Home About us Contact
|
Home About us Contact | ||
|
|
||
Venous Circulation (venous + circulation)
Selected AbstractsCalcium Channel Blocker-Related Peripheral Edema: Can It Be Resolved?JOURNAL OF CLINICAL HYPERTENSION, Issue 4 2003Domenic A. Sica MD Calcium channel blocker (CCB)-related edema is quite common in clinical practice and can effectively deter a clinician from continued prescription of these drugs. Its etiology relates to a decrease in arteriolar resistance that goes unmatched in the venous circulation. This disproportionate change in resistance increases hydrostatic pressures in the precapillary circulation and permits fluid shifts into the interstitial compartment. CCB-related edema is more common in women and relates to upright posture, age, and the choice and dose of the CCB. Once present it can be slow to resolve without intervention. A number of strategies exist to treat CCB-related edema, including switching CCB classes, reducing the dosage, and/or adding a known venodilator such as a nitrate, an angiotensin-converting enzyme inhibitor, or an angiotensin-receptor blocker to the treatment regimen. Angiotensin-converting enzyme inhibitors have been best studied in this regard. Diuretics may alter the edema state somewhat, but at the expense of further reducing plasma volume. Traditional measures such as limiting the amount of time that a patient is upright and/or considering use of graduated compression stockings are useful adjunctive therapies. Discontinuing the CCB and switching to an alternative antihypertensive therapy will resolve the edema. [source] Post-thrombotic syndrome, recurrence, and death 10 years after the first episode of venous thromboembolism treated with warfarin for 6 weeks or 6 monthsJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2006S. SCHULMAN Summary.,Background: The influence of the duration of anticoagulant therapy after venous thromboembolism (VTE) on the long-term morbidity and mortality is unclear. Aim: To investigate the long-term sequelae of VTE in patients randomized to different duration of secondary prophylaxis. Methods: In a multicenter trial comparing secondary prophylaxis with vitamin K antagonists for 6 weeks or 6 months, we extended the originally planned 2 years follow-up to 10 years. The patients had annual visits and at the last visit clinical assessment of the post-thrombotic syndrome (PTS) was performed. Recurrent thromboembolism was adjudicated by a radiologist, blinded to treatment allocation. Causes of death were obtained from the Swedish Death Registry. Results: Of the 897 patients randomized, 545 could be evaluated at the 10 years follow-up. The probability of developing severe PTS was 6% and any sign of PTS was seen in 56.3% of the evaluated patients. In multivariate analysis, old age and signs of impaired circulation at discharge from the hospital were independent risk factors at baseline for development of PTS after 10 years. Recurrent thromboembolism occurred in 29.1% of the patients with a higher rate among males, older patients, those with permanent triggering risk factor , especially with venous insufficiency at baseline , signs of impaired venous circulation at discharge, proximal deep vein thrombosis, or pulmonary embolism. Death occurred in 28.5%, which was a higher mortality than expected with a standardized incidence ratio (SIR) of 1.43 (95% CI 1.28,1.58), mainly because of a higher mortality than expected from cancer (SIR 1.83; 95% CI 1.44,2.23) or from myocardial infarction or stroke (SIR 1.28; 95% CI 1.00,1.56). The duration of anticoagulation did not have a statistically significant effect on any of the long-term outcomes. Conclusion: The morbidity and mortality during 10 years after the first episode of VTE is high and not reduced by extension of secondary prophylaxis from 6 weeks to 6 months. A strategy to reduce recurrence of VTE as well as mortality from arterial disease is needed. [source] Budd,Chiari-like syndrome in a dog with a chondrosarcoma of the thoracic wallJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 2 2007Megan F. Whelan DVM Abstract Objective: To describe a dog with Budd,Chiari-like syndrome secondary to caudal vena cava compression from a thoracic wall chondrosarcoma. Case summary: A 9-year-old spayed female Shetland Sheepdog cross with a recent history of non-productive cough developed severe abdominal distension and dyspnea. Marked ascites and enlarged hepatic veins were identified with ultrasonography. At surgery, a right thoracic wall mass was found to be compressing the caudal vena cava. Fluid analysis of the ascites revealed a modified transudate with elevated protein concentration, consistent with Budd,Chiari-like syndrome. Clinical signs resolved following thoracotomy and complete resection of the mass. New or unique information provided: Obstruction of venous blood flow can result from compression exerted by a space-occupying thoracic wall mass on the caudal vena cava. Clinical resolution can be achieved with return of adequate venous circulation by removal of the mass and alleviation of the external pressure. [source] Prenatal diagnosis of ductus venosus agenesis and its association with cytogenetic/congenital anomaliesPRENATAL DIAGNOSIS, Issue 11 2002Paolo Volpe Abstract Objectives We present an observational study of 12 cases of anomalies of the umbilical and portal vein systems associated with absence of the ductus venosus (DV) diagnosed over the past 5 years. The hemodynamic implications of each pattern of umbilico-portal system anomalies associated with absence of the DV have been investigated, as well as the frequency and types of associated anomalies and their embryological origin. Methods In all cases ultrasound, color Doppler, and cytogenetic investigations were performed. Results Four main patterns of abnormal venous circulation were documented: (1) the umbilical vein (UV) bypasses the liver and drains into the right atrium directly or through a dilated coronary sinus (three cases); (2) the UV bypasses the liver, with an infrahepatic or suprahepatic connection directly to the inferior vena cava (IVC) (two cases); (3) the UV bypasses the liver and drains directly into the iliac or renal veins (four cases); and (4) the UV drains directly into the portal veins (three cases). Among seven cases with other associated anomalies (58%), there were three cases of Turner's and Noonan's syndromes. Two fetuses and two neonates died and there were two terminations of pregnancy (TOP). Conclusions In utero diagnosis of ultrasound patterns associated with DV anomalies is feasible. Fetal karyotyping should be considered, serial ultrasound examinations recommended and, in the presence of heart failure, delivery can be anticipated. Copyright © 2002 John Wiley & Sons, Ltd. [source] Vascular Development and Differentiation During Human Liver OrganogenesisTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 6 2008Sophie Collardeau-Frachon Abstract The vascular architecture of the human liver is established at the end of a complex embryological history. The hepatic primordium emerges at the 4th week and is in contact with two major venous systems of the fetal circulation: the vitelline veins and the umbilical veins. The fetal architecture of the afferent venous circulation of the liver is acquired between the 4th and the 6th week. At the end of this process, the portal vein is formed from several distinct segments of the vitelline veins; the portal sinus, deriving from the subhepatic intervitelline anastomosis, connects the umbilical vein, which is the predominant vessel of the fetal liver, to the portal system; the ductus venosus connects the portal sinus to the vena cava inferior. At birth, the umbilical vein and the ductus venosus collapse; the portal vein becomes the only afferent vein of the liver. The efferent venous vessels of the liver derive from the vitelline veins and are formed between the 4th and the 6th week. The hepatic artery forms at the 8th week; intrahepatic arterial branches progressively extend from the central to the peripheral areas of the liver between the 10th and the 15th week. Hepatic sinusoids appear very early, as soon as hepatic cords invade the septum transversum at the 4th week. They then progressively acquire their distinctive structural and functional characters, through a multistage process. Vascular development and differentiation during liver organogenesis is, therefore, a unique process; many of the cellular and molecular mechanisms involved remain poorly understood. Anat Rec, 291:614,627, 2008. © 2008 Wiley-Liss, Inc. [source] New Technique for Fenestration of the Interatrial SeptumJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2006MUTHUKUMARAN SIVAPRAKASAM M.R.C.P.C.H. Achieving controlled flow between the systemic and pulmonary venous circulations is desirable in many complex congenital heart diseases. This includes the Fontan circulation, primary pulmonary hypertension, double inlet ventricles, or hypoplastic left heart with obstruction to the atrioventricular valve. As no specific device is available for this purpose, we developed a balloon-mounted stent technique to achieve a predetermined-sized fenestration of an atrial baffle in a patient with Fontan circulation. The details of the technique are described. [source] | |||||||||||||