Prevalencia de resistencia plaquetaria a clopidogrel en pacientes sometidos a intervencion coronaria percutanea

Los agentes antiplaquetarios son el principal tratamiento para pacientes con síndromes coronarios agudos, han demostrado reducción en el riesgo de muerte, infarto del miocardio, y necesidad de revascularización urgente. Algunos pacientes presentan eventos cardiacos mayores a pesar de recibir estos medicamentos. El impacto de la resistencia a los medicamentos ha sido material de múltiples estudios. En Colombia no existen estadísticas sobre la resistencia al Clopidogrel.En nuestro estudio la prevalencia de resistencia a Clopidogrel por el método de agregometria plaquetaria por transferencia de luz con muestras tomadas entre el día 7 y el 10 post angioplastia, está por encima del promedio internacional en nuestra población, lo que amerita la realización de nuevos estudios por las implicaciones pronosticas que pudieran tener en términos de eventos cardiovasculares adversos.

Adherencia a criterios de pertinencia de revascularización coronaria del colegio americano de cardiología, servicio de hemodinamia Fundación Cardioinfantil- Bogotá 2011

Titulo: Adherencia a criterios de pertinencia de revascularización coronaria del colegio americano de cardiología 2009, en el servicio de hemodinámica de la fundación cardioinfantil Bogotá 2011. Introducción: La enfermedad cardiovascular es la principal causa de morbimortalidad a nivel mundial, teniendo mayor prevalencia enfermedad coronaria. Existen guías especificas para el manejo de esta enfermedad sin embargo su aplicación se entorpece por factores diversos. Este estudio quiere evaluar la adherencia, en el laboratorio de hemodinamia de la Fundación Cardioinfantil, a las guías de pertinencia de intervencionismo coronario de la ACCF (American college of cardiology foundation). Objetivo General: Evaluar el nivel de adherencia a criterios de pertinencia de revascularización coronaria del colegio americano de cardiología 2009, en el servicio de hemodinámia de la fundación cardioinfantil Bogotá 2011. Métodos: Se revisaron 200 historias clínicas pacientes con diagnóstico de síndrome coronario agudo, llevados a intervención coronaria, según características de pacientes , intervención, y nivel de adherencia se clasifico la intervención como apropiada, incierta e inadecuada . Resultados: De la población analizada, el 71% (n=142) de las intervenciones fueron clasificados como apropiadas, 20% (N=40) como inapropiadas y 8,5% (n=17) como inciertas. Los desenlaces y complicaciones no tuvieron asociación estadísticamente significativa (p> 0,005) con la adherencia a los criterios de pertinencia. Conclusiones: Respecto a la literatura existente el número de intervenciones inapropiadas es mayor en la FCI, comparado con estudios practicados en América Latina y Norte América, sin embargo una adherencia del 80 %, ubica a esta institución en un adecuado nivel de adherencia.

Prevalencia de anormalidades estructurales cardiacas en pacientes con enfermedad isquémica. Bogotá 2007 – 2009

Introducción: Las enfermedades cardiovasculares son la causa de muerte más frecuente en el mundo desarrollado, la mayoría de éstas se relacionan con alteraciones de las arterias coronarias, sin embargo un subgrupo de pacientes presentan como causa de isquemia cardiaca alteraciones estructurales. Material y métodos: Estudio Descriptivo. Se utilizó la base de datos recolectada en un servicio de hemodinamia de Bogotá durante dos años. Se aplicaron criterios de inclusión y exclusión y se determinaron cuatro grupos etáreos, a todos los pacientes se les practicó cateterismo cardiaco diagnóstico. Las variables analizadas fueron: diagnóstico de referencia, antecedentes y resultados del cateterismo incluyendo presencia de anomalías estructurales como las valvulopatias, el origen anómalo de las coronarias y los puentes miocárdicos. Para el análisis descriptivo se utilizó reporte de prevalencias y para el análisis de asociaciones se utilizaron tablas de contingencia y el estadístico de prueba Chi cuadrado, no se realizó análisis multivariado debido a que no se encontraron asociaciones estadísticamente significativas. Resultados: La edad promedio de los pacientes fue de 62 años (DS= 10,5), la representación del género masculino fue del 61,7%, la prevalencia de angina estable fue del 61,6%, los 3 antecedentes más prevalentes fueron: hipertensión arterial (41,4%), la hiperlipidemia (19,1%) y la Diabetes Mellitus (17,7%). La prevalencia de las alteraciones estructurales en la población de estudio de manera general fue del 12,9%, y su distribución por tipo fue: 1,4% para puentes miocárdicos, 0,7% para origen anómalo de las arterias coronarias y 10,8% de enfermedad valvular. Conclusiones: Se encontró una asociación entre los antecedentes médicos y la presencia de valvulopatias cardiacas. Se evidenció que el género no tiene relación con la presencia de alteraciones cardíacas a pesar de la mayor participación de hombres en la población de estudio. Las limitantes de este estudio se relacionaron con el tamaño de muestra, debido a la baja prevalencia de las anomalías estructurales medidas.

Factores asociados con la duración del circuito extracorpóreo en terapias continúas de reemplazo renal en la Fundación Cardioinfantil

Introducción: las terapias continuas de reemplazo renal son una importante medida a utilizar en los pacientes con lesión renal aguda que ingresan a la unidad de cuidado intensivo, la pérdida temprana del circuito por coagulación del mismo es una situación que afecta a este grupo de pacientes. Materiales y métodos: se realizo un estudio de casos y controles de una duración de tres meses tomando los pacientes que eran sometidos a terapia continua de reemplazo renal en la fundación Cardioinfantil, se eligieron como casos aquellos pacientes que no lograban completar 72 horas de terapia por perdida del circuito relacionada con coagulación, y aquellos que si se tomaron como controles, se analizaron ambos grupos en función de diferentes variables demográficas, clínicas y del circuito, tomando como análisis primario el primer filtro utilizado y haciendo un análisis secundario incluyendo todos los filtros. Resultados: se recolectaron 24 pacientes para el análisis primario y 101 filtros para el análisis secundario, el 37,5% de los filtros duró > 72 horas y 62,5%, menos de este tiempo. El puntaje APACHE II (OR: 0,76, p 0.003) y sitio de inserción femoral derecho (OR: 0.14, p 0.007) se encontraron protectoras para la disfunción temprana. Discusión: aunque no se alcanzó la muestra total, se encontró asociación protectora del acceso femoral derecho, que fue novedosa, pero requiere confirmación. El APACHE II, también protector, puede corresponder a un sesgo, se necesitan más estudios para aclarar estos hallazgos y determinar la presencia de otras variables que intervengan.

Marine omega-3 fatty acids and coronary heart disease

Purpose of review: To provide an overview of the key earlier intervention studies with marine omega-3 fatty acids and to review and comment on recent studies reporting on mortality outcomes and on selected underlying mechanisms of action. Recent findings: Studies relating marine omega-3 fatty acid status to current or future outcomes continue to indicate benefits, for example, on incident heart failure, congestive heart failure, acute coronary syndrome, and all-cause mortality. New mechanistic insights into the actions of marine omega-3 fatty acids have been gained. Three fairly large secondary prevention trials have not confirmed the previously reported benefit of marine omega-3 fatty acids towards mortality in survivors of myocardial infarction. Studies of marine omega-3 fatty acids in atrial fibrillation and in cardiac surgery-induced atrial fibrillation have produced inconsistent findings and meta-analyses demonstrate no benefit. A study confirmed that marine omega-3 fatty acids reduce the inflammatory burden with advanced atherosclerotic plaques, so inducing greater stability. Summary: Recent studies of marine omega-3 fatty acids on morbidity of, and mortality from, coronary and cardiovascular disease have produced mixed findings. These studies raise new issues to be addressed in future research.

Anti-platelet effect of aspirin is substantially reduced after administration of heparin during carotid endarterectomy

OBJECTIVES: Aspirin therapy is usually continued throughout the perioperative period to reduce the risk for thromboembolic stroke and myocardial infarction after carotid endarterectomy (CEA). Aspirin irreversibly binds cyclooxygenase-1, thereby reducing platelet aggregation for the lifetime of each platelet. However, recent research from this unit has shown that aggregation in response to arachidonic acid increases significantly, but transiently, during CEA, which suggests that the anti-platelet effect of aspirin is temporarily reversed. The purpose of the current study was to determine when this phenomenon occurs and to identify the possible mechanisms involved. METHODS: Platelet aggregation was measured in platelet-rich plasma from 41 patients undergoing CEA who were stabilized with 150 mg of aspirin daily. Blood was taken at 8 time points: before anesthesia, after anesthesia, before heparinization, 3 minutes after heparinization, 3 minutes after shunt insertion, 10 minutes after flow restoration, 4 hours postoperatively, and 24 hours postoperatively. Platelet aggregation was also measured at similar times in a group of 18 patients undergoing peripheral angioplasty without general anesthesia. RESULTS: All patient platelets were effectively inhibited by aspirin at the start of the operation. There was a significant intraoperative increase in platelet response to arachidonic acid in both groups of patients, which occurred within 3 minutes of administration of unfractionated heparin. In the CEA group this resulted in a greater than 10-fold increase in mean aggregation, to 5 mmol/L of arachidonic acid (5 mmol/L), rising from 3.9% +/- 2.2% preoperatively to 45.1% +/- 29.3% after administration of heparin ( P <.0001). This increased aggregation persisted into the early postoperative period, but by 24 hours post operation aggregation had returned to near preoperative values. Aggregation in response to other platelet agonists (adenosine diphosphate, thrombin receptor agonist peptide) showed only a small increase at the same time, which could be accounted for by a parallel increase in the level of spontaneous aggregation. CONCLUSION: Administration of heparin significantly increases platelet aggregation in response to arachidonic acid, despite adequate inhibition by aspirin administered preoperatively. This apparent reversal in anti-platelet activity persisted into the immediate early postoperative period, and could explain why a small proportion of patients are at increased risk for acute cardiovascular events after major vascular surgery, despite aspirin therapy.

Effects of losartan on ventricular remodeling in experimental infarction in rats

OBJECTIVE: To evaluate the effects of losartan on ventricular remodeling and on survival after myocardial infarction in rats. METHODS: After surgical occlusion of left coronary artery, 84 surviving male Wistar rats were divided into two groups: LO treated with losartan (20mg/kg/day, n=33) and NT (n=51), without medication. After 3 months, we analyzed mortality; ventricular to body mass ratio (VM /BM); myocardial hydroxyproline concentration (HOP); isovolumetric pressure, +dp/dt, -dp/dt, and diastolic volume/left ventricle mass ratio (VO/LV). RESULTS: Mortality was: LO = 22%, and NT = 47% (p<0.05). Ventricular mass,(VM/BM, mg/g) was 4.14 ± 0.76 and 3.54±0.48, in the NT and LO groups, respectively (p<0.05). HOP (median) was 4.92 upsilong/mg in the LO and 5.54 upsilong/g in the NT group (p>0.05). The V0/LV values (median) were 0.24 mL/g in group LO and 0.31 mL/g in group NT (p<0.05) compared to NT group. There were no differences between the groups for +dp/dt and -dp/dt parameters. CONCLUSION: 1- The use of losartan myocardial infarction causes an attenuation of ventricular remodeling, bringing about an increased survival, an attenuation of ventricular hypertrophy and dilation, and an improvement of the isovolumetric pressure; 2- the treatment does not modify the myocardial collagen concentration.

A administração precoce de hormônio de crescimento resulta em efeitos deletérios na remodelação ventricular após o infarto agudo do miocárdio

Objective: To assess the effect of growth hormone (GH) on myocardial remodeling in infarcted rats. Methods: This study comprised 24 Wistar rats divided into 3 groups as follows: 1) AMI-GH group - comprising 8 rats that underwent infarction and were treated with GH; 2) AMI group - comprising 8 rats that underwent infarction and received only the diluent of the GH solution; and 3) control group (C group) - comprising 8 rats that underwent simulated infarction. After 30 days, the animals underwent functional study through echocardiography, and the changes in myocardial contractility of the isolated left ventricular (LV) papillary muscle were studied. Results: The echocardiography identified an increase in the diastolic (C=7.32±0.49; AMI=8.50±0.73; AMI-GH=9.34±0.73; P<0.05) and systolic (C=3.38±0.47, AMI=5.16±1.24; AMI-GH=5.96±1.54; P<0.05) diameters (mm) in the LV of the infarcted animals. The AMI-GH group animals had a lower ejection fraction (%) (C=0.9±0.03; AMI=0.76±0.12; AMI-GH=0.72± 0.14; P<0.05 for C vs AMI-GH) compared with those in controls. The study of the isolated left ventricular papillary muscle showed that the AMI-GH group had changes (C=1.50±0.59; AMI= 1.28±0.38; AMI-GH=1.98±0.41; P<0.05 for C vs AMI-GH) only in the tension at rest (TR - g/mm2) and in the time delta for a 50% decrease in the tension developed (TR50, ms) after stimulation with calcium (C=23.75±9.16; AMI=-16.56±14.82; AMI-GH=-4.69±8.39; P<0.05 for C vs AMI-GH) and in the delta of tension developed (TD, g/mm2) after stimulation with isoproterenol (C=0.99±0.17; AMI=0.54±0.62; AMI-GH=0.08±0.75; P<0.05 for C vs AMI-GH) compared with those in control animals. Conclusion: The early administration of GH in the experimental infarction model in rats may result in adverse effects on the process of ventricular remodeling.

Avaliação da função cardíaca em cães com anemia normovolência aguda experimental

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Estratificação de risco e desfechos clínicos em pacientes com síndrome coronariana aguda em classe funcional de Killip I ou II

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Influência da suplementação de tomate e licopeno na remodelação cardíaca após infarto agudo do miocárdio

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Production of Human Antibody Fragments Binding to Melittin and Phospholipase A2 in Africanised Bee Venom: Minimising Venom Toxicity

The hybrid created from the crossbreeding of European and African bees, known as the Africanised bee, has provided numerous advantages for current beekeeping. However, this new species exhibits undesirable behaviours, such as colony defence instinct and a propensity to attack en masse, which can result in serious accidents. To date, there is no effective treatment for cases of Africanised bee envenomation. One promising technique for developing an efficient antivenom is the use of phage display technology, which enables the production of human antibodies, thus avoiding the complications of serum therapy, such as anaphylaxis and serum sickness. The aim of this study was to produce human monoclonal single-chain Fv (scFv) antibody fragments capable of inhibiting the toxic effects of Africanised bee venom. We conducted four rounds of selection of antibodies against the venom and three rounds of selection of antibodies against purified melittin. Three clones were selected and tested by enzyme-linked immunosorbent assay to verify their specificity for melittin and phospholipase A2. Two clones (C5 and C12) were specific for melittin, and one (A7) was specific for phospholipase A2. In a kinetic haemolytic assay, these clones were evaluated individually and in pairs. The A7-C12 combination had the best synergistic effect and was chosen to be used in the assays of myotoxicity inhibition and lethality. The A7-C12 combination inhibited the in vivo myotoxic effect of the venom and increased the survival of treated animals.

US Food and Drug Administration approval of generic versions of complex biologics: implications for the practicing physician using low molecular weight heparins

Low-molecular-weight heparins (LMWHs) have shown equivalent or superior efficacy and safety to unfractionated heparin as antithrombotic therapy for patients with acute coronary syndromes. Each approved LMWH is a pleotropic biological agent with a unique chemical, biochemical, biophysical and biological profile and displays different pharmacodynamic and pharmacokinetic profiles. As a result, LMWHs are neither equipotent in preclinical assays nor equivalent in terms of their clinical efficacy and safety. Previously, the US Food and Drug Administration (FDA) cautioned against using various LMWHs interchangeably, however recently, the FDA approved generic versions of LMWH that have not been tested in large clinical trials. This paper highlights the bio-chemical and pharmacological differences between the LMWH preparations that may result in different clinical outcomes, and also reviews the implications and challenges physicians face when generic versions of the original/innovator agents are approved for clinical use.

Adipose Tissue-Derived Stem Cell Treatment Prevents Renal Disease Progression

Adipose tissue-derived stem cells (ASCs) are an attractive source of stem cells with regenerative properties that are similar to those of bone marrow stem cells. Here, we analyze the role of ASCs in reducing the progression of kidney fibrosis. Progressive renal fibrosis was achieved by unilateral clamping of the renal pedicle in mice for 1 h; after that, the kidney was reperfused immediately. Four hours after the surgery, 2 x 10(5) ASCs were intraperitoneally administered, and mice were followed for 24 h posttreatment and then at some other time interval for the next 6 weeks. Also, animals were treated with 2 x 10(5) ASCs at 6 weeks after reperfusion and sacrificed 4 weeks later to study their effect when interstitial fibrosis is already present. At 24 h after reperfusion, ASC-treated animals showed reduced renal dysfunction and enhanced regenerative tubular processes. Renal mRNA expression of IL-6 and TNF was decreased in ASC-treated animals, whereas IL-4. IL-10, and HO-1 expression increased despite a lack of ASCs in the kidneys as determined by SRY analysis. As expected, untreated kidneys shrank at 6 weeks, whereas the kidneys of ASC-treated animals remained normal in size, showed less collagen deposition, and decreased staining for FSP-1, type I collagen, and Hypoxyprobe. The renal protection seen in ASC-treated animals was followed by reduced serum levels of TNF-alpha, KC, RANTES, and IL-1 alpha. Surprisingly, treatment with ASCs at 6 weeks, when animals already showed installed fibrosis, demonstrated amelioration of functional parameters, with less tissue fibrosis observed and reduced mRNA expression of type I collagen and vimentin. ASC therapy can improve functional parameters and reduce progression of renal fibrosis at early and later times after injury, mostly due to early modulation of the inflammatory response and to less hypoxia, thereby reducing the epithelial-mesenchymal transition.

Myocardial Remodeling after Large Infarcts in Rat Converts Post Rest-Potentiation in Force Decay

Background: Post-rest contraction (PRC) of cardiac muscle provides indirect information about the intracellular calcium handling. Objective: Our aim was to study the behavior of PRC, and its underlying mechanisms, in rats with myocardial infarction. Methods: Six weeks after coronary occlusion, the contractility of papillary muscles (PM) obtained from sham-operated (C, n = 17), moderate infarcted (MMI, n = 10) and large infarcted (LMI, n = 14) rats was evaluated, following rest intervals of 10 to 60 seconds before and after incubation with lithium chloride (Li+) substituting sodium chloride or ryanodine (Ry). Protein expression of SR Ca(2+)-ATPase (SERCA2), Na+/Ca2+ exchanger (NCX), phospholamban (PLB) and phospho-Ser(16)-PLB were analyzed by Western blotting. Results: MMI exhibited reduced PRC potentiation when compared to C. Opposing the normal potentiation for C, post-rest decays of force were observed in LMI muscles. In addition, Ry blocked PRC decay or potentiation observed in LMI and C; Li+ inhibited NCX and converted PRC decay to potentiation in LMI. Although MMI and LMI presented decreased SERCA2 (72 +/- 7% and 47 +/- 9% of Control, respectively) and phospho-Ser(16)-PLB (75 +/- 5% and 46 +/- 11%, respectively) protein expression, overexpression of NCX (175 +/- 20%) was only observed in LMI muscles. Conclusion: Our results showed, for the first time ever, that myocardial remodeling after MI in rats may change the regular potentiation to post-rest decay by affecting myocyte Ca(2+) handling proteins. (Arq Bras Cardiol 2012;98(3):243-251)