A 72-year-old man with a background history of hypertension, hypercholesterolaemia and osteoarthritis, was brought to the emergency department complaining of acute retrosternal chest pain followed by transient syncope. There was no history of previous chest pain. The patient was usually in good health. His regular medications included simvastatin 10 mg once daily, aspirin 75 mg once daily, and atenolol 50 mg once daily.
At presentation he was noted to be peripherally shut down. His blood pressure was initially 130/97 mm Hg. This deteriorated to a systolic blood pressure between 90–110 mm Hg. Admission blood results were as follows: haemoglobin 8.9 g/dl, white blood cell count 10.3×109/l, platelets 116×109/l, mean corpuscular volume (MCV) 95 fl, sodium 141 mmol/l, potassium 4.4 mmol/l, urea 8.0 mmol/l, and creatinine 147 umol/l. Cardiac enzymes were not requested in the absence of electrocardiographic (ECG) changes.
ECG revealed sinus rhythm at 60 beats/min with no significant abnormality. A chest radiograph showed bibasal atelectasis only, with normal mediastinal size and contour.
Transthoracic echocardiography (TTE) was performed revealing a 3.0 cm pericardial effusion with “fibrinous stranding and thrombus” suggestive of haemopericardium. There was also significant right ventricular collapse ().
(A) Transthoracic echocardiogram: subcostal view showing 3.0 cm pericardial effusion with haematoma. (B) Transoesophageal echocardiogram: undilated ascending aorta. (C) Normal aortic angiogram.
The primary differential diagnosis at this stage was aortic dissection. Other causes of spontaneous haemopericardium causing tamponade include coronary artery rupture secondary to coronary intervention (which this patient had never had before presentation).
An urgent computed tomography (CT) scan of the thorax showed no evidence of an aortic dissection flap, although there was haematoma around the ascending aorta as well as haemopericardium. The descending aorta and aortic arch appeared normal.
Transoesophageal echocardiography (TOE) showed no evidence of a dissection flap. The proximal aorta measured 3.4 cm in diameter, hence was not dilated. There was a possibility of intramural haematoma in the proximal aorta but this was not conclusive of an aortic dissection (). As clinical suspicion was still high, a transfemoral aortogram was performed to evaluate the possibility of aortic dissection further. Aortic angiography revealed no intraluminal dissection and coronary angiography revealed no significant coronary artery disease or evidence of fistula ().
The patient remained haemodynamically unstable. In view of the echocardiographic features of the pericardial effusion suggesting thrombus, it was felt that percutaneous drainage would not be successful and possibly run the risk of even more haemodynamic instability. After discussion with an off-site cardiothoracic surgeon, he was transferred to emergency theatres for thoracotomy and evacuation of pericardial haematoma to relieve tamponade. A vascular surgeon and subsequently a cardiothoracic surgeon were in attendance. Operative findings included a tense pericardium with substantial blood clot. On visual inspection the ascending aorta and pulmonary artery appeared bruised, consistent with a likely aortic plaque rupture. Bleeding from the aorta had ceased. Epi-aortic echocardiography confirmed no dissection flap in the ascending aorta, but there was evidence of plaque disease. The diagnosis was felt to be a highly localised aortic plaque rupture causing haemopericardium and tamponade.
After a prolonged stay in intensive care, the patient made a full recovery. Follow-up TTE revealed no pericardial effusion. There was marginal aortic root dilatation with a maximum diameter of 4 cm at the sinus of Valsalva. The likelihood of re-rupture is unknown but he has continued on statin treatment to attempt to prevent further plaque rupture. Good blood pressure control has been achieved with augmentation of his β-blocker dosage. This in turn will also help reduce progression of aortic root dilatation.