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A Da Costa

Publications and source records attributed to A Da Costa.

At least 19 recordsLinked to original sources

Spectrum of pathogenic mutations and associated polymorphisms in a cohort of 44 unrelated patients with long QT syndrome.

Long QT syndrome (LQTS) is a rare and clinically heterogeneous inherited disorder characterized by a long QT interval on the electrocardiogram, increased risk of syncope and sudden death caused by arrhythmias. This syndrome is mostly caused by mutations in genes encoding various cardiac ion channels. The clinical heterogeneity is usually attributed to variable penetrance. One of the reasons for this variability in expression could be the coexistence of common single nucleotide polymorphisms (SNPs) on LQTS-causing genes and/or unknown genes. Some synonymous and nonsynonymous exonic SNPs identified in LQTS-causing genes may have an effect on the cardiac repolarization process and modulate the clinical expression of a latent LQTS pathogenic mutation. We report the molecular pattern of 44 unrelated patients with LQTS using denaturing high-performance liquid chromatography analysis of the KCNQ1, KCNH2, SCN5A, KCNE1 and KCNE2 genes. Forty-five disease-causing mutations (including 24 novel ones) were identified in this cohort. Most of our patients (84%) showed complex molecular pattern with one mutation (and even two for four patients) associated with several SNPs located in several LQTS genes.

Adolescent↗

[Evaluation and surveillance of patients with an implantable defibrillator].

The implantable cardioverter-defibrillator became in some years the reference treatment of ventricular arrhythmias in association with heart disease. Recently, this technique showed its efficiency in primary prevention for patients at high risk of sudden death. The follow-up of patients with automatic defibrillator requires a detailed knowledge of both electrophysiology and stimulation. This training is based on a practical and theoretical formation. In France, a specific diploma validation is necessary and centres organisation is required. The purpose of this general review is to supply a set of updated data necessary for the coverage and the follow-up of patients with an implantable cardioverter-defibrillator.

Atrial Fibrillation↗

Polysaccharide lyases: recent developments as biotechnological tools.

Polysaccharide lyases, which are polysaccharide cleavage enzymes, act mainly on anionic polysaccharides. Produced by prokaryote and eukaryote organisms, these enzymes degrade (1,4) glycosidic bond by a beta elimination mechanism and have unsaturated oligosaccharides as major products. New polysaccharides are cleaved only by their specific polysaccharide lyases. From anionic polysaccharides controlled degradations, various biotechnological applications were investigated. This review catalogues the degradation of bacterial, plant and animal polysaccharides (neutral and anionic) by this family of carbohydrate acting enzymes.

Animals↗

Factors associated with early atrial fibrillation after ablation of common atrial flutter. A single centre prospective study.

BACKGROUND: The occurrence of early atrial fibrillation (< or = 6 months) after ablation of common atrial flutter is of clinical significance. Variables predicting this evolution in ablated patients without a previous atrial fibrillation history have not been fully investigated. OBJECTIVES: The aim of the present study was: (1) to identify predictive factors of early atrial fibrillation (< or = 6 months) in the overall population following atrial flutter catheter ablation; (2) to identify predictive variables of early atrial fibrillation following (< or = 6 months) atrial flutter catheter ablation within a subgroup of patients without documented prior atrial fibrillation. METHODS: This study prospectively included 96 consecutive patients (age 65 +/- 13 years; 18 women) over a 12-month period. Their counterclockwise flutter was ablated by radiofrequency, by the same operator, with an 8-mm-tip catheter. Clinical, electrophysiological and echocardiographic data were collected and 27 variables were retained for analysis: age; gender; type of atrial flutter (permanent vs paroxysmal); symptom duration (months +/- SD); pre-ablation history of atrial fibrillation; structural heart disease; left ventricular ejection fraction (%); left atrial size (mm); cava--tricuspid isthmus dimension; septal isthmus dimension; systolic pulmonary pressure > or < or = 30 mmHg; right atrial area; left atrial area; isthmus block; number of radiofrequency applications (+/- SD); antiarrhythmic drugs at discharge; left ventricular diastolic diameter; left ventricular systolic diameter; left ventricular telediastolic volume; left ventricular telesystolic volume; A-wave velocity (cm . s(-1)); E-wave velocity (cm . s(-1)); E/A; isovolumetric relaxation time; E-wave deceleration time; significant mitral regurgitation and flutter cycle length (ms). RESULTS: Of the 96 consecutive ablated patients, early atrial fibrillation was documented in 16 patients (17%). Atrial fibrillation occurred 30 +/- 46 days (range 1 to 171 days) after ablation. Univariate analysis associated an early occurrence of atrial fibrillation with: atrial fibrillation history, left ventricular ejection fraction, left atrial size, left ventricular telesystolic volume, A-wave velocity, significant mitral regurgitation and flutter cycle length. Multivariate analysis using a Cox model found that the only independent predictors of early atrial fibrillation were left ventricular ejection fraction and pre-ablation history of atrial fibrillation. In the subgroup without prior atrial fibrillation history (n=63; 66%), the only independent predictor of early atrial fibrillation was the presence of a significant mitral regurgitation. CONCLUSIONS: In a subgroup of patients without atrial fibrillation history, 8% of patients revealed an early atrial fibrillation. Mitral regurgitation is a strong predictive factor of early atrial fibrillation occurrence with 80% sensitivity, 78% specificity and 98% negative predictive value. These data should be considered in post-ablation management.

Adult↗

Chronotropic incompetence response to exercise in congestive heart failure, relationship with the cardiac autonomic status.

In chronic congestive heart failure (CHF), attenuated heart rate response to exercise, a manifestation of chronotropic incompetence (CI), contributes to limiting exercise capacity. The present study was thus conducted to evaluate the respective role of chronic attenuation of cardiac vagal tone associated with depressed baroreflex sensitivity or affected cardiac sympathetic responsiveness in CHF patients with CI. Spontaneous cardiac baroreflex sensitivity (BRS) assessed by sequence method and spectral- and time-domain analysis of heart rate variability (HRV) were analysed in 21 chronic CHF patients. All patients performed a symptom-limited exercise test with measurement of gas exchange. Chronic incompetence which was defined as failure to achieve > or =80% of the heart rate reserve (%HRR) given by (HRpeak - HRrest)/(predictive maximal heart rate - HRrest) was observed in 14 (66%) patients. There was no significant difference in age, heart rate, peak oxygen uptake or left ventricular ejection fraction between the patients with and without CI. Although there was no significant difference in BRS, low frequency power of HRV in normalized units (LFnu) and SDNN were significantly lower in CI patients. Percentage of HRR correlated significantly with LFnu on 15 min (r=0.64, P<0.005) and, with LFnu on 24 h (r=0.52, P<0.01), SDNN (r=0.48, P=0.03) and SDANN (r=0.48, P=0.03), but not BRS (r=0.04, P=NS). Autonomic nervous system derangement is a complex process in CHF. The role of basal depressed cardiac sympathetic tone seems to contribute more closely than depressed baroreflex sensitivity to the impaired heart rate response to exercise frequently observed in CHF patients.

Adult↗

Clinical characteristics, aetiological factors and long-term prognosis of myocardial infarction with an absolutely normal coronary angiogram; a 3-year follow-up study of 91 patients.

OBJECTIVES: The purpose of this study was to evaluate the clinical outcome of a large cohort of patients who suffered an acute myocardial infarction with absolutely normal epicardial coronary arteries at the post-myocardial infarction coronary angiogram. The aetiological and prognostic factors in this population were also analysed. BACKGROUND: Few data exist concerning the outcome, and aetiological and prognostic factors, of patients with myocardial infarction and angiographically absolutely normal coronary arteries. METHODS: Ninety-one patients (34 females/57 males; mean age 50+/-13 years, range 24--78 years) admitted with an acute myocardial infarction had absolutely normal coronary arteries at the angiogram performed 6.2+/-4 days (range 1--15 days) after the myocardial infarction, defined by smooth contours and no focal reduction (NC). Of the 91 NC patients, 71 were evaluated prospectively, alongside a systematic search of all aetiological factors reported in the literature. The NC patients were matched for age, sex, and the same period of myocardial infarction onset with a group of 91 patients with coronary artery stenosis (>50% diameter stenosis) at the angiogram performed 7.3+/-4 days (range 1--15 days) after the myocardial infarction (SC). RESULTS: The percent of smokers was similar between the two groups; higher prevalence rates of coronary heart disease family history, obesity, hypertension, hypercholesterolaemia and diabetes mellitus were found in SC (P=0.043 to 0.0001). In NC, coronary spasm was found in 15.5%, congenital coagulation disorders in 12.8%, collagen tissue disorders in 2.2%, embolization in 2.2%, and oral contraceptive use in 1.1%. Left ventricular ejection fraction at hospital discharge was higher in NC (60%+/-13%) than in SC (55%+/-13%, P=0.04). The mean follow-up was 35 months (range 1--100 months). Kaplan-Meier event-free survival, with the combined end-point defined as death, reinfarction, heart failure and stroke was 75% in NC vs 50% in SC (P<0.0001). Survival rate was 94.5% in NC compared to 92% in SC (ns). Univariate predictors of events in NC were left ventricular ejection fraction (P=0.03), age (P=0.02), diabetes (P=0.01), and smoking (P=0.03). Using Cox multivariate analysis, independent predictors of long-term outcome in NC patients were left ventricular ejection fraction (P=0.003) and diabetes (P=0.004). CONCLUSION: Aetiological factors, predominantly coronary spasm and inherited coagulation disorder, can be detected in only one third of the patients with myocardial infarction and absolutely normal coronary angiograms despite a systematic search in a prospective population. Mortality rates are similar but morbidity is lower in myocardial infarction patients with absolutely normal coronary angiography compared with those with coronary artery stenosis. The only two independent factors predictive of poor outcome in myocardial infarction patients with normal coronary arteries are left ventricular function and diabetes.

Adult↗

Influence of atrial flutter ablation on right to left inter-atrial conduction.

AIMS: Ablation of the atrial isthmus between the tricuspid annulus and the inferior vena cava changes P-wave morphology during low lateral right atrial pacing. For better understanding of the mechanism of this alteration, the sequence of activation of the inter-atrial septum and the left atrium were compared before and after ablation of the isthmus between the inferior vena cava and the tricuspid annulus. METHODS AND RESULTS: In 13 patients, left atrial mapping was performed using a duodecapolar electrode catheter advanced to the far distal coronary sinus. The inter-atrial septum was mapped using a right atrial duodecapolar electrode catheter. Conduction times were measured during low lateral right atrial pacing from the pacing artefact and during sinus rhythm from the earliest right atrial electrogram to every intra-cardiac electrogram before and after the ablation. During low lateral right atrial pacing, isthmus ablation resulted in a significant delay in every left atrial lead. Changes were maximal at the posterior aspect of the left atrium and minimal at its anterior aspect. No significant change was discernible on the inter-atrial septum. During sinus rhythm, atrial activations remained unchanged. CONCLUSION: Electrocardiographic changes of P-wave morphology result from alteration in the sequence of left atrial activation rather than that of the inter-atrial septum.

Atrial Flutter↗

Purification and properties of a glucuronan lyase from Sinorhizobium meliloti M5N1CS (NCIMB 40472).

A glucuronan lyase extracted from Sinorhizobium meliloti strain M5N1CS was purified to homogeneity by anion-exchange chromatography. The purified enzyme corresponds to a monomer with a molecular mass of 20 kDa and a pI of 4.9. A specific activity was found only for polyglucuronates leading to the production of 4,5-unsaturated oligoglucuronates. The enzyme activity was optimal at pH 6.5 and 50 degrees C. Zn(2+), Cu(2+), and Hg(2+) (1 mM) inhibited the enzyme activity. No homology of the enzyme N-terminal amino acid sequence was found with any of the previously published protein sequences. This enzyme purified from S. meliloti strain M5N1CS corresponding to a new lyase was classified as an endopolyglucuronate lyase.

Amino Acid Sequence↗

Glucose competence of the hepatoportal vein sensor requires the presence of an activated glucagon-like peptide-1 receptor.

Activation of the hepatoportal glucose sensors by portal glucose infusion leads to increased glucose clearance and induction of hypoglycemia. Here, we investigated whether glucagon-like peptide-1 (GLP-1) could modulate the activity of these sensors. Mice were therefore infused with saline (S-mice) or glucose (P-mice) through the portal vein at a rate of 25 mg/kg. min. In P-mice, glucose clearance increased to 67.5 +/- 3.7 mg/kg. min as compared with 24.1 +/- 1.5 mg/kg. min in S-mice, and glycemia decreased from 5.0 +/- 0.1 to 3.3 +/- 0.1 mmol/l at the end of the 3-h infusion period. Coinfusion of GLP-1 with glucose into the portal vein at a rate of 5 pmol/kg. min (P-GLP-1 mice) did not increase the glucose clearance rate (57.4 +/- 5.0 ml/kg. min) and hypoglycemia (3.8 +/- 0.1 mmol/l) observed in P-mice. In contrast, coinfusion of glucose and the GLP-1 receptor antagonist exendin-(9-39) into the portal vein at a rate of 0.5 pmol/kg. min (P-Ex mice) reduced glucose clearance to 36.1 +/- 2.6 ml/kg. min and transiently increased glycemia to 9.2 +/- 0.3 mmol/l at 60 min of infusion before it returned to the fasting level (5.6 +/- 0.3 mmol/l) at 3 h. When glucose and exendin-(9-39) were infused through the portal and femoral veins, respectively, glucose clearance increased to 70.0 +/- 4.6 ml/kg. min and glycemia decreased to 3.1 +/- 0.1 mmol/l, indicating that exendin-(9-39) has an effect only when infused into the portal vein. Finally, portal vein infusion of glucose in GLP-1 receptor(-/-) mice failed to increase the glucose clearance rate (26.7 +/- 2.9 ml/kg. min). Glycemia increased to 8.5 +/- 0.5 mmol/l at 60 min and remained elevated until the end of the glucose infusion (8.2 +/- 0.4 mmol/l). Together, our data show that the GLP-1 receptor is part of the hepatoportal glucose sensor and that basal fasting levels of GLP-1 sufficiently activate the receptor to confer maximum glucose competence to the sensor. These data demonstrate an important extrapancreatic effect of GLP-1 in the control of glucose homeostasis.

Animals↗

[Secondary infections after pacemaker implantation].

INTRODUCTION: Infectious complications following pacemaker implantation are not common but may be particularly severe. Localized wound infections at the site of implantation have been reported in 0.5% of the cases in the most recent series, with an average of about 2%. The incidence of septicemia and infectious endocarditis is lower, about 0.5% of the cases. The operator's experience, the duration of the procedure and repeat procedures are considered to be predisposing factors. CURRENT KNOWLEDGE AND KEY POINTS: The main cause of these infections has been recently demonstrated to be local contamination during implantation. The commonest causal organism is Staphylococcus (75 to 92% of the cases), Staphylococcus aureus being the cause of acute infections (less than 6 weeks), whereas Staphylococcus epidermidis is associated with cases of secondary infection (more than 2 months). The usual clinical presentation is infection at the site of the pacemaker but other forms such as abscess, endocarditis, rejection of the implanted material, septic emboli or phlebitis have been described. The diagnosis is confirmed by local and systemic biological investigations and by echocardiography (especially transesophageal echocardiography) in cases of right heart endocarditis. There are two axes of treatment: bactericidal double antibiotherapy and surgical ablation of the infected material either percutaneously or by cardiotomy. FUTURE PROSPECTS AND PROJECTS: A recent meta-analysis supported the role of systematic, preoperative, prophylactic antibiotic therapy in the prevention of these complications. These data should be confirmed by suitably powered clinical trials.

Aged↗

Safe and effective placement of two bipolar silicone leads in the cephalic vein using a hydrophilic guidewire and a split introducer.

The cephalic vein (CV) is preferable to the subclavian vein for implanting permanent pacing leads because of fewer complications. Unfortunately, this access is unusable in a substantial number of patients. This prospective study evaluates a technique to increase CV access for the placement of two silicone bipolar leads used in DDD pulse generator implants. A standard cephalic cutdown was performed under local anesthesia and a hydrophilic guidewire (HGW) threaded in the CV. The first (ventricular) bipolar lead was then introduced and positioned. When possible, introduction of the second (atrial) lead followed the same direct access. A failed introduction led to a modified procedure (MP) relying on a "split" introducer (8-9 Fr Plastimed) advanced with a circular motion over the HGW, then removal of the dilator, removal of the HGW, insertion of the pacing lead into the sheath with placement in the right atrium, followed by sheath withdrawal. Over an 18-month period, 90 consecutive patients had DDD pacemakers implanted. The CV was accessible in 76 (84.5%) of 90 patients and the direct introduction of the ventricular lead was obtained in 74 (97.4%) of these. Atrialization proceeded as follows: direct access CV in 14 (18%) of 76 patients, MP access in 54 (71%) of 76 patients, and MP failure in 8 (11%) of 76 patients. Overall, this approach allowed cephalic dual insertion in 68 (89%) of 76 patients. In conclusion, the modified procedure presented in this study allows a dual catheterization with bipolar leads in 89% of patients when a CV is available. This significantly improves the success rate for dual bipolar lead implants in this configuration.

Adult↗

Predictive factors of ventricular fibrillation triggered by pause-dependent torsades de pointes associated with acquired long QT interval: role of QT dispersion and left ventricular function.

INTRODUCTION: Death due to acquired torsades de pointes usually is caused by ventricular fibrillation (VF), but the contributing factors to VF triggered by pause-dependent torsades de pointes are not understood. METHODS AND RESULTS: We evaluated 91 patients who fulfilled four criteria: (1) pause-dependent torsades de pointes; (2) prolonged QT interval and/or corrected QT (QTc) (>0.44 sec); (3) long-short initiation sequence; and (4) conditions known to induce pause-dependent torsades de pointes. There were 38 patients with a documented VF (group I) and 53 without VF (group II). Absolute and relative dispersions of QT and QTc were calculated based on the 12-lead standard ECG. Group I differed from group II with regard to myocardial infarction history (32% vs 13%; P = 0.035), left ventricular ejection fraction (44% +/- 14% vs 65% +/- 9%; P < 0.0001), presence of structural heart disease (100% vs 20.8%; P < 0.0001), QT mean (591 +/- 73 msec vs 514 +/- 78 msec; P < 0.0001), QTc mean (563 +/- 76 msec vs 508 +/- 90 msec; P = 0.002), absolute QT dispersion (166 +/- 56 msec vs 84 +/- 49 msec; P < 0.0001), relative QT dispersion (9.9% +/- 3.5% vs 6.3% +/- 3.2%; P < 0.0001), absolute QTc dispersion (158 +/- 57 msec vs 81 +/- 44 msec; P < 0.0001), and relative QTc dispersion (9.9% +/- 3.6% vs 6.2% +/- 3%; P < 0.0001). Multiple regression analysis showed that ejection fraction (P = 0.0001), presence of structural heart disease (P < 0.0001), and relative QTc dispersion (P = 0.038) were the only independent predictors of VF. CONCLUSION: Left ventricular function, presence of structural heart disease, and QTc relative dispersion should be evaluated carefully in patients with conditions susceptible to inducing torsades de pointes.

Aged↗

Prevalence of factor V Leiden in patients with myocardial infarction and normal coronary angiography.

Factor V Leiden is associated with an increased risk of venous thrombosis and myocardial infarction in young women, but not in men in this latter case. The aim of this study was to evaluate the prevalence of this mutation in patients with myocardial infarction but normal coronary angiography. We compared 3 groups of patients: one group consisted of 107 patients with premature myocardial infarction but no significant coronary artery stenosis; another group of 244 patients with myocardial infarction and significant coronary artery stenosis; a third group of 400 healthy controls. Factor V Leiden was found in 13 patients (12.1%) who had a myocardial infarction without significant coronary artery stenosis, 11 patients (4.5%) who had a myocardial infarction with significant coronary artery stenosis (p = 0.01) and in 20 controls (5%) (p = 0.01). Odds ratio associated with factor V Leiden were respectively 2.93 (CI95: 1.18-7.31 ) and 2.63 (CI95: 1.19-5.78) when we compared myocardial infarction patients without significant coronary artery stenosis to controls or to patients with significant coronary artery stenosis. In myocardial infarction patients without significant coronary artery stenosis, prevalence of factor V Leiden is significantly higher than in controls. This new finding supports the hypothesis that thrombosis plays a key role in this selected situation.

Adult↗

Role of the preaxillary flora in pacemaker infections: a prospective study.

BACKGROUND: Infection remains a severe complication after pacemaker implantation. The purpose of our prospective study was to evaluate the role of the local bacteriologic flora in its occurrence. METHODS AND RESULTS: Specimens were collected at the site of implantation for culture from the skin and the pocket before and after insertion in a consecutive series of patients who underwent elective permanent pacemaker implantation. Microorganisms isolated both at the time of insertion and of any potentially infective complication were compared by using conventional speciation and ribotyping. There were 103 patients (67 men and 36 women) whose age ranged from 16 to 93 years (mean+/-SD, 67+/-15). At the time of pacemaker implantation, a total of 267 isolates were identified. The majority (85%) were staphylococci. During a mean follow-up of 16.5 months (range, 1 to 24), infection occurred in four patients (3.9%). In two of them, an isolate of Staphylococcus schleiferi was recognized by molecular method as identical to the one previously found in the pacemaker pocket. In one patient, Staphylococcus aureus, an organism that was absent at the time of pacemaker insertion, was isolated. In another patient, a Staphylococcus epidermidis was identified both at the time of pacemaker insertion and when erosion occurred; however, their antibiotic resistance profiles were different. CONCLUSIONS: This study strongly supports the hypothesis that pacemaker-related infections are mainly due to local contamination during implantation. S schleiferi appears to play an underestimated role in infectious colonization of implanted biomaterials and should be regarded as an important opportunistic pathogen.

Abscess↗

Antibiotic prophylaxis for permanent pacemaker implantation: a meta-analysis.

BACKGROUND: Infection remains a serious complication after permanent pacemaker implantation. Antibiotic prophylaxis is frequently prescribed at the time of insertion to reduce its incidence, although results of well-designed, controlled studies are lacking. METHODS AND RESULTS: We performed a meta-analysis of all available randomized trials to evaluate the effectiveness of antibiotic prophylaxis to reduce infection rates after permanent pacemaker implantation. Reports of trials were identified through a Medline, Embase, Current Contents, and an extensive bibliography search. Trials that met the following criteria were included: (1) prospective, randomized, controlled, open or blind trials; (2) patients assigned to a systemic antibiotic group or a control group; (3) end point events related to any infection after pacemaker implantation: wound infection, septicemia, pocket abscess, purulent secretion, right infective endocarditis, inflammatory signs, a positive culture, septic pulmonary embolism, or repeat operation for an infective complication. Seven trials met the inclusion criteria. They included 2023 patients with established permanent pacemaker implantation (new implants or replacements). The incidence of end point events in control groups ranged from 0% to 12%. The meta-analysis suggested a consistent protective effect of antibiotic pretreatment (P=.0046; common odds ratio: 0.256, 95% confidence interval: 0.10 to 0.656). CONCLUSIONS: Results of the present meta-analysis suggest that systemic antibiotic prophylaxis significantly reduces the incidence of potentially serious infective complications after permanent pacemaker implantation. They support the use of prophylactic antibiotics at the time of pacemaker insertion to prevent short-term pocket infection, skin erosion or septicemia.

Adult↗

[Infections secondary to implantation of cardiac pacemakers].

Infectious complications of pacemaker implantation are not common but may be particularly severe. Localised wound infections at the site of implantation have been reported in 0.5% of cases in the most recent series with an average of about 2%. The incidence of septicaemia and infectious endocarditis is lower, about 0.5% of cases. The operator's experience, the duration of the procedure and repeat procedures are considered to be predisposing factors. The main cause of these infections is though to be local contamination during the implantation. The commonest causal organism is the staphylococcus (75 to 92%), the staphylococcus aureus being the cause of acute infections whereas the staphylococcus epidermis is associated with cases of secondary infection. The usual clinical presentation is infection at the site of the pacemaker but other forms such as abscess, endocarditis, rejection of the implanted material, septic emboli and septic phlebitis have been described. The diagnosis is confirmed by local and systemic biological investigations and by echocardiography (especially transoesophageal echocardiography) in cases of right heart endocarditis. There are two axes of treatment: bactericidal double antibiotherapy and surgical ablation of the infected material either percutaneously or by cardiotomy. Though controversial, and unsupported by scientific evidence, the role of systematic, preoperative, prophylactic antibiotic therapy in the prevention of these complications seems to be increasing.

Abscess↗

Symptomatic inferior vena cava filter thrombosis: clinical study of 30 consecutive cases.

Inferior vena cava (IVC) filter thrombosis has not been described as a clinical entity. Thirty patients with IVC percutaneous filter thrombosis were assessed by cavography, computed tomographic (CT) scan and/or duplex ultrasonography. All patients had proximal venous thrombosis when the filter was placed, and the indication for filter placement was a contraindication to anticoagulant therapy in eight patients (27%). Filter thrombosis occurred within 6 months following filter placement in 15 patients (early filter thrombosis group). Among these patients, 10 were not treated with oral anticoagulant, and none of the other five received adjusted anticoagulation. No patients with late filter thrombosis received anticoagulant at the time of the diagnosis. Early filter thrombosis was mainly associated with LGM filters (12 of the 15 cases). Occlusion was revealed by recurrent venous thrombosis in 18 cases. A thrombus above the filter and pulmonary embolism was found in 10 patients (33%). Thrombolytic therapy failed in 5 out of 7 cases, and all but two patients were treated with anticoagulant therapy. In conclusion, early filter thrombosis appears to be due to intracaval extension of deep vein thrombosis, and this emphasizes the need for appropriate anticoagulation. In the case of temporary contraindication to anticoagulation at the time of the filter placement, anticoagulant should be reassessed later.

Adult↗