Following reperfusion therapy for acute myocardial infarction, at times blood can extravasate into the interstitial space leading to intramyocardial hemorrhage (IMH) within myocardial infarction (MI). This results in the most severe form of myocardial injury in reperfused MI, which is captured as Stage IV injury in the recently released CCS-AMI classification [1]. Studies have shown that IMH is associated with larger MIs, delayed infarct healing, persistent microvascular obstruction, higher left ventricular volumes, compromised left-ventricular ejection fraction and late-arrhythmogenic risk [[2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14]]. Therefore, accurate detection of IMH is crucial for identifying hemorrhagic MI patients and in the potential development of therapies against its adverse effects. To date, MRI-based approaches have been used to detect IMH and consequential iron deposition in the convalescent phase of myocardial infarction. These approaches take advantage of the observation that IMH creates local susceptibility-induced distortions in the static magnetic field and accelerates transverse magnetization decay. Notably, T2*-based MRI techniques have emerged as the standard method for detecting hemorrhagic MI as they have high sensitivity for detecting and quantifying the iron content within MI [10,15].

Cardiac T2* imaging can be performed with either bright-blood or dark-blood. Dark-blood [16] cardiac T2* was developed based on the conventional segmented, multi-gradient-echo bright-blood cardiac T2* technique by adding a double-inversion-recovery (DIR) preparation at R-wave. The DIR preparation consists of one non-selective 180° inversion adiabatic pulse, which is immediately followed by a slice-selective 180° inversion adiabatic pulse to invert the magnetization within the slice of interest. In this scheme, blood within the slice of interest is replaced by the blood with inverted magnetization within left ventricle after R-wave. And readout takes place at the blood-nulling point to ensure that the blood pool appears dark, which allows for clear blood/myocardium interface.

The dark-blood cardiac T2* technique [16] was initially used for assessment of global iron overload diseases [[17], [18], [19]], such as thalassemia [20], since it can suppress blood signal for better delineation of myocardium. More recently, dark-blood technique has become the common choice in the application of cardiac T2* imaging for assessment of myocardial iron overload including local iron overload such as IMH [12,21,22].

However, evidence showed that dark-blood technique may not provide equivalent diagnostic accuracy for assessment of myocardial infarctions as bright-blood techniques [23,24]. In our previous studies [15,23], we have systematically evaluated the capability of bright-blood and dark-blood cardiac T2* imaging techniques for assessment of IMH. We demonstrated [23] that the conspicuity of IMH is significantly reduced on dark-blood T2* images compared to that observed on bright-blood T2* images, across infarct age in clinical and preclinical settings at 1.5 T and 3.0 T. Comparing to bright-blood T2* images, dark-blood T2* images showed lower signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR) and higher Coefficient of Variation (COV), which led to underestimated IMH extent and impaired diagnostic performance. In this work, we further investigated the mechanisms of the previous findings.

In dark-blood techniques, the DIR preparation uses adiabatic inversion pulses to minimize sensitivity to B1 inhomogeneity. However, adiabatic RF pulses are much longer (10–20 ms, depending on static field strength) than conventional RF pulses, which can have a non-negligible impact of relaxation [25] on magnetization during the excitation process given the short T2 of myocardial tissue (T2 of myocardial tissue is about 45 ms at 3.0 T) [26]. Particularly the impact is doubled by the use of two consecutive adiabatic RF pulses for magnetization preparation in DIR-prepared dark-blood techniques. Accordingly, we hypothesize that the loss of signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) on dark-blood cardiac T2* images of IMH stems from signal loss [25,27] during the double inversion preparation. To test our hypothesis, we performed phantom studies and validated our results with an animal model.