Rediscovery of Infarct Imaging by Cardiac CT

• computed tomography
• myocardial infarction
• left ventricular function

In the 1990s, imaging of delayed enhancement by the use of magnetic resonance (MR), which allows one to predict recovery of infarction or revascularization, developed into one of the most successful applications of cardiac magnetic resonance (CMR) (1). However, in the late seventies and early eighties computed tomography (CT) already was used to assess the value of contrast enhancement patterns of the left ventricular myocardium after coronary occlusion in animal models (2–5). At that time only single-slice CT scanners were available, and because of the obvious limitations of these scanners, CT contrast enhancement investigation was not further pursued as a clinical tool. Nearly 20 years later, the availability of fast rotating, multislice CT technology sparked renewed interest in myocardial-enhancement imaging to assess the magnitude of ischemic injury, identify viable myocardium, and predict recovery of left ventricular dysfunction after myocardial infarction and restoration of antegrade coronary flow (6–9).

As a result of altered contrast medium kinetics, a number of characteristic enhancement patterns can be observed in acute and chronic myocardial infarction, varying with the delay between contrast injection and CT or CMR (10–12). Early hypoenhancement is a hypoenhanced (black) zone that can be observed during the first pass of contrast medium at the core of an area of infarcted myocardium. Late hypoenhancement is a hypoenhanced (black) zone that can be observed on a CT scan performed 5 to 15 min after contrast injection at the area of infarcted myocardium. Finally, late or delayed hyperenhancement is a hyperenhanced (bright) zone that is observed on a CT scan performed 5 to 15 min after contrast injection within the infarcted area.

Early and late hypoenhancement is caused by absent or delayed myocardial perfusion (slow wash-in of contrast) and, hence, there is a lower attenuation compared with normal contrast-enhanced myocardium. This is due to obstruction of the microvasculature located within the subendocardial core of the infarcted myocardium and is associated with the “no-reflow phenomenon.” The cause of microvascular obstruction is multifactorial and includes distal embolization, vasoconstriction, interstitial edema, capillary leak, and reperfusion injury. This early hypoenhancement zone at the core of the necrotic myocardium is an independent predictor of poor clinical outcome.

Late hyperenhancement in the acute and subacute phase of myocardial infarction is caused by myocyte membrane dysfunction. The normal cell membrane is impermeable to contrast medium, but when damaged there is intracellular accumulation of contrast medium. Because the intracellular volume is 75% of the total myocardial volume, loss of membrane integrity is associated with a large increase of additional intracellular volume now filled by contrast, which causes a marked hyperenhancement. In addition there is delayed in-flow and out-flow of contrast, which enforces delayed enhancement (7). Delayed-enhancement CT imaging of myocardial infarction in animals has shown good correlation with pathology (8,9). In addition, the authors of studies (7,10) comparing CT and CMR in humans demonstrated good correlation. Delayed enhancement represents necrotic, dead tissue that is irreversibly damaged but may contain a peripheral zone that may recover function after restoration of coronary blood flow.

Late enhancement in the chronic phase of infarction is due to the accumulation of contrast medium in the interstitial space between the collagen fibers of the scarred tissue. Because the collagen fibers are loosely distributed, contrary to normal tightly packed myocytes, an increased volume is created that, filled by delayed wash-in and wash-out kinetics of contrast, is associated by marked delayed contrast enhancement (8). The presence and size of delayed contrast enhancement is predictive of left ventricular remodeling and viability upon revascularization.

In several earlier trials (13,14), CT myocardial enhancement imaging in the setting of primary percutaneous coronary intervention (PCI) for acute myocardial infarction was used by the institution of CT coronary angiography immediately (within 25 min) after primary PCI (without necessity of iodine reinjection because the contrast medium used during primary PCI had already accumulated in the infarcted myocardium). These authors showed that CT enhancement allowed the accurate evaluation of the injured myocardium and provided valuable information of myocardial viability, left ventricular remodeling, and prognosis.

In this issue of iJACC, Rodriquez-Granillo et al. (15) expand these observations by using the same CT protocol in patients undergoing primary PCI. They demonstrate that the presence and extent of delayed enhancement directly correlated with a low Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion flow grade (0 to 1), limited electrocardiographic ST-segment elevation resolution (to <50% of ST-segment elevation at admission), greater peak creatine kinase increase, lower left ventricular ejection fraction, and more frequent in-hospital complications. Interesting was the observation that although post-PCI TIMI flow grade 3 was achieved in all patients, nevertheless nearly half of the patients exhibited delayed enhancement, thereby demonstrating that the extent of myocardial necrosis probably was diminished but that myocardial necrosis was not always prevented.

The drawbacks of the CT enhancement technique are the relatively high radiation exposure inherent to the CT investigation, which requires the operator to make 2 scans (in the acute phase of a myocardial infarction, only 1 scan is needed) and the rather low contrast-to-noise ratio, which may hinder the accurate assessment of presence and size of infarcted myocardium. In case of performance of CT scanning immediately after percutaneous treatment of acute MI, a CT scanner should be situated quite close to the catheterization laboratory because CT scanning without reinjection of iodine must be performed within 15 to 20 min after contrast injection (8).

It is yet unclear to which extent differences in total contrast dose, procedure time, and delay until CT acquisition affect the display of delayed myocardial enhancement. Although impressive images of delayed enhancement can be produced, image quality is generally considered inferior to CMR in terms of the contrast-to-noise ratio. Considering this superior image quality, the excellent functional imaging abilities and the lack of radiation it would seem unlikely that CT will replace CMR for this application in the foreseeable future. Improvement of image contrast between infarcted and normal myocardium, may be possible by lowering the tube voltage or perhaps by the use of duel-energy CT scanning.

Although noninvasive coronary angiography is likely to remain the core business of cardiac CT in the foreseeable future, various noncoronary applications of this fascinating technique are (re-)discovered. In addition to coronary imaging, the assessment of global and regional ventricular function, and even stress perfusion imaging, imaging of myocardial infarction and assessment of viability would add to the comprehensive cardiac evaluation by CT. It remains to be seen whether CT scanning is robust enough to claim its place amongst various other imaging modalities that offer post-infarction viability assessment.

• American College of Cardiology Foundation