sábado, 19 de mayo de 2012

como me veo yo

sE han dado cuenta que las personas mas conspirativas son las que toleran menos las criticas y reclaman confianza  tolerancia y paciencia cuando cuando se trata de ellos mismos. Que las personas mas intolerantes son las que que menos se exigen  asi mismos y se toleran toda clase de cosas incluso la mediocridad.la negligencia la falta de conocimiento. Pueden ver cosas en los demas que no ven en ellos mismos. Tienen definitivamente un problema de percepcion. Pero no contentos con eso tratan de convencer o forzar a los demas para que los vean como ellos quieren que los vean. Como ellos se ven asimismos. Una vision que no concuerda con la realidad que no pueden soportar. Necesitan in ventar una ficcion. Y fuerzan a los demas a vivir dentro de esa ficcion. Como la anorexia nervosa que un desorden de la percepcion. Hay una sreie de desordenes parecidos.

viernes, 2 de marzo de 2012

amandatina para TEC grave

Original Article

Placebo-Controlled Trial of Amantadine for Severe Traumatic Brain Injury

Joseph T. Giacino, Ph.D., John Whyte, M.D., Ph.D., Emilia Bagiella, Ph.D., Kathleen Kalmar, Ph.D., Nancy Childs, M.D., Allen Khademi, M.D., Bernd Eifert, M.D., David Long, M.D., Douglas I. Katz, M.D., Sooja Cho, M.D., Stuart A. Yablon, M.D., Marianne Luther, M.D., Flora M. Hammond, M.D., Annette Nordenbo, M.D., Paul Novak, O.T.R., Walt Mercer, Ph.D., Petra Maurer-Karattup, Dr.Rer.Nat., and Mark Sherer, Ph.D.

N Engl J Med 2012; 366:819-826March 1, 2012

Abstract
Article
References

Background

Amantadine hydrochloride is one of the most commonly prescribed medications for patients with prolonged disorders of consciousness after traumatic brain injury. Preliminary studies have suggested that amantadine may promote functional recovery.

Methods

We enrolled 184 patients who were in a vegetative or minimally conscious state 4 to 16 weeks after traumatic brain injury and who were receiving inpatient rehabilitation. Patients were randomly assigned to receive amantadine or placebo for 4 weeks and were followed for 2 weeks after the treatment was discontinued. The rate of functional recovery on the Disability Rating Scale (DRS; range, 0 to 29, with higher scores indicating greater disability) was compared over the 4 weeks of treatment (primary outcome) and during the 2-week washout period with the use of mixed-effects regression models.

Results

During the 4-week treatment period, recovery was significantly faster in the amantadine group than in the placebo group, as measured by the DRS score (difference in slope, 0.24 points per week; P=0.007), indicating a benefit with respect to the primary outcome measure. In a prespecified subgroup analysis, the treatment effect was similar for patients in a vegetative state and those in a minimally conscious state. The rate of improvement in the amantadine group slowed during the 2 weeks after treatment (weeks 5 and 6) and was significantly slower than the rate in the placebo group (difference in slope, 0.30 points per week; P=0.02). The overall improvement in DRS scores between baseline and week 6 (2 weeks after treatment was discontinued) was similar in the two groups. There were no significant differences in the incidence of serious adverse events.

Conclusions

Amantadine accelerated the pace of functional recovery during active treatment in patients with post-traumatic disorders of consciousness. (Funded by the National Institute on Disability and Rehabilitation Research; ClinicalTrials.gov number, NCT00970944.)

Media in This Article

Figure 1Mean Disability Rating Scale (DRS) Scores during the 6-Week Assessment Period, According to Study Group.
Figure 2Post hoc Analysis of the Distribution of DRS Scores by Outcome Category.

Severe traumatic brain injury is a catastrophic event that frequently has devastating familial, economic, and societal consequences. Traumatic brain injury is the most common cause of death and disability in persons between 15 and 30 years of age.1 The most severe injuries can result in prolonged disorders of consciousness. Approximately 10 to 15% of patients with severe traumatic brain injury are discharged from acute care in a vegetative state,2 a condition in which there is wakefulness without behavioral evidence of conscious awareness.3 The estimated prevalence of a minimally conscious state,4 which is distinguished from a vegetative state by the presence of at least one clearly discernible behavioral sign of consciousness, is 8 times as high as the prevalence of a vegetative state.5 Of patients who are in a vegetative state for at least 4 weeks, approximately 50% will regain consciousness by 1 year.2 Outcomes are generally more favorable for patients who are in a minimally conscious state, although approximately 50% remain severely disabled at 1 year.6-9

No intervention has been shown in rigorous studies to alter the pace of recovery or improve the functional outcome. Neuropharmacologic therapies are commonly used off label to enhance arousal and behavioral responsiveness, on the premise that injury induced derangements in dopaminergic and noradrenergic neurotransmitter systems can be improved through supplementation.

Amantadine hydrochloride is one of the most commonly prescribed medications for patients with disorders of consciousness who are undergoing inpatient neurorehabilitation.10 The mechanism of action is unclear, although amantadine appears to act as an N-methyl-D-aspartate antagonist and indirect dopamine agonist.11 The results of two randomized trials involving patients with traumatic disorders of consciousness suggested that amantadine was effective,12,13 although methodologic limitations, including small samples and unbalanced groups, precluded definitive conclusions.14,15

In 1998, a consortium of brain-injury rehabilitation centers conducted an observational pilot study designed to establish the rate of spontaneous recovery from vegetative and minimally conscious states and provide the basis for a multicenter clinical trial.10 A multiple-regression analysis exploring the effect of cognition-enhancing medications at 16 weeks after injury on scores on the Disability Rating Scale (DRS),16 a measure of functional outcome that is specific to traumatic brain injury, showed better scores at 16 weeks after injury in patients who received amantadine than in those who did not.

On the basis of these findings, we designed the current multicenter, prospective, double-blind, randomized, placebo-controlled trial to determine the effectiveness of amantadine in promoting recovery from a post-traumatic vegetative or minimally conscious state. We hypothesized that 4 weeks of treatment with amantadine administered between 4 and 16 weeks after injury in patients with traumatic disorders of consciousness would improve the rate of functional recovery during the treatment interval, that the improvement would be maintained 2 weeks after drug washout, and that amantadine would be well tolerated.

Methods

Patients and Sites

We conducted this study at 11 clinical sites in three countries. Eligible patients were 16 to 65 years of age, had sustained a nonpenetrating traumatic brain injury 4 to 16 weeks before enrollment, and were receiving usual inpatient rehabilitation at each site. Additional eligibility criteria were a vegetative state or a minimally conscious state, as indicated by a DRS score greater than 11, and an inability both to follow commands consistently and to engage in functional communication, as assessed by the score on the Coma Recovery Scale–Revised (CRS-R).17

The DRS includes measures of eye opening, verbalization, and motor response (derived from the Glasgow Coma Scale); cognitive understanding of feeding, dressing, and grooming; degree of assistance and supervision required; and employability.16 Scores range from 0 to 29, with higher values indicating greater disability (see the Supplementary Appendix, available with the full text of this article at NEJM.org, for details). The CRS-R is a standardized neurobehavioral assessment tool comprising six hierarchically organized subscales (i.e., auditory, visual, motor, oromotor–verbal, communication, and arousal); scores range from 0 to 23, with higher scores indicating a higher level of neurobehavioral function.

Exclusion criteria were any disability related to the central nervous system that predated the traumatic brain injury, medical instability, pregnancy, serious renal disease (estimated creatinine clearance, less than 60 ml per minute), more than one seizure in the previous month, prior treatment with amantadine, and allergy to amantadine. In the case of patients who were undergoing evaluation for ventricular shunt placement or receiving a psychoactive medication, enrollment was deferred until shunt placement had been completed or psychoactive medications discontinued.

Demographic characteristics and baseline functional scores on the DRS and CRS-R were submitted to the data coordinating center through an online portal. Treatment was assigned within centers in random blocks of four or six, with stratification for diagnosis (vegetative state vs. minimally conscious state) and interval between injury and enrollment (28 to 70 days vs. 71 to 112 days), which are factors shown to be predictive of outcomes.3,6,10

Study Oversight

The protocol was approved by the institutional review boards at all participating sites, and written informed consent was obtained from each patient's legally authorized representative. Independent oversight was provided by an external data and safety monitoring board. All data were stored and analyzed by a data coordinating center at Columbia University. The study was conducted in adherence to the protocol, available at NEJM.org. The first and second authors designed the study. All the authors vouch for the accuracy and completeness of the data and for the analysis. The National Institute on Disability and Rehabilitation Research provided all financial support for this study, including funds to purchase amantadine.

Study Procedures

Amantadine and a visually identical placebo were supplied by four compounding pharmacies serving the different study regions. On randomization, the data coordinating center assigned coded medication bottles to patients enrolled at each clinical site. The patients began receiving treatment at a dose of 100 mg twice daily on the day after randomization, with this dose continued for 14 days. The dose was increased to 150 mg twice daily at week 3 and to 200 mg twice daily at week 4 if the DRS score had not improved by at least 2 points from baseline (see Table S1 in the Supplementary Appendix for a breakdown of the drug doses received by patients in each study group). After the week 4 assessment, the study drug was tapered over a period of 2 to 3 days, with assessment of the patients continued through week 6. Additional procedural details are provided in the study protocol.

To minimize exposure to confounding psychoactive medications during the treatment phase, a list of suggested treatments for commonly observed medical problems was compiled. This list was ordered roughly from the least to the most potentially confounding treatment. Treating physicians were requested to follow the order in this list, when possible, in choosing treatments.

Outcomes

The primary outcome was the rate of improvement in the DRS score during the 4 weeks of treatment. DRS scores were collected at baseline and weekly through week 6 on the basis of consensus ratings compiled by the interdisciplinary treatment team.

To gauge the clinical significance of the effects of amantadine, clinically relevant behavioral benchmarks were assessed by study personnel using the CRS-R. We used the CRS-R as a qualitative measure to better understand the effects of the study drug on key behaviors associated with a vegetative state, a minimally conscious state, and emergence from a minimally conscious state.17 We also assessed whether the rate of recovery was altered in the amantadine group during the 2-week washout period. All DRS and CRS-R assessments were conducted by study personnel who were unaware of the group assignments. Adverse events were documented throughout the 6-week assessment period and were coded with respect to their severity, whether they were expected, and whether they were thought by the investigator to be related or possibly related to the study drug. Exposure to other psychoactive drugs was recorded for all patients throughout the 6-week period. All outcome assessments and the final data analysis were conducted without knowledge of group assignments.

Statistical Analysis

The planned sample size of 184 was estimated, on the basis of our previously described pilot study,10 to provide 80% power to detect a difference in the rate of change in the DRS score of 0.3 points per week, or 1.2 points by the end of the 4-week treatment interval. This sample size also provided 90% power to detect an unforeseen adverse event with an incidence of at least 2.5% and allowed estimation of the incidence of adverse events to an accuracy of ±10%. Two blinded interim analyses were conducted after the enrollment of 60 and 120 participants, with the use of the O'Brien–Fleming boundaries and with alpha levels set at 0.0005 and 0.014, respectively. An alpha level of 0.045 was set for the final analysis.

We used t-tests for continuous variables and a chi-square analysis for categorical variables for comparison of the study groups at baseline. We used mixed-effect regression models with random intercepts to test the primary and secondary hypotheses of a difference in the rate of change in the DRS score between the amantadine and placebo groups overall and in stratified subgroups.

The first hypothesis (primary outcome) was assessed by comparing the slope of change in the DRS score over the 4-week treatment period between the two groups, with a negative slope reflecting functional improvement. We conducted a post hoc descriptive analysis of behavioral recovery as defined by the six CRS-R behavioral benchmarks associated with the highest level of cognitive processing on each subscale. Because this analysis was not prespecified in the protocol and was conducted for descriptive purposes only, a statistical comparison of the percentage of patients within each group who were able to engage in these behaviors was not conducted.

The second hypothesis (durability of the treatment effect) was assessed by comparing the slope of change in the DRS score between weeks 4 and 6 in the two groups. Preplanned subgroup analyses were conducted to determine the consistency of the results across the strata of diagnosis (vegetative state vs. minimally conscious state) and interval between injury and enrollment (28 to 70 days vs. 71 to 112 days). An analysis of residuals was conducted to determine model fit. Fisher's exact test was used to compare the proportions of patients who had adverse events in the two groups. The Wilcoxon signed-rank test was used to compare non-normally distributed variables. All analyses were conducted according to the intention-to-treat principle.

Results

Study Participants

Of 1170 patients who were screened for eligibility, 350 met all eligibility criteria and 184 were enrolled (Figure S2 in the Supplementary Appendix). Of these 184 patients, all but 3 (2 assigned to the placebo group and 1 to the amantadine group) completed the study. The amantadine and placebo groups were well matched with respect to major demographic variables and prognostic factors, including the DRS score at baseline, interval between injury and enrollment, and diagnosis at enrollment (Table 1Table 1Demographic and Clinical Characteristics at Baseline.). Of the 184 patients, 154 (84%) missed no more than 4 of the 56 total doses of study medication. The remaining 30 patients (16%) missed between 5 and 52 doses, in most cases owing to transfer to an acute care facility where it was not feasible or was medically inadvisable to continue the study treatment. Approximately one third of the patients received potentially confounding medications (Table S3 in the Supplementary Appendix). Exposure to stimulants and open-label amantadine was uncommon. Antiepileptic drug use was more frequent in the amantadine group (P=0.04), whereas use of narcotic analgesic agents was more frequent in the placebo group (P=0.08).

Outcomes

Both groups had significant improvement in the DRS score over the 4-week treatment interval, but the amantadine group had significantly faster recovery (difference in slope, −0.24 points per week; P=0.007) (Figure 1Figure 1Mean Disability Rating Scale (DRS) Scores during the 6-Week Assessment Period, According to Study Group.) and had fewer dose increases at weeks 2 and 3. Although in both study groups, patients who were enrolled earlier after injury versus later (i.e., 28 to 70 days vs. 71 to 112 days) and those who were in a minimally conscious state rather than a vegetative state at enrollment had faster recovery rates, the treatment effect was consistent across subgroups. The advantage of exposure to amantadine was most pronounced for patients who were enrolled later as compared with those who were enrolled earlier (effect size, −0.40 points vs. −0.19 points). The effect size was similar between diagnostic subgroups (vegetative state, −0.25 points; minimally conscious state, −0.24 points). However, all subgroup effect sizes fell within the 95% confidence interval for the overall effect (95% confidence interval, −0.41 to −0.07 points) (Figure S4 and S5 in the Supplementary Appendix).

More patients in the amantadine group than in the placebo group had favorable outcomes on the DRS, fewer remained in a vegetative state (Figure 2Figure 2Post hoc Analysis of the Distribution of DRS Scores by Outcome Category.), and a greater percentage had recovery of key behavioral benchmarks on the CRS-R at the end of the 4-week treatment period. Statistical comparison of the behavioral benchmarks was not prespecified and therefore was not performed (Figure 3Figure 3Frequency of Recovery of Key Behavioral Benchmarks on the Coma Recovery Scale–Revised (CRS-R).).

During the 2-week washout period, only the placebo group had significant improvement in the DRS score (slope, −0.44 points per week; P<0.001 for the change from the beginning of week 5 to the end of week 6). Although behavioral improvements were generally maintained in the amantadine group, the pace of recovery was significantly slower in the amantadine group (slope, −0.14 points per week; between-group difference in slope, 0.30 points; P=0.02) (Figure 1). The percentage of patients who were able to engage in each of the six clinically relevant behaviors was higher in the amantadine group than in the placebo group at 4 weeks, but the difference was smaller at the 6-week follow-up assessment (Figure 3).

Adverse Events

As expected, medical complications were common (median number of adverse events per patient, 2), with no significant difference in the incidence of adverse events between groups (P>0.20) (Table 2Table 2Adverse Events, According to Treatment Group.). During the course of the trial, one patient in the amantadine group died from cardiac arrest (see Table S6 in the Supplementary Appendix for a list of all serious adverse events).

Discussion

In this international, multicenter, randomized, controlled trial involving patients with post-traumatic disorders of consciousness, we found that the administration of amantadine between 4 and 16 weeks after injury significantly improved the rate of functional recovery over the 4-week period of treatment, as compared with placebo. In keeping with evidence on the rate of change during inpatient rehabilitation,10,18 both groups had improvement during the 4-week period. However, the rate of recovery was more rapid in the amantadine group, affecting functionally meaningful behaviors such as consistent responses to commands, intelligible speech, reliable yes-or-no communication, and functional-object use.

The benefit of amantadine appeared to be consistent, regardless of the interval since injury or whether patients were in a vegetative state or a minimally conscious state at enrollment. Although gains were generally well maintained in the amantadine group after the washout period, the rate of recovery attenuated substantially after treatment was discontinued, and scores on the DRS were largely indistinguishable between the amantadine and placebo groups at the 6-week follow-up assessment. During the 6-week observation period, exposure to amantadine did not increase the risk of adverse medical, neurologic, or behavioral events, including those of greatest concern to clinicians treating this population (e.g., seizure). These findings suggest that amantadine can be used safely at doses between 200 mg and 400 mg in patients with severe traumatic brain injury.

Our findings are consistent with observational reports12,19 suggesting the acceleration of recovery in patients who are receiving amantadine and the deceleration or loss of function after treatment is discontinued. The acute phase of recovery from severe traumatic brain injury is characterized by a brief period of neuronal excitability followed by a longer period of hypoexcitability, involving depletion of multiple neurotransmitters, including dopamine. Amantadine may promote dopaminergic activity by facilitating presynaptic release and blocking reuptake postsynaptically.20,21 The favorable neurobehavioral effects of amantadine may reflect enhanced neurotransmission in the dopamine-dependent nigrostriatal, mesolimbic, and frontostriatal circuits that are responsible for mediating arousal, drive, and attentional functions.

Two case studies that used serial 18F-fluorodeoxyglucose–positron-emission tomography to evaluate the effects of amantadine showed significant increases in prefrontal cortical metabolism22,23 and a nonsignificant increase in striatal D2 dopamine–receptor availability, supporting this proposed mechanism of action. The extent to which the treatment effect was mediated by general improvements in arousal cannot be discerned from this study because arousal functions generally recover in parallel with cognition.

Our study has some limitations. The sample comprised patients admitted to inpatient rehabilitation centers, raising the possibility of selection bias because decisions about admission to a rehabilitation center may be influenced by the probability of further improvement. In addition, nonwhites were underrepresented, potentially limiting the generalizability of the results to nonwhite populations. Second, practical and ethical constraints required the use of a brief treatment interval and a short term assessment of the outcome, because we anticipated that caregivers would withdraw patients who were not making gains in order to try other treatments. Thus, our findings do not address the effects of prolonged treatment on long-term outcomes. Third, we did not restrict standard rehabilitation interventions, so we cannot determine the degree to which the benefits of amantadine are independent of or synergistic with such standard treatments. Fourth, despite attempts to limit the use of potentially confounding psychoactive drugs, such drugs were used frequently. However, exposure to other psychoactive drugs would be expected either to block the benefits of amantadine in treated patients or to provide alternative mechanisms for similar benefits in the placebo group, thereby reducing rather than exaggerating the magnitude of the difference between the groups. Finally, we did not use continuous electroencephalographic monitoring to detect seizures; however, a high incidence of amantadine-induced subclinical seizures would be expected to slow rather than accelerate functional recovery.

We conclude that amantadine is effective in accelerating the pace of recovery during acute rehabilitation in patients with prolonged post-traumatic disturbances in consciousness. Exposure to amantadine is associated with more rapid emergence of cognitively mediated behaviors that serve as the foundation for functional independence. The rate of recovery in the amantadine group slowed and between-group behavioral differences diminished during the washout period, suggesting that the response is drug-dependent. Whether treatment with amantadine, as compared with placebo, improves the long-term outcome or simply accelerates recovery en route to an equivalent level of function remains unknown. In view of health care cost constraints and declining lengths of stay for inpatient rehabilitation,24 amantadine-induced acceleration of recovery may represent an important advance. Future research should focus on determining the pathophysiological characteristics of patients who have a response to amantadine, the most effective dosage and duration of treatment and timing of its initiation, and the effectiveness of amantadine in patients with nontraumatic brain injuries.

Supported by a grant from the National Institute on Disability and Rehabilitation Research (H133A031713).

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

Drs. Giacino and Whyte contributed equally to this article.

Source Information

From the JFK Johnson Rehabilitation Institute, Edison, NJ (J.T.G., K.K., A.K.); Spaulding Rehabilitation Hospital and Department of Physical Medicine and Rehabilitation, Harvard Medical School (J.T.G.), and Department of Neurology, Boston University School of Medicine (D.I.K.) — all in Boston; Moss Rehabilitation Research Institute, Albert Einstein Healthcare Network, Elkins Park (J.W., S.C.), and Brain Injury Program, Bryn Mawr Rehab Hospital, Malvern (D.L.) — both in Pennsylvania; Department of Biostatistics, Mailman School of Public Health, Columbia University, New York (E.B.); Texas NeuroRehab Center, Austin (N.C., W.M.); SRH Fachkrankenhaus Neresheim, Neresheim (B.E., P.M.-K.), and Schön Klinik Bad Aibling, Bad Aibling (M.L.) — both in Germany; Braintree Rehabilitation Hospital, Braintree, MA (D.I.K.); Methodist Rehabilitation Center, Jackson, MS (S.A.Y., M.S.); Division of Physical Medicine and Rehabilitation, University of Alberta, Edmonton, Canada (S.A.Y.); Department of Physical Medicine and Rehabilitation, Carolinas Rehabilitation, Charlotte, NC (F.M.H.); Indiana University School of Medicine, Indianapolis (F.M.H.); Department of Neurorehabilitation, Traumatic Brain Injury Unit at Copenhagen University Hospital, Glostrup, and Hvidovre Hospital, Hvidovre — both in Denmark (A.N.); Sunnyview Rehabilitation Hospital, Schenectady, NY (P.N.); and TIRR Memorial Hermann, Houston (M.S.).

Address reprint requests to Dr. Giacino at the Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, 125 Nashua St., Boston, MA 02114, or at .

viernes, 23 de diciembre de 2011

Re: Saludos Navideños

y donde estas?
con razon que no vas a jugar fulbito
 cmori

El 22 de diciembre de 2011 15:53, Juan Carlos Carril Alvarez <carrilalvarezjc@hotmail.com> escribió:
Buenas tardes amigos :  en esta oportunidad les envio un fuerte abrazo y saludos por estas fiestas navideñas , espero que lo pasen con mucha felicidad y amor para uds y sus familias y que  a pesar de la distancia los llevo  muy presente , saludos para el resto de amigos de la Familia Casimirina .
Un saludo muy fuerte para uds.
 
        Juan Carlos Carril Alvarez

domingo, 20 de noviembre de 2011

ketorolaco

digemid HA retirado ketorolaco 60 mg endovenoso no sabemos con que criterios. El asunto es que se recomienda para crisis de migraña siendo muy efectivo y mucho mas barato que los triptanos.Sn embargo en casimiro ulloa hay ketorolaco de 30 mg ev.
Y que?  no puede comprar directamente esterptokinasa en el extranjero
 cmori
 
 
 

First page of article

First page of 2008: The Year in Review
 
 

First page of article

First page of 2008: The Year in Review

sábado, 12 de noviembre de 2011

no hay estrepto

El TASK FORCE de infarto de miocardio dice que si un infartocon supradesnivel del ST    es pequeno se debe usar estreptoquinaza, si es grande alteplase si es extenso o esta shocado el paciente angioplastia. Sin embargo el hospital solo tiene alteplase. Refieren que la esterptokinasa ha sido retirada del mercado?. Acaso el estado no la puede comprar directamente. Acaso solo los ricos se pueden trombolizar. El alteplase esta costando 5000 soles. Y una angioplastia puede llegar a costar hasta 20,000  25,000 dolares

martes, 8 de noviembre de 2011

VI CURSO DE CARDIOLOGIA INTERVENCIONISTA


 

VI CURSO INTERNACIONAL DE INTERVENCIONISMO CARDIOVASCULAR


 
Organizado por la Sociedad Peruana de Cardiología
Sábado 19 de Noviembre de 2011
Plaza del Bosque Hotel
 
INSCRIPCION DE CORTESIA

 

 


P R O G R A M A
 
08:45 - 09:00       Inauguración por el Presidente de la Sociedad Peruana de Cardiología
                    Dr. Mario Zubiate 
 
MODERADOR   Dra. Bertha Gonzáles
 
09:00 -09.30 Inflamación, ateroesclerosis y aterotrombosis 
              Dr. Félix Medina
 
09:30 - 10:00 Terapia coadyuvante en intervencionismo  
         Dr. Aldo Castañeda
 
10:00 – 10:30       Stent medicados y no medicados
                            Dr. Jorge Casana
 
10:30 – 11:00  Intervencionismo periférico
                            Dr. Bernardo Treistman (USA)
 
11:00 – 11:30 Carótidas y circulación intracraneal
                            Dr. Michel Mawad (USA)
 
11:30 – 11:45       Preguntas
 
11:45 – 12:00       Break
 
MODERADOR   Dr. Federico Osores
 
12:00 – 12:30      Intervención Percutánea SCASTNE 
Dr. Ricardo Coloma
 
12:30 – 13:00 Intervención Percutánea  SCASTE
Dr. Enrique Bustos
 
13:00 – 13:30       Lesiones en bifurcaciones 
                            Dr. José Ercilla
 
13:30-15:30 Almuerzo
 
 
MODERADOR   Dr.  Plinio Obregón
 
15:30 – 16:00 Intervención Percutánea en  Tronco de Coronaria Izquierda
Dr. Walter Mogrovejo
 
16.00 -16:30 Intervención en  Múltiples vasos
Dr. Orestes Salazar
 
16:30 – 17:00 Intervención Coronaria Percutánea Transradial
  Dr. Luis Mejía
 
17:00 – 17:15 Preguntas
 
17:15 – 17:30       Break
 
MODERADOR   Dr. Carlos Sánchez
 
17:30 – 18:00 Infarto Miocárdico en el periprocedimiento y protección
  de embolismos
                              Dr. César Conde
 
18:00 – 18:30 Intervención en territorios vasculares distales
  Dr. Rodolfo Rojas
 
18:30 – 18:45 Preguntas
 
18:45 – 19:45 SIMPOSIUM
          Prótesis valvular aórtica por vía percutánea
                                     Dr. 
                                  
19:45  Clausura por el Vocal de Acción Científica
      Dr. Guillermo Bustamante

 


CONFIRMAR ASISTENCIA, SE ADJUNTA FICHA DE INSCRIPCION.


E-MAIL:   sopecard@hotmail.com


TELEFONOS:   4216999    -   4415932

---------- Mensaje reenviado ----------
De: Sociedad Peruana de Cardiologia <sopecard@hotmail.com>
Fecha: 7 de noviembre de 2011 13:07
Asunto: VI CURSO DE CARDIOLOGIA INTERVENCIONISTA
Para: Sociedad Peruana de Cardiologia <sopecard@hotmail.com>



VI CURSO INTERNACIONAL DE INTERVENCIONISMO CARDIOVASCULAR

 

Organizado por la Sociedad Peruana de Cardiología

Sábado 19 de Noviembre de 2011

Plaza del Bosque Hotel

 

INSCRIPCION DE CORTESIA




P R O G R A M A

 

08:45 - 09:00       Inauguración por el Presidente de la Sociedad Peruana de Cardiología

                    Dr. Mario Zubiate 

 

MODERADOR   Dra. Bertha Gonzáles

 

09:00 -09.30 Inflamación, ateroesclerosis y aterotrombosis 

              Dr. Félix Medina

 

09:30 - 10:00 Terapia coadyuvante en intervencionismo  

         Dr. Aldo Castañeda

 

10:00 – 10:30       Stent medicados y no medicados

                            Dr. Jorge Casana

 

10:30 – 11:00  Intervencionismo periférico

                            Dr. Bernardo Treistman (USA)

 

11:00 – 11:30 Carótidas y circulación intracraneal

                            Dr. Michel Mawad (USA)

 

11:30 – 11:45       Preguntas

 

11:45 – 12:00       Break

 

MODERADOR   Dr. Federico Osores

 

12:00 – 12:30      Intervención Percutánea SCASTNE 

Dr. Ricardo Coloma

 

12:30 – 13:00 Intervención Percutánea  SCASTE

Dr. Enrique Bustos

 

13:00 – 13:30       Lesiones en bifurcaciones 

                            Dr. José Ercilla

 

13:30-15:30 Almuerzo

 

 

MODERADOR   Dr.  Plinio Obregón

 

15:30 – 16:00 Intervención Percutánea en  Tronco de Coronaria Izquierda

Dr. Walter Mogrovejo

 

16.00 -16:30 Intervención en  Múltiples vasos

Dr. Orestes Salazar

 

16:30 – 17:00 Intervención Coronaria Percutánea Transradial

  Dr. Luis Mejía

 

17:00 – 17:15 Preguntas

 

17:15 – 17:30       Break

 

MODERADOR   Dr. Carlos Sánchez

 

17:30 – 18:00 Infarto Miocárdico en el periprocedimiento y protección

  de embolismos

                              Dr. César Conde

 

18:00 – 18:30 Intervención en territorios vasculares distales

  Dr. Rodolfo Rojas

 

18:30 – 18:45 Preguntas

 

18:45 – 19:45 SIMPOSIUM

          Prótesis valvular aórtica por vía percutánea

                                     Dr. 

                                  

19:45  Clausura por el Vocal de Acción Científica

      Dr. Guillermo Bustamante



CONFIRMAR ASISTENCIA, SE ADJUNTA FICHA DE INSCRIPCION.


E-MAIL:   sopecard@hotmail.com 


TELEFONOS:   4216999    -   4415932








domingo, 30 de octubre de 2011

Pediatrics in Review & NeoReviews all 2011 issues

Soplo cardiaco

De Wikipedia, la enciclopedia libre

Los soplos cardiacos (o soplos del corazón) son ruidos patológicos que se perciben a la auscultación con el uso del estetoscopio y se originan por aumento de flujo a través de una válvula cardiaca normal, por alteraciones de dichas válvulas (estenosis, insuficiencia, doble lesión), por ciertas anomalías intracardiacas (comunicación interventricular) o extracardiacas (estenosis arteriales, ductus arterioso persistente, fístulas arteriovenosas).

Contenido

[editar] Clasificación

Auscultograma con sonidos normales y anormales

Los soplos pueden ser clasificados por 7 diferentes características: Tiempo, forma, posición, irradiación, intensidad, calidad y tono.

  • El tiempo se refiere a si es sistólico o diastólico.
  • La forma se refiere al patrón de intensidad que tiene el soplo. Puede ser, constante, en crescendo, decrescendo o una mezcla de estos dos últimos.
  • La localización se refiere al lugar en donde el soplo tiene su mayor intensidad. Existen 6 lugares de auscultación en la cara anterior del tórax:
    • Segundo espacio intercostal derecho
    • Segundo a quinto espacio intercostal izquierdo
    • Quinto espacio intercostal en línea medioclavicular izquierdo.
  • La irradiación se refiere al lugar hacia donde el soplo se irradia. En general, el sonido se irradia siguiendo la dirección del flujo sanguíneo.
  • La intensidad se refiere a la potencia del sonido, el cual va de 0 a 6 (se escribe con números romanos Ejemplo: II/VI)
  • El tono puede variar según sea bajo o alto
  • La calidad se refiere a las características especiales que pueda tener cada soplo (por ejemplo, musical, en rodada, soplante etc...)

[editar] Clasificación según intensidad

Grading of Murmurs[1] La plantilla {{ref}} está obsoleta, véase el nuevo sistema de referencias.
Grado Descripción
Grado 1 Muy tenue
Grado 2 Suave
Grado 3 Audible en todo la región precordial
Grado 4 Ruidoso, con frémito palpable
Grado 5 Muy ruidoso, con frémito palpable. Puede ser escuchado con el estetoscopio alejado de la piel.
Grado 6 Muy ruidoso, con frémito palpable. Puede ser audible con el estetoscopio totalmente alejado del pecho del paciente.


[editar] Véase también



---------- Forwarded message ----------
From: Edwin Villacorta <evillitaz@yahoo.com>
Date: 2011/10/29
Subject: [SALUD_LORETO] Rv: [medicpass] Pediatrics in Review & NeoReviews all 2011 issues
To: Salud Loreto <salud_loreto@yahoogroups.com>


 



Edwin Villacorta Vigo
 


--- El sáb, 10/29/11, tamer ibrahim <drtameribrahim@gmail.com> escribió:

NeoReviews

Pediatrics in Review

    all 2011 issues

 

Download from our sharing folder:

http://NeoReviews.4shared.com/

http://PediatricsInReview.4shared.com/

--

no mires la paja en el ojo ajeno cuando tienes la viga en el tuyo

es un rasgo del ser humano ver en los demas los errores o defectos que no ve en el mismo. O reconocer defectos en los demas que no ve en si mismo. El corrupto llama corrupto al corrupto. El escapero de la guardia llama escapero al otro escapero. El que no esta capacitado llama incapacitado al otro incapacitado. El impuntual llama impuntual al otro impuntual. Cree que porque guarda las apariencias no es como el otro. No importa si te portas bien en realidad. Lo que importa es aparentar que lo haces, ser solapa. Es pegado al pie de la letra con las reglas pero solo cuando le conviene. Solo para aparentar para enganar a los demas que lo es o para enganarse a si mismo que lo es. Cuando sus amigos cometen faltas graves se sale y viola las normas. Ahi no es pegado a las reglas. Doble moral. Honestidad  de barro.En algunos casos la inclinacion a ver errores en los demas que uno tambien tiene  es obsesiva alcanzando el nivel neurotico. Cuando alguien con estas caracteristicas tiene poder delegado por alguna institucion se generan muchos problemas.  El tiene problemas para ser un lider. Y las instituciones  sin lideres tendran problemas. Todos tenemos afan de reconocimiento. Dicen que eso es mas fuerte que el hambre o el deseo de libertad. Por eso florecen los nacionalismos sobre todo en sociedades con individuos no individualistas.
El critica y sanciona al que llega tarde pero el se escapa de la guardia. Es muy peruano, el cree que tiene privilegios, que esta por encima de las reglas pero no los demas. O protege a sus amigos que lo hacen. O protege a sus amigos que cometen graves faltas de negligencia que le cuestan la vida a personas. Al mismo tiempo te critica cuando tu cometes una negligencia que no le cuesta la vida a nadie. Por supuesto que en ambos casos no hay disculpa. Te critica y raja de ti porque llegas  tarde. Pero el llega cochino al hospital impresentable. Por supuesto que ambos casos no tienen disculpa.
Te critica porque llegas tarde pero el es un medico parasito. Siempre esta buscando que lo programen en areas de poco trabajo o poco stress. Siempre esta buscando diluir sus responsabilidades trabajar menos lo menos posible  comprometiendo en sus propias responsabilidades a otros medicos cuando el podria y debiera resolver sus problemas solo. Te critica cuando tu cometes un error medico pero el nunca hace nada para no cometer errores. El continuamente comete errores por omision que a veces cuestan vidas pero el no lo ve o no quiere verlo. Total en Peru no existen auditorias de nada para que preocuparse. A veces llega al nivel sociopatico cinico de creer que los demas no se dan cuenta de como es o como actua. El cree que porque los demas son educados y lo sobrellevan no se dan cuenta. Claro este ya es otro nivel, el nivel sociopatico. El nivel del cinico del manipulador, del que trata de matarte moralmente porque es demasiado cobarde para hacerlo fisicamente.


cmori

miércoles, 26 de octubre de 2011

martes, 4 de octubre de 2011

Revisan el Tratamiento de Control del Asma en los Niños [Archivo adjunto 1]

[Más abajo se incluyen archivos adjuntos de johnny sandoval garay]
 
Adjunto revisión original
                 Atentamente
               Johny Sandoval Garay
                        Pediatra
                         RNE 21209


----- Mensaje reenviado -----
De: "wolfmdped@yahoo.com" <wolfmdped@yahoo.com>
Para: Salud Loreto <SALUD_LORETO@yahoogroups.com>
Enviado: martes 4 de octubre de 2011 14:54
Asunto: [SALUD_LORETO] Revisan el Tratamiento de Control del Asma en los Niños


 
Saludos amigos,

http://www.bago.com/BagoArg/Biblio/pediatweb581.htm

Enviado desde mi BlackBerry de Claro.

 

 

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Archivos adjuntos de johnny sandoval garay
Archivo 1 de 1
 Pediatric_Asthma_Controller_Therapy.2.pdf

---------- Mensaje reenviado ----------
De: johnny sandoval garay <johnysanga@yahoo.es>
Fecha: 4 de octubre de 2011 15:52
Asunto: Rv: [SALUD_LORETO] Revisan el Tratamiento de Control del Asma en los Niños [Archivo adjunto 1]
Para: salud loreto <Salud_loreto@yahoogroups.com>, Pediatras <PEDIATRIA_PERU@yahoogroups.com>, ramirez felix mechato <beto1355@hotmail.com>, Huanca David <dhuancap@gmail.com>, Santos Aida Saby Borcic <aidaborcic@hotmail.com>, Roncal Marco <antonioroncal@yahoo.com>, Calle Carlos Enrique Checa <drcarloscheca@yahoo.es>, Flores Vigo Admer <aflovi100@gmail.com>, Valera Lazo Tomas <tomasvalera25@hotmail.com>, Pardo Marìa <maripardo74@hotmail.com>, Roncal Marco <marcoroncal@yahoo.es>, Rojas David <darogue1111@yahoo.es>, Vite Juarez Nora <noravitejuarez@hotmail.com>, Martinez Delgado Humberto <beto1244@hotmail.com>, OMAR JHON <jhomgavi11@hotmail.com>, Guffanti Giancarlo <gjguffantia@hotmail.com>, Contreras Carreño Jose julian <pepeju8@hotmail.com>, prado julio <juliopradoa.q.p@hotmail.com>, gonzalesS luis <Lgdlav@yahoo.com>, gonzales luis <lgdlav@yahoo.com>, Baltazar Luis <luisbar2000@hotmail.com>, flores nube <nubeflores@hotmail.com>, "carmen.armas@hotmail.com" <carmen.armas@hotmail.com>, LAVI ROSARIO REATEGUI <charlav3@hotmail.com>, Millones LLorca Luz Melina <sheccid_224@hotmail.com>, more clara <cl_more@hotmail.com>, Fernandez Loperz Graciela Angela <graciela_enf@hotmail.com>, Cordova Dersy <dersy160975@hotmail.com>, Calderon Patricia <recalmen_40@hotmail.com>, Maribel <rosamari78@hotmail.com>, Alcedo Mariella <ela_ac@hotmail.com>, Susana <susan1180@hotmail.com>, Bertha <enferberlu_2@hotmail.com>, Dioselinda <yossy882@hotmail.com>, Chapoñan Claudia <sagi18_73@hotmail.com>, Sarita <saritac19@hotmail.com>, Rubio Rubio Sonia <soniarubiorubio@yahoo.com>, Lorena <loemi01@hotmail.com>, Simbaña Rivera Aurora <asir755@hotmail.com>, ITURRIA Deysi <empera_2010@hotmail.com>, Tecnica Rosa <rosa_rpv55@hotmail.com>, Briceño Infante Cecilia Elvira <miel_y_jazmin@hotmail.com>, Pouicon Roxana <roxy312@hotmail.com>, "tatiaagu@hotmail.com" <tatiaagu@hotmail.com>


 
[Más abajo se incluyen archivos adjuntos de johnny sandoval garay]

Adjunto revisión original
                 Atentamente
               Johny Sandoval Garay
                        Pediatra
                         RNE 21209

----- Mensaje reenviado -----
De: "wolfmdped@yahoo.com" <wolfmdped@yahoo.com>
Para: Salud Loreto <SALUD_LORETO@yahoogroups.com>
Enviado: martes 4 de octubre de 2011 14:54
Asunto: [SALUD_LORETO] Revisan el Tratamiento de Control del Asma en los Niños

 
Saludos amigos,

http://www.bago.com/BagoArg/Biblio/pediatweb581.htm

Enviado desde mi BlackBerry de Claro.



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Archivos adjuntos de johnny sandoval garay

Archivo 1 de 1

 

lunes, 26 de septiembre de 2011

Guías salud mental MINSA-PERU


Maximo Cuadros Chavez posted in cibermedicos.
Maximo Cuadros Chavez12:02pm Sep 26
Guías salud mental MINSA-PERU
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Fecha: 26 de septiembre de 2011 12:02
Asunto: [cibermedicos] Guías salud mental MINSA-PERU
Para: cibermedicos <internetymedicos@groups.facebook.com>


Maximo Cuadros Chavez posted in cibermedicos.
Guías salud mental MINSA-PERU...
Maximo Cuadros Chavez 12:02pm Sep 26
Guías salud mental MINSA-PERU
http://www.minsa.gob.pe/portada/est_san/saludmental.htm
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lunes, 19 de septiembre de 2011

Acute Myocardial Ischaemia Update 2011


Acute Myocardial Ischaemia Update 2011

Link
http://www.mediafire.com/?mavm1nd4yttdaxc


Murillo Santucci Cesar de Assunção
Unidade de Terapia Intensiva adulto
Disciplina de Anestesiologia, Dor e Terapia Intensiva
Escola Paulista de Medicina
Rua Napoleão de Barros,715
Vila Clementino - São Paulo - CEP: 04024-002
Tel/Fax: +55-11-55757768
Tel/Fax: +55-11- 55764069
m.assuncao@unifesp.br
murilloassuncao@gmail.com

---------- Forwarded message ----------
From: Murillo Santucci Cesar de Assunção <murilloa@uol.com.br>
Date: 2011/9/19
Subject: [interno_residente_medico_PERU] Acute Myocardial Ischaemia Update 2011
To: UTI - Anestesiologia UNIFESP <uti-anestesiologia@yahoogrupos.com.br>


Acute Myocardial Ischaemia Update 2011

pact.jpg 
Acute Myocardial Ischaemia Update 2011

Link
http://www.mediafire.com/?mavm1nd4yttdaxc
Murillo Santucci Cesar de Assunção
Unidade de Terapia Intensiva adulto
Disciplina de Anestesiologia, Dor e Terapia Intensiva
Escola Paulista de Medicina
Rua Napoleão de Barros,715
Vila Clementino - São Paulo - CEP: 04024-002
Tel/Fax: +55-11-55757768
Tel/Fax: +55-11- 55764069




domingo, 11 de septiembre de 2011

] Captado por una cámara del transito.. Reflexión!!!



---------- Mensaje reenviado ----------
De: Mauricio Oyuela Pavón <dr.maoy.blackberry@gmail.com>
Fecha: 8 de septiembre de 2011 23:15
Asunto: [SALUD_LORETO] Captado por una cámara del transito.. Reflexión!!!
Para: Salud Loreto <salud_loreto@yahoogroups.com>


 


 
La vida es solo un soplo, adios a los resentimientos, hay que aprovechar las segundas oportunidades, y mantenerce en paz con DIOS y las personas que quieres.
 
ESPERA QUE CARGE PARA QUE LO OBSERVES BIEN  

Son 3 segundos para que nuestra vida termine, y sin tener la culpa.




La vida es tan corta para levantarnos en la mañana con tristezas Así es que, comienza tu día con una oración, ama a tu familia que se preocupa por ti sinceramente, atesora a tus amigos, Olvida a los que te hacen daño, manténte en paz con Dios por sobre todo. Y cree que las cosas suceden por una razón. Si te dan una oportunidad aprovéchala, existen las segundas oportunidades, si hiciste algo mal reivindícate y no lo vuelvas a hacer. Nadie dice que será fácil.  Solo te puedo asegurar que valdrá la pena.
 

__._,_.___