Imaging is playing an increasingly important role in the risk stratification of patients presenting with acute coronary syndromes (ACS). Microvascular damage is frequently observed in the setting of ACS. Imaging techniques that identify the severity of microvascular dysfunction allow increased understanding about coronary microcirculatory patho-physiology in this setting, which, in time may allow the development of potential cardio-protective measures to aid current therapies.¹

 

Several techniques and modalities have been described to identify microvascular injury following ACS. Of these, cardiac magnetic resonance (CMR) imaging has become the reference standard for assessment of myocardial injury as it allows accurate assessment of function, perfusion abnormalities, extent of infarction, oedema, and myocardial salvage² (a composite marker of adverse outcome), as well as delineation of microvascular obstruction (MVO) in a single examination.³ The most frequently used CMR techniques to delineate and differentiate microvascular damage are described in the remainder of this article.

 

Gadolinium-based contrast media are extracellular agents, with rapid distribution within the intravascular and interstitial space, but are excluded from the intracellular space of intact myocytes. In the context of acute myocardial injury, the cell membranes can no longer exclude the contrast from the intracellular space and injured myocardium therefore takes up and retains more contrast agent than viable myocardium. In addition, clearance of contrast agent from injured myocardium is reduced. The CMR technique of late-gadolinium enhancement (LGE) makes use of these differences in the distribution volume of the contrast agent and with appropriate imaging parameters depicts acutely infarcted myocardium as an area of hyper-enhanced myocardium compared to regions of non-infarcted myocardium.⁴ Due to its high spatial resolution and tissue contrast LGE imaging can accurately depict the extent and transmurality of myocardial injury after acute myocardial infarction including microinfarcts as low as 1 gram of tissue.⁵ In the presence of MVO, MRI contrast media do not reach the infarct core affected by the reperfusion injury. On LGE images, the MVO zone therefore appears as a dark core residing within a hyper-enhanced infarct zone. The transmurality of LGE and the amount MVO present are both inversely related to the eventual left ventricular (LV) ejection fraction and predicts the likelihood of recovery of regional wall motion.⁶

 

 

One of the patho-physiological consequences of acute ischaemia is an increase in unbound water in the ischaemic tissue.⁷ T2-weighted CMR (T2w CMR) is sensitive to the water content of tissue and therefore allows the delineation of acutely ischaemic myocardium. The area of high signal on T2w CMR has been shown to accurately correlate with the area at risk assessed by microspheres.⁷ Additionally, increased myocardial T2 signal may be observed within 30 minutes of ischemia onset detecting myocardial injury prior to both troponin and LGE.⁸

 

 

Mortality following myocardial infarction is related to several factors, one of which is the amount of myocardium subtended by the infarct-related vessel; the hypoperfused area at risk (AAR) as a result of the ischaemic insult.⁹ Combined, LGE and T2 weighted CMR allow the distinction between infarcted and potentially viable myocardium; LGE delineates the former, whilst T2- imaging determines the latter. These methods therefore permit the calculation of a myocardial salvage index (MSI) by CMR, by correcting the amount of necrotic myocardium for the extent of AAR. Eitel et al have recently prospectively demonstrated that MSI is a strong independent predictor of both major adverse cardiovascular events and mortality at six months and in the longer term (median of 19 months) following reperfused STEMI.^{2, 10}

 

Dynamic contrast-enhanced myocardial perfusion-CMR is based on the monitoring of contrast medium wash-in kinetics into the myocardium. Data can be acquired at rest and during a hyperaemic state, which is most frequently pharmacologically induced with a concurrent intravenous adenosine infusion. One of the key advantages of perfusion-CMR over other imaging methods is its high spatial resolution of <3mm or even higher with recent methods, allowing the differentiation of perfusion to the subendocardial and subepicardial myocardial layers.¹¹ In myocardial regions supplied by arteries with haemodynamically significant coronary disease, myocardial perfusion CMR during hyperaemia shows delayed and reduced wash-in of contrast agent compared to regions with normal myocardial perfusion.¹² Resting perfusion sequence also remains a valuable tool in delineating areas of MVO, and is synergistic with oedema and scar imaging, in this setting.¹³

 

 

The coronary microcirculation is critical in the perfusion and mechanical functioning of the myocardium. Increased understanding of the importance of this vascular compartment has allowed improvements in therapeutic strategies in the management of various conditions such as acute myocardial infarction.  Non-invasive imaging, particularly with the advent and advancement of CMR, has allowed improved risk stratification of patients, with greater understanding about possible prognosis and likely recovery in function following ischaemic injury.  The numerous facets to CMR imaging are synergistic to one another, in assessing and differentiating myocardial necrosis from injured but viable myocardium.