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 7-week-old male infant was noted to be hypoxemic prior to repair of an inguinal hernia. A postoperative echocardiogram demonstrated a large membranous VSD and a long segment coarctation of the aorta. Three months after repair of the coarctation the infant was in congestive heart failure and was brought to the operating room for VSD repair. Preoperative transesophageal echocardiography (TEE) demonstrated a large membranous VSD that extended into the inlet septum and a widely patent left ventricular outflow tract ().\nVSD repair was performed using aortobicaval cannulation with mild hypothermia and antegrade cardioplegeic arrest. The echocardiographic findings were confirmed at surgery, and the VSD was closed in the standard manner using a Dacron patch and 5–0 Prolene pledgeted suture. The initial suture line was carried clockwise avoiding the crest of the ventricular septum. Near the septal leaflet of the tricuspid valve, sutures were placed superficially to avoid the conduction system. The VSD was then closed in a counterclockwise fashion staying away from the crest of the ventricular septum, across the ventricular infundibular fold avoiding the aortic annulus, and eventually transitioning to the septal leaflet of the tricuspid valve. The remainder of the VSD underneath the septal leaflet of the tricuspid valve was closed by weaving in and out of the valve leaflet and the VSD patch. The suture was then tied over an autologous pericardial patch.\nPostoperative TEE (), performed immediately after coming off of cardiopulmonary bypass, demonstrated an echo lucent region beneath the VSD patch that was surrounded by a thin membrane protruding into the LVOT, findings consistent with a DVSH. During systole the anterior mitral leaflet/chordal apparatus came in contact with the DVSH resulting in severe LVOT obstruction with a peak instantaneous Doppler gradient between 70–80 mmHg which was confirmed by direct pressure measurement. The patient was placed back on cardiopulmonary bypass and an oblique aortotomy was made allowing retraction of the aortic valve leaflets to inspect the ventricular septum. The hematoma was identified and the thin membrane overlying the hematoma was incised and evacuated. The remainder of the hematoma was unroofed and LVOT patency was confirmed with a 9 mm dilator. Postevacuation TEE confirmed a widely patent LVOT with no residual gradient (). The LVOT remained widely patent on transthoracic echocardiography performed five days later.