Contractile reserve can be assessed by CMR using low dose dobutamine stress testing. Similar to echocardiography, CMR allows visualisation of cardiac motion but is characterised by superior endocardial border definition, facilitating more accurate wall motion and wall thickening assessment (fig 11).
Figure Direct comparison of a low dose dobutamine transthoracic echo (TTE) and low dose dobutamine cardiovascular magnetic resonance (CMR) study to assess viability in the septal and lateral wall after myocardial infarction in the same patient.
There is a large body of evidence that an increase in regional systolic function with low dose dobutamine is indicative of myocardial viability. Dobutamine CMR compared favourably to positron emission tomography (PET) in 35 patients with mild left ventricular dysfunction, with a sensitivity of 88% and a specificity of 87% for detecting regions of viable myocardium.1 When the recovery of regional improvement of wall thickening after revascularisation was considered to be the gold standard, the majority of studies showed a relatively modest sensitivity but high specificity of dobutamine CMR for detection of viable myocardium, ranging from 50–90% and 73–94%, respectively. Analogous to the limitations of other viability tests, the reported accuracy of CMR depends on the studied population, since it is known that contractile reserve has a reduced predictive accuracy if more severe dysfunction is present at rest. Whereas Baer et al1 found a good sensitivity and specificity in patients with mild left ventricular (LV) dysfunction (mean (SD) ejection fraction was 42 (16)%), Gunning et al,2 who studied 30 patients with more severe LV dysfunction (mean ejection fraction 24 (8)%), confirmed the high specificity of 81% but found a sensitivity of only 50%. This reduced sensitivity may relate to the development of ischaemia at even low levels of inotropic stress, and/or the pathophysiology of hibernating myocardium in which cellular dedifferentiation may occur with dropout of myofibrillar units. In both cases, viable myocardium would be unable to respond to inotropic stimulation. Consequently, if contractile function improves after inotropic stimulation, it is safe to assume that there is a significant amount of viability; the converse, however, is not necessarily true.
Figure Direct comparison of a low dose dobutamine transthoracic echo (TTE) and low dose dobutamine cardiovascular magnetic resonance (CMR) study to assess viability in the septal and lateral wall after myocardial infarction in the same patient.
There is a large body of evidence that an increase in regional systolic function with low dose dobutamine is indicative of myocardial viability. Dobutamine CMR compared favourably to positron emission tomography (PET) in 35 patients with mild left ventricular dysfunction, with a sensitivity of 88% and a specificity of 87% for detecting regions of viable myocardium.1 When the recovery of regional improvement of wall thickening after revascularisation was considered to be the gold standard, the majority of studies showed a relatively modest sensitivity but high specificity of dobutamine CMR for detection of viable myocardium, ranging from 50–90% and 73–94%, respectively. Analogous to the limitations of other viability tests, the reported accuracy of CMR depends on the studied population, since it is known that contractile reserve has a reduced predictive accuracy if more severe dysfunction is present at rest. Whereas Baer et al1 found a good sensitivity and specificity in patients with mild left ventricular (LV) dysfunction (mean (SD) ejection fraction was 42 (16)%), Gunning et al,2 who studied 30 patients with more severe LV dysfunction (mean ejection fraction 24 (8)%), confirmed the high specificity of 81% but found a sensitivity of only 50%. This reduced sensitivity may relate to the development of ischaemia at even low levels of inotropic stress, and/or the pathophysiology of hibernating myocardium in which cellular dedifferentiation may occur with dropout of myofibrillar units. In both cases, viable myocardium would be unable to respond to inotropic stimulation. Consequently, if contractile function improves after inotropic stimulation, it is safe to assume that there is a significant amount of viability; the converse, however, is not necessarily true.
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