Az iszkémiás és posztiszkémiás vaszkuláris és kardiorespiratorikus károsodások tanulmányozása = Investigation of apparent injury in the vascular and cardiorespiratory system due to ischemia and reperfusion

((1) A szívhipertrófiát irányító GATA-4 transzkripciós faktort a mitogén-aktiválta protein kinázok (p38, ERK) aktiválják mechanikai feszítés során. (2) Kamrai falfeszülés az endogén endothelin-1 és az angiotenzin II révén váltja ki a BNP expressziójának fokozódását. (3) Az endogén ouabain-szerű anyag szerepet játszik az ANP bal kamrai génexpressziójának szabályozásában. (4) A nukleáris faktor-kappaB transzkripciós faktor gátlása kivédi a bal kamrai remodellinget annak előrehaladott fázisában. (5) A szívizom-kontraktilitás szabályozásában döntő szerepet játszanak a mitogén aktiválta protein kinázok. (6) Viabilitás, coronária occlusios idő okozta bal kamra funkció változás vizsgálata MRI-vel. Az occlusios idő 45 és 90 perc között változtatvan proporcionálisan rontotta a bal kamra funkciót, mely mögött okként az arányos infarctus méret áll. (7) Humán mitrokondriumok nem termelnek relevans mennyiségű nitrogén oxidot iszkémiás szívbetegekben. (8) A flavonoid szupplementáció előnyös hatású krónikus obstruktív tüdőbetegségben. (9) Invazív módon validáltuk az artériás stifness meghatározására szolgáló non-invazív Arteriográf készüléket. (10) Jellemeztük a szérum asszimmetrikus dimetil-arginin változását katéteres revascularizatios eljáráson átesett betegeknél. (11) A poli-ADP-ribóz polimeráz enzim gátlása javítja a bal kamrai funkciót akut és krónikus experimentális szívelégtelenségben. (12) A szívritmus variabilitás vizsgálatára hatékony elemző rendszert fejlesztettünk ki. | (1) Our results suggest that the prohypertrophic transcription factor GATA-4 is activated by mitogen-activated protein kinases (p38, ERK) in response to mechanical stretch. (2) Stretch-induced activation of B-type natriuretic peptid gene expression is regulated by endogenous endothelin-1 and angiotensin II. (3) Adrenal-derived endogenous ouabain-like compound is involved in the activation of atrial natriuretic peptide in the left ventricle. (4) Inhibition of nuclear factor kappa-B attenuates severe left ventricular remodeling. (5) Mitogen-activated protein kinases play pivotal role in the regulation of myocardial contractility. (6) MRI study of LV function: dependence on coronary occlusion time and viability. Occlusion time between 45 and 60 minutes induced larger infarct and consequent heart failure proportionally. (7) Human heart mitochondria do not produce physiologically relevant quantities of nitric oxide. (8) Dietary flavonoids are beneficial in chronic obstructive pulmonary disease. (9) A new, oscillometric, portable device for measuring augmentation index and aortic pulse wave velocity (Areteriograph) has been validated invasively. (10) The response of asymetric dimethylarginine levels to stent placement has been characterized in patients with coronary heart disease. (11) Inhibition of poly(ADP-ribose) polymerase improves cardiac function in acute and chronic heart failure. (12) A data analysis system has been developed for analysis of heart rate variability

Vaszkuláris ultrahangvezérelt vena femoralis punkciók szív-elektrofiziológiai beavatkozások során = Vascular ultrasound guided femoral vein puncture in cardiac electrophysiology procedures

Az invazív szív-elektrofiziológia vizsgálatok és katéterablációk leggyakoribb szövődményei a vaszkuláris behatolással kapcsolatosak. Szemben a hagyományos anatómiai alapokon nyugvó, palpáció-irányított technikával, az ultrahangvezérléssel végzett punkciók potenciális előnyöket biztosíthatnak, amelyekkel a vaszkuláris szövődmények aránya csökkenthető. Összefoglaló közleményünk célja az elektrofiziológiai beavatkozások során ultrahangvezérléssel végzett vena femoralis punkciókkal kapcsolatos tudományos adatok áttekintése, saját eredményeink ismertetése, továbbá a saját laboratóriumukban alkalmazott metódus bemutatása

Lateralized rhythmic acoustic stimulation during daytime NREM sleep enhances slow waves

Slow wave sleep (SWS) is characterized by the predominance of delta waves and slow oscillations, reflecting the synchronized activity of large cortical neuronal populations. Amongst other functions, SWS plays a crucial role in the restorative capacity of sleep. Rhythmic acoustic stimulation (RAS) during SWS has been shown a cost-effective method to enhance slow wave activity. Slow wave activity can be expressed in a region-specific manner as a function of previous waking activity. However, it is unclear whether slow waves can be enhanced in a region-specific manner using RAS. We investigated the effects of unilaterally presented rhythmic acoustic sound patterns on sleep electroencephalographic (EEG) oscillations. Thirty-five participants received during SWS 12-second long rhythmic bursts of pink noise (at a rate of 1 Hz) that alternated with non-stimulated, silent periods, unilaterally delivered into one of the ears of the participants. As expected, RAS enhanced delta power, especially in its low-frequency components between 0.75 and 2.25 Hz. However, increased slow oscillatory activity was apparent in both hemispheres regardless of the side of the stimulation. The most robust increases in slow oscillatory activity appeared during the first 3-4 seconds of the stimulation period. Furthermore, a short-lasting increase in theta and sigma power was evidenced immediately after the first pulse of the stimulation sequences. Our findings indicate that lateralized RAS has a strong potential to globally enhance slow waves during daytime naps. The lack of localized effects suggests that slow waves are triggered by the ascending reticular system and not directly by specific auditory pathways

Coronary-artery bypass surgery in patients with left ventricular dysfunction

The role of coronary-artery bypass grafting (CABG) in the treatment of patients with coronary artery disease and heart failure has not been clearly established.Between July 2002 and May 2007, a total of 1212 patients with an ejection fraction of 35% or less and coronary artery disease amenable to CABG were randomly assigned to medical therapy alone (602 patients) or medical therapy plus CABG (610 patients). The primary outcome was the rate of death from any cause. Major secondary outcomes included the rates of death from cardiovascular causes and of death from any cause or hospitalization for cardiovascular causes.The primary outcome occurred in 244 patients (41%) in the medical-therapy group and 218 (36%) in the CABG group (hazard ratio with CABG, 0.86; 95% confidence interval [CI], 0.72 to 1.04; P=0.12). A total of 201 patients (33%) in the medical-therapy group and 168 (28%) in the CABG group died from an adjudicated cardiovascular cause (hazard ratio with CABG, 0.81; 95% CI, 0.66 to 1.00; P=0.05). Death from any cause or hospitalization for cardiovascular causes occurred in 411 patients (68%) in the medical-therapy group and 351 (58%) in the CABG group (hazard ratio with CABG, 0.74; 95% CI, 0.64 to 0.85; P<0.001). By the end of the follow-up period (median, 56 months), 100 patients in the medical-therapy group (17%) underwent CABG, and 555 patients in the CABG group (91%) underwent CABG.In this randomized trial, there was no significant difference between medical therapy alone and medical therapy plus CABG with respect to the primary end point of death from any cause. Patients assigned to CABG, as compared with those assigned to medical therapy alone, had lower rates of death from cardiovascular causes and of death from any cause or hospitalization for cardiovascular causes. (Funded by the National Heart, Lung, and Blood Institute and Abbott Laboratories; STICH ClinicalTrials.gov number, NCT00023595.)

Myocardial viability and survival in ischemic left ventricular dysfunction

The assessment of myocardial viability has been used to identify patients with coronary artery disease and left ventricular dysfunction in whom coronary-artery bypass grafting (CABG) will provide a survival benefit. However, the efficacy of this approach is uncertain.In a substudy of patients with coronary artery disease and left ventricular dysfunction who were enrolled in a randomized trial of medical therapy with or without CABG, we used single-photon-emission computed tomography (SPECT), dobutamine echocardiography, or both to assess myocardial viability on the basis of prespecified thresholds.Among the 1212 patients enrolled in the randomized trial, 601 underwent assessment of myocardial viability. Of these patients, we randomly assigned 298 to receive medical therapy plus CABG and 303 to receive medical therapy alone. A total of 178 of 487 patients with viable myocardium (37%) and 58 of 114 patients without viable myocardium (51%) died (hazard ratio for death among patients with viable myocardium, 0.64; 95% confidence interval [CI], 0.48 to 0.86; P=0.003). However, after adjustment for other baseline variables, this association with mortality was not significant (P=0.21). There was no significant interaction between viability status and treatment assignment with respect to mortality (P=0.53).The presence of viable myocardium was associated with a greater likelihood of survival in patients with coronary artery disease and left ventricular dysfunction, but this relationship was not significant after adjustment for other baseline variables. The assessment of myocardial viability did not identify patients with a differential survival benefit from CABG, as compared with medical therapy alone. (Funded by the National Heart, Lung, and Blood Institute; STICH ClinicalTrials.gov number, NCT00023595.)