The effect of a myocardial infarction on the normalized time-varying elastance curve

1 Laboratory of Haemodynamics and Cardiovascular Technology, Ecole Polytechnique Fédérale de Lausanne, Lausanne; 2 Department of Cardiovascular Surgery, Centre Hospitalier Universitaire Vaudois, Lausanne; 3 Department of Cardiovascular Surgery, Inselspital, Bern; and 4 Department of Cardiology, Cent...

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Published inJournal of applied physiology (1985) Vol. 102; no. 3; pp. 1123 - 1129
Main Authors Jegger, David, Mallik, Ajit S, Nasratullah, Mohammed, Jeanrenaud, Xavier, Silva, Rafaela da, Tevaearai, Hendrik, von Segesser, Ludwig K, Stergiopulos, Nikolaos
Format Journal Article
LanguageEnglish
Published Bethesda, MD Am Physiological Soc 01.03.2007
American Physiological Society
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Summary:1 Laboratory of Haemodynamics and Cardiovascular Technology, Ecole Polytechnique Fédérale de Lausanne, Lausanne; 2 Department of Cardiovascular Surgery, Centre Hospitalier Universitaire Vaudois, Lausanne; 3 Department of Cardiovascular Surgery, Inselspital, Bern; and 4 Department of Cardiology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland Submitted 4 September 2006 ; accepted in final form 4 December 2006 It has been suggested that the shape of the normalized time-varying elastance curve [E n ( t n )] is conserved in different cardiac pathologies. We hypothesize, however, that the E n ( t n ) differs quantitatively after myocardial infarction (MI). Sprague-Dawley rats ( n = 9) were anesthetized, and the left anterior descending coronary artery was ligated to provoke the MI. A sham-operated control group (CTRL) ( n = 10) was treated without the MI. Two months later, a conductance catheter was inserted into the left ventricle (LV). The LV pressure and volume were measured and the E n ( t n ) derived. Slopes of E n ( t n ) during the preejection period ( PEP ), ejection period ( EP ), and their ratio ( = EP / PEP ) were calculated, together with the characteristic decay time during isovolumic relaxation ( ) and the normalized elastance at end diastole (E min n ). MI provoked significant LV chamber dilatation, thus a loss in cardiac output (–33%), ejection fraction (–40%), and stroke volume (–30%) ( P < 0.05). Also, it caused significant calcium increase (17-fold), fibrosis (2-fold), and LV hypertrophy. End-systolic elastance dropped from 0.66 ± 0.31 mmHg/µl (CTRL) to 0.34 ± 0.11 mmHg/µl (MI) ( P < 0.05). Normalized elastance was significantly reduced in the MI group during the preejection, ejection, and diastolic periods ( P < 0.05). The slope of E n ( t n ) during the PEP and were significantly altered after MI ( P < 0.05). Furthermore, and end-diastolic E min n were both significantly augmented in the MI group. We conclude that the E n ( t n ) differs quantitatively in all phases of the heart cycle, between normal and hearts post-MI. This should be considered when utilizing the single-beat concept. compliance; ischemia; contractility; ventricular function; hemodynamics; conductance volumetry Address for reprint requests and other correspondence: D. Jegger, Laboratory of Haemodynamics and Cardiovascular Technology, Swiss Federal Institute of Technology, Batiment AAB.026, 1015 Lausanne, Switzerland (e-mail: David.Jegger{at}epfl.ch )
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ISSN:8750-7587
1522-1601
DOI:10.1152/japplphysiol.00976.2006