C13 AT THE ROOT OF HYPOXIA: NEVER UNDERESTIMATE THE CLINICAL

Abstract A 74–year–old woman arrived to the ER for syncope, reporting episodes of atypical chest pain for a few months. The initial ECG showed negative T waves in the lateral leads; an echocardiogram documented lower–limit systolic function due to akinesia of the antero–lateral segments and the presence of an ascending aorta aneurysm (AAA). The woman, with multiple cardiovascular risk factors, had previous transmural myocardial ischemia documented by MRI and never investigated with coronary angiography (ICA). Admitted to ICCU for suspected ischemic heart disease, she experienced a sudden clinical deterioration with onset of acute respiratory failure, initially stabilized with noninvasive ventilation. A chest angioCT excluded acute events (pulmonary embolism, aortic dissection) and confirmed the presence of AAA with bovine arch. Given the persistent need for oxygen therapy, closer clinical observation allowed objectification of platypnea–orthodeoxia syndrome (POS) that presented with desaturation, dyspnea, and mental confusion in the orthostatic position that improved with supine position. A bubble test in the two positions documented worsening intracardiac shunt in the sitting position, and a transesophageal echocardiogram showed the presence of a tunnel–like patent foramen ovale (PFO). The patient then underwent ICA that found a stenosis–free vascular tree, but a marked fusiform common trunk aneurysm (CTA) was appreciated. After exclusion of altered cardiopulmonary hemodynamic balance, percutaneous closure of the PFO was performed, which allowed progressive improvement of respiratory exchanges and subsequent complete weaning from oxygen. Typically, PFO occurs in the case of a pulmonary ventilo–perfusory mismatch or right–left shunt (rlS), associating mainly with atrial congenital defects and, to a lesser extent, pulmonary arteriovenous malformations. Sometimes, for POS to occur, the presence of a functional component facilitating rlS is necessary. In our case, it is conceivable that such a contribution was both ab–extrinsic compression of the right atrium by the AAA and compression of the pulmonary trunk at the level of the pulmonary valve by the CTA. This diagnostic hypothesis is compatible with the late presentation.