Although many physicians think about gadolinium enhanced CMR as a method for assessing viability, dobutamine stress CMR was the first validated method. The very concept of hibernating myocardium originated in the early days of bypass surgery when it was noticed that some patients with left ventricular dysfunction had substantial improvement of left ventricular function after revascularization.1,2
The concept of hibernating myocardium was crystallized out of this observation of reversible, ischemic left ventricular dysfunction.3
Many aspects of the pathophysiology of hibernating myocardium were described by 1986 and recovery of global or regional function became a central tenet in the entity.4
The concept that hibernating myocardium showed a “biphasic response” characterized by an improvement in regional function during low-dose dobutamine infusions but ischemic deterioration at high doses of dobutamine.5
This biphasic response has become an important refinement in the non-invasive diagnosis of the hibernating myocardium.
Dobutamine stress CMR is performed following doses and imaging protocols that are comparable to dobutamine stress echocardiography.6
After baseline imaging, graded doses of dobutamine are infused and left ventricular function is imaged at each stage. A low-dose dobutamine stress test typically looks for improvement of regional wall motion abnormalities with a submaximal dose of the catecholamine. Some groups use low and high doses of dobutamine to have the specificity of the biphasic response as an indicator of hibernating myocardium. Most clinicians would use either type of response as a sign of viability to maximize sensitivity of the test.
Dobutamine stress CMR is accurate for detecting significant coronary artery stenosis7–9
and for characterizing hibernating myocardium. Baer et al published a series of studies exploring the feasibility and accuracy of dobutamine stress CMR as a non-invasive test of myocardial viability. In comparisons of dobutamine stress CMR and 18
F-deoxyglucose PET, dobutamine induced wall thickening was a better predictor of residual metabolic activity than end diastolic wall thickness but grading a segment as viable if at least one of both CMR parameters fulfilled viability criteria improved the sensitivity of CMR to 88% for 18
F-deoxyglucose PET assessed metabolic activity without adversely affecting specificity (87%) or positive predictive accuracy (92%).10
Dobutamine stress CMR and dobutamine stress echocardiography had similar diagnostic accuracy for viable myocardium relative to 18
Dobutamine stress CMR predicted recovery of function after revascularization in patients with chronic regional wall motion abnormalities.12
In a head-to-head comparison of dobutamine stress transesophageal echocardiography and dobutamine stress CMR for predicting functional recovery of hibernating myocardium with a reference standard that included successful revascularization of the ischemic territory, both tests were highly accurate.13
Thus, dobutamine stress CMR can be used to characterize the likelihood of functional recovery of regional wall motion abnormalities in patients with ischemic heart disease. One particular advantage of this method is that gadolinium contrast is not needed so the method can be used in patients with severe kidney disease. There is some evidence that dobutamine stress MRI is a better predictor of functional recovery than late gadolinium enhancement (LGE).14
The discrepancies in predicting recovery of function may represent analogous differences between dobutamine echo and SPECT mechanisms of assessing viability as described by Arrighi and Dilsizian.15
The use of regional wall thickening as the reference standard for assessing viability may also introduce a bias favoring dobutamine wall motion tests to assess viability. Not withstanding of these issues, dobutamine is a powerful method for enabling viability assessment by CMR.