Primarily, this chapter will focus on using cardiovascular magnetic resonance (CMR) to understand myocardial viability; that is the detection and distinction between scar and recoverable myocardium. We note that, myocardial perfusion strategies have predated the more recent use of delayed hyperenhancement (DHE). A considerable amount of data has been amassed concerning perfusion sequences designed to detect single, double, and triple vessel coronary artery disease (CAD) in a manner not dissimilar to current nuclear strategies. However, CMR differs strikingly from nuclear metabolic radionuclide tracer methods, because CMR perfusion strategies detects alterations in myocardial blood flow (typically related to epicardial vessels) whereas nuclear methods are sensitive to radiotracer interaction with a particular cellular domain, related to integrity of either cellular membranes or metabolism. Distinct differences exist chiefly in that CMR requires no radionuclide injection, has higher imaging resolution than current nuclear techniques, and retains the ability to detect subendocardial defects, and appears able to detect microvascular disease, especially in women, in the absence of epicardial disease.

CMR contrast agents, which are typically gadolinium based-chelates, generally have similar relaxivity rates, with the possible exception of for gadobenate dimeglumine (Gd-BOPTA), which produces approximately twice the 1/T1 effect. The critical action of contrast agents is that they increase the resident myocardial signal because of changing the T1-relaxation rate, and are generally safe in their pharmacokinetics and metabolism when cleared from the body by normally functioning kidneys.

Multiple methods for analyzing and processing CMR perfusion data exist. Typically, the first pass contrast kinetics are visually detectable, allowing comparison of rest and stress perfusion images. Alternatively, strategies exist to quantify myocardial uptake, using prototypic algorithms, most incorporating a measure of the input flow waveform to the myocardium, allowing normalization for underlying cardiac function. Typically, myocardial segmental analysis is performed on the slope of the time intensity curve. Myocardial segment time intensity curve metrics are compared for differences to determine the likelihood for territorial disease within the myocardium. More recently, attempts to improve the already reasonable sensitivity and specificity has led to considerations of double bolus strategies utilizing a low, followed by a high, dose contrast administration.

Paradoxically, low-dose gadolinium for detecting perfusion defects yields the best receiver-operator-characteristic (ROC) curve when using angiography as the “gold standard” for the detection of CAD. Therefore, doses of 0.5 mmol/kg are used to (a) maximize accuracy; (b) increase reproducibility among readers; (c) reduce susceptibility artifacts, which are a major source of error, especially at the interface between low and high regions of concentration of gadolinium such as those that exist along the intraventricular septum; (d) detect perfusion defects that exist at least 8 seconds after contrast injection in two or more contiguous slices, which has been shown to be a measure of maximum sensitivity in recent studies; and (e) detect microvascular disease.

CMR stress testing has now become an accepted protocol, with the following being the indications for stress testing:

Contraindications for stress testing include the following:

Numerous protocols are available for stress testing:

It is important to monitor the patient during stress testing to detect any untoward event:

DHE imaging is often performed following perfusion imaging for viability evaluation. Gadolinium (see Fig. 12-1) is introduced that accumulates in infarcted tissue. The contrast agent is a chelate that decreases T1 of blood approximately threefold when administered IV with the following ideal characteristics: