Methods: From 1992 to 2008, 2,415 patients receiving an ICD at the Leiden University Medical Center were analyzed. Pocket-related complications requiring surgical re-intervention following ICD... Show moreMethods: From 1992 to 2008, 2,415 patients receiving an ICD at the Leiden University Medical Center were analyzed. Pocket-related complications requiring surgical re-intervention following ICD implantation or replacement were noted. Elective device replacement, lead failure, and device malfunction were not considered pocket-related complications. Results: A total of 3,161 ICDs were included in the analysis. In total, 145 surgical re-interventions were required in 122 (3.9%) ICDs implanted in 114 (4.7%) unique patients. Three-year cumulative incidence for first surgical re-intervention in all ICDs was 4.7% (95% confidence interval [CI] 3.9-5.5%). Replacement ICDs exhibited a doubled requirement for surgical re-intervention (rate ratio 2.2, 95% CI 1.5-3.0). Compared to first implanted ICDs, the occurrence of surgical re-intervention in replacements was 2.5 (95% CI 1.6-3.7) times higher for infectious and 1.7 (95% CI 0.9-3.0) for noninfectious causes. Subdivision by the number of ICD replacements showed an increase in the annual risk for surgical re-intervention, ranging from 1.5% (95% CI 1.2-1.9%) for the first, to 8.1% (95% CI 1.7-18.3%) for the fourth implanted ICD. Conclusions: ICD replacement is associated with a doubled risk for pocket-related surgical re-interventions. Furthermore, the need for re-intervention increases with every consecutive replacement. (PACE 2010; 1013-1019). Show less
P>Epidemiological research throughout the last 50 years has provided the long list of risk factors for venous thrombosis that are known today. Although this has advanced our current... Show moreP>Epidemiological research throughout the last 50 years has provided the long list of risk factors for venous thrombosis that are known today. Although this has advanced our current understanding about the aetiology of thrombosis, it does not give us all the answers: many people have several of these risk factors but never develop thrombosis; others suffer from thrombosis but have none. In this review, we discuss how risk factors for venous thrombosis can be interpreted with use of several epidemiological models. We comment on how to explain why risk factors for first venous thrombosis differ from recurrent venous thrombosis, and use a causal model to better understand risk of first and recurrent venous thrombosis. Show less
A hypercoagulable state exists in hyperthyroidism, but the association with venous thrombosis (VT) is not fully explored. We aimed to investigate VT risk for different plasma levels of thyroid... Show moreA hypercoagulable state exists in hyperthyroidism, but the association with venous thrombosis (VT) is not fully explored. We aimed to investigate VT risk for different plasma levels of thyroid hormones and thyroid antibodies. We used a case-control study on leg vein thrombosis conducted between September 1999 and August 2006 at the Academic Medical Center, Amsterdam, The Netherlands. Parameters of thyroid function were assessed in 190 cases (mean age, 57 years; range, 19-90 years) and 379 sex-matched controls (mean age, 56 years; range, 18-93 years). Odds ratios (ORs) and 95% confidence intervals (CIs) for VT risk were estimated according to several cutoff levels derived from plasma levels observed in controls. We found the risk of VT to gradually rise with increasing levels of free thyroxine (FT4). In the absence of traditional acquired risk factors, FT4 levels above 17 pmol/L yielded a sex- and age-adjusted OR of 2.2 (95% CI, 1.2-4.2) for deep VT, which further increased up to an OR of 13.0 (95% CI, 1.1-154.1) for FT4 levels above reference range. Our data suggest increasing levels of FT4 to be a risk factor for VT and may have implications for both the prevention and management of this disease. (Blood. 2010; 115(22): 4344-4349) Show less
Background: It is unknown whether venous thrombosis after long haul air travel is exclusively attributable to immobilization. Objectives: We determined whether the following mechanisms were... Show moreBackground: It is unknown whether venous thrombosis after long haul air travel is exclusively attributable to immobilization. Objectives: We determined whether the following mechanisms were involved: hypoxia, stress, inflammation or viral infection. Patients/Methods: In a case crossover setting in 71 healthy volunteers who were exposed to an 8-h flight, 8-h movie marathon and 8 h of regular activities, we compared markers for several hypothetical pathways: plasminogen activator inhibitor-1 (PAI-1), stress, plasma factor (F)VIII coagulant activity (FVIIIc), soluble P-selectine (sP-selectine), interleukin-8 (IL-8) and neutrophil elastase. We reported earlier an activated clotting system, as evidenced by thrombin generation, in 17% of volunteers after the flight. Results: PAI-1 increased by 4.2 ng mL-1 (CI95:-49.5 to 6.5) in volunteers with an activated clotting system whereas it decreased in those without (-20.0 ng mL-1, CI95:-33.2 to -14.0). FVIIIc levels rose more in individuals with clotting activation (18.0%, CI95:-1.0 to 33.0) than in those without (2.0%, CI95:-2.0 to 5.0). The increases in FVIIIc were not associated with stress, which appeared unrelated to clotting activation. sP-selectin increased in those with clotting activation (3.5 mu g L-1, CI95: -3.0 to 10.0), but decreased in those without (-0.5 mu g L-1, CI95: -2.0 to 2.0). Changes in levels of neutrophil elastase or IL-8 were not different between the subjects with and without clotting activation. Conclusions: Our results do not support the hypotheses that stress, infection or air pollution are involved in the development of a prothrombotic state in air travellers. After long haul air travel, this state is more pronounced in patients with risk factors and may be caused by hypoxia, triggering systemic inflammation and platelet activation, leading to coagulation induction and degranulation of platelets. Show less
Background An explanation for the increased risk of myocardial infarction and stroke in patients with venous thrombosis is lacking. The objective of this study was to investigate whether risk... Show moreBackground An explanation for the increased risk of myocardial infarction and stroke in patients with venous thrombosis is lacking. The objective of this study was to investigate whether risk factors for arterial cardiovascular disease also increase the risk of venous thrombosis. Design and Methods Cases who had a first venous thrombosis (n=515) and matched controls (n=1,505) were identified from a population-based, nested, case-cohort study (the HUNT 2 study) comprising 71% (n=66,140) of the adult residents of Nord-Trondelag County in Norway. Results The age- and sex-adjusted odds ratio of venous thrombosis for subjects with concentrations of C-reactive protein in the highest quintile was 1.6 (95% confidence interval: 1.2-2.2) compared to subjects with C-reactive protein in the lowest quintile. This association was strongest in subjects who experienced venous thrombosis within a year after blood sampling with a three-fold increased risk of participants in the highest versus the lowest quintile. Having first degree relatives who had a myocardial infarction before the age of 60 years was positively associated with venous thrombosis compared to not having a positive family history [odds ratio 1.3 (95% confidence interval: 1.1-1.6)]. Subjects with blood pressure in the highest quintile had half the risk of developing venous thrombosis compared to subjects whose blood pressure was in the lowest quintile. There were no associations between the risk of venous thrombosis and total cholesterol, low density lipoprotein-cholesterol, high density lipoprotein-cholesterol, triglycerides, glucose or smoking. We confirmed the positive association between obesity and venous thrombosis. Conclusions C-reactive protein and a family history of myocardial infarction were positively associated with subsequent venous thrombosis. Blood pressure was inversely correlated to venous thrombosis. These findings should be confirmed by further investigations. Show less
Background: Legg-Calve-Perthes disease is a pediatric disorder characterized by osteonecrosis of the proximal femoral epiphysis. The etiology probably involves successive vascular occlusions, in... Show moreBackground: Legg-Calve-Perthes disease is a pediatric disorder characterized by osteonecrosis of the proximal femoral epiphysis. The etiology probably involves successive vascular occlusions, in which hypercoagulable disorders may play a role. We evaluated the etiologic role of thrombophilia in Legg-Calve-Perthes disease in a pediatric population. Methods: One hundred and sixty-nine consecutive patients who had been diagnosed with Legg-Calve-Perthes disease at two centers in Rotterdam, the Netherlands, when they were between 1.5 and 13.5 years of age were identified between 2000 and 2003. The study also included two control groups: 474 subjects (16.3 to 73.1 years of age) from a population-based case-control study on the etiology of venous thrombosis as well as thirty-eight children (1.8 to 18.8 years of age) who were treated for asthma at one of the centers. We determined levels of protein C, protein S, factor VIII, and fibrinogen and tested for the factor V Leiden and prothrombin G20210A mutations. We calculated age and sex-adjusted odds ratios as measures of the relative risk of the development of Legg-Calve-Perthes disease. Results: The incidence of Legg-Calve-Perthes disease was increased in the presence of the factor V Leiden mutation (odds ratio, 3.3; 95% confidence interval, 1.6 to 6.7), in the presence of the prothrombin G20210A mutation (odds ratio, 2.6; 95% confidence interval, 1.0 to 6.3), in association with elevated levels of factor VIII (>150 IU/dL) (odds ratio, 7.5; 95% confidence interval, 2.2 to 25.2), and in association with protein S deficiency (<67 U/dL) (odds ratio, 2.8; 95% confidence interval, 0.7 to 10.8). Neither high levels of fibrinogen (>4.0 g/L) nor protein C deficiency (! 55 U/dL) had an apparent effect on the risk of Legg-Calve-Perthes disease. (Odds ratios were adjusted forage and sex.) Overall, males had a 2.4 times higher risk of Legg-Calve-Perthes disease developing than did females. The effect of the factor V Leiden mutation, high levels of fibrinogen, and increasing levels of factor VIII was stronger in males than in females. The risk of Legg-Calve-Perthes disease increased with an increasing number of coagulation abnormalities in males but not in females. Conclusions: There appears to be a thrombotic component in the etiology of Legg-Calve-Perthes disease. Show less
