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      A novel clinical method for quantification of regional left ventricular pressure–strain loop area: a non-invasive index of myocardial work

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          Abstract

          Aims

          Left ventricular (LV) pressure–strain loop area reflects regional myocardial work and metabolic demand, but the clinical use of this index is limited by the need for invasive pressure. In this study, we introduce a non-invasive method to measure LV pressure–strain loop area.

          Methods and results

          Left ventricular pressure was estimated by utilizing the profile of an empiric, normalized reference curve which was adjusted according to the duration of LV isovolumic and ejection phases, as defined by timing of aortic and mitral valve events by echocardiography. Absolute LV systolic pressure was set equal to arterial pressure measured invasively in dogs ( n = 12) and non-invasively in patients ( n = 18). In six patients, myocardial glucose metabolism was measured by positron emission tomography (PET). First, we studied anaesthetized dogs and observed an excellent correlation ( r = 0.96) and a good agreement between estimated LV pressure–strain loop area and loop area by LV micromanometer and sonomicrometry. Secondly, we validated the method in patients with various cardiac disorders, including LV dyssynchrony, and confirmed an excellent correlation ( r = 0.99) and a good agreement between pressure–strain loop areas using non-invasive and invasive LV pressure. Non-invasive pressure–strain loop area reflected work when incorporating changes in local LV geometry ( r = 0.97) and showed a strong correlation with regional myocardial glucose metabolism by PET ( r = 0.81).

          Conclusions

          The novel non-invasive method for regional LV pressure–strain loop area corresponded well with invasive measurements and with directly measured myocardial work and it reflected myocardial metabolism. This method for assessment of regional work may be of clinical interest for several patients groups, including LV dyssynchrony and ischaemia.

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          Most cited references17

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          Mapping of regional myocardial strain and work during ventricular pacing: experimental study using magnetic resonance imaging tagging.

          The purpose of this study was to determine the spatial distribution of myocardial function (myofiber shortening and work) within the left ventricular (LV) wall during ventricular pacing. Asynchronous electrical activation, as induced by ventricular pacing, causes various abnormalities in LV function, perfusion and structure. These derangements may be caused by abnormalities in regional contraction patterns. However, insight into these patterns during pacing is as yet limited. In seven anesthetized dogs, high spatial and temporal resolution magnetic resonance-tagged images were acquired in three orthogonal planes. Three-dimensional deformation data and LV cavity pressure and volume were used to determine midwall circumferential strain and external and total mechanical work at 192 sites around the left ventricle. During ventricular pacing, systolic fiber strain and external work were approximately zero in regions near the pacing site, and gradually increased to more than twice the normal value in the most remote regions. Total mechanical work, normalized to the value during right atrial pacing, was 38 +/- 13% (right ventricular apex [RVapex] pacing) and 61 +/- 23% (left ventricular base [LVbase] pacing) close to the pacing site, and 125 +/- 48% and 171 +/- 60% in remote regions, respectively (p < 0.05 between RVapex and LVbase pacing). The number of regions with reduced work was significantly larger during RVapex than during LVbase pacing. This was associated with a reduction of global LV pump function during RVapex pacing. Ventricular pacing causes a threefold difference in myofiber work within the LV wall. This difference appears large enough to regard local myocardial function as an important determinant for abnormalities in perfusion, metabolism, structure and pump function during asynchronous electrical activation. Pacing at sites that cause more synchronous activation may limit the occurrence of such derangements.
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            Total mechanical energy of a ventricle model and cardiac oxygen consumption.

            H Suga (1979)
            Mechanical energy (ENG) required by a time-varying elastance model of the ventricle was compared with oxygen consumption per beat (VO2) of the canine left ventricle contracting under a variety of loading conditions. ENG needed for this model to increase its elastance during systole is shown to be equal to the sum of the potential energy built in the elastance during systole plus the external mechanical stroke work. This ENG is equivalent to the area (PVA) bounded by the end-systolic and end-diastolic P-V curves and the systolic limb of the P-V loop trajectory in the P-V plane. There was a high correlation (r = 0.89) between VO2s documented in the literature and PVAs assessed by the author from the accompanying P-V data from both isovolumic and ejecting contractions in 11 hearts. A linear regression analysis yielded an empirical equation: VO2 (ml O2/beat) = a . PVA (mmHg . ml/beat) + b, where a = 1.37 X 10(-5) and b = 0.027, which can be used to predict VO2 from PVA. A preliminary experimental study in my laboratory confirmed the validity of this empirical equation.
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              Asynchronous electrical activation induces asymmetrical hypertrophy of the left ventricular wall.

              Asynchronous electrical activation, induced by ventricular pacing, causes regional differences in workload, which is lower in early- than in late-activated regions. Because the myocardium usually adapts its mass and structure to altered workload, we investigated whether ventricular pacing leads to inhomogeneous hypertrophy and whether such adaptation, if any, affects global left ventricular (LV) pump function. Eight dogs were paced at physiological heart rate for 6 months (AV sequential, AV interval 25 ms, ventricular electrode at the base of the LV free wall). Five dogs were sham operated and served as controls. Ventricular pacing increased QRS duration from 47.2+/-10.6 to 113+/-16.5 ms acutely and to 133.8+/-25.2 ms after 6 months. Two-dimensional echocardiographic measurements showed that LV cavity and wall volume increased significantly by 27+/-15% and 15+/-17%, respectively. The early-activated LV free wall became significantly (17+/-17%) thinner, whereas the late-activated septum thickened significantly (23+/-12%). Calculated sector volume did not change in the LV free wall but increased significantly in the septum by 39+/-13%. In paced animals, cardiomyocyte diameter was significantly (18+/-7%) larger in septum than in LV free wall, whereas myocardial collagen fraction was unchanged in both areas. LV pressure-volume analysis showed that ventricular pacing reduced LV function to a similar extent after 15 minutes and 6 months of pacing. Asynchronous activation induces asymmetrical hypertrophy and LV dilatation. Cardiac pump function is not affected by the adaptational processes. These data indicate that local cardiac load regulates local cardiac mass of both myocytes and collagen.
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                Author and article information

                Journal
                Eur Heart J
                eurheartj
                ehj
                European Heart Journal
                Oxford University Press
                0195-668X
                1522-9645
                March 2012
                6 February 2012
                6 February 2012
                : 33
                : 6
                : 724-733
                Affiliations
                [1 ]simpleInstitute for Surgical Research, Oslo University Hospital, Rikshospitalet, University of Oslo , Oslo, simpleNorway
                [2 ]Department of Cardiology, simpleOslo University Hospital, Rikshospitalet, University of Oslo , N-0027 Oslo, simpleNorway
                [3 ]Center for Cardiological Innovation, Oslo University Hospital, University of Oslo, Oslo, Norway
                [4 ]KG Jebsen Cardiac Research Centre, Oslo, Norway
                [5 ]Department of Radiology and Nuclear Medicine, simpleOslo University Hospital, University of Oslo , Oslo, simpleNorway
                Author notes
                [* ]Corresponding author. Tel: +47 23070000/+47 23073271, Fax: +47 23073917, Email: osmiseth@ 123456ous-hf.no
                Article
                ehs016
                10.1093/eurheartj/ehs016
                3303715
                22315346
                eb838785-5314-4727-a109-fae45687dc69
                Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2012.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 9 November 2011
                : 22 December 2011
                : 16 January 2012
                Categories
                Fasttrack Clinical
                Fast Track

                Cardiovascular Medicine
                heart failure,cardiac resynchronization therapy,dyssynchrony
                Cardiovascular Medicine
                heart failure, cardiac resynchronization therapy, dyssynchrony

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