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. 2022 Apr;70(2):148-159.
doi: 10.23736/S2724-5683.20.05304-9. Epub 2020 Jul 10.

Feasibility and value of two-dimensional volumetric stress echocardiography

Tonino Bombardini  1 Angela Zagatina  2 Quirino Ciampi  3 Lauro Cortigiani  4 Antonello D'Andrea  5 Clarissa Borguezan Daros  6 Nadezhda Zhuravskaya  2 Jaroslaw D Kasprzak  7 Karina Wierzbowska-Drabik  7 José L de Castro E Silva Pretto  8 Ana Djordjevic-Dikic  9 Branko Beleslin  9 Marija Petrovic  9 Nikola Boskovic  9 Milorad Tesic  9 Ines P Monte  10 Iana Simova  11 Martina Vladova  11 Alla Boshchenko  12 Tamara Ryabova  12 Rodolfo Citro  13 Miguel Amor  14 Paul E Vargas Mieles  14 Rosina Arbucci  15 Claudio Dodi  16 Fausto Rigo  17 Suzana Gligorova  18 Milica Dekleva  19 Sergio Severino  20 Marco A Torres  21 Alessandro Salustri  22 Hugo Rodrìguez-Zanella  23 Fabio M Costantino  24 Albert Varga  25 Gergely Agoston  25 Eduardo Bossone  26 Francesco Ferrara  26 Nicola Gaibazzi  27 Granit Rabia  27 Jelena Celutkiene  28 Maciej Haberka  29 Fabio Mori  30 Maria G D'Alfonso  30 Barbara Reisenhofer  31 Ana C Camarozano  32 Michael Salamé  14 Ewa Szymczyk  7 Paulina Wejner-Mik  7 Katarzyna Wdowiak-Okrojek  7 Tamara Kovacevic Preradovic  1 Fabio Lattanzi  33 Doralisa Morrone  33 Maria C Scali  34 Miodrag Ostojic  35 Aleksandra Nikolic  35 Federica Re  36 Andrea Barbieri  37 Giovanni DI Salvo  38 Paolo Colonna  39 Michele DE Nes  40 Marco Paterni  40 Pablo M Merlo  15 Jorge Lowenstein  15 Clara Carpeggiani  40 Dario Gregori  41 Eugenio Picano  42 Stress Echo 2020 Study Group of the Italian Society of Echocardiography and Cardiovascular Imaging
Affiliations

Feasibility and value of two-dimensional volumetric stress echocardiography

Tonino Bombardini et al. Minerva Cardiol Angiol. 2022 Apr.

Abstract

Background: Stroke volume response during stress is a major determinant of functional status in heart failure and can be measured by two-dimensional (2-D) volumetric stress echocardiography (SE). The present study hypothesis is that SE may identify mechanisms underlying the change in stroke volume by measuring preload reserve through end-diastolic volume (EDV) and left ventricular contractile reserve (LVCR) with systolic blood pressure and end-systolic volume (ESV).

Methods: We enrolled 4735 patients (age 63.6±11.3 years, 2800 male) referred to SE for known or suspected coronary artery disease (CAD) and/or heart failure (HF) in 21 SE laboratories in 8 countries. In addition to regional wall motion abnormalities (RWMA), force was measured at rest and peak stress as the ratio of systolic blood pressure by cuff sphygmomanometer/ESV by 2D with Simpson's or linear method. Abnormal values of LVCR (peak/rest) based on force were ≤1.10 for dipyridamole (N.=1992 patients) and adenosine (N.=18); ≤2.0 for exercise (N.=2087) or dobutamine (N.=638).

Results: Force-based LVCR was obtained in all 4735 patients. Lack of stroke volume increase during stress was due to either abnormal LVCR and/or blunted preload reserve, and 57% of patients with abnormal LVCR nevertheless showed increase in stroke volume.

Conclusions: Volumetric SE is highly feasible with all stresses, and more frequently impaired in presence of ischemic RWMA, absence of viability and reduced coronary flow velocity reserve. It identifies an altered stroke volume response due to reduced preload and/or contractile reserve.

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