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PubMed1998

Intravascular ultrasound-guided optimized stent deployment. Immediate and 6 months clinical and angiographic results from the Multicenter Ultrasound Stenting in Coronaries Study (MUSIC Study)

OBJECTIVES: A study was set up to validate the safety and feasibility of intravascular ultrasound-guided stenting without subsequent anticoagulation, and its impact on the 6 months restenosis rate. METHODS: The study was designed to be multicentred, prospective, and observational. RESULTS: One hundred and sixty-one patients with stable angina and a de novo coronary artery lesion were enrolled. In four patients, the implantation of a Palmaz-Schatz (with spiral bridge) stent had failed. One of these four patients died 3 days following bypass surgery. In two other patients, intravascular ultrasound assessment was not performed. One hundred and twenty-five of the remaining 155 patients (81%) were treated with aspirin (100 mg x day(-1)), because all three criteria for optimized stent expansion were met. Twenty-two of the remaining 38 patients (25%), in whom at least one criterion was not met were treated with aspirin and acenocoumarol (3 months, INR 2.5-3.5), while 16 patients only received aspirin. Stent thrombosis was documented in two patients (1.3%) for which repeat angioplasty was performed. During the hospital stay, there were no deaths or Q-wave myocardial infarctions. Five patients (3.2%) sustained a non-Q-wave myocardial infarction. During the follow-up period (198+/-38 days, complete for all patients, except one), one patient (0.6%) sustained a Q-wave myocardial infarction, one (0.6%) underwent bypass surgery, and repeat angioplasty was performed in nine patients (5.7%). In two of the nine patients, repeat angioplasty involved another lesion. Therefore, the target lesion revascularization rate during follow-up was 4.5% (seven patients). At quantitative coronary angiography, the minimal lumen diameter (mean+/-SD) increased from 1.12+/-0.34 mm before to 2.89+/-0.35 mm after stenting. Repeat angiography at 6 months was performed in 144 patients (92%). The minimal lumen diameter at follow-up was 2.12+/-0.67 mm. Restenosis (diameter stenosis of 50% or more) was documented in 12 patients or 8.3%. When the two patients with documented stent thrombosis are included, the restenosis rate amounts to 97%. CONCLUSIONS: These data confirm that, in selected patients, stents can safely be implanted without the use of systemic anticoagulation, provided optimal stent expansion is achieved. The exact role of intravascular ultrasound in the achievement of these results needs to be established by appropriately designed studies. In the meantime, intravascular ultrasound coupled with the Palmaz-Schatz stent incorporating a spiral bridge, may have contributed considerably to the immediate angiographic outcome, which in turn may explain the favourable clinical and angiographic outcome at 6 months.

Aged↗
PubMed1979

[Interaction of rifampicin with phenprocoumon (author's transl)].

Prothrombin time and plasma phenprocoumon levels were serially controlled, at short intervals, in three tubercular patients receiving both tuberculostatic drugs and phenprocoumon. The required phenprocoumon dose was continuously adapted to the prothrombin time values. During and after treatment with rifampicin optimal levels of prothrombin time were difficult or even impossible to achieve in two of the three patients. This confirms the known loss of effectiveness of the coumarins induced by rifampicin. This action has a slower onset and disappears more gradually than after acenocoumarol or warfarin. It is, therefore, likely that these two latter drugs are more suitable in patients treated with rifampicin than phenprocoumon.

4-Hydroxycoumarins↗
PubMed2000

Pharmacokinetics of recombinant activated factor VII (rFVIIa).

Recombinant coagulation factor VIIa (NovoSeven, Novo Nordisk Pharmaceuticals, Inc., Princeton NJ, USA) is a new drug for treatment of bleeding in patients with hemophilia and inhibitors. The pharmacokinetic profiles of rFVIIa have been evaluated in healthy adult volunteers who were pretreated with acenocoumarol, in adult and pediatric patients with hemophilia A or B, and in adult patients with cirrhosis and a prolonged prothrombin time (PT). The clearance (CL) and half-life (t1/2) values of rFVIIa after bolus injection were in the same range in the adult populations studied: patients with hemophilia, patients with cirrhosis, and healthy volunteers. The volume of distribution at steady state (Vss), on the other hand, was slightly smaller in healthy adult volunteers than in patients with hemophilia. The pharmacokinetic profile of rFVIIa seems to be independent of bleeding or nonbleeding conditions in adult hemophilic patients; however, the patients in these studies did not suffer from major bleeding episodes. The values of CL and t1/2 were also dose independent in adult patients with hemophilia and in patients with cirrhosis. Pediatric patients with hemophilia had shorter t1/2 and higher CL values than the adults with hemophilia. The administration of rFVIIa by continuous infusion is still experimental and a number of practical issues remain to be resolved.

Adult↗
PubMed2003

Genetic regulation of warfarin metabolism and response.

Genetic factors make an important contribution to the wide interindividual variation in warfarin dose requirement. Several cytochromes P450, each of which shows genetic polymorphism leading to interindividual variation in levels of activity, contribute to oxidative metabolism of warfarin. The most important of these is CYP2C9, which 7-hydroxylates S-warfarin. In clinical studies, possession of the CYP2C9*2 or CYP2C9*3 variant alleles, which result in decreased enzyme activity, has been associated with a significant decrease in mean warfarin dose requirement in at least eight studies. Several studies also suggest that possession of a variant allele is associated with an increased risk of adverse events. Other genetic factors such as polymorphisms affecting CYP3A4 or CYP1A2 may also be relevant to warfarin dose requirement. The molecular basis of warfarin resistance remains unclear but could be due to unusually high CYP2C9 activity (pharmacokinetic resistance) or to abnormal vitamin K epoxide reductase (pharmacodynamic resistance). There is less information available on genetic factors affecting other anticoagulants, but the CYP2C9 genotype is also relevant to acenocoumarol dose.

Anticoagulants↗
PubMed1999

Pharmacokinetic and pharmacodynamic properties of oral anticoagulants, especially phenprocoumon.

Anticoagulants of the cumarin-type (warfarin, phenprocoumon, and acenocoumarol) are drugs for the long-term treatment and prevention of thromboembolic disorders. Because of their narrow therapeutic range, many patients have bleedings of variable severity or have recurrent thrombotic events. For this reason, the study of the pharmacokinetic parameters of phenprocoumon (PPC), considering its influence on blood clotting factors, is of high interest. The elimination kinetics of PPC, its interaction with phytomenadion (vitamin K), and the pharmacokinetic behavior of the anticoagulant under steady-state conditions have been investigated in studies with healthy volunteers and patients taking anticoagulants. The maintenance dose and the plasma levels of PPC were correlated with prothrombin time (PT) in 89 patients treated with PPC. Varying parameters in each patient (e.g., elimination kinetics of PPC, activity of the cumarin-dependent blood-clotting factors, endogenous phytomenadion stores), render it impossible to use a different means of monitoring than that of PT determination.

Administration, Oral↗
PubMed1999

Pharmacology of warfarin and clinical implications.

The history of oral anticoagulants started in the 1920s in North Dakota and Alberta when a new type of hemorrhagic disease struck cattle in these areas. The group of Karl Paul Link finally succeeded in isolating the causative agent, dicumarol. It was not before the 1940s, that dicumarol or its derivatives were introduced to medicine. Acenocoumarol, phenprocoumon, and warfarin are the most commonly used oral anticoagulants. There is no known difference in the pharmacodynamic activity of these agents on the vitamin K metabolism. They are completely absorbed from the gastrointestinal tract and are firmly bound to plasma albumin and metabolized in the liver. The different elimination half-lives of the coumarins have several implications for patient management. Absorption, protein binding, and anticoagulant activity of oral anticoagulants are affected in many different ways. Also the different pharmacological properties of coumarins require different strategies in the clinical management of patients.

Animals↗
PubMed1999

Liver damage induced by coumarin anticoagulants.

Except for bleeding complications, relevant adverse effects of coumarin anticoagulants are comparatively rare considering the widespread use of these substances. Here we present the case of a 56-year-old woman who developed recurrent episodes of severe hepatitis following repeated exposure to phenprocoumon (Marcumar; Roche, Grenzach-Wyhlen, Germany) and warfarin (Coumadin; DuPont Pharma, Bad Homburg, Germany) after replacement of the mitral valve with a mechanical prosthesis. The diagnosis of "coumarin-induced hepatitis" is compatible with the time relationship between start of the drug and the onset of hepatopathy (first episode 8 months, second episode 4 weeks, and third episode 7 days), the rapid improvement following discontinuation of the drug, recurrence of liver dysfunction after re-exposure to the drug, and liver histology. After anticoagulant therapy was changed to heparin and acenocoumarol (Sintrom; Ciba-Geigy, Basel, Switzerland), the patient's general state was markedly improved and her liver values became almost normal. This case will be discussed and compared with other reports of coumarin-induced hepatic lesions. Although liver damage induced by coumarin derivates is rare, it is important to be aware of the hepatotoxic potential of these drugs, which, in most cases, mimics the clinical presentation of viral hepatitis.

Anticoagulants↗
PubMed2002

Factors predictive of failure of Brescia-Cimino arteriovenous fistulas.

OBJECTIVE: To evaluate patency rates of Brescia-Cimino fistulas and to find out which independent factors were predictors of failure. DESIGN: Retrospective clinical study. SETTING: University hospital, The Netherlands. SUBJECTS: 150 consecutive patients (mean age 56 years, range 17-80) who had 153 primary Brescia-Cimino fistulas created during the 5-year period January 1995-December 1999. MAIN OUTCOME MEASURES: Patency rates calculated by the Kaplan-Meier method and the possible predictive value of 20 different variables assessed by Cox's proportional hazard model. RESULTS: The primary patency rate was 70% at 3 months, and 7 distinct factors were significantly associated with failure of the fistula. The ones with a hazard ratio (HR) for failure greater than 2.5 were: the start of dialysis before creation of the fistula (HR 2.79, p < 0.01), moderate or poor quality of both the artery (HR 2.54, p < 0.01) and vein (HR 3.55, p < 0.001), and postoperative use of acenocoumarol instead of acetylsalicylic acid (HR 3.14. p < 0.01). CONCLUSION: The major determinants for a successfully created Brescia-Cimino fistula were creation of the fistula before the start of dialysis, as well as good quality of both the artery and the vein. This argues for timely creation of such fistulas in patients with end-stage renal disease and for accurate preoperative examination to establish the quality of the vessels.

Arm↗
PubMed2006

Isolated ventricular non-compaction: clinical study and genetic review.

Isolated non-compaction of the ventricular myocardium (INVM), sometimes referred to as 'spongy myocardium', is a congenital and exceedingly rare cardiomyopathy. Isolated ventricular non-compaction occurs in the absence of other structural heart diseases and, hypothetically, it is due to the arrest of myocardial morphogenesis. Isolated non-compaction of the ventricular myocardium may manifest itself from infancy to young adulthood with a high mortality rate. Both sexes are affected. In our study, we present a case of INVM (left and right ventricles) in a 3-year-old girl, diagnosed by two-dimensional echocardiography. The anomaly presented as a restrictive cardiomyopathy. The girl was admitted to our hospital with heart failure, when she was 10 months old. She was treated with dopamine, digoxin, furosemide, spironolactone, and acenocoumarol and her condition improved. Presently, the girl remains asymptomatic and for 3 years of follow-up, her development has been almost normal. We here describe the genetic background of this disorder (based on a literature review).

Acyltransferases↗
PubMed2006

Acute bromadiolone intoxication.

A 55-year-old man came to the hospital with a bleeding wound on his tongue. The coating of his tongue was green, and his sputum was red. Because an increased international normalized ratio-value was measured, a blood sample was sent to our laboratory with the suspicion of coumarin intoxication. Liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) analysis confirmed the poisoning was by bromadiolone, with its maximum serum concentration at 440 microg/L. The analysis of further samples resulted in a calculated elimination half-life of 140 h. The analytical method described was developed for the determination and quantitation of bromadialone using LC-MS. This method is suitable for the simultaneous identification and quantitation of 10 indirect anticoagulants in human serum, which include five superwarfarins (brodifacoum, bromadiolone, difenacoum, difethialone, and flocoumafen) as rodenticides licenced in Germany and five other vitamin K antagonists (acenocoumarol, coumatetralyl, coumachlor, phenprocoumon, and warfarin). The method is based on an acidic (pH 4.2) liquid-liquid extraction followed by LC-ESI-MS analysis. Analytical separation was carried out using an Atlantis C18 column (2.1 x 20 mm, 3 microm). The mobile phase consisted of methanol/0.1% formic acid; the flow rate was 0.6 mL/min, and the time needed for analysis was 5 min. The lower limit of quantitation was 5 microg/L (signal-to-noise > 10).

4-Hydroxycoumarins↗
PubMed1995

Cancer incidence and mortality in patients with heart disease. Effect of oral anticoagulant therapy.

Cancer incidence and mortality were reviewed in patients (683) who, during the period 1969-1988, had been attending the Cardiological Center of Pisa University for more than 1 year for valvular (494), ischemic (183), or myocardial (6) disease. Oral anticoagulant therapy (tromexan, acenocoumarol or warfarin) was administered to 312 of these 693 patients and regulated to prolong prothrombin time to a value between 20% and 40% of normal controls. The duration of treatment ranged from 1 to 14 years, with a mean of 4 years. As clinical and radiological controls were performed on all the patients at regular intervals (2-12 months), cancer incidence and mortality were recorded. Cancer incidence and mortality in the 312 patients treated with anticoagulants were compared with that of the 381 patients who did not receive this therapy. Furthermore, cancer mortality in the patients on anticoagulants was compared to that expected on the basis of national tumor registry rates. The age of the patients varied from 20 or under to 80 or over in both groups. The total observation period was 1415 patient-years (555 for males and 860 for females) in the former and 1617 patient-years (735 males and 882 females) in the latter. The proportion of the patient-years of the men over 45 (with the highest risk of cancer mortality) was higher in the group treated with anticoagulants (83%) than in the controls (72%) (p < .001). The proportion of the patient-years of the women over 45 was also higher in the former (84% vs 62%; p < .001). Six cancers were observed in the patients treated with oral anticoagulants (3 men, 3 women), while 12 cancers occurred in the control group (9 men, 3 women). There were 3 deaths in the former (1 man, 2 women) and 6 in the latter (5 men, 1 woman). On the basis of the national tumor registry rates, deaths expected in men and women on oral anticoagulants were 3 and 2. These data are compatible with the hypothesis that oral anticoagulants might reduce cancer incidence and mortality in humans.

Administration, Oral↗
PubMed2004

Effects of CYP2C9 polymorphisms on the pharmacokinetics of R- and S-phenprocoumon in healthy volunteers.

CYP2C9 catalyses the biotransformation of the oral anticoagulants S-warfarin and R- and S-acenocoumarol. According to data obtained in vitro, phenprocoumon is also metabolized by CYP2C9 but the impact of the CYP2C9 polymorphism on phenprocoumon pharmacokinetics has not been studied. Twenty-six healthy heterozygous and homozygous carriers of the CYP2C9 alleles *1 (wild-type), *2 (Arg144Cys), and *3 (Ile359Leu) received a single oral dose of 12 mg of racemic phenprocoumon. Plasma and 12 h urine concentrations of both enantiomers and their monohydroxylated metabolites were measured by high-performance liquid chromatography with mass spectrometry detection. No significant effect of the CYP2C9 variants *2 and *3 on R-phenprocoumon pharmacokinetic parameters was detected, but S-phenprocoumon clearance tended to decrease with increasing number of CYP2C9*2 and *3 alleles. The ratios of S- to R-phenprocoumon plasma clearances were higher with a median of 0.95 in carriers of *1/*1 versus 0.65 in *3/*3 (P < 0.001 for trend). Plasma and urine concentrations of 4'-, 6- and 7-hydroxyphenprocoumon were significantly lower in homozygous carriers of the CYP2C9*2 and *3 variants compared to CYP2C9*1/*1. Carriers of CYP2C9*3/*3 had a median AUC of (R,S) 7-OH-phenprocoumon of only approximately 25% compared to the wild-type genotype. The AUC of (R,S) 6-OH-phenprocoumon was only approximately 50% in CYP2C9*3/*3 compared to the homozygous wild-type genotype. In conclusion, carriers of CYP2C9*2 and *3 alleles had a lower metabolic capacity regarding phenprocoumon hydroxylation than those with CYP2C9*1/*1. However, regarding phenprocoumon hydroxylation CYP2C9 genotypes had only marginal effects on S- and R-phenprocoumon total clearance in healthy volunteers.

Alleles↗
PubMed2006

Bullous pemphigoid in a patient with psoriasis during the course of PUVA therapy: study by ELISA test.

A 65-year-old woman had a history of deep vein thrombosis and depression. Psoriasis was diagnosed in 1986 and various topical and systemic therapies, singly or in combination, were prescribed: tar, topical corticosteroids, cyclosporine, etretinate, and methotrexate. Two courses of oral and one course of bath psoralen plus UVA (PUVA) therapy (cumulative dose, 467 J/cm(2)) and UVB (2.96 J/cm(2)) had been given. In January 1999, she developed a flare of generalized psoriasis. In May 1999, therapy with PUVA (8-methoxypsoralen) plus topical acetonide triamcinolone 0.1% was initiated. At the time, she was taking acenocoumarol, lorazepam, and hydroxyzine chlorhydrate. In August 1999, at session 30, when the dose of UVA was 9 J/cm(2), and the total dose was 205 J/cm(2), a bulla appeared on the dorsum of the toe and was controlled with topical antibiotics. Five further sessions of PUVA were given and a generalized itching bullous eruption appeared all over the body. PUVA was stopped and the patient was hospitalized. On physical examination, extensive psoriatic plaques plus vesicles and bullae on the normal skin and on psoriatic lesions were observed all over the body (Fig. 1). Histopathologic study of a lesion showed a subepidermal vesicle containing fibrin, neutrophils, and a few eosinophils. No sunburn cells were observed (Fig. 2). The direct immunofluorescence (DIF) test of perilesional uninvolved skin revealed immunoglobulin G (IgG) (Fig. 3) and C3 at the dermal-epidermal junction. The DIF study using the patient's skin, previously treated with 1 m NaCl, localized the IgG at both the epidermal and dermal sides of the basement membrane zone (Fig. 4). Bullous pemphigoid (BP) was diagnosed and therapy with prednisone (60 mg/day) was started. The disease was well controlled in 3 weeks. The dose of prednisone was tapered and stopped 20 months later, without any recurrence. Study of the antibodies by the indirect immunofluorescence (IIF) test, using monkey esophagus and guinea pig as substrate, was positive at a titer of 1/160 in September 1999. The titer decreased to 1/10 in January 2000, and was negative in July 2000. An enzyme-linked immunosorbent assay (ELISA) test, performed using the commercial kit MBL, which identifies antibodies directed against epitopes of the extracellular fragment NC16 of antigen 2 of BP, was positive at 15 U/mL (normal value, < 9 U/mL) in September 1999, and negative in July 2000 (Table 1).

Aged↗
PubMed2004

Bullous systemic lupus erythematosus with antiphospholipid syndrome.

We report the case of a 44-year-old male with a 10-year history of manifestations of the rare form of bullous systemic lupus erythematosus (SLE) with coexisting antiphospholipid syndrome (APS) that remained undiagnosed until thrombotic-embolic episodes appeared and high titres of anticardiolipin (ACL) antibodies were detected. The patient fulfilled the criteria for SLE and the atypical cutaneous manifestations together with histopathological changes and a favourable response to sulphones were the grounds for the diagnosis of the bullous variety of SLE. Treatment with prednisolone, acenocoumarol and dapsone resulted in marked clinical improvement, reduction in antinuclear antibodies (ANAs) and normalization of ACL antibody titres.

Adult↗
PubMed2005

Factor XIII Val34Leu polymorphism and gamma-chain cross-linking at the site of microvascular injury in healthy and coumadin-treated subjects.

Fibrin (Fn) cross-linking by activated factor (F) XIII is essential for clot stability. In vitro, a common Leu34 polymorphism of the FXIIIA-subunit increases the rate of thrombin-mediated FXIII activation, but not cross-linking activity upon complete FXIII activation. The effect of FXIII Val34Leu polymorphism on fibrin(ogen) cross-linking in vivo when vascular injury triggers the blood coagulation has not been studied yet. Using quantitative immunoblotting with antibodies raised against FXIIIA-subunits, fibrinogen, and gamma-gamma-dimers, the rates of FXIIIA cleavage and fibrin(ogen) cross-link formation in the fluid phase of 30-s blood samples collected at the site of microvascular injury were compared in the Leu34-positive and -negative healthy individuals and patients on long-term oral anticoagulation. In addition to accelerated FXIII activation, in healthy subjects the presence of FXIII Leu34 allele was associated with increased soluble gamma-gamma-dimer formation by 40% (1355 +/- 17 microg L(-1) for Leu34 carriers vs. 804.3 +/- 17 microg L(-1) for Leu34 non-carriers; P = 0.028) at the site of microvascular injury. This solution phase effect was abolished in coumadin-treated patients (369.4 +/- 75.9 microg L(-1) for Leu34 carriers vs. 290.5 +/- 35.9 microg L(-1) for Leu34 non-carriers; P > 0.05). The present study indicates that the Leu34 allele affects soluble gamma-gamma-dimer formation in untreated individuals, but not in those receiving acenocoumarol. Our data may help elucidate the impact of the FXIII Val34Leu polymorphism on Fn cross-linking in vivo and its modulation by oral anticoagulants.

Adult↗
PubMed1998

Suppression of torsades de pointes by atropine.

A 67 year old woman with a history of chronic atrial fibrillation presented with asthma cardiale. She took no medication and there was no family history of long QT syndrome. She was treated with furosemide, nitroprusside, acenocoumarol, and digoxin. Two days later excessively prolonged RR intervals, which were terminated by escape beats with a right bundle branch block morphology, suggested impending total AV block. There was also severe QT (0.48 s) and QTc (0.56) interval prolongation with bizarre inverted TU waves and multifocal premature ventricular complexes within the U waves. The patient experienced angina pectoris followed by episodes of torsades de pointes, which were interpreted as the result of bradycardia, and the bradycardia as the result of high grade AV block induced by increased vagal tone caused by ischaemia in the presence of digoxin intoxication (serum digoxin was 2.5 micrograms/l). Subsequent atropine infusion sped up the ventricular rate and shortened the QT (0.39) and QTc (0.51) intervals. Digoxin was replaced by metoprolol to control ventricular rate and angina pectoris. Within days, QT and QTc intervals became normal and the U waves disappeared. Neither torsades de pointes nor angina pectoris recurred. Based on a review of the literature, it is suggested that the electrophysiological mechanism of this effect is not only an increase of the heart rate, but also a direct action of muscarinic receptor antagonism on Purkinje cells and ventricular refractoriness.

Aged↗
PubMed1989

Treatment of femoropopliteal stenoses by means of self-expandable endoprostheses: midterm results.

An endovascular mechanical support that can be introduced percutaneously could be an attractive approach to preventing acute occlusion and restenosis following angioplasty. The self-expandable metallic endoprosthesis is characterized by its flexibility and elasticity. The authors report the results of 40 femoropopliteal implantations in 36 patients; the follow-up period was greater than 6 months in all patients. Lesion length exceeded 7 cm in 25% of cases and was 3-7 cm in 75%. Thirty percent of lesions were total occlusions. At hemodynamic and angiographic study, two types of complications were noted. In patients not receiving orally administered anticoagulants, six thromboses occurred early; no early thromboses were noted in the nine patients treated with acenocoumarol. Restenosis occurred in 10% of cases (maximum follow-up, 2 years) and was noted even in long lesions (greater than 7 cm). The authors believe that placement of this type of prosthesis is an attractive approach to preventing postangioplasty restenosis, provided that the conditions of anticoagulation are well controlled.

Adult↗
PubMed2005

[Upper limb deep venous thrombosis. Risk factors, outcome, and posthrombotic syndrome].

OBJECTIVE: Our objective was that of describing a series of episodes of upper limb deep venous thrombosis, with special emphasis on the incidence of posthrombotic syndrome and its impact in the quality of life of the patients. METHODS: 33 episodes (29 patients) of upper limb deep venous thrombosis were studied, between January 1995 and January 2002; episodes until September 1999 (18 episodes) were considered retrospectively while those which took place starting in this date (15 episodes) were considered prospectively. In all, 24 patients were cared in hospital clinic. It was possible to obtain complete data in 16 cases, in which evolution toward posthrombotic syndrome, venous revascularization, and impact of the pathological process in the global quality of life of patients were studied. RESULTS: Average age of patients was 58.9 years. In 25 episodes (75.8%) some risk factor for venous thrombosis existed, the presence of a venous catheter being the most frequent. Subclavian axillary affectation was predominant (18 episodes, 55%) and in the left side (25 episodes, 76%). Twenty-eight episodes were diagnosed with echography (84.8%). Mean D-dimers concentration (N = 16) was 1,046 ng/ml (standard deviation [SD]: 826.9). One of the episodes (3%) was associated to lung thromboembolism. Treatment consisted on the administration of low molecular weight heparin during the acute phase in 70% of the cases. In 13 episodes (39%) additional treatment of thrombosis (endovascular in most) was carried out. In 29 episodes (88%) chronic treatment was administered with acenocoumarol, while in 4 episodes (12%) the administration of low molecular weight heparin was kept. No patient died during hospitalization. In 15 patients (52%) control of revascularizacion was performed. We detected complete revascularization in 6 patients (40%), revascularization with collateral circulation in 4 patients (27%), partial revascularization in other 4 patients (27%) and presence of permeability but with expansion and tortuosity of deep venous system in 1 case (6%). Posthrombotic syndrome was considered mild or nonexistent in 10 patients (62.5%) and moderate in 6 patients (37.5%). Quality of life of patients with moderate posthrombotic syndrome was significantly worse than that of patients with mild posthrombotic syndrome (73 vs 90, p < 0.035). CONCLUSIONS: Most of upper limb deep venous thrombosis are associated to the use of intravenous catheters. Echography is the primary diagnostic technique. At the time of the diagnosis, patients tend to show elevation in D-dimers levels. Evolution toward posthrombotic syndrome is frequent; this syndrome does not use to be serious but indeed influences the quality of life of patients.

Adolescent↗