El control de la hipertensión arterial: precoz y diligente / Controlling high blood pressure: Early and diligent

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Un ensayo clínico que compara control intensivo de presión arterial versus control estándar / A randomized trial of intensive versus standard blood pressure control

Introducción: El objetivo de presión arterial sistólica (PAS) a alcanzar con el tratamiento, para reducir la morbimortalidad cardiovascular (CV) en sujetos sin diabetes no está claramente definido. Objetivo: Comparar 2 estrategias de control de PAS. Métodos: Se aleatorizaron 9.361 sujetos con una PAS igual o mayor de 130mmHg y riesgo elevado, no diabéticos, a un objetivo de PAS menor de 120mmHg (control intensivo) o menor de 140mmHg (control estándar). La variable principal del estudio fue un combinado de infarto agudo de miocardio (IAM), otros síndromes coronarios agudos, ictus, insuficiencia cardíaca o muerte por causa CV. Resultados: Al cabo de un año, los valores medios de PAS eran de 121,4mmHg en el grupo de control intensivo y de 136,2 en el grupo de control estándar. El ensayo se paró antes de los previsto, al cabo de 3,2 años, por una reducción significativa de la variable principal combinada en el grupo de control intensivo (1,65 por año vs. 2,19%; RR: 0,75; IC 95%: 0,64-0,89; p<0,0001). La mortalidad por todas las causas fue también significativamente más baja en el grupo de control intensivo (RR: 0,73; IC 95%: 0,60-0,90; p=0,003). Los efectos secundarios como hipotensión, síncope, alteraciones de electrolitos y fallo renal agudo fueron también más frecuentes en el grupo de tratamiento intensivo. Conclusiones: En los pacientes de alto riesgo CV, no diabéticos, un objetivo de PAS menor de 120mmHg comparado con un objetivo menor de 140mmHg supone un menor riesgo de morbimortalidad CV y mortalidad total con una mayor frecuencia de algunos efectos adversos (AU)

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Health-related quality of life in hypertrophic cardiomyopathy patients with implantable defibrillators.

BACKGROUND: Health-related quality of life (HRQL) in hypertrophic cardiomyopathy (HCM) patients with implantable cardioverter-defibrillators (ICDs) is largely unknown. The aim was to assess HRQL, including comparisons between groups, using the questionnaire SF-36, and compare it to a Swedish age- and sex-matched population. METHODS AND RESULTS: Validated data on adult HCM patients with ICDs were used. The SF-36 response rate was 82.5 % and 245 patients (mean age 55.9 years, 70.2 % men) were analyzed using the Mann-Whitney U-test, t-test, Spearman correlation and effect size calculations. In all SF-36 domains the patients' score was lower (p-value of <0.0001) than norms except for bodily pain. The general health domain showed the highest effect size (0.77) and the impact was more pronounced in the SF-36 physical component summary score (0.62) than the mental component summary score (0.46). Older age was correlated with lower scores on the physical component and higher scores on the mental component. Atrial fibrillation and/or systolic heart failure were associated with worse physical health. HRQL was similar in primary vs secondary prevention cases. Inappropriate ICD shock was associated with worse mental health while appropriate therapy trended toward better mental health. CONCLUSION: HCM patients with ICDs suffer from poor HRQL regardless of age, sex, or primary vs secondary prevention indication. Atrial fibrillation and systolic heart failure are determinants of poor physical health. Inappropriate shocks, but not appropriate therapies, are associated with poorer mental health.

Réplica a «Comentarios al artículo "Tratamiento anestesiológico de la fractura de pelvis 'en libro abierto' secundario a explosión"» / Reply to «Comment on article "Anesthesiology treatment of an 'open book' pelvic fracture due to an explosión"»

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Micropartículas de pequeño tamaño como indicadores del estado agudo en la insuficiencia cardiaca sistólica / Small-size microparticles as indicators of acute decompensated state in ischemic heart failure

Introducción y objetivos. Las micropartículas son marcadores de la activación celular y la apoptosis y podrían aportar una información muy valiosa e inasequible con los datos clínicos. En este estudio se evalúa la relación clínica y biológica entre las micropartículas de pequeño tamaño presentes en diferentes formas de la insuficiencia cardiaca sistólica isquémica y los marcadores de la inflamación y la reparación. Métodos. Se compararon 49 pacientes con insuficiencia cardiaca aguda, 39 con insuficiencia cardiaca estable y 25 pacientes con enfermedad coronaria estable. Se cuantificaron las micropartículas de pequeño tamaño mediante citometría de flujo de alta resolución. Se analizaron también tres subpoblaciones monocitarias diferentes y su expresión de receptores barredores de la inflamación y la adhesión empleando un citómetro de flujo convencional. Resultados. El recuento de micropartículas CD144+ de origen endotelial mostró reducción en los grupos con insuficiencia cardiaca (p = 0,008). Se observó que el recuento de micropartículas unidas a anexina V aumentaban en la insuficiencia cardiaca (p = 0,024) y en los pacientes con peor clase funcional (p = 0,013). El recuento de micropartículas CD42b+ de origen plaquetario presentaron una correlación positiva con la fracción de eyección del ventrículo izquierdo (p = 0,006), y los de micropartículas unidas a anexina V presentaron correlación positiva con la concentración de interleucina 6 en la insuficiencia cardiaca estable (p = 0,034). En el estado agudo, el recuento de micropartículas unidas a anexina V mostró intensa correlación con la expresión del receptor toll-like-4 en todos los subgrupos de monocitos (p < 0,01 en todos los casos). Tres meses después del ingreso por insuficiencia cardiaca aguda, el recuento de micropartículas unidas a anexina V tenía correlación positiva con los receptores de interleucina 6, CD163 y CD204 (p < 0,05 en todos los casos). Conclusiones. El recuento de micropartículas unidas a anexina V es una valiosa característica distintiva del estado agudo descompensado en la insuficiencia cardiaca sistólica. La relación observada entre las micropartículas de pequeño tamaño unidas a anexina V y los receptores barredores respalda su intervención en la progresión de la respuesta aguda a la lesión y, por lo tanto, su contribución en la patogenia de la insuficiencia cardiaca aguda descompensada (AU)

Introduction and objectives. Microparticles are markers for cell activation and apoptosis and could provide valuable information that is not available from clinical data. This study assesses the clinical and biological relationship of small-sized microparticles in different forms of ischemic systolic heart failure and their relation to markers of inflammation and repair. Methods. We compared 49 patients with acute heart failure, 39 with stable heart failure and 25 patients with stable coronary artery disease. Small-size microparticles counts were determined by high-resolution flow cytometry. Moreover, 3 different monocyte subpopulations and their expression of inflammatory and adhesive scavenger receptors were analyzed using a conventional flow cytometer. Results. Endothelial CD144+ microparticle counts were decreased in heart failure groups (P = .008). Annexin V-binding microparticle counts were found increased in heart failure (P = .024) and in patients with lower functional class (P = .013). Platelet CD42b+ microparticle counts positively correlated with left ventricular ejection fraction (P = .006), and annexin V-binding microparticle counts with interleukin-6 levels in stable heart failure (P = .034). Annexin V-binding microparticle counts in the acute status strongly correlated with toll-like receptor-4 expression on all monocyte subsets (all P < .01). Three months after admission with acute heart failure, annexin V-binding microparticle counts were positively correlated with receptors for interleukin-6, CD163 and CD204 (all P < .05). Conclusions. Annexin V-binding microparticle counts constitute valuable hallmarks of acute decompensated state in systolic heart failure. The observed relationship between small-size annexin V-binding microparticles and scavenger receptors supports their involvement in the progression of the acute response to injury, and thus their contribution to the pathogenesis of acute decompensated heart failure (AU)

Blood pressure in hypertensive women after aerobics and hydrogymnastics sessions / Presión arterial en mujeres hipertensas tras sesiones de gimnasia aeróbica y acuática

Introduction: regular exercise has been recommended as an important behavior in controlling blood pressure. In recent years it has been demonstrated that a single session of exercise can lower blood pressure levels compared to pre-exercise period, becoming an effective non-pharmacological therapy for the treatment of hypertension. Objective: the purpose of this study was to analyze the levels of blood pressure in post-exercise period of controlled hypertension women after an aerobics session and a hydrogymnastics session. Methods: twelve elderly (65±3.6 years) who practice regular physical activity for at least two months had their levels of blood pressure measured during 60 minutes after the end of each session. Blood pressure was measured every five minutes after the end of each session until the twentieth minute of recovery. Following, blood pressure was measured every ten minutes. T-student test was used to compare mean and the level of significance adopted was 5%. Results: the mean values of hypotension found during the recovery period after the hydrogymnastics session were not significantly different when compared to blood pressure levels of the pre-exercise period (p=0.260). However, the result of the same comparison for the aerobics session was statistically significant (p<0.001). The lowest values of systolic blood pressure reached in the recovery period for hydrogymnastics (120 mmHg) and aerobics (106 mmHg) were significantly different (p0.001). Conclusions: the aerobics session showed to be more effective in reducing post-exercise blood pressure compared to the hydrogymnastics. After practice aerobics, the participants presented lower blood pressure levels and longer duration of the hypotensive effect (AU)

Introducción: la práctica regular de ejercicios ha sido recomendada como conducta importante en el control de la presión arterial. En los últimos años se ha demostrado que una sola sesión de ejercicio físico puede disminuir la presión arterial comparada a los niveles del periodo pre-ejercicio, convirtiéndose en una terapia no farmacológica efectiva para el tratamiento de la hipertensión. Objetivo: analizar el comportamiento de la presión arterial post-ejercicio en mujeres hipertensas controladas tras la realización de una sesión de gimnasia acuática y una sesión de gimnasia aeróbica. Métodos: participaron en el estudio 12 mujeres mayores con edad de 65±3.6 años y practicantes de actividad física por un periodo superior a dos meses. La presión arterial fue medida durante 60 minutos tras el final de cada clase. Este procedimiento fue realizado cada 5 minutos tras el esfuerzo hasta el vigésimo minuto de la recuperación, seguido de mediciones cada 10 minutos hasta el sexagésimo minuto. Fue utilizado el test T-Student para la comparación de los promedios y fue adoptado un nivel de significación del 5%. Resultados: los promedios de hipotensión encontrados durante la recuperación tras la clase de gimnasia acuática no fueron significativamente diferentes comparados con los promedios obtenidos en el pre-ejercicio (p=0,260). Sin embargo, en la sesión de gimnasia aeróbica la diferencia entre esos valores fue estadísticamente significativa (p<0,001). Los menores valores de presión arterial sistólica alcanzados en la recuperación para gimnasia acuática (120 mmHg) y gimnasia aeróbica (106 mmHg) también fueron significativamente diferentes (p<0,001). Conclusión: la gimnasia aeróbica se mostró más eficiente para la reducción de la presión arterial post-ejercicio con respecto a la gimnasia acuática, presentando menores valores y mayor duración del efecto hipotensor (AU)

La hora del ejercicio en la cronodisrupción, la salud y la enfermedad / No disponible

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Recent progress in end-stage hypertrophic cardiomyopathy.

Within the diverse spectrum of hypertrophic cardiomyopathy (HCM), a unique subgroup characterized by left ventricular enlargement and systolic dysfunction has emerged (defined as end-stage HCM [ES-HCM]). This underestimated entity provides challenging treatment strategies for extremely high risk of refractory heart failure and sudden cardiac death. Over the last 2 decades, the clinical features of ES-HCM have expanded and the underlying mechanisms gradually elucidated. Moreover, there is increasing evidence for early recognition of ES-HCM. New insights into early prevention and management will improve the clinical outcomes of this entity.

[Systolic heart failure in elderly patients]. / Systolische Herzinsuffizienz bei älteren Patienten.

Heart failure is becoming more and more important because of an increasing prevalence in elderly people. Even in healthy elderly individuals there are physiological changes in the cardiovascular system which can be modified by cardiac risk factors and comorbidities and trigger the onset of heart failure. The symptoms in the elderly are often atypical and can be difficult to diagnose in the presence of comorbidities. Echocardiography is important for the diagnosis of heart failure and can be easily and non-invasively performed. This can be complemented by further imaging methods and serological tests, such as determination of the concentrations of brain natriuretic peptide (BNP) and n-terminal pro-brain natriuretic peptide (NTproBNP). In elderly patients the problem of polypharmacy often arises. Therapeutic goals are in particular improvement in the quality of life and of symptoms.

Risk factors for late right ventricular systolic dysfunction in pediatric patients with repaired tetralogy of Fallot.

To evaluate independent risk factors for late right ventricular systolic dysfunction after correction of Tetralogy of Fallot (TOF) in a single-centre, retrospective and observational clinical trial.Patients less than 3 years of age who underwent correction of TOF and subsequently routine clinical follow-up of more than 36 months were included in this study and were divided either into an experimental group (right ventricular systolic dysfunction) or a control group (normal right ventricular systolic function) according to the tricuspid annular peak systolic velocity (TAPSV) value measured by pulsed wave-tissue Doppler imaging (pulsed wave-TDI). The relevant data of all selected patients were investigated and analyzed. From January 2012 to December 2012, a total of 113 consecutive eligible patients were enrolled in this study and were divided either into an experimental group (n = 41) or control group (n = 72). Through univariate analysis and subsequent logistic regression, low preoperative arterial oxygen saturation (OR = 1.66, 95%CI 1.22-4.58, P = 0.0163), age less than 6 months at the time of surgery (OR = 3.45, 95%CI 1.87-9.17, P = 0.0021), and transannular patch (OR = 2.15, 95%CI 1.31-5.38, P = 0.0015) were 3 independent risk factors for late right ventricular systolic dysfunction after correction of TOF.This clinical trial suggested low preoperative arterial oxygen saturation was associated with late right ventricular systolic dysfunction after correction of TOF, and appropriate age at the time of surgery and selection of a proper surgical method to reconstruct the right ventricular outflow tract contributed to improving late right ventricular systolic function in pediatric patients with repaired TOF.

Metformin protects against systolic overload-induced heart failure independent of AMP-activated protein kinase α2.

Activation of AMP-activated protein kinase (AMPK)-α2 protects the heart against pressure overload-induced heart failure in mice. Although metformin is a known activator of AMPK, it is unclear whether its cardioprotection acts independently of an AMPKα2-dependent pathway. Because the role of AMPKα1 stimulation on remodeling of failing hearts is poorly defined, we first studied the effects of disruption of both the AMPKα1 and AMPKα2 genes on the response to transverse aortic constriction-induced left ventricular (LV) hypertrophy and dysfunction in mice. AMPKα2 gene knockout significantly exacerbated the degree of transverse aortic constriction-induced LV hypertrophy and dysfunction, whereas AMPKα1 gene knockout had no effect on the degree of transverse aortic constriction-induced LV hypertrophy and dysfunction. Administration of metformin was equally effective in attenuating transverse aortic constriction-induced LV remodeling in both wild-type and AMPKα2 knockout mice, as evidenced by reduced LV and lung weights, a preserved LV ejection fraction, and reduced phosphorylation of mammalian target of rapamycin (p-mTOR(Ser2448)) and its downstream target p-p70S6K(Thr389). These data support the notion that activation of AMPKα1 plays a negligible role in protecting the heart against the adverse effects of chronic pressure overload, and that metformin protects against adverse remodeling through a pathway that seems independent of AMPKα2.

A pilot study of systolic dyssynchrony index by real time three-dimensional echocardiography and Doppler tissue imaging parameters predicting the hemodynamic response to biventricular pacing in the early postoperative period after cardiac surgery.

OBJECTIVE: To evaluate systolic dyssynchrony index (SDI) measured by real time three-dimensional echocardiography (RT3DE) and Doppler tissue imaging (DTI) dyssynchrony parameters in predicting the hemodynamic response to biventricular (BIV) pacing in the early postoperative period after cardiac surgery. To compare right ventricular (RV) and BIV pacing using invasively measured hemodynamic values. METHODS: A prospective randomized clinical study enrolling 11 patients with ischemic heart disease, concomitant valvular heart disease, and left ventricular ejection fraction (LVEF) ≤ 35% comparing preoperative SDI by RT3DE and DTI LV dyssynchrony parameters to hemodynamic values obtained during RV or BIV sequential (DDD) epicardial pacing in the first 72 hours after cardiac surgery. RESULTS: BIV pacing produced a statistically significant higher cardiac output (CO) (6.27 ± 1.55 L/min) and cardiac index (CI) (3.44 ± 0.93 L/min per m(2) ) than RV pacing (CO 5.44 ± 0.97 L/min, CI 3.03 ± 0.83 L/min per m(2) , P < 0.05). We found a statistically moderate correlation between preoperative SDI by RT3DE and CO (r = 0.596, P < 0.05) and a nonsignificant correlation to CI (r = 0.535, P < 0.10) during BIV pacing. No correlation was observed between DTI dyssynchrony parameters and measured hemodynamic values. BIV pacing reduced the ICU stay and inotropic support requirements of patients after heart surgery. CONCLUSIONS: SDI measured preoperatively using RT3DE can predict CO during BIV pacing in the early postoperative period after cardiac surgery. BIV pacing is more hemodynamically effective than RV pacing in patients with LV dysfunction after coronary artery bypass grafting with or without a valve procedure.

Different determinants of improvement of early and late systolic mitral regurgitation contributed after cardiac resynchronization therapy.

BACKGROUND: Functional mitral regurgitation (MR) at different phases of the regurgitant period may respond differently to cardiac resynchronization therapy (CRT). The aims of this study were to examine the impact of CRT on the phasic changes of MR (early vs late systole) and to explore the mechanisms of such changes. METHODS: Instantaneous MR flow rate and total MR volume were evaluated in 60 patients who had more than mild functional MR before and 3 months after CRT. In addition, indices of global left ventricular (LV) remodeling, mitral deformation, and LV systolic dyssynchrony were assessed. RESULTS: CRT diminished MR volume (38 ± 18 vs 32 ± 20 mL) by reducing both the early (72 ± 47 vs 58 ± 48 mL/sec) and late (48 ± 42 vs 40 ± 42 mL/sec) systolic components (all p values < .01). In patients with ≥10% reductions in total MR volume but not in patients without this improvement, there were significant reductions in LV end-systolic volume, increases in LV +dP/dt, decreases in mitral valvular tenting, and improvements of systolic dyssynchrony at 3 months (all P values < .05). By multivariate regression, the reductions in LV end-systolic volume and tenting area were independent determinants of a reduction in total MR volume: the reductions in LV end-systolic volume and global dyssynchrony determined the reduction in early systolic MR, and the reductions in tenting area and global dyssynchrony determined reduction in late systolic MR. CONCLUSIONS: CRT decreases MR volume by reducing both early and late systolic MR. The determinants of the phasic improvement in functional MR are different.

Insuficiencia cardíaca con función sistólica conservada: fisiopatología / No disponible

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Hypertension and cardiac failure in its various forms.

Hypertension clearly increases the risk of systolic or diastolic heart failure. With aging population and advancements in treatment of cardiovascular diseases, the prevalence of heart failure is ever-increasing and is a principal cause of cardiovascular morbidity and mortality. Treating hypertension has been shown to decrease the risk of development of heart failure and hence underscores the early recognition and treatment of hypertension and hypertensive heart disease. Antihypertensive treatment with drugs from all classes except direct vasodilators is effective in reversing LVH and preventing heart failure. Also, all of the major classes of antihypertensive drugs, particularly beta-blockers and RAS antagonists, with the exception of calcium antagonists, have been shown to improve survival in patients who have LV systolic dysfunction. However, phenotyping and identifying the pathophysiology and appropriate treatments for patients who have diastolic dysfunction and heart failure with preserved ejection fraction has been a daunting task. At this time, treatment of these patients is largely empiric, focusing on BP control, and treating or avoiding intravascular volume overload.

Resolution of established cardiac hypertrophy and fibrosis and prevention of systolic dysfunction in a transgenic rabbit model of human cardiomyopathy through thiol-sensitive mechanisms.

BACKGROUND: Cardiac hypertrophy, the clinical hallmark of hypertrophic cardiomyopathy (HCM), is a major determinant of morbidity and mortality not only in HCM but also in a number of cardiovascular diseases. There is no effective therapy for HCM and generally for cardiac hypertrophy. Myocardial oxidative stress and thiol-sensitive signaling molecules are implicated in pathogenesis of hypertrophy and fibrosis. We posit that treatment with N-acetylcysteine, a precursor of glutathione, the largest intracellular thiol pool against oxidative stress, could reverse cardiac hypertrophy and fibrosis in HCM. METHODS AND RESULTS: We treated 2-year-old beta-myosin heavy-chain Q403 transgenic rabbits with established cardiac hypertrophy and preserved systolic function with N-acetylcysteine or a placebo for 12 months (n=10 per group). Transgenic rabbits in the placebo group had cardiac hypertrophy, fibrosis, systolic dysfunction, increased oxidized to total glutathione ratio, higher levels of activated thiol-sensitive active protein kinase G, dephosphorylated nuclear factor of activated T cells (NFATc1) and phospho-p38, and reduced levels of glutathiolated cardiac alpha-actin. Treatment with N-acetylcysteine restored oxidized to total glutathione ratio, normalized levels of glutathiolated cardiac alpha-actin, reversed cardiac and myocyte hypertrophy and interstitial fibrosis, reduced the propensity for ventricular arrhythmias, prevented cardiac dysfunction, restored myocardial levels of active protein kinase G, and dephosphorylated NFATc1 and phospho-p38. CONCLUSIONS: Treatment with N-acetylcysteine, a safe prodrug against oxidation, reversed established cardiac phenotype in a transgenic rabbit model of human HCM. Because there is no effective pharmacological therapy for HCM and given that hypertrophy, fibrosis, and cardiac dysfunction are common and major predictors of clinical outcomes, the findings could have implications in various cardiovascular disorders.

Chemotherapy and cardiotoxicity.

Newer cancer therapies have improved the survival of patients with cancer and, in some cases, turned cancer into a chronic disease. Patients are now surviving long enough for the adverse cardiovascular effects of some cancer therapies to become apparent. The anthracyclines are perhaps the most notorious offenders. Acute reactions include chest discomfort and shortness of breath consistent with a myopericarditis. Toxicity can also develop months after the last chemotherapy dose and typically presents as new onset heart failure with left ventricular systolic dysfunction. Late reactions are seen years after presentation as new-onset cardiomyopathy, often in patients who were treated for childhood neoplasms. 5-Fluorouracil, its prodrug capecitabine, and trastuzumab, a tumor-specific antibody, have also been associated with cardiotoxicity. Until adequate predictive models, prevention modalities, and treatments can be identified, the clinician's focus should be on aggressive monitoring for early signs of cardiac dysfunction in order to prevent severe systolic dysfunction and its concomitant morbidity and mortality.