Left Ventricular Pressure-Strain-Derived Myocardial Work at Rest and during Exercise in Patients with Cardiac Amyloidosis

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Fältnamn	Indikatorer	Metadata
000		04732naa a2200409 4500
001		oai:DiVA.org:uu-412283
003		SwePub
008		200625s2020 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4122832 URI
024	7	a https://doi.org/10.1016/j.echo.2019.11.0182 DOI
040		a (SwePub)uu
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Clemmensen, Tor Skibstedu Aarhus Univ Hosp, Dept Cardiol, Skejby, Denmark.4 aut
245	1 0	a Left Ventricular Pressure-Strain-Derived Myocardial Work at Rest and during Exercise in Patients with Cardiac Amyloidosis
264	1	b MOSBY-ELSEVIER,c 2020
338		a print2 rdacarrier
520		a Background: Left ventricular pressure-strain-derived myocardial work index (LVMWI) is a novel, noninvasive method for left ventricular (LV) function evaluation in relation to LV pressure dynamics. LV global longitudinal strain (LVGLS) has proven benefit for diagnosis and risk stratification in patients with cardiac amyloidosis (CA), but LVGLS does not adjust for loading conditions. The aim of the present study was to characterize LVMWI at rest and during exercise in patients with CA. Methods: A total of 155 subjects were retrospectively included. These subjects comprised 100 patients with CA and 55 healthy control subjects. All patients had previously undergone comprehensive two-dimensional echocardiographic examinations at rest. Furthermore, a subgroup 27 patients with CA and 41 control subjects was examined using sennisu pine exercise stress echocardiography. Results: Patients with CA had significantly lower LVGLS, LVMWI, and LV myocardial work efficiency (LVMWE) than control subjects (P < .0001 for all). The reduction in LV myocardial performance was more pronounced in the basal segments, which led to significant alterations in the average apical-to-basal segmental ratios between patients with CA and control subjects (LVGLS, 2.6 [1.9 to 4.1] vs 1.3 [1.2 to 1.5]; LVMWI, 2.6 [1.7 to 3.8] vs 1.3 [1.1 to 1.5]; LVMWE, 1.1 [1.0 to 1.3] vs 1.0 [1.0 to 1.1]; P < .0001 for all). The average increase in LVMWI from rest to peak exercise was 1,974 mm Hg% (95% CI, 1,699 to 2,250 mm Hg%; P < .0001) in control subjects and 496 mm Hg% (95% CI, 156 to 835 mm Hg%; P < .01) in patients with CA. The absolute numeric LVGLS increase was 5.6% (95% CI, 3.9% to 7.3%; P < .0001) in control subjects and only 1.2% (95% CI, -0.9% to 3.3%; P = .26) in patients with CA (between groups, P < .0001) from rest to peak exercise. The LVMWI increase in patients with CA was mediated by improvement in the apical segments (P < .0001), whereas there was no significant LVMWI alterations in the midventricular or basal segments. LVMWE remained stable during exercise in control subjects (Delta -0.6%; 95% CI, -2.5% to 1.2%; P = .50) but decreased significantly in patients with CA (Delta -2.5%; 95% CI, -4.8% to -0.2%; P < .05). Conclusions: Patients with CA have significantly reduced magnitude of LVMWI compared with healthy control subjects. With exercise, the differences are even more pronounced. Even though LVMWI increased with exercise, LVMWE decreased, suggesting inefficient myocardial energy exploitation in patients with CA.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Kardiologi0 (SwePub)302062 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cardiac and Cardiovascular Systems0 (SwePub)302062 hsv//eng
653		a Cardiac amyloidosis
653		a Exercise echocardiography
653		a Strain imaging
653		a Speckle-tracking imaging
653		a Myocardial work
700	1	a Eiskjaer, Hansu Aarhus Univ Hosp, Dept Cardiol, Skejby, Denmark.4 aut
700	1	a Mikkelsen, Fabianu Aarhus Univ Hosp, Dept Cardiol, Skejby, Denmark.4 aut
700	1	a Granstam, Sven-Olof,d 1963-u Uppsala universitet,Klinisk fysiologi4 aut0 (Swepub:uu)svolgran
700	1	a Flachskampf, Frank,d 1957-u Uppsala universitet,Klinisk fysiologi,Kardiologi4 aut0 (Swepub:uu)frafl698
700	1	a Sörensen, Jensu Uppsala universitet,Radiologi,Aarhus Univ Hosp, Dept Nucl Med, Skejby, Denmark.;Aarhus Univ Hosp, PET Ctr, Skejby, Denmark4 aut0 (Swepub:uu)jenssore
700	1	a Poulsen, Steen Hvitfeldtu Aarhus Univ Hosp, Dept Cardiol, Skejby, Denmark.4 aut
710	2	a Aarhus Univ Hosp, Dept Cardiol, Skejby, Denmark.b Klinisk fysiologi4 org
773	0	t Journal of the American Society of Echocardiographyd : MOSBY-ELSEVIERg 33:5, s. 573-582q 33:5<573-582x 0894-7317x 1097-6795
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-412283
856	4 8	u https://doi.org/10.1016/j.echo.2019.11.018

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