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Biomedical subjects

J Mateo

Publications and source records attributed to J Mateo.

At least 19 recordsLinked to original sources
PubMed2006

[Severe cervical skin and soft tissue infections and necrotizing fasciitis].

Cervical severe skin and soft tissue infections and necrotizing fasciitis originate from dental or pharyngeal infections. When compared to other forms of skin and soft tissue infections, they are recognized late, usually after one week of evolution often in a patient receiving antibiotic treatments. Extensions toward adjacent anatomical structures including mediastinum lead to a life-threatening prognosis. The cutaneous appearance of these severe infections is usually inflammatory cervical signs combined to facial oedema. These moderate clinical signs require immediate surgery after CT scan imaging.

Adult↗
PubMed2003

Risk of ischemic stroke associated with functional thrombin-activatable fibrinolysis inhibitor plasma levels.

BACKGROUND AND PURPOSE: Recently, a novel procarboxypeptidase B-like proenzyme, called thrombin-activatable fibrinolysis inhibitor (TAFI), has been described. It plays an important role in the delicate balance between coagulation and fibrinolysis. TAFI leads to potent inhibition of tissue plasminogen activator-induced fibrinolysis. The relevance of TAFI in thromboembolic disease is unclear. We have investigated the risk of ischemic stroke (IS) in relation to plasma levels of functional TAFI. METHODS: In a case-control study, we enrolled 264 individuals; 114 had IS, and 150 were recruited as controls who were age and sex matched and had no history of arterial disease. The individuals supplied information on their personal and family histories of cardiovascular diseases and conventional cardiovascular risk factors. Functional TAFI assays were performed by use of a method based on the activation of TAFI with thrombin-thrombomodulin and the measure of the TAFI activity generated. Other hemostatic parameters assayed were factor VIIIc, anti-phospholipid antibodies,fibrinogen, factor V Leiden, and the prothrombin gene G20210A mutations (PT20210A). RESULTS: Functional TAFI levels were significantly higher in patients with IS (113.7+/-25%; range, 57% to 209%) than in controls (102.6+/-19%). The odds ratio for IS in patients with functional TAFI levels >120% was 5.7 (95% confidence interval, 2.3 to 14.1). CONCLUSIONS: We found that functional TAFI levels in plasma (>120%) increased the risk of IS approximately 6-fold. Further studies should elucidate the physiological role of TAFI in arterial disease and possibly provide clues to therapeutic approaches.

Adult↗
PubMed2003

Coronary artery disease diagnosis based on exercise electrocardiogram indexes from repolarisation, depolarisation and heart rate variability.

Several indexes have been reported to improve the accuracy of exercise test electrocardiogram (ECG) analysis in the diagnosis of coronary artery disease (CAD), compared with the classical ST depression criterion. Some of them combine repolarisation measurements with heart rate (HR) information (such as the so-called ST/HR hysteresis); others are obtained from the depolarisation period (such as the Athens QRS score); finally, there are heart rate variability (HRV) indexes that account for the nervous system activity. The aim of this study was to identify the best exercise ECG indexes for CAD diagnosis. First, a method to automatically estimate repolarisation and depolarisation indexes in the presence of noise during a stress test was developed. The method is divided into three stages: first, a preprocessing step, where QRS detection, filtering and baseline beat rejection are applied to the raw ECG, prior to a weighted averaging; secondly, a post-processing step in which potentially noisy averaged beats are identified and discarded based on their noise variance; finally, the measurement step, in which ECG indexes are computed from the averaged beats. Then, a multivariate discriminant analysis was applied to classify patients referred for the exercise test into two groups: ischaemic (positive coronary angiography) and low-risk (Framingham risk index < 5%). HR-corrected repolarisation indexes improved the sensitivity (SE) and specificity (SP) of the classical exercise test (SE = 90%, SP = 79% against SE = 65%, SP = 66%). Depolarisation indexes also achieved an improvement over ST depression measurements (SE = 78%, SP = 81%). HRV indexes obtained the best classification results in our study population (SE = 94%, SP = 92%) by means of the very high-frequency power (VHF) (0.4-1 Hz) at stress peak.

Adult↗
PubMed2001

Physical training decreases plasma thrombomodulin in type I and type II diabetic patients.

AIMS/HYPOTHESIS: Endothelial damage is an early step in the pathogenesis of atherosclerosis and its improvement through physical training can contribute to the known reduction of cardiovascular risk associated with exercise. An increase in some endothelium-dependent haemostatic parameters, considered as markers of endothelial damage, has been observed in diabetic patients. METHODS: The effect of a three-month physical exercise programme on thrombomodulin, tissue factor pathway inhibitor, plasminogen activator inhibitor, tissue-type plasminogen activator and von-Willebrand factor was evaluated in 14 well-controlled patients with Type I (insulin-dependent) diabetes mellitus and 13 patients with Type II (non-insulin-dependent) diabetes mellitus (HbA1c 6.5 +/- 0.8 and 7.4 +/- 0.8%, respectively). A matched control group was also studied. RESULTS: Thrombomodulin at baseline was higher in both Type I and Type II diabetic patients than in their respective matched control subjects (50.0 +/- 16 vs 31.1 +/- 8.7 microg/l, p < 0.05; 51.0 +/- 10 vs 28.5 +/- 11 microg/l, p <0.05, respectively). After the exercise programme, thrombomodulin plasma concentrations had decreased (p < 0.05) in both groups of patients, with final thrombomodulin values being similar to those observed in their control groups (38.2 +/- 11 microg/l for Type I and 34.6 +/- 12 microg/l for Type II patients). The thrombomodulin decrement correlated with baseline thrombomodulin and VO2max increase in Type I diabetic patients. A decrease in tissue factor pathway inhibitor was also observed in Type II diabetic patients. CONCLUSION/INTERPRETATION: We conclude that the normalisation of plasma thrombomodulin concentrations in Type I and Type II diabetic patients after physical training might reflect the improvement in endothelial function associated with physical exercise.

Adolescent↗
PubMed2001

Genetic regulation of plasma levels of vitamin K-dependent proteins involved in hematostatis: results from the GAIT Project. Genetic Analysis of Idiopathic Thrombophilia.

Vitamin K-dependent proteins play a critical role in hemostasis. We have analysed the genetic and environmental correlations between measures of several vitamin K-dependent proteins in 21 Spanish extended families, including 397 individuals. Plasma functional levels of factors II, VII, IX, X, protein C and functional protein S were assayed in an automated coagulometer. Antigenic levels of total and free protein S were measured using an ELISA method. A maximum likelihood-based covariance decomposition analysis was used to assess the heritability of each trait and the genetic and environmental correlations between all possible pairs. All of the plasma levels had a significant genetic component (heritability) ranging from 22% to 52% of the phenotypic variance. Among the 28 possible pairs of genetic correlations, 18 were significant at a level of p < 0.05 and six exhibited a p-value between 0.05 and 0.10. Positive environmental correlation was observed for 25 of the pairs (p < 0.05). We conclude that genetic effects account for a large proportion of the observed phenotypic variation in vitamin K-dependent proteins. Some of the genes appear to pleiotropically influence all of these traits, since most pairs of phenotypes exhibit significant genetic correlation. However, since these phenotypes show a high degree of environmental correlation, it is also likely that the same environmental factors influence them co-jointly.

Adolescent↗
PubMed2001

Risk of thrombosis associated with oral contraceptives of women from 97 families with inherited thrombophilia: high risk of thrombosis in carriers of the G20210A mutation of the prothrombin gene.

BACKGROUND AND OBJECTIVES: Oral contraceptives (OC) and inherited thrombophilia are well-known risk factors associated with venous thromboembolism (VTE). However, there are only few studies on the risk of VTE in women with inherited thrombophilia who use oral contraceptives. DESIGN AND METHODS: We performed a retrospective family cohort study of 325 women belonging to 97 families with inherited thrombophilia, including antithrombin, protein S and C deficiencies, the factor V Leiden mutation (FVL) and the G20210A mutation of the prothrombin gene (PT20210A) to determine the risk of VTE associated with OC intake. RESULTS: For carriers of the PT20210A mutation, the risk of VTE in OC users was 3-fold higher (95% CI 1.3-6.8) than that in non-carriers. Carriers of FVL mutation taking OC showed an OR of 1.4 (95% CI 0.6-3.3), indicating a tendency to increase the risk of VTE. INTERPRETATION AND CONCLUSIONS: Because of the high prevalence of the PT20210A (6.5%) and FVL (2%) mutations in the general Spanish population and the increased risk of VTE associated with OC intake, genetic screening for these mutations should be considered in potential OC users belonging to families with thrombophilia.

Adolescent↗
PubMed2001

Contribution of prothrombin 20210A allele and factor V Leiden mutation to thrombosis risk in thrombophilic families with other hemostatic deficiencies.

BACKGROUND AND OBJECTIVES: The aims of this study were to compare the lifetime probability of developing thrombosis in 722 relatives of 132 thrombophilic families of symptomatic probands with recognized thrombophilic defects and to determine the prevalence of the factor V Leiden (FVL) mutation and the 20210A allele of the prothrombin gene (PT20210A) in these families. DESIGN AND METHODS: The study included 722 members belonging to 132 unrelated families. The propositi were patients who had been referred to our Thrombosis Unit. The families were selected through a symptomatic proband. Once a patient with a deficiency or mutation was identified, family members were screened for the same defect. RESULTS: The prevalence of FVL and PT20210A in families with other thrombophilic defects was higher than expected. Compared with non-deficient individuals, the risk of venous thrombosis was increased in subjects with antithrombin (AT), protein S (PS) and protein C (PC) deficiencies, and in carriers of FVL and PT20210A mutations. The risk of thrombosis was significantly increased for individuals with combined genetic defects (PC-FVL, PS-FVL, PS-PT20210A and FVL-PT20210A). The ages at the time of 50% thrombosis-free survival were as follows: 34 years for AT deficiency, (19 years with FVL, 21 years with PT20210A), 62 years for PC deficiency (33 years with FVL, 44 years with PT20210A), 37 years for PS deficiency (24 years with FVL, 36 years with PT20210A), 50 years for the FVL mutation (52 years with PT20210A), and 65 years for the PT20210A mutation. As for clinical characteristics, no differences were observed except for the higher frequency of oral contraceptive-related thrombosis in women who were carriers of PT20210A or FVL. INTERPRETATION AND CONCLUSIONS: Based on these results, screening for FVL and PT20210A mutation is recommended in patients with other thrombophilic defects. To the best of our knowledge, this is the first family study, including the PT20210A mutation, that compares genetic risk factors for thrombosis and the lifelong probability of developing thrombosis.

Adolescent↗
PubMed2000

Genetic susceptibility to thrombosis and its relationship to physiological risk factors: the GAIT study. Genetic Analysis of Idiopathic Thrombophilia.

Although there are a number of well-characterized genetic defects that lead to increased risk of thrombosis, little information is available on the relative importance of genetic factors in thrombosis risk in the general population. We performed a family-based study of the genetics of thrombosis in the Spanish population to assess the heritability of thrombosis and to identify the joint actions of genes on thrombosis risk and related quantitative hemostasis phenotypes. We examined 398 individuals in 21 extended pedigrees. Twelve pedigrees were ascertained through a proband with idiopathic thrombosis, and the remaining pedigrees were randomly ascertained. The heritability of thrombosis liability and the genetic correlations between thrombosis and each of the quantitative risk factors were estimated by means of a novel variance component method that used a multivariate threshold model. More than 60% of the variation in susceptibility to common thrombosis is attributable to genetic factors. Several quantitative risk factors exhibited significant genetic correlations with thrombosis, indicating that some of the genes that influence quantitative variation in these physiological correlates also influence the risk of thrombosis. Traits that exhibited significant genetic correlations with thrombosis included levels of several coagulation factors (factors VII, VIII, IX, XI, XII, and von Willebrand), tissue plasminogen activator, homocysteine, and the activated protein C ratio. This is the first study that quantifies the genetic component of susceptibility to common thrombosis. The high heritability of thrombosis risk and the significant genetic correlations between thrombosis and related risk factors suggest that the exploitation of correlated quantitative phenotypes will aid the search for susceptibility genes.

Adolescent↗
PubMed2000

Linkage analysis demonstrates that the prothrombin G20210A mutation jointly influences plasma prothrombin levels and risk of thrombosis.

Association studies suggest that the G20210A mutation (G to A substitution at nucleotide position 20210) in the prothrombin gene (PT) is associated with increased plasma prothrombin activity and with increased risk for venous thromboembolism. To test directly for linkage between this PT variant and plasma prothrombin activity we performed a family-based study. The G20210A genotypes and plasma prothrombin activity levels were determined in 435 individuals belonging to 22 extended Spanish families. The sample was composed of 388 homozygous (G/G) normal individuals and 43 heterozygote (G/A) and 4 homozygote (A/A) carriers for the G20210A mutation. The results of variance-component linkage analysis yielded a highly significant lod score of 3.6 (P = 2.4 x 10(-5)) between this mutation and a quantitative trait locus (QTL) that influences prothrombin activity. Importantly, a conditional linkage analysis that simultaneously accounted for association with the G20210A variant completely eliminated the linkage signal, which indicates that this mutation affects the function of the prothrombin gene. Additionally, a bivariate linkage analysis of plasma prothrombin activity and thrombosis significantly improved the linkage signal for prothrombin activity (lod score = 4.7; P = 1.5 x 10(-6)) and provided strong evidence that this QTL has a pleiotropic effect on the risk of thrombosis (lod score = 2.43; P =.0004). These results represent the first direct genetic evidence that a QTL in the PT gene influences prothrombin activity levels and susceptibility to thrombosis and strongly support the conclusion that G20210A is a functional polymorphism. (Blood. 2000;95:2780-2785)

Adult↗
PubMed2000

Genetic determinants of hemostasis phenotypes in Spanish families.

BACKGROUND: Recent studies have described genetic mutations that affect the risk of thrombosis as a result of abnormal levels of such hemostatic parameters as protein C, protein S, and the activated protein C resistance ratio. Although these mutations suggest that genes play a part in determining variability in some hemostasis-related phenotypes, the relative importance of genetic influences on these traits has not been evaluated. METHODS AND RESULTS: The relative contributions of genetic and environmental influences to a panel of hemostasis-related phenotypes were assessed in a sample of 397 individuals in 21 extended pedigrees. The effects of measured covariates (sex, age, smoking, and exogenous sex hormones), genes, and environmental variables shared by members of a household were quantified for 27 hemostasis-related measures. All of these phenotypes showed significant genetic contributions, with the majority of heritabilities ranging between 22% and 55% of the residual phenotypic variance after correction for covariate effects. Activated protein C resistance ratio, activated partial thromboplastin time, and Factor XII showed the strongest heritabilities, with 71.3%, 83.0%, and 67.3%, respectively, of the residual phenotypic variation attributable to genetic effects. CONCLUSIONS: These results clearly demonstrate the importance of genetic factors in determining variation in hemostasis-related phenotypes that are components of the coagulation and fibrinolysis pathways and that have been implicated in risk for thrombosis. The presence of such strong genetic effects suggests that it will be possible to localize previously unknown genes that influence quantitative variation in these hemostasis-related phenotypes that may contribute to risk for thrombosis.

Adolescent↗
PubMed2000

D-Dimer is an early diagnostic marker of coronary ischemia in patients with chest pain.

BACKGROUND: Chest pain is a frequent symptom in the emergency department and often presents a diagnostic challenge. Because coronary thrombosis is a hallmark of acute ischemic syndromes, the substrates of the coagulation and fibrinolysis cascades may be markers of coronary ischemia. The objective of this study was to determine the diagnostic value of several hemostatic markers in patients presenting to the emergency department (ED) with chest pain syndromes. METHODS: Two hundred fifty-seven consecutive patients with acute chest pain were studied in this prospective study conducted in an urban ED. D-Dimer levels were measured at admission to the ED in all patients. We also measured thrombin-antithrombin complexes, prothrombin fragment 1+2, activated factor VII, and fibrinogen. We used regression analysis to estimate the likelihood of myocardial infarction and the diagnostic value of D-dimer. RESULTS: D-Dimer and fibrinogen levels were significantly higher in patients with acute ischemic events (myocardial infarction and unstable angina) than in nonischemic patients (P <.01 and P =.02, respectively). The other hemostatic markers were not significantly elevated in patients with ischemic events. D-Dimer level >500 microg/L had an independent diagnostic value for myocardial infarction and increased the diagnostic sensitivity of the electrocardiogram and history from 73% to 92%. CONCLUSION: D-Dimer, an expression of ongoing thrombus formation and lysis, is a marker of substantial incremental value for the early diagnosis of acute coronary syndromes presenting with chest pain. It adds independent information to the traditional assessment for myocardial infarction. D-Dimer can be incorporated into clinical decision models in the ED.

Adult↗
PubMed2000

Evolution of leukotriene B4, peptide leukotrienes, and interleukin-8 plasma concentrations in patients at risk of acute respiratory distress syndrome and with acute respiratory distress syndrome: mortality prognostic study.

OBJECTIVE: To compare the evolution of plasma concentrations of leukotriene (LT) B4, LTC4, LTD4, and interleukin (IL)-8 in patients with acute respiratory distress syndrome (ARDS) and in patients at risk of ARDS and to assess the value of these mediators in predicting mortality rate from ARDS. DESIGN: A case-control study comparing ARDS patients and patients at risk of ARDS as well as survivors and nonsurvivors with ARDS. SETTING: Hospital intensive care unit, laboratory, and department of hematology. PATIENTS: Twenty-one patients with ARDS and 14 patients at risk of ARDS. INTERVENTION: Arterial blood samples were collected on days 0, 1, and 5 after admission to the intensive care unit. MEASUREMENTS AND MAIN RESULTS: LTs were extracted, separated by high-pressure liquid chromatography and quantified by enzyme immunoassay. IL-8 was analyzed by ELISA. Plasma concentrations of LTB4 and LTC4 plus LTD4 were significantly higher in ARDS patients than in patients at risk of ARDS during the first 24 hrs. Concentrations of IL-8 were also higher in ARDS patients than in patients at risk throughout the study, although the differences between the two groups were only significant on day 5. Only the plasma concentration of LTB4 on day 1 was a marker of ARDS (72.2% sensitivity, 84.6% specificity). A logistic regression analysis showed that LTB4 and IL-8, on day 1, were markers of mortality rate in patients with ARDS (70.0% sensitivity, 87.5% specificity). CONCLUSIONS: LTs are elevated during the early phases of ARDS, whereas IL-8 increases throughout the study. The evaluation of LTB4 and IL-8 may be useful prognostic indices in patients with early phase ARDS after admission to the intensive care unit.

Biomarkers↗
PubMed2000

Improved heart rate variability signal analysis from the beat occurrence times according to the IPFM model.

The heart rate variability (HRV) is an extended tool to analyze the mechanisms controlling the cardiovascular system. In this paper, the integral pulse frequency modulation model (IPFM) is assumed. It generates the beat occurrence times from a modulating signal. This signal is thought to represent the autonomic nervous system action, mostly studied in its frequency components. Different spectral estimation methods try to infer the modulating signal characteristics from the available beat timing on the electrocardiogram signal. These methods estimate the spectrum through the heart period (HP) or the heart rate (HR) signal. We introduce a new time domain HRV signal, the Heart Timing (HT) signal. We demonstrate that this HT signal, in contrast with the HR or HP, makes it possible to recover an unbiased estimation of the modulating signal spectra. In this estimation we avoid the spurious components and the low-pass filtering effect generated when analyzing HR or HP.

Analysis of Variance↗
PubMed2000

Functional effects of the ABO locus polymorphism on plasma levels of von Willebrand factor, factor VIII, and activated partial thromboplastin time.

Lower levels of factor VIII and von Willebrand factor (vWF) have been reported in individuals with blood type O compared with individuals with other ABO blood types. However, this relationship has been demonstrated only by association studies and not by linkage studies. Also, it is not clear whether the ABO locus exerts a functional effect directly on these plasma factors or whether the ABO locus is in linkage disequilibrium with another locus that controls these factors. To distinguish between these 2 possibilities, we applied new statistical methods combining linkage and association tests in a pedigree-based sample. In contrast to most previous studies that used the ABO phenotypes, our study used the ABO genotypes, permitting us to distinguish AO from AA and BO from BB. Our results clearly showed significant linkage between the ABO locus and vWF antigen (P=0.00075). In addition, factor VIII coagulant activity and activated partial thromboplastin time showed suggestive linkage with the ABO locus (P=0.10 and P=0.13). All 3 plasma phenotypes showed significant differences between OO and non-OO genotypes. In addition, vWF antigen exhibited significant differences between O heterozygotes and non-OO homozygotes. This study is unique because it used a combined linkage and association test, which indicated that the ABO locus itself has a functional effect on these plasma phenotypes.

ABO Blood-Group System↗
PubMed2000

Platelet function during cardiopulmonary bypass not changed by two different doses of aprotinin.

BACKGROUND AND OBJECTIVE: Bleeding is one of the major complications of cardiopulmonary bypass (CBP) during cardiac surgery. A platelet function defect seems to be the main cause of the hemostatic problems associated with CBP. Controversial results have been reported concerning the possible protective mechanism of action of aprotinin on platelets. DESIGN AND METHODS: In this study we investigated the effect of two different dosages of aprotinin (high and pump-prime-only dose) on platelet reactivity in vitro and adhesion, activation and aggregation receptors on the platelet surface. RESULTS: The results obtained from 53 patients undergoing CBP showed a significantly deficient platelet aggregation in response to agonist in all groups without differences between aprotinin treated or not treated patients. No changes in platelet surface expression of glycoprotein (GP) IIb-IIIa, GPIb, GPIV and P-selectin, were observed during CBP between patients treated with aprotinin or not. INTERPRETATION AND CONCLUSIONS: These data suggest that inadequate platelet function induced by CBP is not a defect intrinsic to the platelet. We conclude that the hemostatic effect of aprotinin, regardless of the dose employed, is not mediated by protection of platelet function.

Adult↗
PubMed2000

Platelet ultrastructural morphometry for diagnosis of partial delta-storage pool disease in patients with mild platelet dysfunction and/or thrombocytopenia of unknown origin. A study of 24 cases.

BACKGROUND AND OBJECTIVE: Exact diagnosis is sometimes difficult in patients presenting with a slight bleeding diathesis, prolonged bleeding times, non-specific aggregometric abnormalities, and/or mild thrombocytopenia. The objective of this study was to evaluate the use of platelet ultrastructural morphometry in detecting a partial d-storage pool disease in such patients. DESIGN AND METHODS: Platelets from 52 patients and 15 controls were fixed immediately in glutaraldehyde in White's saline without anticoagulant and processed for transmission electron microscopy. Using computer-assisted morphometry, the size and shape of the platelets were measured, as were the size and number per platelet of the dense- and a-granules. Ultrastructural morphology of the above and other intraplatelet structures was observed. RESULTS: Twenty-four cases were diagnosed as having a partial d-storage pool disease. Mean platelet area (2.28 microm(2)) and maximum diameter (2.58 microm) were significantly greater in patients than in control subjects (1.64 microm(2) and 2. 25 microm, respectively) but discoid shape was preserved. Mean dense-granule number was decreased, both per platelet and per microm(2) of platelet area (patients 0.22 and 0.09; controls 0.42 and 0.24). Seven patients also had a marked decrease in a-granules, resulting in a significantly lower mean number of granules per microm(2 )(patients 2.43; controls 3.15). Additionally, the patients' platelets had significant increases in both lipid droplets and surface-connected canalicular system. INTERPRETATION AND CONCLUSIONS: A partial dense-granule deficiency, sometimes associated with partial a-granule deficiency, should be borne in mind faced with patients who have a slight bleeding diathesis, non-specific platelet dysfunction tests and/or mild thrombocytopenia of unknown origin. Platelet ultrastructural morphometry is useful in diagnosing this condition.

Adolescent↗