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Right ventricular-pulmonary arterial coupling describes the relation between right ventricular contractility and its afterload and is estimated as the ratio of the tricuspid annular plane systolic excursion (TAPSE) to pulmonary arterial systolic pressure (PASP) by way of echocardiography. Whether TAPSE/PASP is reflective of invasive hemodynamics or occult shock in acute pulmonary embolism (PE) is unknown. This was a single-center retrospective study over a 3-year period of consecutive patients with PE who underwent mechanical thrombectomy and simultaneous pulmonary artery catheterization with echocardiograms performed within 24 hours before the procedure. A total of 70 patients (81% intermediate risk) had complete invasive hemodynamic profiles and echocardiograms, with TAPSE/PASP calculated. The optimal cutoff for TAPSE/PASP as a predictor of a reduced cardiac index (CI) (CI ≤2.2 L/min/m 2 ) was 0.34 mm/mm Hg, with an area under the curve of 0.97 and sensitivity, specificity, positive predictive value, and negative predictive value of 97.3%, 90.9%, 92.3%, and 96.8%, respectively. Every 0.1 mm/mm Hg decrease in TAPSE/PASP was associated with a 0.24-L/min/m 2 decrease in the CI. This relation was similar when restricted to intermediate-risk PE. The TAPSE/PASP ratio was predictive of normotensive shock with an odds ratio of 2.63 (95% confidence interval 1.42 to 4.76, p = 0.002) per unit decrease in the ratio. In conclusion, in patients with acute PE who underwent mechanical thrombectomy, TAPSE/PASP was a strong predictor of a reduced CI and normotensive shock. This means that noninvasive point-of-care assessment of hemodynamics may have added value in PE risk stratification., Competing Interests: Declaration of competing interest Dr. Bangalore reports being part of the advisory board for Abbott Vascular, Boston Scientific, Biotronik, Amgen, Pfizer (New York, New York), Merck, REATA, Inari, Truvic, and Argon. Dr. Horowitz receives funding from Inari Medical. The remaining authors have no competing interests to declare., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Competing Interests: Declaration of competing interest Dr. Bangalore: Advisory board for Abbott Vascular, Boston Scientific, Biotronik, Amgen, Pfizer, Merck, REATA, Inari, Truvic. The remaining authors have no competing interests to declare.

Discrepancy between computed tomography (CT) and transthoracic echocardiography (TTE) regarding pericardial effusion (PEff) size is common, but there is limited data regarding the correlation between these 2 imaging methods. The aim of this study is to examine the real-world concordance of observed PEff size between CT and TTE. We performed a retrospective analysis of all imaging reports available from 2013 to 2019 and identified patients with a PEff who underwent both a chest CT and TTE within a 24-hour period. We evaluated the agreement between CT and TTE in assessing PEff size. Of 1,118 patients included in the study, mean age was 66 (±17 years) and 54% were female. The median time interval between the 2 studies was 9.4 hours (interquartile range 3.5 to 16.6). Patients within a half-grade or full-grade of agreement were 71.9% and 97.2%, respectively. The mean difference in grade of agreement (TTE minus CT) between the 2 imaging methods was -0.1 (±0.6, p <0.0001). CT was more likely to report a higher grade (i.e. larger PEff size) when compared with TTE (261 patients vs 157 patients, p <0.001). The weighted kappa was 0.73 (95% confidence interval 0.69 to 0.76). After excluding patients with trace/no effusion, 42.3% and 94.1% of patients' studies were within a half-grade or full-grade of agreement, respectively. Of the 18 patients who had large discrepancies, 9 patients had loculated effusions, 2 patients had large pleural effusions, and 6 patients had suboptimal TTEs images. In conclusion, TTE and CT showed relatively strong agreement in estimation of PEff size, with CT sizes larger than TTE, on average. Large discrepancies in size may be related to reduced image quality, large pleural effusions, and loculated PEff., Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest to declare., (Published by Elsevier Inc.)

Purpose: To determine whether hyperglycemia affects pancreatic islet microcirculation in vivo and whether nitric oxide is a mediator., Methods: Islet blood flow was measured before and after infusion of glucose during in vivo microscopy of mouse pancreatic islet. The pancreas of male BALB/c mice was exteriorized and viewed under the microscope utilizing monochromatic transmitted light. The carotid artery and tail vein were cannulated and systemic blood pressure was monitored continuously. Under fluorescent light, a 0.02 mL bolus of 2% fluorescein isothyocyanate (FITC-albumin) was injected intra-arterially and the first pulse of FITC-albumin through an islet capillary was videorecorded. Following equilibration, either glucose or normal saline 300 mg/g of body weight was given intravenously. Five minutes later, a second bolus was given and the second pulse was videorecorded. The study was repeated in the presence of N omega-nitro-L-arginine methyl ester (L-NAME). The FITC-albumin bolus mean transit time (TT) and observed cross time (OCT) through the islet were calculated using slow-motion video analysis of the recorded images., Results: Infusion of glucose resulted in a significant increase in islet blood flow with no change in systemic blood pressure: baseline TT was 20 +/- 1.3 pixel/0.03 sec and baseline OCT was 0.6 +/- 0.04 seconds; during hyperglycemia, TT was 16.1 +/- 1 pixel/0.03 sec, and OCT was 0.48 +/- 0.03 seconds (n = 11, P < 0.05 versus basal via paired t-test). Continuous infusion of L-NAME negated the effect of hyperglycemia on islet blood flow: baseline TT was 20 +/- 1.8 pixel/0.03 sec and OCT was and 0.6 +/- 0.05 seconds; during hyperglycemia, TT was 20 +/- 1.1 pixel/0.03 sec and OCT was 0.6 +/- 0.33 seconds (n = 10; P < 0.05 versus glucose via unpaired t-test).