Background: Atherosclerosis, thromboembolism and hemodynamic mechanism, via cerebral hypoperfusion, are the main causes of acute ischemic stroke. In watershed infarcts, which represent 10% of all ischemic brain infarcts, the regional and global hemodynamic disturbances which lead to a low cerebral blood flow, are responsible of affecting the junction area of the distal territories of two nonanastomosing large cerebral arteries.
Case presentation: We present the case of a 50 year old male patient, with multiple atherosclerotic risk factors: smoking, hypertension, dyslipidemia, insulin necessary type 2 diabetes, with clinical, biological, electrical and echocardiographic findings of anterior Killip IV STEMI at presentation, necessitating endotracheal intubation and mechanical ventilation 48 hours in the intensive care unit. The emergency coronary angiography identi-fied trivascular atherosclerotic coronary artery disease, the patient undergoing primary percutaneous coronary angioplasty with drug-eluting stent placement in the culprit lesion of the medium-proximal segment of the left anterior descending artery, with left circumflex and right coronary arteries’ lesions without an interventio-nal treatment ( RCA chronic occlusion and 60% LCX stenosis, <2.5 mm vessel diameter). At the admission at the Cardiology department, the patient developed sud-den aphasia and right brachial monoparesis. The emer-gency cerebral computed tomography showed acute ischemic stroke involving two different cerebral territories- left MCA and MCA-PCA borderline territory. The cervical-cerebral Doppler ultrasound described left internal carotid artery occlusion and right carotid artery „insignificant” stenosis. The echocardiographic reassessment identified severe left ventricular dysfunc-tion, diffuse hypokinesis and apical, posterior and ba-sal inferior walls akinesis, with apical thrombosis; no vegetation was identified by the the transesophageal echocardiography; the blood cultures were negative. In the context of acute neurological event, the initial dual antiplatelet therapy and low-molecular-weight heparin treatment were replaced by mono antiplatelet therapy (P₂Y₁₂ inhibitor) and LMWH, the neurology specialist recommending a 14 day cessation of aspirin post-acute ischemic stroke.
Case particularity: We raised the problem of the the-rapeutic management and the measures for preventing recurrence after cerebral infarction, in an complex etio-logy of a left acute ischemic stroke in a young individual, with traditional atherosclerosis risk factors, with left internal carotid artery occlusion , with cardiac conditions likely to produce cardioembolism (acute myocar-dial infarction with invasive cardiac procedures, severe left ventricular dysfunction, intracavitary thrombus) and also cerebral hypoperfusion, in context of low cardiac output (acute MI with cardiogenic shock at onset, severe left ventricular dysfunction).
Conclusions: T he causes of an acute ischemic stroke in a patient with acute coronary syndrome are multiple and can be superimposable. The presence of a carotid artery occlusion is not always edifying for establishing a certain etiology of an acute neurological event; mo-reover, patients with carotid occlusion and poor he-modynamic reserve carry a high risk of subsequent stroke. Taking everything into account, identifying all the mechanisms prone to develop an acute stroke post-acute MI, by a thorough clinical and paraclinical data collection, becomes mandatory for adequate treatment strategy, prognosis and reducing risk of recurrence.