1
Introduction
Aortic atheroma is a common finding in patients with ischemic heart disease and is associated with traditional risk factors for atherosclerosis, such as increasing age, hypertension, dyslipidemia, and smoking. It is frequently observed during coronary angiography, but rarely precludes the passage of endovascular equipment required to engage the coronary ostia. Can it provide a physical barrier to percutaneous coronary intervention (PCI)?
2
Case report
A 75-year-old woman presented to the emergency department via ambulance 2 h after the onset of ischemic chest pain. The patient had multiple cardiac risk factors including hypertension, hypercholesterolemia, and a history of prior smoking but no known prior cardiac history. She was diaphoretic and nauseated. Physical examination was unremarkable; she was in sinus rhythm with a heart rate of 90 bpm, blood pressure was 118/80 mmHg, and there was no evidence of heart failure or aortic dissection. Peripheral pulses, although weak, were present bilaterally. An electrocardiograph ( Fig. 1 ) confirmed inferior ST-elevation consistent with an evolving inferior myocardial infarction. A narrow mediastinum with a well-demarcated aortic knuckle was noted on chest X-ray with no features to suggest aortic dissection.
She was transferred to the cardiac catheter laboratory for urgent diagnostic catheterisation. Following the uncomplicated insertion of a right femoral artery sheath, the guide wire and catheter were unable to traverse the upper descending thoracic aorta into the aortic arch. An aortogram was performed with the diagnostic 6F JL4 catheter and demonstrated a severely calcified and tortuous aorta, with lucency in the descending aorta, suspicious for a dissection flap or mobile atheroma ( Fig. 2 ).
At this point, an urgent ‘on-table’ transoesophageal echocardiography was performed to exclude aortic dissection. This revealed an intact aortic wall (no dissection flap) with severe atheroma extending from proximal to the right brachiocephalic artery, around the arch and into the descending aorta with multiple mobile elements. There was extensive layering of presumed atheroma to the aortic intima (in combination with extensive mobile atheroma), making an alternative diagnosis of intramural haematoma unlikely ( Fig. 3 ).
Conversion to an arm approach was considered but not undertaken due to the extent of atheroma proximal to the right brachiocephalic artery in the ascending aorta. As the patient remained haemodynamically stable with minimal ongoing pain and preserved left ventricular function, a difficult decision was reached by the coronary interventionalist to abort further attempts at coronary angiography. A radio focus (slime) wire would have been required for diagnostic or guide catheter positioning and this was felt to be associated with excess risk of plaque disruption and potential stroke. At this point, thrombolysis was also considered but not administered due to the recent right femoral arterial puncture. Furthermore, while delineation of the coronary anatomy would be important for prognostication, it was felt that the extensive aortic atheroma would preclude any future surgical revascularisation.
The patient remained stable in the ensuing days with no further chest pain and no haemodynamic compromise. The creatinine kinase level peaked at 1200 U/l and Q waves developed in the inferior leads (II, III, and AVF). Transthoracic echocardiography on Day 4 showed only mild segmental LV systolic impairment with inferobasal wall akinesis. She was discharged 6 days later on appropriate pharmacotherapy, and 3 months post discharge remains well.
2
Case report
A 75-year-old woman presented to the emergency department via ambulance 2 h after the onset of ischemic chest pain. The patient had multiple cardiac risk factors including hypertension, hypercholesterolemia, and a history of prior smoking but no known prior cardiac history. She was diaphoretic and nauseated. Physical examination was unremarkable; she was in sinus rhythm with a heart rate of 90 bpm, blood pressure was 118/80 mmHg, and there was no evidence of heart failure or aortic dissection. Peripheral pulses, although weak, were present bilaterally. An electrocardiograph ( Fig. 1 ) confirmed inferior ST-elevation consistent with an evolving inferior myocardial infarction. A narrow mediastinum with a well-demarcated aortic knuckle was noted on chest X-ray with no features to suggest aortic dissection.
