Acute changes of left ventricular function during surgical revascularization by 3D speckle tracking.

BACKGROUND: Detecting early impact of coronary artery bypass grafting (CABG) on left ventricular (LV) function is important because such measures may contribute to meaningful improvement in clinical outcomes. We aimed to gain knowledge about acute changes of LV performance during surgical revascularization using three-dimensional speckle tracking echocardiography (3D STE). METHODS: Thirty-five patients scheduled for CABG surgery who underwent intraoperative transesophageal echocardiography (TEE) were enrolled (mean age 68.9 ± 7.3 years). TEE was performed before and after surgery, as well as before and after grafting. 3D LV ejection fraction (LVEF), tissue motion annular displacement (TMAD) of the mitral valves, 3D global longitudinal strain (GLS), global circumferential strain (GCS), twist, and torsion were quantified. Regional longitudinal strain (LS) was calculated based on coronary perfusion territories in a 16-segment LV model. RESULTS: Despite the absence of change in TMAD and 3D LVEF, 3D GLS (-18.6 ± 4.3% at baseline vs -16.0 ± 4.0% after surgery, P = .01) was significantly decreased, followed with no significant effect on GCS, twist, and torsion during surgery. 3D GLS correlated significantly with 3D LVEF (r between -0.34 and -0.51, P < .05 for all) under the whole operation. Territorial LS did not increase immediately after surgery. CONCLUSION: 3D speckle tracking imaging allows for detailed and direct evaluation of myocardial deformation, though impaired LV longitudinal function is still apparent immediately after surgery. GLS is more sensitive to an acute reduction in LV function than conventional parameters, which can be potentially useful for serial monitoring of functional recovery.

Protein kinase C regulates alpha(2A/D)-adrenoceptor constitutive activity.

We investigated a possible role for protein kinases in the constitutive activity of alpha(2A/D) adrenoceptors in membranes from transfected PC12 cells, using a [35S]GTPgammaS binding assay. After treatment of intact cells with various protein kinase inhibitors, constitutive activity was assessed by the reduction in basal GTP binding caused by the inverse agonist rauwolscine (RAU). Inhibitors of protein kinase C (PKC) caused the loss of RAU-sensitive GTP binding, while inhibitors of other protein kinases were ineffective. Anti-G(alpha) antibody treatments showed that constitutive alpha(2A/D)-receptor activity is directed toward different G proteins than agonist-stimulated activity. T373A mutant receptors exhibited increased constitutive activity, including a component that was insensitive to PKC inhibition. Since T373 is located within a putative G(i/o) activator sequence, these results suggest that PKC-dependent phosphorylation of T373 increases alpha(2A/D)-adrenergic receptor constitutive activity and causes a switch in G protein preference.