This reversible post-ischaemic dysfunction is known as myocardial stunning.
More recently, we have reported initial findings from a follow up study, where GLP-1 (7–36) administered during DSE under hyperglycaemic conditions again improved tolerance to ischaemia and abolished post-ischaemic dysfunction [ 84].
These data contrast prior studies in hearts from obese insulin-resistant rats exhibiting exaggerated post-ischaemic dysfunction (du Toit et al., 2005; du Toit et al., 2008) and infarction (Clark et al., 2011; du Toit et al., 2005; du Toit et al., 2008; Essop et al., 2009; Maarman et al., 2012).
Such ischaemia-reperfusion injury (IRI), with resultant apoptosis, necrosis and post-ischaemic dysfunction remains a key determinant of the final extent of infarction, degree of myocardial salvage and the overall associated morbidity and mortality of MI (illustrated in Figure 1a) [ 4, 5].
Background: ischaemic renal dysfunction is present in many clinical settings, including cardiovascular surgery.
Intramyocardial cellular delivery provides a promising therapeutic strategy for ischaemic cardiac dysfunction.
Initial results from the follow up study have showed GLP-1 (7–36) administered before the first balloon occlusion protected against ischaemic LV dysfunction and attenuated stunning compared to controls [ 86].
Throughout this work we have observed increased tolerance of the myocardium to ischaemia with attenuation of post-ischaemic LV dysfunction (i.e. reduction in stunning) with GLP-1 (7–36).
Although leptin might contribute to post-ischaemic myocardial dysfunction (Moro et al., 2011; Ren et al., 2010), leptin and IGF-1 are also implicated as triggers of cytoprotection (Lisa et al., 2011; Smith and Yellon, 2011).
In patients with ischaemic left ventricular dysfunction, MPS can define the need for revascularisation by determining the presence and extent of ischaemia and of viable but hibernating myocardium [ 193, 194, 195, 196] (Table 9).
Predictors of mortality are listed in Table 2. Significant univariate predictors were age, NYHA class IV, AF, renal dysfunction, ischaemic cardiomyopathy, LVEF, severe mitral regurgitation, and type of CRT device.
