A 79-year-old, hypertensive, diabetic, male patient with a thoracic aortic aneurysm and aortic valve stenosis was scheduled for total aortic arch replacement and simultaneous aortic valve replacement. Following sternal entry, CPB was established by right axillary and femoral arterial cannulation with bicaval cannulation. After aortic cross-clamping, myocardial protection was achieved with antegrade, retrograde, and selective cold blood cardioplegia without any technical problem. The aortic valve was replaced with a 21-mm bioprosthesis (Inspiris Resilia, Edwards Life Sciences, Irvine, CA). Subsequent total aortic arch replacement was performed under antegrade selective cerebral perfusion with moderate hypothermic circulatory arrest. After aortic declamping, a small point of oozing hemorrhage was identified on the epicardial surface of the right ventricular outflow tract. The oozing was controlled by hemostatic agent application, followed by the reconstruction of the arch vessels. The surgical maneuver was completed without any technical difficulty; however, we noticed the progressively expanding hematoma at the right ventricular surface to the size of a Japanese rice ball measuring 50 × 50 mm (Fig. ). The hematoma was hard, and the epicardial surface was dark red and notably swollen with multiple oozing ruptures. There was no evidence of ST-T changes on electrocardiogram. No cardiac wall motion abnormalities were observed on transesophageal echocardiography. Because of the rapid growth of the hematoma, we decided that early discontinuation of CPB and protamine administration should be mandatory. After termination of CPB, followed by the administration of protamine and fresh frozen plasma/platelet transfusion, manual compression with hemostatic agents such as Surgicel (Ethicon, Somerville, NJ, USA) and Tachosil (CSL Behring, Tokyo, Japan) were applied for 15 min. Thereafter, hemostasis was achieved on the epicardial surface, and the hematoma did not expand further without hemodynamic deterioration. The patient showed uneventful postoperative course. Postoperative computed tomography showed hematoma absorption, and transthoracic echocardiography revealed normal ventricular function of both the right and left ventricles. He is doing well 1 year after surgery.
A 60-years-old male patient admitted to our centre as a case of anterior wall myocardial infarction with pulmonary oedema. He had a history of ischaemic heart disease, no history of hypertension, and he is not diabetic.\nBedside TTE was performed on the same day of admission and showed () & () LV apical cavitary lesion with internal heterogeneity (likely to be thrombosed content). The neocavity was separated from the LV cavity by a contracting wall displaying paradoxical diastolic contraction, indicating that it is an endomyocardial layer. There was no detectable communication between the LV cavity and the neocavity in the contrast echocardiography. Doppler images showed no flow inside the neocavity. The estimated LV ejection fraction (EF) was 20–25%. No pericardial effusion was detected. Conventional coronary angiography revealed a severe three-vessel disease.\nCMR was performed on the next day of admission on a 1.5 T system (SignaHDx Series, GE Healthcare, Chicago, IL). Retrospectively gated breath-hold steady-state free precession sequences (SSFP-FIESTA) were obtained in the four-chamber and two-chamber long axes, then in the short axis slabs from the LV base to the apex and axial chest slabs covering the heart. T1 weighted double inversion recovery and T2 weighted double inversion recovery with fat suppression were applied in the axial chest plane. Contrast MRA (magnetic resonance angiography) was performed with hree-dimensional reformates then late gadolinium enhancement (LGE) images were acquired in the short axis, four-chamber, and two-chamber planes.\nCMR images are presented in () & ( and ). CMR showed enhanced infarcted five LV segments in LAD (left anterior descending coronary artery) territory (mid-anterior, mid-anteroseptal, apical anterior, apical septal, and apex segments) with a large intramyocardial dissecting cystic lesion delineated by endomyocardial flap toward the LV cavity (clearly appreciated on FIESTA images) and by the enhanced infarcted myocardium toward the pericardial space. The dissecting hematoma displayed heterogeneous signal intensity, the thrombus that was of isointense signal to the myocardium, and high signal intensity to the myocardium of the blood products in T1 weighted and T2 weighted images. On the LGE sequence, the cystic lesion displayed homogenous signal void signal intensity outlined by the enhanced myocardium toward the pericardium. There was no detectable endomyocardial tear. Contrast-enhanced MRA showed no contrast leakage from the LV cavity into the hematoma. A rim of pericardial effusion was noted. The patient was treated conservatively according to the consensus of the heart team, including cardiologists, cardiovascular surgeons, interventional cardiologists, and anaesthesiologist. They went with the conservative approach due to the high risk of surgery, the large size and wide extension of the IMDH, and the poor LV function.\nThe patient was treated medically with anti-failure medications. Anticoagulants were not used for fear of increasing the size of the hematoma. Follow-up TTE after 4 months showed no significant change as regards the size and the echo pattern of the hematoma in the last TTE before discharge. The patient was haemodynamically stable.\nThe worldwide incidence of IMDH has not been adequately reported. It is an uncommon but under recognised complication of myocardial infarction. LV free wall rupture is the third most common cause of death after acute myocardial infarction, and immediate surgical repair is the treatment of choice. In such cases, a tear from the endocardium through the myocardium and epicardium leads to cardiac tamponade, imminent left ventricle failure, and death. If the tear is confined to the myocardium, an intramyocardial hematoma (IMH) can be formed as a neocavitation enclosed by the myocardium. The hematoma was thought to be due to the rupture of the intramyocardial vessels, diminished tensile strength of the infarcted myocardium, or due to sudden increased perfusion pressure.\nTTE is the most commonly used first-time imaging modality, but CT or CMR is advised if the patient is clinically stable. Some previous variable publications suggested the establishment of IMDH diagnosis echocardiographically if the patient had at least three of the following supporting findings:(1) formation of a neocavitation with central echolucency (2) mobile contracting endomyocardial border (3) the neocavity is outlined by the myocardium from outside (4) continuity between the ventricular cavity and the dissecting hematoma (5) detection of Doppler coloured flow within the cavity (6) changing of the echo pattern of the neocavity on follow-up (7) partial or complete absorption of the cystic cavity.\nCMR is the only imaging modality that can detect precisely IMH owing to the characteristic signal intensity of the blood products. However, the optimal CMR sequences to identify IMDH are still a matter of debate. Kumar et al, in his paper, concluded that T2*-CMR could adequately quantify the myocardium reperfusion haemorrhage. Kali et al reported that T2* is more suitable than T2 weighted CMR in the detection of the acute IMH. While Pedersen et al study concluded that T1 weighted inversion recovery sequences (T1WIR) have high sensitivity and specificity in the detection of experimental IMH in porcine myocardium as compared to T2 short tau inversion recovery and T2*-weighted sequences. In our case, the IMDH was well-depicted in the cine FIESTA, and in the DIR (both T1- and T2 weighted). In the conventional LGE, the enhanced infarcted inner endomyocardial layer could not be differentiated from the adjacent bright LV blood. So, we recommend using the novel dark-blood LGE method to nullify the LV blood magnetisation for better detection of the ischaemic myocardial scar in such similar cases. It had been published that dark blood LGE imaging improved the depiction of myocardial fibrosis in the cases with low contrast with the contiguous blood pool.\nThe management of patients with IMDH, either via surgical or conservative approach, depends on various factors: the haemodynamic stability status of the patient, the size of the dissecting hematoma, LV function, and the experience of each surgical centre. Conservative management is a suitable viable approach for patients with haemodynamic stability, large-sized dissecting area, or those with reduced LV function and dilated cardiomyopathy. Till now, the short-to-midterm prognosis of IMDH in patients who were not treated surgically is poor. However, many IMDH cases treated conservatively were published showed a fair mid-to-long-term survival.\nHerein, we represent a rare case of a large LV partially thrombosed IMDH. The lesion is suspected by TTE and very well characterised in CMR.