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      Invasive left ventricle pressure–volume analysis: overview and practical clinical implications

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          Abstract

          Ventricular pressure–volume (PV) analysis is the reference method for the study of cardiac mechanics. Advances in calibration algorithms and measuring techniques brought new perspectives for its application in different research and clinical settings. Simultaneous PV measurement in the heart chambers offers unique insights into mechanical cardiac efficiency. Beat to beat invasive PV monitoring can be instrumental in the understanding and management of heart failure, valvular heart disease, and mechanical cardiac support. This review focuses on intra cardiac left ventricular PV analysis principles, interpretation of signals, and potential clinical applications.

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          Most cited references47

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          Hemodynamics of Mechanical Circulatory Support.

          An increasing number of devices can provide mechanical circulatory support (MCS) to patients with acute hemodynamic compromise and chronic end-stage heart failure. These devices work by different pumping mechanisms, have various flow capacities, are inserted by different techniques, and have different sites from which blood is withdrawn and returned to the body. These factors result in different primary hemodynamic effects and secondary responses of the body. However, these are not generally taken into account when choosing a device for a particular patient or while managing a patient undergoing MCS. In this review, we discuss fundamental principles of cardiac, vascular, and pump mechanics and illustrate how they provide a broad foundation for understanding the complex interactions between the heart, vasculature, and device, and how they may help guide future research to improve patient outcomes.
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            Noninvasive single-beat determination of left ventricular end-systolic elastance in humans.

            The goal of this study was to develop and validate a method to estimate left ventricular end-systolic elastance (E(es)) in humans from noninvasive single-beat parameters. Left ventricular end-systolic elastance is a major determinant of cardiac systolic function and ventricular-arterial interaction. However, its use in heart failure assessment and management is limited by lack of a simple means to measure it noninvasively. This study presents a new noninvasive method and validates it against invasively measured E(es). Left ventricular end-systolic elastance was calculated by a modified single-beat method employing systolic (P(s)) and diastolic (P(d)) arm-cuff pressures, echo-Doppler stroke volume (SV), echo-derived ejection fraction (EF) and an estimated normalized ventricular elastance at arterial end-diastole (E(Nd)): E(es(sb)) = [P(d) - (E(Nd(est)) x P(s) x 0.9)[/(E(Nd(est)) x SV). The E(Nd) was estimated from a group-averaged value adjusted for individual contractile/loading effects; E(es(sb)) estimates were compared with invasively measured values in 43 patients with varying cardiovascular disorders, with additional data recorded after inotropic stimulation (n = 18, dobutamine 5 to 10 microg/kg per min). Investigators performing noninvasive analysis were blinded to the invasive results. Combined baseline and dobutamine-stimulated E(es) ranged 0.4 to 8.4 mm Hg/ml and was well predicted by E(es(sb)) over the full range: E(es) = 0.86 x E(es(sb)) + 0.40 (r = 0.91, SEE = 0.64, p < 0.00001, n = 72). Absolute change in E(es(sb)) before and after dobutamine also correlated well with invasive measures: E(es(sb)): DeltaE(es) = 0.86 x DeltaE(es(sb)) + 0.67 (r = 0.88, p < 0.00001). Repeated measures of E(es(sb)) over two months in a separate group of patients (n = 7) yielded a coefficient of variation of 20.3 +/- 6%. The E(es) can be reliably estimated from simple noninvasive measurements. This approach should broaden the clinical applicability of this useful parameter for assessing systolic function, therapeutic response and ventricular-arterial interaction.
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              Role of left ventricular stiffness in heart failure with normal ejection fraction.

              Increased left ventricular stiffness is a distinct finding in patients who have heart failure with normal ejection fraction (HFNEF). To elucidate how diastolic dysfunction contributes to heart failure symptomatology during exercise, we conducted a study using an invasive pressure-volume loop approach and measured cardiac function at rest and during atrial pacing and handgrip exercise. Patients with HFNEF (n=70) and patients without heart failure symptoms (n=20) were enrolled. Pressure-volume loops were measured with a conductance catheter during basal conditions, handgrip exercise, and atrial pacing with 120 bpm to analyze diastolic and systolic left ventricular function. During transient preload reduction, the diastolic stiffness constant was measured directly. Diastolic function with increased stiffness was significantly impaired in patients with HFNEF during basal conditions. This was associated with increased end-diastolic pressures during handgrip exercise and with decreased stroke volume and a leftward shift of pressure-volume loops during atrial pacing. Increased left ventricular stiffness contributed to increased end-diastolic pressure during handgrip exercise and decreased stroke volume during atrial pacing in patients with HFNEF. These data suggest that left ventricular stiffness modulates cardiac function in HFNEF patients and suggests that diastolic dysfunction with increased stiffness is a target for treating HFNEF.
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                Author and article information

                Journal
                Eur Heart J
                Eur. Heart J
                eurheartj
                European Heart Journal
                Oxford University Press
                0195-668X
                1522-9645
                21 March 2020
                21 August 2019
                21 August 2019
                : 41
                : 12 , Focus Issue on Heart Failure
                : 1286-1297
                Affiliations
                [1 ] Department of Cardiology, Thoraxcenter, Erasmus University Medical Centre , Office Nt 645, Dr Molewaterplein 40 3015 GD, Rotterdam, The Netherlands
                [2 ] Cardiovascular Research Foundation , New York, NY, USA
                [3 ] Department of Cardiac and Transplant Surgery , IKEM, Prague, Czech Republic
                [4 ] Department of Intensive Care Medicine, Thoraxcenter, Erasmus University Medical Centre , Rotterdam, The Netherlands
                [5 ] Department of Internal Medicine III, Cardiology, Angiology, Intensive Care Medicine, Saarland University Hospital , Homburg/Saar, Germany
                Author notes
                Corresponding author. Tel: +31(0)107035260, Fax: +31(0)104369154, Email: n.vanmieghem@ 123456erasmusmc.nl
                Author information
                http://orcid.org/0000-0003-2269-8983
                http://orcid.org/0000-0003-3995-2466
                http://orcid.org/0000-0001-8628-1410
                http://orcid.org/0000-0003-0635-2843
                http://orcid.org/0000-0001-7071-8825
                Article
                ehz552
                10.1093/eurheartj/ehz552
                7084193
                31435675
                d6637b80-2bab-42cf-8034-be43e9cab0f0
                © The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 12 January 2019
                : 22 April 2019
                : 7 August 2019
                Page count
                Pages: 12
                Categories
                Clinical Reviews
                Basic Science for the clinician

                Cardiovascular Medicine
                pressure-volume loop,left ventricular haemodynamics,myocardial energetics

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