A 77-year-old male patient presented to a secondary care hospital with persistent left-sided chest pain during exercise for one week with mild dyspnoea. His past medical history included coronary artery disease with previous coronary artery bypass surgery in 2009, chronic obstructive pulmonary disease on inhaler steroid therapy, dyslipidaemia, and arterial hypertension. The clinical examination showed no abnormality on respiratory examination, normal heart sounds, and normal abdominal findings. The initial electrocardiogram (ECG) showed sinus rhythm, a heart rate of 79 b.p.m. with a right bundle branch block as well as isolated ventricular extrasystoles (). The initial echocardiography showed a mildly reduced LV systolic function with moderate tricuspid valve insufficiency. Coronary angiography was organized because of typical chest pain and elevated cardiac biomarkers on Day 1, including troponin I at a level of 22 114 pg/mL (normal < 57 pg/mL), CK at a level of 707 U/L (normal < 190 U/L) and CK-MB at a level of 44 ng/mL (normal < 3.6 ng/mL). The patient was diagnosed with a NSTEMI. Coronary intervention with drug-eluting stent implantation (Coroflex® ISAR NEO) into the proximal and mid-right coronary artery (RCA) was performed. An ostial stenosis of the left anterior descending artery (LAD) and a 50% stenosis of the proximal left circumflex artery was left untreated. The venous bypass on the RCA showed a stenosis of the proximal anastomosis, the arterial bypass (left internal mammary artery on LAD) was patent and functional. The patient was loaded on dual anti-platelets with 500 mg aspirin and 600 mg clopidogrel following coronary angioplasty. The post-procedural echocardiogram demonstrated normal findings.\nThe following day transthoracic echocardiography (TTE) showed an unidentified right ventricular (RV) mass occluding the RV cavity. Main differential diagnoses were an intraventricular thrombus or an overlooked myocardial tumour mass like sarcoma or metastasis. Computed tomography confirmed the finding () and demonstrated a widening of the ventricular septum to 40 mm. Intramyocardial haematoma was suspected and confirmed by magnetic resonance imaging ().\nDue to the large, interventricular haematoma, the patient was transferred to our cardiac surgery department because a substantial risk of developing a ventricular septal defect.\nUpon admission to our cardiac surgery intermediate care unit, the patient was clinically stable and asymptomatic. His blood pressure was 90/60 mmHg with a heart rate of 77 beats per minute and oxygen saturation of 91% on room air without added breath sounds on auscultation. In a repeat TTE as performed 2 days later, the intramyocardial haematoma was unchanged (). CK and troponin I levels peaked on Day 1 and then gradually declined with final CK at a level of 93 U/L and final troponin I below 57 pg/mL on Day 7.\nPatient developed atrial fibrillation with a ventricular rate of 110–120 b.p.m. without haemodynamic instability during cardiac monitoring, which lasted for more than 24 h. This was electrically converted to sinus rhythm after a guideline-based exclusion of an intra-atrial thrombus by transoesophageal echocardiography. The decision to perform an electrical cardioversion followed an institutional policy. On Day 11 after the initial diagnosis, a slight decrease of the haematoma and the septal thickness (37 mm) was noted in the four-chamber view of the TTE (). The patient was discharged.\nTransthoracic echocardiography done after 3-month follow-up revealed an almost complete regression of the haematoma (). The patient had remained symptom-free.
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.