La atención urgente al ictus en el "Cinturón del ictus" español / Emergency stroke care in Spain's "Stroke Belt"

No disponible

Ictus cardioembólico / Cardioembolic stroke

Hombre de 77 años que consulta por debilidad del brazo izquierdo y disartria. Refiere haber sido diagnosticado de hipertensión arterial y estar recibiendo enalapril/hidroclorotiazida, sin un control adecuado de su presión arterial. Ha sido fumador de 2 paquetes/día y sigue fumando en la actualidad. Ingresa en urgencias unos 90min después del comienzo de sus síntomas. No refiere cefalea, náuseas o vómitos. Su presión arterial es de 182/104mmHg con pulso irregular a 88 latidos por minuto. En la exploración neurológica se objetiva disartria, hemianopsia homónima izquierda, debilidad muscular e hipoestesia de miembros izquierdos. ¿Cómo debe ser evaluado y tratado este enfermo?(AU)

A 77-year old man who consulted due to left arm weakness and dysarthria. He reported having been diagnosed of high blood pressure and that he was taking enalapril/hydrochlorothiazide without adequate blood pressure control. He had smoked 2 packs of cigarettes a day and continues to smoke at present. He was admitted to the emergency service about 90min after the onset of his symptoms. He did not report headache, nausea or vomiting. His BP was 182/104mmHg, with irregular pulse at 88 beats per minute. The neurological examination revealed dysarthria, left homonymous hemianopsia, muscle weakness and hypoesthesia of the left limbs. How should this patient be evaluated and treated?(AU)

[Cardioembolic stroke]. / Ictus cardioembólico.

A 77-year old man who consulted due to left arm weakness and dysarthria. He reported having been diagnosed of high blood pressure and that he was taking enalapril/hydrochlorothiazide without adequate blood pressure control. He had smoked 2 packs of cigarettes a day and continues to smoke at present. He was admitted to the emergency service about 90 min after the onset of his symptoms. He did not report headache, nausea or vomiting. His BP was 182/104 mmHg, with irregular pulse at 88 beats per minute. The neurological examination revealed dysarthria, left homonymous hemianopsia, muscle weakness and hypoesthesia of the left limbs. How should this patient be evaluated and treated?

[Non-pharmacological measures in the secondary prevention of atherothrombic stroke of the elderly. Current status of the subject]. / Medidas no farmacológicas en la prevención secundaria del ictus aterotrombótico del anciano. Estado actual de la cuestión.

Stroke represents a primary health problem in the elderly population. It is the first cause of mortality in women over 65 years, and that of men over 75 years in our country. Atheromatous carotid disease (ACD) is a fundamental etiological factor for the development of ischemic stroke. It is known that approximately 10% of the subjects with stroke have carotid stenosis of 50% or greater. Non-pharmacological management of the ACD in elderly subjects is an increasingly more frequent clinical problem in the daily practice and a subject that is traditionally under debate. The aim of this article is to review the current status of knowledge on this controversial subject and to be able to apply it to our clinical practice.

Medidas no farmacológicas en la prevención secundaria del ictus aterotrombótico del anciano. Estado actual de la cuestión / Non-pharmacological measures in the secondary prevention of atherothrombic stroke of the elderly. Current status of the subject

El ictus representa un problema de salud importante en la población anciana, constituyendo en nuestro país la primera causa de mortalidad en las mujeres mayores de 65 años, y la de los hombres mayores de 75 años. La enfermedad carotídea ateromatosa (ECA) es un factor etiológico fundamental para el desarrollo de ictus isquémico. Se sabe que aproximadamente el 10% de los sujetos con ictus presentan una estenosis carotídea del 50% o superior. El manejo no farmacológico de la ECA en los sujetos ancianos es un problema clínico cada vez más frecuente en la práctica diaria, y un tema tradicionalmente sujeto a debate. El objetivo de este artículo es revisar el estado actual de los conocimientos sobre esta controvertida cuestión, para así poder aplicarlo a nuestra práctica clínica (AU)

Stroke represents a primary health problem in the elderly population. It is the first cause of mortality in women over 65 years, and that of men over 75 years in our country. Atheromatous carotid disease (ACD) is a fundamental etiological factor for the development of ischemic stroke. It is known that approximately 10% of the subjects with stroke have carotid stenosis of 50% or greater. Non-pharmacological management of the ACD in elderly subjects is an increasingly more frequent clinical problem in the daily practice and a subject that is traditionally under debate. The aim of this article is to review the current status of knowledge on this controversial subject and to be able to apply it to our clinical practice (AU)

Procedural outcomes and long-term survival among patients undergoing percutaneous coronary intervention of a chronic total occlusion in native coronary arteries: a 20-year experience.

OBJECTIVES: The study compared procedural outcomes and long-term survival for patients undergoing percutaneous coronary intervention (PCI) of a chronic total coronary artery occlusion (CTO) with a matched non-CTO cohort to determine whether successful PCI of a CTO is associated with improved survival. BACKGROUND: Percutaneous coronary intervention of a CTO is a common occurrence, and the long-term survival for patients with successful PCI of a CTO has not been clearly defined. METHODS: Between June 1980 and December 1999, a total of 2,007 consecutive patients underwent PCI for a CTO. Utilizing propensity scoring methods, a matched non-CTO cohort of 2,007 patients was identified and compared to the CTO group. The cohorts were stratified into successful and failed procedures. RESULTS: The in-hospital major adverse cardiac event (MACE) rate was 3.8% in the CTO cohort. Technical success has improved over the last 10 years (overall 74.4%, slope 1.0%/yr, p = 0.02, R2 = 49.9%) as did procedural success (overall 69.9%, slope 1.2%/yr, p = 0.02, R2 = 51.5%) without a concomitant increase in in-hospital MACE rates (slope 0.1%/yr, p = 0.7). There was a distinct 10-year survival advantage for successful CTO treatment compared with failed CTO treatment (73.5% vs. 65.1%, p = 0.001). The CTO versus non-CTO 10-year survival was the same (71.2% vs. 71.4%, p = 0.9). Diabetics in the CTO cohort had a lower 10-year survival compared with nondiabetics (58.3% vs. 74.3%, p < 0.0001). CONCLUSIONS: These data represent follow-up of the largest reported series of patients undergoing PCI for a CTO. The 10-year survival rates for matched non-CTO and the CTO cohorts were similar. Success rates have continued to improve without an accompanying increase in MACE rates. A successfully revascularized CTO confers a significant 10-year survival advantage compared with failed revascularization.

Shear stress stimulation of p130(cas) tyrosine phosphorylation requires calcium-dependent c-Src activation.

Fluid shear stress (flow) modulates endothelial cell function via specific intracellular signaling events. Previously we showed that flow activated ERK1/2 in an integrin-dependent manner (Takahashi, M., and Berk, B. C. (1996) J. Clin. Invest. 98, 2623-2631). p130 Crk-associated substrate (Cas), a putative c-Src substrate, was originally identified as a highly phosphorylated protein that is localized to focal adhesions and acts as an adapter protein. Recent reports have shown that Cas is important in cardiovascular development and actin filament assembly. Flow (shear stress = 12 dynes/cm(2)) stimulated Cas tyrosine phosphorylation within 1 min in human umbilical vein endothelial cells. Phosphorylation peaked at 5 min (3.5 +/- 0.7-fold) and was sustained to 20 min. Tyrosine phosphorylation of Cas was functionally important because flow stimulated association of Cas with Crk in a time- and force-dependent manner. Flow-mediated activation of c-Src, phosphorylation of Cas, and association of Cas with Crk were all inhibited by calcium chelation and pretreatment with the Src family-specific tyrosine kinase inhibitor PP1. To determine the role of c-Src in flow-stimulated phosphorylation of Cas, we transduced cells with adenovirus encoding kinase-inactive Src. Expression of kinase-inactive Src prevented flow-induced Cas tyrosine phosphorylation but not ERK1/2 activation. Calcium-dependent activation of c-Src and tyrosine phosphorylation of Cas defines a new flow-stimulated signal pathway, different from ERK1/2 activation. This pathway may be involved in focal adhesion remodeling and actin filament assembly.

Agonist-stimulated cytoskeletal reorganization and signal transduction at focal adhesions in vascular smooth muscle cells require c-Src.

Thrombin and angiotensin II (angII) have trophic properties as mediators of vascular remodeling. Focal adhesions and actin cytoskeleton are involved in cell growth, shape, and movement and may be important in vascular remodeling. To characterize mechanisms by which thrombin and angII modulate vessel structure, we studied the effects of these G protein-coupled receptor ligands on focal adhesions in vascular smooth muscle cells (VSMCs). Both thrombin and angII stimulated bundling of actin filaments to form stress fibers, assembly of focal adhesions, and protein tyrosine phosphorylation at focal adhesions, such as p130Cas, paxillin, and tensin. To test whether c-Src plays a critical role in focal adhesion rearrangement, we analyzed cells with altered c-Src activity by retroviral transduction of wild-type (WT) and kinase-inactive (KI) c-Src into rat VSMCs, and by use of VSMCs from WT (src+/+) and Src-deficient (src-/-) mice. Tyrosine phosphorylation of Cas, paxillin, and tensin were markedly decreased in VSMCs expressing KI-Src and in src-/- VSMCs. Expression of KI-Src did not inhibit stress fiber formation by thrombin. Surprisingly, actin bundling was markedly decreased in VSMCs from src-/- mice both basally and after thrombin stimulation, compared with src+/+ mice. We also studied the effect of KI-Src and WT-Src on VSMC spreading. Expression of KI-Src reduced the rate of VSMC spreading on collagen, whereas WT-Src enhanced cell spreading. In conclusion, c-Src plays a critical role in agonist-stimulated cytoskeletal reorganization and signal transduction at focal adhesions in VSMCs. c-Src kinase activity is required for the cytoskeletal turnover that occurs in cell spreading, whereas c-Src appears to regulate actin bundling via a kinase-independent mechanism.

Alterations in the mechanical properties of the lung during dyspnea in chronic obstructive pulmonary disease.

The mechanical properties of the lungs in seven patients with chronic obstructive pulmonary disease (COPD) were measured before and during dyspnea on exertion, as well as when relief with added oxygen was obtained. Mean pulmonary dynamic compliance was 0.091 liters/cm of H(2)O before dyspnea, 0.057 during dyspnea, and 0.101 liters/cm H(2)O during relief. During dyspnea there was an increase in the total respiratory work (both elastic and nonelastic work) and this fell during relief with oxygen. Nonelastic resistance and respiratory rate were not significantly different during the three periods. In five similar patients a progressive increase in the instantaneous rate of change of transpulmonary pressure (dP/dt) was observed during exercise and this was markedly increased during dyspnea. These changes in dP/dt during exercise could explain the observed fall of pulmonary dynamic compliance.