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This chapter will focus on acute and chronic ischemic heart disease (IHD); the underlying pathophysiology; and the assessment of myocardial function, perfusion, infarct size, and myocardium at risk, all by cardiovascular magnetic resonance (CMR).


Understanding of CMR imaging in both acute and chronic IHD necessitates understanding of the sequence of pathophysiologic events that occur during ischemia. IHD is a dominating cause of death in Western countries and an emerging problem in developing countries. The development of IHD is related to both hereditary factors and lifestyle factors including smoking, diet, and lack of exercise. This section provides an overview of pathophysiology of ischemia with a focus on the mechanisms relevant to the etiology, diagnosis, and treatment of acute myocardial ischemia, stress-induced ischemia, myocardial stunning, hibernation, and infarction. These mechanisms are discussed in relation to the ischemic cascade, findings of myocardial perfusion and function at rest and stress, and the assessment of myocardial viability and the need for coronary revascularization.


The temporal sequence of events referred to as the ischemic cascade1 is illustrated in Fig. 6–1. Ischemia can be described as an imbalance between myocardial oxygen supply and demand. Ischemia can thus be conceptualized in two different ways. Reduced supply in the resting condition is exemplified by myocardial ischemia in the setting of plaque rupture, thrombus formation, and acute coronary occlusion. By comparison, a person may have adequate myocardial perfusion at rest despite having a stenosis in a coronary artery. Upon physical exertion, demand is increased, and myocardial ischemia may ensue despite unchanged supply, or rather, inability to increase supply in order to meet increased demand. In terms of treatment, a situation where myocardial oxygen supply is insufficient in relation to demand (ischemia) can be alleviated by increasing supply (ie, increased perfusion following surgical or percutaneous revascularization), but also by reducing demand (ie, β-blocker therapy). If possible, both the supply and the demand sides of the ischemic imbalance can be therapeutically targeted.

Figure 6–1.
Graphic Jump Location

The ischemic cascade. As ischemia progresses, information on the severity is most sensitive when using imaging modalities that depict ischemia followed by imaging modalities that depict function. Electrocardiographic changes are usually a late-stage sign of ischemia preceding chest pain.


Acute Coronary Syndrome


Acute coronary syndrome2 (ACS) refers to clinical symptoms related to acute myocardial ischemia, sometimes called unstable coronary artery disease. If myocardium is affected by severe enough ischemia for a sufficient duration of time, the ultimate consequence is irreversible cell death. This is represented by infarction, seen at the top extreme of the ischemic cascade (see Fig. 6–1). During the healing process, the dead myocytes are replaced by connective tissue, forming a fibrotic scar, and myocardial contraction in the affected region cannot be restored. Furthermore, patients undergoing myocardial infarction are often subject to repeated infarction and, dependent on infarct size ...

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