Abstract

Abstract We present the case of an 81 year old man suffering from hypertensive heart disease with dilated evolution, dyslipidemia and previous TIAs; on one occasion documentation of cardioembolic origin of the event: AF paroxysm. CHA2DS2–VASc Score = 6. In therapy with DOAC: Dabigatran 110 mg x 2. Placed in therapy with Mysoline for inconstant tremors of the limbs and doubt of absences. Three days after the start of this therapy, the patient was hospitalized for dysarthria (2 h); NIHSS: 0 and ABCD2 score: 4; Brain CT: not acute lesions; centralization to Hub stroke not indicated and DOAC dosage not performed in the PS; at the verification of the DOAC concentration at the peak, during the infra–hospital intake, values of 123 ng / ml; no changes in blood pressure at onset, unchanged CHA2DS2 Vasc Score and HAS–BLED, unchanged blood tests, verified correct intake (CP count), kept the original packaging of the drug, there were no changes in body weight and there was no associated GE pathology; however, primidone was found to be a drug able to decreasing the plasma levels of Dabigatran as an inducer of P–gp glycoprotein. Tp confirmed with Dabigatran and Mysoline replaced with Clonazepam. Subsequent new hospitalization for dysarthria (2 h); centralized in Hub stroke; NIHSS: 1 (slight deviation of the buccal rim–outcome); pressure rise upon access to the PS; peak DOAC concentration 53 ng / ml; CT angiography of the neck and intracranial vessels with evidence of significant underlying vascular lesion load already in itself a contraindication to reperfusion tp which has been excluded; no brain CT lesions; hypothesized in the acute phase switch to another DOAC that has been performed; switch to Apixaban 5 mg 1 tablet x 2 and potentiation of antihypertensive treatment. NMR program of brain in sedation for claustrophobia. Subsequent new hospitalization for septic state and profound drowsiness; severe alteration of blood tests; subacute ischemic hypodensity in the peripheral territory of the left posterior brain; exitus of the patient. Many patients with AF remain at high residual risk of stroke despite an apparent appropriate dosage of oral anticoagulant drugs. However, a multidisciplinary and integrated investigation strategy of all known risk factors does not always give an effective answer, as in the case presented, and there is a lack of information in the literature regarding management options in such circumstances.

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