NEW FINDINGS: What is the central question of this study? While the load dependence of the diastolic function is established for the normal heart, little is known about the response of the acutely ischaemic and reperfused myocardium to alterations in afterload. What is the main finding and its importance? Using a model that simulates the clinical scenario of acute ischaemia-reperfusion, we show that increased afterload aggravates @entity67 during both acute ischaemia and reperfusion. In addition, increased afterload induces @entity15071 , which might be the underlying mechanism of the @entity67 of the @entity1562 . These findings provide us with new information regarding how better to manage @entity1 who undergo revascularization therapy after acute @entity583 . The effects of changes in left ventricular (LV) afterload on diastolic function of acutely ischaemic and reperfused myocardium have not been studied in depth. We examined the following factors: (i)  the consequences of increasing the LV afterload on LV diastolic function during acute ischaemia and reperfusion; (ii)  whether the myocardial response to afterload elevation is stable throughout a 2  h reperfusion period; and (iii)  the role of LV wall synchrony in the development of afterload-induced @entity67 . We instrumented 12 anaesthetized, open-chest @entity1707 with Millar pressure catheters and piezoelectric crystals before ligating mid-left anterior descending coronary artery for 1  h, followed by reperfusion for 2  h. Six of the animals survived throughout the 2  h of reperfusion, and their data were used for comparisons across the different experimental phases. Left ventricular afterload was increased by inflating an intra-aortic balloon. Data were recorded at baseline, after 20  min of @entity1563 and at 30 and 90  min of myocardial reperfusion. The increased afterload for 2  min lengthened the isovolumic relaxation during ischaemia and during early and late reperfusion but had no significant effect on isovolumic relaxation before @entity1563 . Increasing the afterload aggravated LV @entity15071 during @entity1563 , but not during reperfusion. The afterload-induced prolongation of isovolumic relaxation was positively correlated with afterload-induced @entity15071 . These observations indicate that, during @entity296 and throughout reperfusion, LV diastolic function is afterload dependent. Afterload-induced @entity15071 might be an underlying mechanism of @entity67 during acute ischaemia.

Afterload-induced left ventricular diastolic dysfunction during XXXX and reperfusion.

@entity1 :: ('9606', 'Species') :: ['patients'] @entity1707 :: ('9823', 'Species') :: ['pigs'] @entity296 :: ('MESH:D009202', 'Disease') :: ['myocardial ischaemia'] @entity583 :: ('MESH:D009203', 'Disease') :: ['myocardial infarction'] @entity1563 :: ('MESH:D054059', 'Disease') :: ['coronary artery occlusion', 'coronary occlusion'] @entity1562 :: ('MESH:D017682', 'Disease') :: ['ischaemic myocardium'] @entity15071 :: ('MESH:C563897', 'Disease') :: ['diastolic dyssynchrony'] @entity67 :: ('MESH:D018754', 'Disease') :: ['diastolic dysfunction']
@entity296 :: (MESH:D009202,Disease) :: ['myocardial ischaemia']
