Do left atrial strain and strain rate reflect intrinsic atrial function, or are they determined by left ventricular function?

Background: Left atrial (LA) strain (S) and strain rate (SR) are reported as measures of intrinsic function. Aim: Since the LA and left ventricle (LV) are connected through the mitral annulus, we investigated: (1) if deformation indices in the LA are mostly predicted by deformation of the LV; (2) if timings of S and SR events are similar in both the LA and LV; and (3) if alteration of S and SR in patients with primarily LV dysfunction would be similar in the LA and LV. Methods: We retrospectively assessed 50 asymptomatic women (Group 1) and 20 patients with recent (< 96 h) acute pulmonary oedema (10 women) (Group 2). Using speckle tracking, the amplitude and timings of S and SR were averaged from three apical views, for one cardiac cycle, starting from the P-wave. Results: In Group 1, all deformation indices were higher in the LA compared with the LV (p < 0.001 for all). In Group 2, S and SR during LA contraction were higher in the LA vs. LV (p < 0.05 for both), but all other deformation indices were not different in the LA vs. LV. All timings of S and SR occurred simultaneously in LA and LV in both groups, except S during LA contraction in Group 1, which occurred slightly earlier in LA than in LV. By multiple regression analysis, the most important predictors of LA deformation indices were the corresponding LV deformation indices, especially in patients with LV dysfunction (Group 1: r = 0.35–0.52; Group 2: r = 0.76–0.85; p < 0.05 by Fisher r-to-z transform). Conclusions: LA deformation strongly reflects LV deformation both in asymptomatic subjects and in patients with LV dysfunction. With the possible exception of LA contraction in asymptomatic individuals, discriminating intrinsic LA function from LV influence is difficult using deformation analysis

Method-specific serum cortisol responses to the adrenocorticotrophin test: comparison of gas chromatography-mass spectrometry and five automated immunoassays

Objective: The serum cortisol response to the ACTH test is known to vary significantly by assay but lower reference limits (LRL) for this response have not been established by the reference gas chromatography-mass spectrometry (GC-MS) method or modern immunoassays. We aimed to compare the normal cortisol response to ACTH stimulation using GC-MS with five widely used immunoassays. Design, Patients and Measurements: An ACTH test (250 micrograms iv ACTH1-24) was undertaken in 165 healthy volunteers (age 20-66yrs; 105 female, 24 of whom were taking an oestrogencontaining oral contraceptive pill [OCP]). Serum cortisol was measured using GC-MS, Advia Centaur (Siemens), Architect (Abbott), Modular Analytics E170 (Roche), Immulite 2000 (Siemens) and Access (Beckman) automated immunoassays. The estimated LRL for the 30min cortisol response to ACTH was derived from the 2.5th percentile of log-transformed concentrations. Results: The GC-MS-measured cortisol response was normally distributed in males but not females, with no significant gender difference in baseline or post-ACTH cortisol concentration. Immunoassays were positively biased relative to GC-MS, except in samples from women on the OCP, who showed a consistent negative bias. The LRL for cortisol was method-specific (GC-MS: 420 nmol/l; Architect: 430 nmol/l; Centaur: 446 nmol/l; Access 459 nmol/l; Immulite (2000) 474 nmol/l) and, for the E170, also gender-specific (Female: 524 nmol/l; Male 574 nmol/l). A separate LRL is necessary for women on the OCP. Conclusions: Normal cortisol responses to the ACTH test are influenced significantly by assay and oestrogen treatment. We recommend the use of separate reference limits in premenopausal women on the OCP, and warn users that cortisol measurements in this subgroup are subject to assay interference