Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 11

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  atrial fibrillation
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Rapid regular atrial pacing (RAP) produces changes in atrial function similar to those caused by atrial fibrillation in animal models. Left atrial appendage (LAA) function represents regional atrial function. The aim of our study was to investigate the influence of RAP on left atrial regional function and to evaluate the reversibility of changes after terminationtermination of pacing in a canine model. Eight dogs were subjected to RAP (400 bpm) for 16 days. Transesophageal echocardiography was performed at baseline, immediately after RAP and weeks after the terminationtermination of RAP. The LAA peak late emptying velocity (LAA-E) and filling wave (LAA-f) were measured. LAA-E velocities were significantly reduced and filling wave velocities (LAA-f) were significantly less negative after RAP compared with the baseline values. Four weeks after terminationtermination of pacing, the LAA-E and LAA-f velocities were normal. RAP results in impaired regional atrial systolic and diastolic function. The changes were completely reversible 4 weeks after terminationtermination of pacing. These results suggest that the LAA is mechanically stunned after RAP.
In animal and human studies, it has been shown that atrial fibrillation shortens the atrial refractory period and impairs its rate adaptation. The objective of this study was to evaluate the effects of high-rate pacing on sinus node function and intra-atrial conduction. Eight dogs were subjected to rapid atrial pacing (AP) at 400 bpm for 16 days. Sinus node recovery time (SNRT) and P-wave duration were measured at baseline, immediately after AP and four weeks after the termination of AP. SNRT immediately after AP was significantly prolonged at all pacing rates compared to the baseline values. P-wave duration was significantly longer after AP relative to the baseline values. All the variables were completely reversible four weeks after the termination of pacing. Rapid AP induces sinus node dysfunction and prolongs the intra-atrial conduction time. It is possible that the electrical remodelling extends to the sinus node as well.
The atria are highly complex multidimensional structures composed of a heterogeneous branching network of subendocardial muscular bundles. The relief of the inner part of the right atrium includes the crista terminalis as well as multiple pectinate muscles that bridge the thinner atrial free walls and appendages. However, a handful of studies have focused attention on the role of the naturally occurring complexities of the atrial subendocardial muscle structures in the mechanisms of cardiac arrhythmias. In accordance with the facts mentioned above, it was decided to examine the morphology and topography of the external interatrial junctions and related structures in order to define the possible anatomical basis of impulse propagation in focal atrial fibrillation. Research was conducted on material consisting of 15 human hearts of both sexes (female — 6, male — 9) from 18 to 82 years of age. In addition we were concerned, on the basis of the history and electrocardiograph tracings, that none of the patients had shown focal and non-focal type of atrial fibrillation. The classic macroscopic methods of anatomical evaluation were used. The walls of the atria were prepared via a stereoscopic microscope, the pericardium and fatty tissue were eliminated from the surface of the atria, visualising muscle fibres linking both of the atria, and the beginnings and the endpoints of fascicles in the right and left atrium were estimated. The structure, large muscle bundle, was present in all examined hearts. The muscle fascicle was descending from the anterior wall of the right atrium just below the orifice of the superior vena cava. The fascicle, running towards the left atrium, divided into two branches, one of which joined with the superior fascicle from the posterior wall and created one running above the interatrial septum and infiltrating into the wall of the left atrium on its superior surface between the superior pulmonary veins. The other branch of the anterior fascicle was running across the anterior wall of the atria and it penetrated into the left atrium muscle in the region of the inferior pole of the left auricle outlet. On the posterior wall of the atria three types of interatrial fascicles were distinguished: unifascicular, bifascicular and trifascicular. The bifascicular type was the most frequent configuration (9 cases — 60.0%), in 5 cases it was trifascicular (33.3%) and finally the unifascicular configuration was observed in just 1 heart (6.7%). On the basis of our study we can conclude that the external interatrial fascicles are the constant structure of the heart, although they may have a variable morphology. Those structures could be responsible for physiological conduction between the atria and may play an important role in patients with atrial fibrillation.
In circulation, platelets may come into contact with both exogenous (cardiac glycoside treatment) and endogenously produced inhibitors of Na+/K+-ATPase. We examined whether blocking of platelet Na+/K+-ATPase by ouabain results in generation of procoagulant activity. It was shown that an in vitro treatment of platelets with ouabain (20-200 µM for 20 to 60 min) is associated with an intracellular accumulation of sodium ([Na+]i), generation of a weak calcium signal, and expression of procoagulant activity. The ouabain-induced procoagulant response was dose- and time-related, less pronounced than that evoked by collagen and similar to that produced by gramicidin, not affected by EDTA or aspirin, and strongly reduced in the absence of extracellular Na+ or by hyperosmolality. Flow cytometry studies revealed that ouabain treatment results in a unimodal left shift in the forward and side scatter of the entire platelet population indicating morphological changes of the plasma membrane. The shift was dose related, weaker than that evoked by collagen and similar to that produced by gramicidin. Ouabain-treated platelets express phosphatidylserine (PS). The ouabain-evoked PS expression was dose- and time-dependent, weaker than that produced by collagen and similar to that evoked by gramicidin. Electronic cell sizing measurements showed a dose-dependent increase in mean platelet volume upon treatment with ouabain. Hypoosmotically-evoked platelet swelling resulted in the appearance of procoagulant activity. Thromboelastography measurements indicate that, in whole blood, nanomolar (50-1000 nM, 15 min) concentrations of ouabain significantly accelerate the rate of clot formation initiated by contact and high extracellular concentration of calcium. We conclude that inefficiently operating platelet Na+/K+-ATPase results in a rise in [Na+]i. An increase in [Na+]i and the swelling associated with it may produce PS exposure and a rise in membrane curvature leading to the generation of a procoagulant activity.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.