Velocity vector imaging (VVI) software permits quantitative assessment of ventricular function through measurement of myocardial strain (S) and strain rate (SR). The purpose of this study was to define a reference range of ventricular S and SR values in normal adults using VVI software, and to describe the variability among observers and systems. Two-dimensional echocardiography was performed in 186 healthy adults free of cardiovascular disease or risk factors, followed by comprehensive ventricular S and SR analysis using VVI software. Images were acquired using three commercial ultrasound systems. The mean age of patients was 44 ± 16 years, and 114 (61 %) were female. Mean global left ventricular (LV) longitudinal, circumferential, and radial S and SR, and right ventricular (RV) longitudinal S and SR values are presented. Significant segmental variation in regional LV and RV S and SR was detected. Multivariate regression analysis demonstrated global longitudinal LV (p = 0.05) and RV (p = 0.002) S values decline significantly with age. The overall variability of S and SR values accounted for by patient demographic and hemodynamic variables was low (16 and 8 % for LV longitudinal S and SR, respectively). Interobserver agreement was very good, but was lowest for LV radial S and SR. There were no significant differences of LV and RV S and SR between ultrasound systems. Comprehensive reference values for the normal ranges of LV and RV S and SR measured using VVI software are presented. The ultrasound system used for image acquisition did not significantly influence results.

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BACKGROUND: Studies comparing left atrial (LA) function after surgical closure or percutaneous closure in patients with an atrial septal defect (ASD) are lacking. METHODS: Between 1 and 3 years after ASD treatment, we retrospectively analyzed the medical records and transthoracic echocardiographic images of patients who had been diagnosed with an ASD after 20 years of age and who had undergone surgical closure (ASD-S) or percutaneous device closure (ASD-D). We measured LA peak systolic, early diastolic, and late diastolic strain values using 2-dimensional (2D) speckle tracking echocardiography (STE) and calculated reservoir, conduit, and contraction strain. RESULTS: The reservoir strain value of the ASD-D groups was 25.2% ± 7.4%, which was lower compared to the control group (33.6% ± 5.5%) (p = 0.004). The LA conduit strain and the LA contraction values of the ASD-D group were also lower compared to the control group (−13.8% ± 5.8% vs. −20.4% ± 4.7%, p = 0.034; −11.3% ± 4.2% vs. −13.2% ± 2.5%, p = 0.037, respectively). The reservoir, conduit, and contraction strains of the ASD-S group were 27.8% ± 8.8%, −15.3% ± 6.4%, and −12.5% ± 5.8%, respectively, and were not different from those of the control group or the ASD-D group. CONCLUSIONS: The 2D STE is a suitable method for evaluating LA function after ASD closure. Our results demonstrate that 1 year after device closure, the LA reservoir, conduit and contraction function were reduced in ASD-D group compared to healthy controls, while there was no difference between the ASD-S and ASD-D groups.

Amitriptyline, a tricyclic antidepressant (TCA) drug, is widely used in treatment of psychiatric disorders. However, the side effects of amitriptyline on vascular K channels remain to be determined. Therefore, we investigated the effect of the tricyclic antidepressant and serotonin reuptake inhibitor amitriptyline on voltage-dependent K (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells, using the whole-cell patch clamp technique. The Kv current amplitudes were inhibited by amitriptyline in a concentration-dependent manner, with an apparent IC value of 2.2 ± 0.14 μmol/L and a Hill coefficient of 0.87 ± 0.03. Amitriptyline shifted the activation curve to a more positive potential, but had no significant effect on the inactivation curve, suggesting that amitriptyline altered the voltage sensitivity of Kv channels. Pretreatment with Kv1.5 and Kv1.2 channel inhibitors did not alter the inhibitory effect of amitriptyline on Kv channels. Additionally, application of train pulses (1 and 2 Hz) did not affect amitriptyline-induced inhibition of Kv currents, which suggested that the action of amitriptyline on Kv channels was not use (state)-dependent. From these results, we concluded that amitriptyline inhibited the channels in a concentration-dependent, but state-independent manner.