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[This corrects the article DOI: 10.1098/rsos.190775.].
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Atherothrombosis is the cornerstone of cardiovascular diseases and the primary cause of death worldwide. Genetic contribution to disturbances in lipid metabolism, coagulation, inflammation and oxidative stress increase the susceptibility to its development and progression. Given its multifactorial nature, the multiloci studies have been proposed as potential predictors of susceptibility. A cross-sectional study was conducted to explore the contribution of nine genes involved in oxidative stress, inflammatory and thrombotic processes in 204 subjects with atherothrombosis matched by age and gender with a healthy group (n = 204). To evaluate the possibility of spurious associations owing to the Mexican population genetic heterogeneity as well as its ancestral origins, 300 unrelated mestizo individuals and 329 Native Americans were also included. ALOX5, LPA, MMP9 and TPO gene polymorphisms, as well as their multiallelic combinations, were twice to four times more frequent in those individuals with clinical manifestations of atherothrombosis than in the healthy group. Once adjusting for population stratification was done, these differences remained. Our results add further evidence on the contribution of ALOX5, LPA, MMP9 and TPO polymorphisms to atherothrombosis development in the middle-aged group, emphasizing the multiethnic studies in search of gene risk polymorphisms.
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BACKGROUND: Ischemic heart disease, cerebrovascular accident, and venous thromboembolism have the presence of a thrombotic event in common and represent the most common causes of death within the population. OBJECTIVE: Since Schiff base copper(II) complexes are able to interact with polyphosphates (PolyP), a procoagulant and potentially prothrombotic platelet agent, we investigated the antiplatelet aggregating properties of two novel tridentate Schiff base ligands and their corresponding copper( II) complexes. METHODS: The Schiff base ligands (L1) and (L2), as well as their corresponding copper(II) complexes (C1) and (C2), were synthesized and characterized by chemical analysis, X-ray diffraction, mass spectrometry, and UV-Visible, IR and far IR spectroscopy. In addition, EPR studies were carried out for (C1) and (C2), while (L1) and (L2) were further analyzed by 1H and 13C NMR. Tests for antiplatelet aggregation activities of all of the four compounds were conducted. RESULTS: X-ray diffraction studies show that (L1) and (L2) exist in the enol-imine tautomeric form with a strong intramolecular hydrogen bond. NMR studies show that both ligands are found as enol-imine tautomers in CDCl3 solution. In the solid state, the geometry around the copper(II) ion in both (C1) and (C2) is square planar. EPR spectra suggest that the geometry of the complexes is similar to that observed in the solid state by X-ray crystallography. Compound (C2) exhibited the strongest antiplatelet aggregation activity. CONCLUSION: Schiff base copper(II) complexes, which are attracting increasing interest, could represent a new approach to treat thrombosis by blocking the activity of PolyP with a potential anticoagulant activity and, most importantly, demonstrating no adverse bleeding events.
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Complejos de Coordinación/química , Complejos de Coordinación/farmacología , Cobre/química , Inhibidores de Agregación Plaquetaria/química , Inhibidores de Agregación Plaquetaria/farmacología , Agregación Plaquetaria/efectos de los fármacos , Adulto , Humanos , Masculino , Persona de Mediana Edad , Bases de Schiff/química , Adulto JovenRESUMEN
Background. Thrombin has been implicated as a key molecule in atherosclerotic progression. Clinical evidence shows that thrombin generation is enhanced in atherosclerosis, but its role as a risk factor for coronary atherosclerotic burden has not been proven in coronary artery disease (CAD) stable patients. Objectives. To evaluate the association between TAT levels and homocysteine levels and the presence of coronary artery disease diagnosed by coronary angiography in patients with stable CAD. Methods and Results. We included 95 stable patients admitted to the Haemodynamics Department, including 63 patients with significant CAD and 32 patients without. We measured the thrombin-antithrombin complex (TAT) and homocysteine concentrations in all the patients. The CAD patients exhibited higher concentrations of TAT (40.76 µg/L versus 20.81 µg/L, p = 0.002) and homocysteine (11.36 µmol/L versus 8.81 µmol/L, p < 0.01) compared to the patients without significant CAD. Specifically, in patients with CAD+ the level of TAT level was associated with the severity of CAD being 36.17 ± 24.48 µg/L in the patients with bivascular obstruction and 42.77 ± 31.81 µg/L in trivascular coronary obstruction, p = 0.002. Conclusions. The level of in vivo thrombin generation, quantified as TAT complexes, is associated with the presence and severity of CAD assessed by coronary angiography in stable CAD patients.
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BACKGROUND: Clopidogrel is a pro-drug and its intestinal absorption is limited by the P-glycoprotein encoded by the ABCB1 gene. It is metabolized hepatically by cytochrome P450 enzymes encoded by CYP genes to produce an active metabolite that antagonizes the P2Y12 platelet receptor. Some patients exhibit poor clopidogrel responsiveness due to polymorphisms, resulting in thrombotic events. The aim of this study was to determine the relationship between poor clopidogrel responsiveness and the ABCB1, CYP and P2RY12 gene polymorphisms among patients undergoing percutaneous coronary intervention (PCI). METHODS AND RESULTS: Two hundred seventy-six patients who underwent PCI were included in this study. Clopidogrel responsiveness was determined via optical aggregometry in platelet-rich plasma using 10 µM ADP. Patients exhibiting a platelet aggregation response higher than 70% were classified as poor responders. The genetic polymorphisms were analyzed via real-time PCR. Poor responsiveness to clopidogrel was noted in 22.1% of the patients. The TT genotype of the C3435T polymorphism of the ABCB1 gene and omeprazole usage were each associated with poor clopidogrel responsiveness (Exp (ß) 2.73, p=0.009 and Exp (ß) 3.86, p=0.04, respectively). CONCLUSION: Poor clopidogrel responsiveness is associated with the TT genotype of the C3435T polymorphism of the ABCB1 gene.
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Intervención Coronaria Percutánea/métodos , Inhibidores de Agregación Plaquetaria/uso terapéutico , Ticlopidina/análogos & derivados , Subfamilia B de Transportador de Casetes de Unión a ATP/genética , Subfamilia B de Transportador de Casetes de Unión a ATP/metabolismo , Clopidogrel , Femenino , Humanos , Masculino , México , Persona de Mediana Edad , Polimorfismo Genético , Ticlopidina/uso terapéuticoRESUMEN
Platelets play a pivotal role in physiological hemostasis. However, in coronary arteries damaged by atherosclerosis, enhanced platelet aggregation, with subsequent thrombus formation, is a precipitating factor in acute ischemic events. Avocado pulp (Persea americana) is a good source of bioactive compounds, and its inclusion in the diet as a source of fatty acid has been related to reduced platelet aggregability. Nevertheless, constituents of avocado pulp with antiplatelet activity remain unknown. The present study aims to characterize the chemical nature of avocado constituents with inhibitory effects on platelet aggregation. Centrifugal partition chromatography (CPC) was used as a fractionation and purification tool, guided by an in vitro adenosine diphosphate (ADP), arachidonic acid or collagen-platelet aggregation assay. Antiplatelet activity was initially linked to seven acetogenins that were further purified, and their dose-dependent effects in the presence of various agonists were contrasted. This process led to the identification of Persenone-C (3) as the most potent antiplatelet acetogenin (IC50=3.4 mM) among the evaluated compounds. In vivo evaluations with Persenone A (4) demonstrated potential protective effects against arterial thrombosis (25 mg kg⻹ of body weight), as coagulation times increased (2-fold with respect to the vehicle) and thrombus formation was attenuated (71% versus vehicle). From these results, avocado may be referred to as a functional food containing acetogenin compounds that inhibit platelet aggregation with a potential preventive effect on thrombus formation, such as those that occur in ischaemic diseases.
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Acetogeninas/aislamiento & purificación , Descubrimiento de Drogas , Fibrinolíticos/aislamiento & purificación , Frutas/química , Alimentos Funcionales/análisis , Persea/química , Inhibidores de Agregación Plaquetaria/aislamiento & purificación , Acetogeninas/química , Acetogeninas/farmacología , Acetogeninas/uso terapéutico , Animales , Animales no Consanguíneos , Coagulación Sanguínea/efectos de los fármacos , Distribución en Contracorriente , Alcoholes Grasos/química , Alcoholes Grasos/aislamiento & purificación , Alcoholes Grasos/farmacología , Alcoholes Grasos/uso terapéutico , Fibrinolíticos/química , Fibrinolíticos/farmacología , Fibrinolíticos/uso terapéutico , Humanos , Cinética , Masculino , México , Ratones , Estructura Molecular , Extractos Vegetales/efectos adversos , Extractos Vegetales/química , Extractos Vegetales/aislamiento & purificación , Extractos Vegetales/farmacología , Agregación Plaquetaria/efectos de los fármacos , Inhibidores de Agregación Plaquetaria/química , Inhibidores de Agregación Plaquetaria/farmacología , Inhibidores de Agregación Plaquetaria/uso terapéutico , Trombosis/prevención & controlRESUMEN
Compounds with estrogenic effects that also inhibit platelet aggregation might be useful in reducing thrombotic events associated with estrogenic therapy. In this study, two aminoestrogens, Buame [N-(3-hydroxy-1,3,5(10)-estratrien-17ß-yl)-butylamine] and Diebud [N,N'-bis-(3-hydroxy-1,3,5(10)-estratrien-17ß-yl)-1,4-butanediamine], were synthesized and characterized using common analytical methods and spectrophotometric analyses. The location and orientation of these molecules on the estrogenic receptor α (ERα) were also evaluated. Platelet inhibitory effects were elucidated ADP-induced platelet aggregation and ADP- and collagen-induced ATP release. Molecular docking demonstrated that Buame can reach and bind to the ERα in the ligand binding domain (LBD) similar to 17ß-estradiol (co-crystallized ligand). On the other hand, Diebud binds only to the surface of ERα due to its high molecular volume compared to 17ß-estradiol and Buame.
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Congéneres del Estradiol/farmacología , Inhibidores de Agregación Plaquetaria/farmacología , Agregación Plaquetaria/efectos de los fármacos , Adenosina Difosfato/farmacología , Adenosina Trifosfato/metabolismo , Adulto , Sitios de Unión , Colágeno/farmacología , Cristalografía por Rayos X , Relación Dosis-Respuesta a Droga , Congéneres del Estradiol/química , Congéneres del Estradiol/metabolismo , Receptor alfa de Estrógeno/química , Receptor alfa de Estrógeno/metabolismo , Humanos , Liposomas/química , Masculino , Persona de Mediana Edad , Modelos Moleculares , Estructura Molecular , Inhibidores de Agregación Plaquetaria/química , Inhibidores de Agregación Plaquetaria/metabolismo , Unión Proteica , Estructura Terciaria de Proteína , Adulto JovenRESUMEN
N-(3-hydroxy-1, 3, 5 (10) estratrien-17beta-yl)-3-hydroxypropylamine (17ß aminoestrogen, prolame) is a steroidal compound with weak estrogen-related trophic-proliferative effects in uterus. Contrasting with 17ß-estradiol (E2) pro-coagulant effects, this compound has high anticoagulant and antiplatelet effects. It has been extensively demonstrated that E2 plays important roles in brain function. However, prolame's influence on central nervous system has not been documented. In this study, we evaluated the effects of prolame replacement in young ovariectomized rats on spatial learning and memory and anxiety, correlating pyramidal cell dendritic spine density changes and neuronal nitric oxide synthase (nNOS) expression in the hippocampus. Ovariectomized young rats were treated with prolame for 4 weeks. Three other groups were used as physiological, pathological, and pharmacological references as follow: gonadally intact cycling females, ovariectomized, and ovariectomized with 17ß-estradiol treatment respectively, for the same time period. Experiment 1 investigated the behavioral effects of prolame on anxiety and spatial learning using elevated plus maze (EPM) and Morris water maze (MWM) paradigms respectively. Experiment 2 studied the dendritic spine density and neuronal nitric oxide synthase expression in the hippocampus of the 4 experimental groups. Similar to estradiol, prolame reversed the anxiogenic effects of ovariectomy, evaluated by EPM, and enhanced MWM performance to the level of gonadally intact subjects. Hippocampi from prolame-treated rats exhibited enhanced nNOS immunoreactivity and its relocation in dendritic compartments, as well as recovery of dendritic spine density loss in pyramidal neurons. Hence, prolame may provide an alternative option for ameliorating neurological symptoms caused by surgical menopause.
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Ansiedad/tratamiento farmacológico , Estrenos/uso terapéutico , Terapia de Reemplazo de Hormonas/psicología , Discapacidades para el Aprendizaje/tratamiento farmacológico , Trastornos de la Memoria/tratamiento farmacológico , Óxido Nítrico Sintasa de Tipo I/biosíntesis , Ovariectomía/efectos adversos , Animales , Espinas Dendríticas/ultraestructura , Modelos Animales de Enfermedad , Evaluación Preclínica de Medicamentos/métodos , Evaluación Preclínica de Medicamentos/psicología , Estradiol/farmacología , Estradiol/uso terapéutico , Estrenos/síntesis química , Estrenos/farmacología , Femenino , Hipocampo/citología , Hipocampo/metabolismo , Terapia de Reemplazo de Hormonas/métodos , Aprendizaje por Laberinto/efectos de los fármacos , Ratas , Ratas WistarRESUMEN
UNLABELLED: Homocysteine is implicated as an early atherosclerotic promoter, which enhances the smooth muscle cell proliferation and produces free radicals that induce cellular damage. These factors must have a role in the progression of atherosclerosis that subsequently leads to vascular mineralization. AIM: Identify a correlation between the plasma concentration of total homocysteine and the amount of minerals that accumulate in the aorta of patients with atherosclerosis. METHODS: We performed a cross-sectional study in 13 patients with three-vessel coronary artery disease, undergoing coronary artery bypass surgery. Aortic and mammary artery specimens were analyzed using a scanning electron microscope with an energy dispersive X-ray spectrometer. The homocysteine was determined using an immunonephelometry method. RESULTS: The amount of minerals in the aorta was greater (300 ± 181.6 particles per 500 µm2 than that in the mammary artery (64 ± 45 particles per 500 µm2 (p < 0.01). The average tHcy was 9.5 ± 2.3 µmol/L. The Spearman's rank correlation coefficient was positive between tHcy, and aortic iron (p < 0.05). CONCLUSIONS: Our study demonstrates that the aorta is dramatically affected by mineralization compared to the mammary artery. In addition, a direct correlation was identified between the levels of tHcy and the iron particles in the aortic wall.
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Calcinosis/etiología , Enfermedad de la Arteria Coronaria/complicaciones , Enfermedades de las Válvulas Cardíacas/etiología , Homocisteína/metabolismo , Arterias Mamarias/patología , Isquemia Miocárdica/complicaciones , Calcinosis/metabolismo , Calcinosis/patología , Enfermedad de la Arteria Coronaria/metabolismo , Enfermedad de la Arteria Coronaria/patología , Estudios Transversales , Femenino , Enfermedades de las Válvulas Cardíacas/metabolismo , Enfermedades de las Válvulas Cardíacas/patología , Humanos , Masculino , Persona de Mediana Edad , Isquemia Miocárdica/metabolismo , Isquemia Miocárdica/patología , PronósticoRESUMEN
Vanadium pentoxide (V(2)O(5)) inhalation effect on platelet function in mice was explored, as well as the in vitro effect on human platelets. Mouse blood samples were collected and processed for aggregometry and flow cytometry to assess the presence of P-selectin and monocyte-platelet conjugates. Simultaneously, human platelets were processed for aggregometry(.) The mouse results showed platelet aggregation inhibition in platelet-rich-plasma (PRP) at four-week exposure time, and normality returned at eight weeks of exposure, remaining unchanged after the exposure was discontinued after four weeks. This platelet aggregation inhibition effect was reinforced with the in vitro assay. In addition, P-selectin preserved their values during the exposure, until the exposure was discontinued during four weeks, when this activation marker increased. We conclude that vanadium affects platelet function, but further studies are required to evaluate its effect on other components of the hemostatic system.
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Plaquetas/efectos de los fármacos , Plaquetas/fisiología , Compuestos de Vanadio/toxicidad , Administración por Inhalación , Contaminantes Atmosféricos/sangre , Contaminantes Atmosféricos/toxicidad , Animales , Células Cultivadas , Humanos , Masculino , Ratones , Ratones Endogámicos , Selectina-P/metabolismo , Activación Plaquetaria/efectos de los fármacos , Agregación Plaquetaria/efectos de los fármacos , Plasma Rico en Plaquetas/efectos de los fármacos , Compuestos de Vanadio/administración & dosificación , Compuestos de Vanadio/sangreRESUMEN
The density of Angiotensin II (Ang) receptors on tissue surfaces is regulated by multiple hormones, cytokines and metabolic factors and is profoundly affected by various pathological conditions, such as age, diet and environmental conditions. The participation of several cardiovascular risk factors in the regulation of Angiotensin II receptor expression has been incompletely studied. We performed an ex-vivo study with human aortic postsurgical specimens to test the hypothesis that Ang AT1 and AT2 receptor expression in human aortic arteries is associated with the presence of cardiovascular risk factors. We included 31 Mexican patients with coronary artery disease. We evaluated Angiotensin II receptor expression by immunostaining and angiotensin converting enzyme insertion/deletion (ACE I/D) polymorphisms by polymerase chain reaction. AT1 and AT2 receptor expression was increased in the aortic segments from the cardiovascular patients compared with control arteries and in patients with the DD genotype. There was a correlation between increased AT1 receptor expression and the number of cardiovascular risk factors present in the patient. Furthermore, reduction of AT1 expression correlated with the number of drug combinations used in the patients. These correlations were not present with respect to AT2 receptor expression. We suggest that increased AT1 receptor expression is associated with the DD genotype. Thus the presence of several cardiovascular risk factors as well as DD genotype, induce AT1 expression increasing the probability to develop coronary occlusive disease.
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Estenosis Coronaria/genética , Predisposición Genética a la Enfermedad , Receptor de Angiotensina Tipo 1/genética , Adulto , Antagonistas de Receptores de Angiotensina/metabolismo , Inhibidores de la Enzima Convertidora de Angiotensina/metabolismo , Aorta/metabolismo , Aorta/patología , Estenosis Coronaria/metabolismo , Estenosis Coronaria/patología , Femenino , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Receptor de Angiotensina Tipo 1/metabolismo , Receptor de Angiotensina Tipo 2/genética , Receptor de Angiotensina Tipo 2/metabolismo , Factores de RiesgoRESUMEN
In this work it is emphasized the presence of the fibrinolitico system in different physiological mechanisms, specially in the antithrombotic regulation of the hemostasis. It is described: the mechanism of activation of plasminogen by their activators as much on the fibrin as in the cells surface; the inhibition of the activators in different metabolic alterations.
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Fibrinólisis/fisiología , Animales , Hemostasis , Humanos , TrombosisRESUMEN
El corazón es el primer órgano que se forma y funciona en el embrión, de tal suerte que todos los eventos subsecuentes en la vida del organismo dependen de la habilidad de este órgano para atender las demandas de oxígeno y nutrientes que éste requiere. Las anormalidades en la formación del corazón, la forma más común de defectos humanos al nacimiento, afecta al 1 % de los nacidos vivos, y su frecuencia en abortos espontáneos se eleva diez veces más. La patofisiología de este tipo de malformaciones congénitas se ha venido enriqueciendo en los últimos años con el conocimiento del Proyecto Genoma Humano; debido al gran avance que se ha producido en el conocimiento genético y molecular de los diferentes genes y cromosomas que suelen ser afectados y muchas veces heredados para producir una enfermedad congénita en general. Esta revisión trata de enfocar su atención sobre la información extraída de los análisis genéticos y moleculares en el diagnóstico, tratamiento y entendimiento de la patogénesis de las enfermedades cardiovasculares pediátricas, dirigidas tanto por los más comunes defectos cardíacos congénitos o heredados, como por los desórdenes esporádicos o adquiridos.
The heart is the first organ to form and function in the embryo, and all subsequent events in the life of the organism depend on the heart's ability to match its output with the organism's demands for oxygen and nutrients. Abnormalities in heart formation, the most common form of human birth defects, afflict nearly 1% of newborns, and their frequency in spontaneously aborted pregnancies is estimated to be tenfold higher. With the completion of the sequencing of the human genome, molecular genetic efforts directed at finding genes for monogenic traits have accelerated dramatically. Breakthroughs in molecular genetic technology have just begun to be applied in pediatric cardiology stemming from the use of chromosomal mapping and the identification of genes involved in both the primary etiology and as significant risk factors in the development of cardiac and vascular abnormalities. This review will focus on information provided by molecular and genetic analysis in the diagnosis, treatment and overall heart disorders.
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Humanos , Cardiopatías/congénito , Cardiopatías/genética , Cardiopatías/diagnóstico , Cariotipificación , Biología Molecular , Técnicas de Diagnóstico MolecularRESUMEN
The heart is the first organ to form and function in the embryo, and all subsequent events in the life of the organism depend on the heart's ability to match its output with the organism's demands for oxygen and nutrients. Abnormalities in heart formation, the most common form of human birth defects, afflict nearly 1% of newborns, and their frequency in spontaneously aborted pregnancies is estimated to be tenfold higher. With the completion of the sequencing of the human genome, molecular genetic efforts directed at finding genes for monogenic traits have accelerated dramatically. Breakthroughs in molecular genetic technology have just begun to be applied in pediatric cardiology stemming from the use of chromosomal mapping and the identification of genes involved in both the primary etiology and as significant risk factors in the development of cardiac and vascular abnormalities. This review will focus on information provided by molecular and genetic analysis in the diagnosis, treatment and overall heart disorders.
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Cardiopatías/congénito , Cardiopatías/genética , Cardiopatías/diagnóstico , Humanos , Cariotipificación , Biología Molecular , Técnicas de Diagnóstico MolecularRESUMEN
Thrombophilia or prothrombotic state appears when activation of blood hemostatic mechanisms overcomes the physiological anticoagulant capacity allowing a thrombotic event. Thrombosis is the leading worldwide mortality cause and due to its high associated morbidity and mortality, it should be insisted in the opportune identification of a thrombophilic state. The study of thrombophilia identifies individuals at high risk for thrombosis. This meeting was conceived first to analyze the current status of the diagnosis of thrombophilia in Mexico and second to create the base for a national consensus for thrombophilia screening and for the establishment of a national center for laboratory reference and quality control for thrombophilia. Since searching of activated protein C resistance (APCR) and FV Leiden seem to have priority either in the clinical setting and in public health services, it was decided to start with these two abnormalities as a model to analyze the current status of thrombophilia diagnosis in the clinical laboratory. At this time, several thrombophilic abnormalities have been described however, APCR remains the most important cause of thrombophilia, accounting for as much as 20% to 60% of all venous thrombosis. APCR is a consequence of the resistance of activated FV to be inactivated by activated protein C. Procoagulant activity of activated FV increases the risk of thrombosis. Hereditary APCR is almost always due to a point mutation at the nucleotide 1691 of the FV gen inducing an Arg506Glu substitution in FV molecule. This mutation is better known as FV Leiden. Heterocygous carriers of FV Leiden have a thrombotic risk 5 to 10 times higher than general population while the risk for the homocygote state is increased 50 to 100-fold. When activated PC is added to plasma from patients with FV Leiden, this last resists the anticoagulant effect of activated PC. Therefore, thrombin production is not inhibited. This phenomenon is called APCR. The functional test evaluates the partially activated thromboplastin time (aPTT) in a plasma sample before and after adding activated PC. The result is reported as a standardized sensibility index: aPTT post-activated PC/aPTT pre-activated PC. The conclusions of this national reunion pretend to optimize the available resources in our country in order to allow a wide and less-expensive diagnosis of patients with thrombosis.
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Resistencia a la Proteína C Activada/diagnóstico , Resistencia a la Proteína C Activada/complicaciones , Resistencia a la Proteína C Activada/epidemiología , Resistencia a la Proteína C Activada/genética , Análisis Mutacional de ADN , Factor V/genética , Genotipo , Laboratorios/normas , Laboratorios/provisión & distribución , Tamizaje Masivo , México/epidemiología , Reacción en Cadena de la Polimerasa , Control de Calidad , Trombofilia/epidemiología , Trombofilia/etiologíaRESUMEN
UNLABELLED: In this prospective, randomized and controlled study, we compare complications in 2 groups of patients: group 1, enoxaparin 0.8 mg/kg, subcutaneous every 12 hours during 5 days, and group 2, intravenous unfractionated heparin during 5 days, by infusion treated to activate partial tromboplastin time 1.5-2 the upper limit of normal. Blood samples were obtained at 4, 12, 24 hours and at day 5 of treatment, to measure anti-Xa levels, and also, evaluated end points at 30 days, between groups. Univariate and multivariate logistic regression analyses were performed with clinical and angiographic variables between groups, with p < 0.05. RESULTS: 203 consecutive patients, average age of 60.5 +/- 11.2 years, and 80% men, were included. There were no differences in clinical and angiographic characteristics. All patients with enoxaparin had therapeutic levels of anti-Xa, of 0.5 to 0.67 U/mL. There was increasing risk of total bleeding in group 2 (18.7%) than in group 1 (5.6%), with RR = 1.72 (95% CI 1.29, 2.29), p = .003. Also, there was 33.3% of MACE in group 2, and only 17.8% in group 1, with RR = 1.88 (CI 95% 1.29, 2.29), p = .011. CONCLUSIONS: 1) Low doses of enoxaparine achieve therapeutic levels, since the first 4 hours of treatment. 2) A significant reduction of total bleeding occurred with the low doses of enoxaparin, with the same efficacy to reduce MACE during follow-up.
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Angina Inestable/tratamiento farmacológico , Anticoagulantes/administración & dosificación , Enoxaparina/administración & dosificación , Hemorragia/prevención & control , Heparina/administración & dosificación , Anciano , Angina Inestable/sangre , Anticoagulantes/sangre , Enoxaparina/sangre , Femenino , Hemorragia/epidemiología , Heparina/sangre , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Factores de RiesgoRESUMEN
Se describe el caso de una lactante menor la cual presentó púrpura fulminante (PF) y coagulación intravascular diseminada (CID) a los dos meses de edad como manifestación de una probable deficiencia homocigota de proteína C (PC). La paciente presentaba además hemorragia del vítreo, sinequia extensa y desprendimiento de retina en el ojo izquierdo. Fue manejada con plasma fresco congelado(PFC) y heparina con buena evolución. En una ocasión, un intento por disminuir la frecuencia de las transfusiones con PFC a un régimen menor de dos veces al día condujo a un nuevo episodio de PF, el cual se controló al reinstituir el régimen de PFC a dos veces al día. Se instituyó tratamiento con warfarina, lo que permitió una supresión paulatina de la terapia con PFC: Se discuten los aspectos relevantes de la deficiencia de PC y se hace la revisión del tema