title: Cardiovascular haemodynamics and ventriculo-arterial coupling in an acute pig model of coronary ischaemia-reperfusion.
abstract: Although reperfusion after coronary occlusion is mandatory for myocardial salvage, reperfusion may trigger a cascade of harmful events (reperfusion injury) adding to myocardial injury. We investigated effects of reperfusion on left ventricular (LV) haemodynamics and ventriculo-arterial (VA) coupling in pigs following acute myocardial ischaemia induced by coronary artery occlusion. Experiments were performed in six animals, with measurements of cardiac and arterial function at baseline, after 60 min of ischaemia (T60) and after 2 (T180) and 4 h of reperfusion (T300). Ventriculo-arterial coupling was assessed using the ventriculo-arterial elastance ratio of paper, as well as using a 'stiffness coupling' and 'temporal coupling' index. Reperfusion following ischaemia (T180 versus T60) induced a progressive decline in cardiovascular function, evidenced by a decrease in mean arterial blood pressure, cardiac output and ejection fraction which was not restored at T300. Although reperfusion also induced an increase in slope of the end-systolic pressure-volume relationship (ESPVR), the ESPVR curve shifted to the right, associated with a depression of contractile function. Histology demonstrated irreversible myocardial damage at T300. The ventriculo-arterial elastance ratio and the 'stiffness coupling' index were unaffected throughout the protocol, but the 'temporal coupling' parameter indicated a relative shift between heart period and the time constant of the arterial system. It is unlikely that these alterations are attributable to ischaemic injury alone. The combination of both the stiffness and temporal coupling index may provide more information when studying ventriculo-arterial coupling than the more commonly used ventricular end-systolic stiffness/effection arterial elastance (E(es)/E(a)) ratio.
authors.affiliation: Hydraulics Laboratory, Institute Biomedical Technology, St-Pietersnieuwstraat 41, 9000 Gent, Belgium. lieve.lanoye@ugent.be
authors.forename: Lieve
authors.initials: L
authors.lastname: Lanoye
authors.forename: Patrick
authors.initials: P
authors.lastname: Segers
authors.forename: Vincent
authors.initials: V
authors.lastname: Tchana-Sato
authors.forename: Stephanie
authors.initials: S
authors.lastname: Rolin
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Dogne
authors.forename: Alexandre
authors.initials: A
authors.lastname: Ghuysen
authors.forename: Bernard
authors.initials: B
authors.lastname: Lambermont
authors.forename: Julien
authors.initials: J
authors.lastname: Hanson
authors.forename: Thomas
authors.initials: T
authors.lastname: Desaive
authors.forename: Pascal
authors.initials: P
authors.lastname: Verdonck
authors.forename: Vincent
authors.initials: V
authors.lastname: D'Orio
authors.forename: Philippe
authors.initials: P
authors.lastname: Kolh
mesh_terms: D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002302:Cardiac Output; D003187:Compliance; D004195:Disease Models, Animal; D019157:Ischemic Preconditioning, Myocardial / Q000009:adverse effects*; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000628:therapy*; D015427:Reperfusion Injury / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D013318:Stroke Volume; D013552:Swine; D013997:Time Factors; D014655:Vascular Resistance; D016277:Ventricular Function, Left; D017725:Ventricular Pressure