Temporal superficial arteritis as differential diagnosis in patients with atherosclerotic changes due to advanced chronic renal disease: case report and review of the literature.

Giant cell arteritis is an autoimmune disease that affects medium and large caliber vessels, creating deposits of inflammatory clusters on the arterial wall. It is the most common form of large vessel vasculitis, but given the variability of biopsy efficiency and of other diagnostic strategies employed, the diagnosis of this disease is challenging. We report the case of a 69-year-old female patient who presented with neurological deficit and increased bilateral sensation in the temporal region associated with excruciating headache. Workup revealed calcification of the superficial temporal, vertebral and ophthalmic arteries, as well as suggestive findings on Doppler ultrasound such as the halo sign, pointing to superficial temporal arteritis though not excluding the possibility of those calcifications being consistent with atherosclerosis in a patient with advanced chronic renal disease, which has been reported as giving rise to false-positive results. Knowledge of the main differences between the 2 diagnoses is important, given the wide range of diagnostic imaging possibilities which can avoid the need for biopsy.

Comprehensive Simulation of Ca2+ Transients in the Continuum of Mouse Skeletal Muscle Fiber Types.

Mag-Fluo-4 has revealed differences in the kinetics of the Ca2+ transients of mammalian fiber types (I, IIA, IIX, and IIB). We simulated the changes in [Ca2+] through the sarcomere of these four fiber types, considering classical (troponin -Tn-, parvalbumin -Pv-, adenosine triphosphate -ATP-, sarcoplasmic reticulum Ca2+ pump -SERCA-, and dye) and new (mitochondria -MITO-, Na+/Ca2+ exchanger -NCX-, and store-operated calcium entry -SOCE-) Ca2+ binding sites, during single and tetanic stimulation. We found that during a single twitch, the sarcoplasmic peak [Ca2+] for fibers type IIB and IIX was around 16 µM, and for fibers type I and IIA reached 10-13 µM. The release rate in fibers type I, IIA, IIX, and IIB was 64.8, 153.6, 238.8, and 244.5 µM ms-1, respectively. Both the pattern of change and the peak concentrations of the Ca2+-bound species in the sarcoplasm (Tn, PV, ATP, and dye), the sarcolemma (NCX, SOCE), and the SR (SERCA) showed the order IIB ≥ IIX > IIA > I. The capacity of the NCX was 2.5, 1.3, 0.9, and 0.8% of the capacity of SERCA, for fibers type I, IIA, IIX, and IIB, respectively. MITO peak [Ca2+] ranged from 0.93 to 0.23 µM, in fibers type I and IIB, respectively, while intermediate values were obtained in fibers IIA and IIX. The latter numbers doubled during tetanic stimulation. In conclusion, we presented a comprehensive mathematical model of the excitation-contraction coupling that integrated most classical and novel Ca2+ handling mechanisms, overcoming the limitations of the fast- vs. slow-fibers dichotomy and the use of slow dyes.

Calibration of mammalian skeletal muscle Ca2+ transients recorded with the fast Ca2+ dye Mag-Fluo-4.

BACKGROUND: Mag-Fluo-4 is increasingly employed for studying Ca2+ signaling in skeletal muscle; however, the lack of information on the Ca2+-Mag-Fluo-4 reaction limits its wider usage. METHODS: Fluorescence and isothermal titration calorimetry (ITC) experiments were performed to determine the binding stoichiometry (n) and thermodynamics (enthalpy (ΔH) and entropy (ΔS) changes), as well as the in vitro and in situ Kd of the Ca2+-Mag-Fluo-4 reaction. Rate constants (kon, koff), fluorescence maximum (Fmax), minimum (Fmin), and the dye compartmentalization were also estimated. Experiments in cells used enzymatically dissociated flexor digitorum brevis fibres of C57BL6, adult mice, loaded at room temperature for 8 min, with 6 µM Mag-Fluo-4, AM, and permeabilized with saponin or ionomycin. All measurements were done at 20 °C. RESULTS: The in vitro fluorescence assays showed a binding stoichiometry of 0.5 for the Ca2+/Mag-Fluo-4 (n = 5) reaction. ITC results (n = 3) provided ΔH and ΔS values of 2.3 (0.7) kJ/mol and 97.8 (5.9) J/mol.K, respectively. The in situ Kd was 1.652 × 105µM2(n = 58 fibres, R2 = 0.99). With an Fmax of 150.9 (8.8) A.U. (n = 8), Fmin of 0.14 (0.1) A.U. (n = 10), and ΔF of Ca2+ transients of 8.4 (2.5) A.U. (n = 10), the sarcoplasmic [Ca2+]peak reached 22.5 (7.8) µM. Compartmentalized dye amounted to only 1.1 (0.7)% (n = 10). CONCLUSIONS: Two Mag-Fluo-4 molecules coalesce around one Ca2+ ion, in an entropy-driven, very low in situ affinity reaction, making it suitable to reliably track the kinetics of rapid muscle Ca2+ transients. GENERAL SIGNIFICANCE: Our results may be relevant to the quantitative study of Ca2+ kinetics in many other cell types.

Efecto de la localización del electrodo ventricular derecho (tracto de salida vs. ápex) sobre la sincronía ventricular mecánica, en pacientes sometidos a terapia de implante de marcapaso cardiaco / Effect of right ventricular electrode location (outflow tract vs. apex) on mechanical ventricular synchrony in patients that underwent pacemaker implant therapy

Objetivo: evaluar a profundidad el efecto de la estimulación ventricular desde el tracto de salida del ventrículo derecho y el ápex, sobre la sincronía ventricular mecánica. Materiales y métodos: estudio analítico de cohorte, en el que se realizó ecocardiograma transtorácico pre y post implante de marcapaso a 20 pacientes (diez por cada grupo) con indicación de marcapaso definitivo, con implante del electrodo en el tracto de salida del ventrículo derecho y el ápex, sin cardiopatía estructural, fracción de eyección > 50 porciento; QRS y conducción aurículo-ventricular normal, con el fin de evaluar la asincronía ventricular mecánica (modo M y Doppler tisular) y los parámetros de implante y programación del dispositivo.Análisis estadístico: los resultados se presentan como promedios, desviación estándar o porcentajes. Las variables continuas se compararon utilizando prueba Chi cuadrado y ANOVA. Se consideró como estadísticamente significativa una p < 0,05.Resultados: en cinco pacientes (25 porciento), se encontró asincronía ventricular pre implante, en siete (70 porciento) asincronía ventricular post implante en el tracto de salida del ventrículo derecho y en cinco (50 porciento) en el ápex. El promedio del retraso interventricular post implante fue de 21,6 ms en el tracto de salida del ventrículo derecho y de 11,5 ms en el ápex (p=0,8). El promedio de retraso septum a pared lateral fue de 73 ms en el tracto de salida del ventrículo derecho y de 26 ms en el ápex (p=0,8). El del QRS post implante fue de 134 ms en el tracto de salida del ventrículo derecho y de 140 ms en el ápex (p=0,1). No hubo diferencias en parámetros de implante y programación del dispositivo. Conclusiones: se evidenció presencia de asincronía ventricular en pacientes con QRS normal y corazón con estructura sana. La estimulación ventricular con marcapaso desde el ápex o el tracto de salida del ventrículo derecho, sugiere asincronía ventricular aguda al menos en 60 porciento de los casos, sin diferencia estadísticamente significativa entre ambos grupos.