This means that long-term asynchronous ventricular activation leads to LV contractile dysfunction that is, at least in part, reversible immediately after the restoration of a normal ventricular activation sequence. In a study by Nielsen et al, it was found that a change in pacing mode from DDD to AAI in patients receiving long-term pacing (ie, mean duration of pacing, 22 ± 8 months) caused an immediate and significant increase in LVEF. Read more »
News - Part 11
The new findings of this study are as follows: (1) the restoration of a normal ventricular activation sequence after long-term right apical stimulation improves LV contractility and ventriculoarterial coupling in the short term but has no significant effect on diastolic function and MV02; and (2) the change from long-term asynchronous ventricular activation to synchronous ventricular activation leads to a significant increase in the flow in the dominant coronary artery, while reducing the flow reserve in the same artery. Read more »
Although dP/ dtmax did not change, its correlation to end diastolic volume (dP/dtmax-Ved), which is a preload-insensitive and afterload-insensitive contractile index, improved during AAI pacing (73.48 ± 3.2 mm Hg/s/mL vs 77.48 ± 4.7 mm Hg/s/mL, respectively; p = 0.002).
There were no statistically significant differences in cardiac and stroke index, SW, LV Pes or Ves, and MVo2 (Table 2). Read more »
All measurements in these arteries were recorded during DDD and AAI pacing modes.
Continuous variables are summarized as the mean ± SD. Changes in the various parameters between DDD and AAI pacing modes were assessed with the t test for dependent samples and the Wilcoxon signed rank test. Both parametric and nonparametric tests gave significant results for the same parameters. The level of significance was set at 5%. Read more »
We determined the LVEF, the LV end-systolic pressure (Pes)-end-systolic volume (Ves) relationship slope (ie, end-systolic elastance [Ees]), the LV stroke work (SW)-end-diastolic volume (Ved) relationship slope (ie, the preload recruitable SW [PRSW]), the ratio of Pes to stroke volume (SV) [ie, effective arterial elastance [Ea]), ventriculaorterial coupling (as the Ees/Ea ratio), and the maximal rate of rise of LV pressure (dP/dtmax)-Ved relationship from the variably loaded beats produced by transient caval occlusion during both DDD and AAI pacing modes. Read more »
Measurements were made during DDD pacing (ie, the mode that was programmed for the long term) and 5 min after a change of pacing mode to AAI, preserving the same pacing frequency. All drugs with a possible negative inotropic and/or chronotropic effect were stopped five half-lives before the study.
All patients provided written, informed consent, and the experimental protocol was approved by the hospital ethics committee. Read more »
This study included patients who were being observed in the pacing clinic and had been referred for coronary angiography because of chest pain. The inclusion criteria were as follows: (1) dual-chamber pacing with optimal AV delay for at least 1 year for sick sinus syndrome; (2) normal intraventricular conduction before pacemaker implantation and throughout the study (QRS, < 110 ms); and (3) a prolonged PR interval allowing complete ventricular pacing capture at rest and during exercise (ie, to a QRS duration similar to that during VVI pacing, as established by 12-lead resting ECG and Holter ECG recordings). Read more »
The right ventricular apex is still the most usual site for the ventricular electrode in patients who have a permanent pacemaker. The asynchronous ventricular activation and contraction that can result from this kind of pacing have a negative effect on left ventricular (LV) systolic and diastolic function, while also causing regional changes in myocardial perfusion and adrenergic innervation, the pathophysiologic significance of which is not yet clear. Read more »
This suggests that the increase in mucus transport after saline solution inhalation is probably due to other factors such as changes in mucus properties or acute secretion of preformed mucus in response to the hyperosmolarity.
We chose concentrations of hyperosmolar solutions based on concentrations used in clinical stud-ies.” We recognize that immersion of a tracheal segment into a solution is different from inhaling the same hyperosmolar solution, as immersion allows equilibration between the intracellular and extracellular spaces; however, we have demonstrated that mucin secretion was stimulated only when the luminal side of the trachea was incubated with hyperosmolar solution. Read more »
Hyperosmolar solutions probably induce secretion through a direct action on secretory cells or by release of mediators that secondarily trigger receptor-mediated secretion. Because all central neural connections are severed in the excised ferret trachea, this secretagogue effect could not be due to central reflexes. Read more »