Numerous devices purport to measure central (aortic) blood pressure (BP) as distinct from conventional brachial BP. This validation study aimed to determine the accuracy of the Sphygmocor Xcel cuff device (AtCor Medical, CardieX, Sydney, Australia) for measuring central BP. 296 patients (mean age 61±12 years) undergoing coronary angiography had simultaneous measurement of invasive central BP and noninvasive cuff-derived central BP using the Xcel cuff device (total n=558 individual comparisons). A subsample (n=151) also had invasive brachial BP measured. Methods were undertaken according to the Artery Society recommendations, and several calibration techniques to derive central systolic BP (SBP) were examined. Minimum acceptable error was ≤5±≤8 mm Hg. Central SBP was significantly underestimated, and with wide variability, when using the default calibration of brachial-cuff SBP and diastolic BP (DBP; mean difference±SD, −7.7±11.0 mm Hg). Similar variability was observed using other calibration methods (cuff 33% form-factor mean arterial pressure and DBP, −4.4±11.5 mm Hg; cuff 40% form-factor mean arterial pressure and DBP, 4.7±11.9 mm Hg; cuff oscillometric mean arterial pressure and DBP, −18.2±12.1 mm Hg). Only calibration with invasive central integrated mean arterial pressure and DBP was within minimal acceptable error (3.3±7.5 mm Hg). The difference between brachial-cuff SBP and invasive central SBP was 3.3±10.7 mm Hg. A subsample analysis to determine the accuracy of central-to-brachial SBP amplification showed this to be overestimated by the Xcel cuff device (mean difference 4.3±9.1 mm Hg, P =0.02). Irrespective of cuff calibration technique, the Sphygmocor Xcel cuff device does not meet the Artery Society accuracy criteria for noninvasive measurement of central BP.

Radial intra-arterial blood pressure (BP) is sometimes used as the reference standard for validation of brachial cuff BP devices. Moreover, there is an emerging wearables market seeking to measure BP at the wrist. However, radial systolic BP may differ when compared with brachial; yet some authors have labeled these differences as a fictional Popeye phenomenon. Indeed, differences between brachial and radial systolic BP have never been accurately quantified, and this was the aim of this study. Intra-arterial BP was measured consecutively at the brachial and radial artery in 180 participants undergoing coronary angiography (aged 61±10 years; 69% men). On average, radial systolic BP was 5.5 mm Hg higher than brachial systolic BP. Only 43% of participants had radial systolic BP within ±5 mm Hg of brachial. Additionally, 46%, 19%, and 13% of participants had radial systolic BP >5, between 5 and 10, and between 10 and 15 mm Hg higher than brachial respectively. A further 14% of participants had radial systolic BP >15 mm Hg higher than brachial, representing the so-called Popeye phenomenon. Finally, 11% of participants had radial systolic BP >5 mm Hg lower than brachial. In conclusion, radial systolic BP is not representative of brachial systolic BP, with most participants having a radial systolic BP >5 mm Hg higher than brachial and many with differences >15 mm Hg. Therefore, validation testing of BP devices utilizing intra-arterial BP as the reference standard should use intra-arterial BP measured at the same site as the brachial cuff or wearable device.

C-type allatostatins (AST-Cs) are pleiotropic neuropeptides that are broadly conserved within arthropods; the presence of three AST-C isoforms, encoded by paralog genes, is common. However, these peptides are hypothesized to act through a single receptor, thereby exerting similar bioactivities within each species. We investigated this hypothesis in the American lobster, Homarus americanus, mapping the distributions of AST-C isoforms within relevant regions of the nervous system and digestive tract, and comparing their modulatory influences on the cardiac neuromuscular system. Immunohistochemistry showed that in the pericardial organ, a neuroendocrine release site, AST-C I and/or III and AST-C II are contained within distinct populations of release terminals. Moreover, AST-C I/III-like immunoreactivity was seen in midgut epithelial endocrine cells and the cardiac ganglion (CG), whereas AST-C II-like immunoreactivity was not seen in these tissues. These data suggest that AST-C I and/or III can modulate the CG both locally and hormonally; AST-C II likely acts on the CG solely as a hormonal modulator. Physiological studies demonstrated that all three AST-C isoforms can exert differential effects, including both increases and decreases, on contraction amplitude and frequency when perfused through the heart. However, in contrast to many state-dependent modulatory changes, the changes in contraction amplitude and frequency elicited by the AST-Cs were not functions of the baseline parameters. The responses to AST-C I and III, neither of which is COOH-terminally amidated, are more similar to one another than they are to the responses elicited by AST-C II, which is COOH-terminally amidated. These results suggest that the three AST-C isoforms are differentially distributed in the lobster nervous system/midgut and can elicit distinct behaviors from the cardiac neuromuscular system, with particular structural features, e.g., COOH-terminal amidation, likely important in determining the effects of the peptides.NEW & NOTEWORTHY Multiple isoforms of many peptides exert similar effects on neural circuits. In this study we show that each of the three isoforms of C-type allatostatin (AST-C) can exert differential effects, including both increases and decreases in contraction amplitude and frequency, on the lobster cardiac neuromuscular system. The distribution of effects elicited by the nonamidated isoforms AST-C I and III are more similar to one another than to the effects of the amidated AST-C II.

Objectives: Accurate assessment of mean arterial pressure (MAP) is crucial in research and clinical settings. Measurement of MAP requires not only pressure waveform integration but can also be estimated via form-factor equations incorporating peripheral SBP. SBP may increase variably from central-to-peripheral arteries (SBP amplification), and could influence accuracy of form-factor-derived MAP, which we aimed to determine. Methods: One hundred and eighty-eight patients (69% men, age 60 ± 10 years) undergoing coronary angiography had intra-arterial pressure measured in the ascending aorta, brachial and radial arteries. Reference MAP was measured by waveform integration, and form-factor-derived MAP using 33 and 40% form-factors. Results: Reference MAP decreased from the aorta to the brachial (−0.7 ± 4.2 mmHg) and radial artery (−1.7 ± 4.8 mmHg), whereas form-factor-derived MAP increased (33% form-factor 1.1 ± 4.2 and 1.7 ± 4.7 mmHg; 40% form-factor 0.9 ± 4.8 and 1.4 ± 5.4 mmHg, respectively). Form-factor-derived MAP was significantly different to reference aortic MAP (33% form-factor −2.5 ± 4.6 and −1.6 ± 5.8, P < 0.001; 40% form-factor 2.5 ± 5.0 and 3.9 ± 6.4 mmHg, P < 0.001, brachial and radial arteries, respectively), with significant variation in the brachial form-factor required (FFreq) to generate MAP equivalent to reference aortic MAP (FFreq range 20–57% brachial; 17–74% radial). Aortic-to-brachial SBP amplification was strongly related to brachial FFreq (r = −0.695, P < 0.001). The 33% form-factor was most accurate with high aortic-to-brachial SBP amplification (33% form-factor MAP vs. reference aortic MAP difference 0.06 ± 3.93 mmHg, P = 0.89) but overestimated reference aortic MAP with low aortic-to-brachial SBP amplification (+5.8 ± 4.6 mmHg, P < 0.001). The opposite was observed for the 40% form-factor. Conclusion: Due to variable SBP amplification, estimating MAP via form-factors produces nonphysiological inaccurate values. These findings have important implications for accurate assessment of MAP in research and clinical settings.