A Very Complex Clinical Case of Acute Coronary Syndrome Complicated by Thrombosis and Intracranial Haemorrhage

Abstract Female patient, 62 years old, with a remote clinical history of colon adenocarcinoma, arrived at the emergency–urgency department for chest pain; clinical, ECG and laboratory evaluation revealed a ACS NSTEMI and was performed angioplasty with DES implantation on the LAD and Cx branch and DAPT was started with ASA 100 mg/day and ticagrelor 90 mg x 2/day. On echocardiographic re–evaluation, the appearance of left ventricular thrombosis was noted, in the absence of obvious ventricular dysfunction, and she underwent parenteral anticolagulant treatment with heparin sodium. In the following days, the patient manifested a right sensory–motor hemisyndromes and aphasia, for which she underwent encephalous CT and cranial AngioTC, which did not show any images referable to steno–occlusive alterations of the intra– and extracranial arterial vessels. After neurological consultation, the indication for thrombolytic and/or interventional neuroradiological treatment was excluded. At the 24–hour CT check–up a large area of cortical–subcortical hypodensity appeared in the left occipito–temporo–parietal area. At subsequent CT scans, hyperdense areolae appeared, which could be attributed to haemorrhagic infarction, for which anticoagulant therapy was postponed and DAPT was suspended due to the very high haemorrhagic risk. In the next days, due to ECGgraphic changes (ST elevated in the anterior leads), the patient underwent a new emergency coronarographic study and intrastent thrombosis of the LAD branch was found, subjected to mechanical thromboaspiration with a good final result. After the procedure we started treatment with ASA 75 mg/day and enoxaparin 4000 IU/day. At subsequent check–ups progressive reduction of haemorrhagic areas in the brain. She therefore underwent neurological re–evaluation with indication to start NAO therapy (dabigatran 110 mg x 2/day) and SAPT with ASA 100 mg/day. The hospital stay was complicated by left femoral–popliteal DVT at the site of previous femoral CVC placement. Haematochemical and genetic screening revealed a positive ANA 1:320 (AC–8/AC–19), a homozygous mutation in the gene for MTHFR C677T and a heterozygous mutation in the gene for Leiden Factor V H1299R. Antithrombotic treatment in the patient with ACS and intracranial haemorrhage represents a challenge for the cardiologist and neurologist. This clinical case is a food for thought on how many obstacles can be encountered on the way to correct antithrombotic therapy.