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Franz H. Messerli Federico Soria 《Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy》1994,8(Z3):557-563
Left ventricular hypertrophy has been documented to be a powerful risk factor for sudden death, acute myocardial infarction, and other cardiovascular morbidity and mortality. The major determinant of left ventricular mass is the hemodynamic burden. However, the hypertrophic process is modified by demographic parameters (age, sex, race), nutritional parameters (salt intake, alcohol, obesity), and neuroendocrine factors (angiotensin, catecholamines, growth hormones, etc.). Ventricular ectopy and more serious arrhythmias are commonly seen in patients with left ventricular hypertrophy. Specific antihypertensive therapy will reduce left ventricular hypertrophy, although not all antihypertensive drugs are equipotent in this regard. A reduction in left ventricular hypertrophy has been shown to diminish left-ventricular-hypertrophy-associated arrhythmias. However, it remains to be shown that patients with left ventricular hypertrophy and ventricular ectopy are at a higher risk of sudden death than those without ventricular ectopy and that the reduction of left-ventricular-hypertrophy-associated ventricular ectopy indeed confers a clinical benefit that exceeds the one from the reduction in arterial pressure alone.Modified with permission. Messerli FH and Soria F: Left ventricular hypertrophy and ventricular ectopy. In Podrid PJ and Kower PR, eds.Arrhythmia: A Clinical Approach. ¢ Williams & Wilkins, 1994. 相似文献
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In some patients, the inflation of balloons through the mitral orifice during percutaneous mitral valvuloplasties may impair intraventricular conduction. In some cases, this appears to correspond to a block of the anterior and middle network within the left branch of the bundle of His. This left "biblock" is characterized by extreme left axial deviation of AQRS, of about -60 to -70 degrees, with a QS aspect on D2 and D3, RS on V1 and R on V6 with no major prolongation of ventricular activation time. If this hypothesis is correct, it would support the "trifascicular" concept of the left branch of the bundle of His. 相似文献
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Vincent L Soria C Mirshahi F Opolon P Mishal Z Vannier JP Soria J Hong L 《Arteriosclerosis, thrombosis, and vascular biology》2002,22(4):623-629
Cerivastatin is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. It inhibits the biosynthesis of cholesterol and its precursors: farnesyl pyrophosphate and geranylgeranyl pyrophosphate (GGPP), which are involved in Ras and RhoA cell signaling, respectively. Statins induce greater protection against vascular risk than that expected by cholesterol reduction. Therefore, cerivastatin could protect plaque against rupture, an important cause of ischemic events. In this study, the effect of cerivastatin was tested on angiogenesis because it participates in plaque progression and plaque destabilization. Cerivastatin inhibits in vitro the microvascular endothelial cell proliferation induced by growth factors, whereas it has no effect on unstimulated cells. This growth arrest occurs at the G(1)/S phase and is related to the increase of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1). These effects are reversed by GGPP, suggesting that the inhibitory effect of cerivastatin is related to RhoA inactivation. This mechanism was confirmed by RhoA delocalization from cell membrane to cytoplasm and actin fiber depolymerization, which are also prevented by GGPP. It was also shown that RhoA-dependent inhibition of cell proliferation is mediated by the inhibition of focal adhesion kinase and Akt activations. Moreover, cerivastatin inhibits in vivo angiogenesis in matrigel and chick chorioallantoic membrane models. These results demonstrate the antiangiogenic activity of statins and suggest that it may contribute to their therapeutic benefits in the progression and acute manifestations of atherosclerosis. 相似文献
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J López-Sendón E López de Sá I Roldán R Fernández de Soria F Ramos L Martín Jadraque 《Journal of the American College of Cardiology》1990,15(4):801-805
Inversion of the normal interatrial septum convexity has been described in patients with right atrial pressure or volume overload, but there is no reference to this abnormality in acute myocardial infarction. A group of 576 consecutive patients with acute infarction and serial echocardiographic studies were prospectively evaluated during a mean follow-up period of 406 days. Inverted interatrial septum convexity was found in 30 patients (5.2%); 29 of the 30 presented with inferior infarction with right ventricular involvement (29 [24.4%] of 119) and the remaining presented with cardiac tamponade secondary to heart rupture. The incidence of inverted interatrial septum convexity rapidly decreased, and after 3 months it was present in only five patients. All patients with inverted interatrial septum convexity had a right atrial pressure greater than or equal to pulmonary capillary pressure, a relation found in only 2 of 43 patients with right ventricular involvement and normal septal convexity. In patients with right ventricular infarction, right atrial pressure was higher in the presence of inverted septal convexity (15.9 +/- 4.1 versus 10.5 +/- 4.1 mm Hg, p less than 0.0001) and the incidence of hypotension (10 [34.4%] of 29 versus 15 [17.4%] of 90, p = 0.04) and third degree atrioventricular block (10 [34.4%] of 29 versus 11 [12.2%] of 90, p = 0.006) as well as the mortality rate after 3 months (9 [31%] of 29 versus 11 [12.2%] of 90, p = 0.04) were higher in the presence of inverted convexity than in patients with normal septal convexity.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
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J. Soria C. Soria U. Hedner I. M. Nilsson D. Bergqvist M. Samama 《British journal of haematology》1985,61(4):727-738
A study has been conducted in a Swedish patient with severe thrombotic disease and repeated miscarriages related to a hypodysfibrinogenaemia with defective thrombin binding to the abnormal fibrin. The hypodysfibrinogenaemia was found in several members of the family. The patient also had an increased concentration of fibronectin in her plasma at two different occasions. This would appear to be unrelated to the abnormal fibrinogen since a normal concentration of fibronectin has been found in her relatives presenting the same fibrinogen anomaly, and in the patient at two other times. In conclusion, the thrombotic disorder in this patient presenting a congenital hypodysfibrinogenaemia may be explained by the defective thrombin binding to fibrin. 相似文献
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Protective role of melatonin and retinol palmitate in oxidative stress and hyperlipidemic nephropathy induced by adriamycin in rats 总被引:2,自引:0,他引:2
Pedro Lopez Montilla Isaac Fiñana Túnez Carmen Muñoz de Agueda Felix Luna Gascón Juan Vicente López Soria 《Journal of pineal research》1998,25(2):86-93
Abstract: We have studied the effects of melatonin and retinol palmitate (RP) on the nephropathy and oxidative stress induced by a single and high dose of adriamycin (AD) in Wistar male rats. A dose of melatonin (75 μg/ kg/day) and a dose of RP (0.25 g oily solution/kg/day, sc) were injected 3 and 9 days before and after the administration of AD (25 mg/kg, i.p.), respectively. After the decapitation, samples were taken from the neck vascular trunk in order to determine the triglycerides, total cholesterol, phospholipids, HDL-cholesterol, total proteins, urea, lipoperoxides, and reduced glutathione (GSH). We estimated the lipoperoxide and glutathione (GSH) contents in renal homogenates, and the excretion of proteins in urine over a 24 hr period. The administration of AD caused significant increases in proteinuria and in the other parameters studied [lipids (triglycerides, total cholesterol, phospholipids, and HDL-cholesterol), nonprotein nitrogen compounds, and lipoperoxides]. AD increased the lipoperoxide content, but it decreased the GSH content in the kidney. Both melatonin and RP, although melatonin more significantly, decreased the intensity of the changes produced by the administration of AD alone. In fact, melatonin was quite efficient in reducing the formation of lipoperoxides, restoring renal GSH content and decreasing remarkably the severity of proteinuria. These results support the powerful antioxidant action of melatonin at renal level and a lower antioxidant action of retinol. Likewise, these data reinforce the hypothesis which supports the pathogenetic role and the close relation between the oxidative stress and the expression of the nephropathy induced by AD. However, in spite of this obvious antioxidant effect of melatonin in the kidney, additional studies are required to establish accurately the role of this pineal indole in the regulation and dynamics of the antioxidative defense enzyme system, which neutralizes the damaging effect of free radicals, both endogenous and exogenous, in this organ. 相似文献
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