ECG-synchronized first-pass cCTA allows us to not just visualize the coronary artery tree and, consequently, grade coronary stenosis but also to characterize areas of decreased myocardial blood flow. Decreased perfusion, shown as hypoattenuated areas on CT images, may be secondary to a critical coronary artery stenosis or occlusion, microvascular obstruction, or myocardial scar. Thus, while a differential diagnosis is difficult to make, the diagnostic value of delineating the areas with deteriorated blood flow (hypoattenuation) is undeniable (Kramer et al. 1984; Gray et al. 1978; Doherty et al. 1981; Georgiou et al. 1992) Fig. 1.

With contrast-enhanced cCTA, chronic MI can ordinarily be recognized as a hypoattenuated region (>50 % HU decrease compared with surrounding myocardium) (Nikolaou et al. 2004) in a subendocardial or transmural distribution that persists in systole and diastole and is concordant with a coronary territory (Rubinshtein et al. 2009).

It is well established in CMR studies that the transmural extent of nonviable myocardium determines the success of functional recovery after revascularization. Thus, accurate and precise quantification of nonviable myocardium is critical for planning a revascularization strategy and for helping the physician assess the risks and benefits of the PCI procedure and/or coronary artery bypass graft surgery (Kim et al. 2000; Choi et al. 2001). In 2004, animal experiments provided evidence of not just delineation but also quantification of hypoattenuated area within acutely infarcted myocardium. Areas of low attenuation within porcine heart showed good correlation with myocardial blood flow reduction and absolute MI size (Hoffmann et al. 2004).

Nikolaou et al. reported clinical correlation in 30 patients. First-pass CT angiography was able to detect all but one (10 out of 11) MI when compared to DE-CMR. Assuming MI size through blood flow defect quantification results in a significant underestimation (19 %) compared to true infarct size determined by DE-CMR.

Differentiation between ischemia and MI is not possible using first-pass cCTA acquisition alone (Nikolaou et al. 2005). Shapiro et al. (2010) investigated prognostic value of the extent of hypodense areas in patients with MI. It was found that the prognostic relevance of hypoperfused areas, as determined from arterial-phase CT, is unclear and remains such, because decreased myocardial attenuation on arterial-phase CT imaging is not necessarily indicative and, more importantly, not specific for MI. However, patients with MI often show hypoattenuation after first-pass iodinated contrast injection in the infarcted area.

Mahnken et al. (2005) showed the importance of arterial-phase detection but the area of hypoattenuation significantly underestimated the true infarct size compared with cardiac MRI. PIS_MRI versus PIS_MDCT were calculated and compared in each patient. Mean infarct size on MRI (PIS) was 31.2 ± 22.5 % per slice compared with 24.5 ± 18.3 % per slice for first-pass arterial-phase acquisition on MDCT. Actual MI on MDCT size was reportedly underestimated by 25 % compared with DE-CMR (k = 0.635). Reported underestimation and discrepancy in infarct size could be explained by the observation that parts of the reperfused necrotic area display normal enhancement on first-pass perfusion but are hyperenhanced on delayed imaging. Thus, in patients with MI, early hypoattenuated regions represent only a fraction of MI.

In 42 subjects, Sanz et al. reported that quantified MI size in arterial-phase CT angiography imaging and DE-CMR were strongly correlated (r = 0.87, p < 0.0001). MI volume by MDCT was again proven to be underestimated in comparison with DE-CMR (2.7 ± 2.5 vs. 25.9 ± 19.9 mL, p < 0.0001) (Sanz et al. 2006).

In summary, first-pass iodinated contrast media MDCT hypoattenuation is not specific and, more importantly, not an accurate tool for securely diagnosing or quantifying myocardial infarct. Clinical correlation can help establishing the etiology (e.g., perfusion, MI, microvascular obstruction) of hypoattenuation on arterial-phase MDCT images. Quantification of areas with low attenuation significantly underestimates true MI size.

The delayed-hyperenhancement phenomenon of CMR is a well-established and widely-acceptable clinical tool for detecting and quantifying infarcted, nonviable myocardium. Contrast-enhanced CMR uses a GdDTPA contrast agent that has myocardial tissue kinetics that is similar to those of iodinated contrast agents. In acute MI, myocyte necrosis results in interstitial edema and membrane rupture, which allows iodinated contrast agents and gadolinium chelates to diffuse into the intracellular space (Jennings et al. 1985; 1990). Thus, just as GdDTPA of CMR, iodinated contrast material accumulates in the infarcted cardiac segments with a similar late-enhancement phenomenon visualized by delayed cardiac CT. Late DE-MDCT acquisition after iodinated contrast agent administration is capable of delineating MI as an area of hyperattenuation, i.e., myocardial region with high Hounsfield unit values. Usually, late-scan acquisition is considered to be 5–15 min after the administration of contrast agent.

GdDTPA and iodinated contrast agent accumulation is observed in both acute and chronic myocardial infarcts. In acute settings, necrosis is identified; in chronic infarcts, a dense collagen-rich scar is identified. Both histopathological entities show expanded extracellular space that delays washout of contrast media (Gerber et al. 2006).

Transmural extent of MI as detected and quantified with DE-MDCT predicts the recovery of regional systolic LV function after revascularization for acute STEMI (ST-elevation myocardial infarct, as observed on ECG) (Shapiro et al. 2010).