colesterolo HDL. Altri lipidi che sono favorevolmente ridotti dai SERMs sono la lipoproteina (a) e l’apolipoproteina B. Il raloxifene riduce i livelli plasmatici di omocisteina ed il tamoxifene quelli di proteina C reattiva. Raloxifene e tamoxifene riducono significativamente il livello di fibrinogeno, questa azione non è associata a variazioni dei livelli del frammento 1-2 della protrombina e del fibrinopeptide A. La precisa azione dei SERMs sulla fibrinolisi e sulla cascata coagulativa non è chiara. I SERMs hanno effetti positivi sui markers biochimici di rischio cardiovascolare, ma non è noto se questi cambiamenti si traducono in favorevoli outcomes clinici. Ulteriori studi sono necessari per chiarire l’azione dei SERMs sulle malattie cardiovascolari
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Endothelial dysfunction in rheumatic autoimmune diseases.
No full textRheumatic autoimmune diseases have been associated with accelerated atherosclerosis and various types of vasculopathies. Atherosclerosis is an inflammatory condition which starts as a “response to injury” favoring endothelial dysfunction which is associated with increased expression of adhesion molecules, pro-inflammatory cytokines, pro-thrombotic factors, oxidative stress upregulation and abnormal vascular tone modulation. Endothelial dysfunction in rheumatic autoimmune diseases involves innate immune responses, including macrophages and dendritic cells expression of scavenger and toll-like receptors for modified or native LDL as well as neutrophil and complement activation, and dysregulation of adaptive immune responses, including proliferation of autoreactive T-helper-1 lymphocytes and defective function of dendritic and regulatory T cells. Specific differences for endothelial function among different disorders include: a) increased amounts of pro-atherogenic hormones, decreased amounts of anti-atherogenic hormones and increased insulin resistance in rheumatoid arthritis; b) autoantibodies production in systemic lupus erythematosus and antiphospholipid syndrome; c) smooth muscle cells proliferation, destruction of internal elastic lamina, fibrosis and coagulation and fibrinolytic system dysfunction in systemic sclerosis. Several self-antigens (i.e. high density lipoproteins, heat shock proteins, β2-glycoprotein1) and self-molecules modified by oxidative events (i.e. low density lipoproteins and oxidized hemoglobin) have been identified as targets of autoimmune responses. Endothelial dysfunction leads to accelerated atherosclerosis in rheumatoid arthritis, systemic lupus erythematosus and spondyloarthropaties whereas obliterative vasculopathy is associated with systemic sclerosis. In this paper, we will briefly review the most relevant information upon endothelial dysfunction and inflammatory mechanisms in atherosclerosis and we will summarize the similarities and differences in vascular disease patterns underlying different rheumatic autoimmune diseases
Autoimmune intrahepatic cholangiopathy associated with antiphospholipid antibody syndrome
No full textWe report the case of a 26-year-old woman who developed thrombophlebitis in her left leg in 2002, followed by fever, asthenia and headache in 2004. Antinuclear antibodies, antimitochondrial antibodies, anti-liver kidney microsome, anti-Smith, antiphospholipid (aPL) and antineutrophil cytoplasmic antibodies, as well as lupus- anticoagulant activity were positive. Systemic lupus erythematosus (SLE) with aPL syndrome was diagnosed and the patient was treated with azathioprine and heparin. Symptoms persisted and itching arose in the following months. The patient was admitted to our department in January 2005 for jaundice and skin rash. Elevated levels of acute phase proteins and cholestasis and liver necrosis indexes were present. Antinuclear antibodies, aPL and antimitochondrial antibodies (M5) antibodies were positive. Liver histology showed minimal focal hepatocyte necrosis, intrahepatic biliary stasis and intralobular inflammatory cell infiltrate. The absence of clinical signs that are characteristic of SLE as well as the failure to confirm antiSmith antibody positivity led us to rule out a diagnosis of SLE. On the basis of clinical, immunological and histological data, autoimmune intrahepatic cholangiopathy associated with primary aPL syndrome was diagnosed. The patient was treated with intravenous methylprednisolone followed by oral prednisone, warfarin and ursodeoxycholic acid. Liver necrosis and cholestasis indexes rapidly improved within 1 month and progressively reached the normal range. To our knowledge, this is the first description of a patient with an association of intrahepatic cholangiopathy and aPL, thus suggesting that autoimmune liver disease might associate with aPL syndrome
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