Introduction: Cardiotoxicity represents one of the major complications of the chemotherapeutic treatment in cancer and it causes a significant risk in the morbidity and mortality of the oncological patients. It may appear early during the treatment, late, in the first year after the therapy and very late, more than one year after finishing the treatment, it’s manifestations varying from subclinical myocardial dysfunction to irreversible heart failure and even death.
Case presentation: A 34 years old patient, with oncological comorbidities (right femur osteosarcoma, surgically treated and chemo-treated with Cisplatin in 2008), who presents for sudden heart palpitations and dyspnea, and also a right hemiplegia with speech disorders, as the expression of an ischemic stroke in the territory of the middle cerebral artery, objectified through a cranial CT. The blood pressure was 120/80 mmHg upon admission, the heart rate 90/min, in sinus rhythm, with negative T waves in the lateral derivations DI, aVL, V₅-V₆. 24 hours Holter EKG showed the presence of 703 monomorphic single ventricular extrasystoles and 129 single supraventricular extrasystoles. The echocardiography revealed a dilated left ventricle with diffuse hypokinesia and light systolic dysfunction, the left atrium slightly dilated, without intra-cavitary thrombi, and also a light mitral and tricuspid regurgitation. Considering the sudden appearance of the ischemic stroke in a young patient, we investigated the hereditary thrombophilia profile, which denoted the presence of 2 mutations on MTHFR gene (methyle-netetrahydrofolate reductase): C677T-homozygote genotype and A1298C-heterozygote genotype. Thus, we consider that the etiology of the ischemic stroke is the association of the patients’ genetic predisposition to hypercoagulability, confirmed through the mutations of the MTHFR gene and the post-chemotherapy dilated cardiomyopathy, that may lead to stroke through embolism. The patient was included in a neuromotor and speech rehabilitation therapy and was given an oral anticoagulant treatment with Apixaban 5 mg twice a day, an antiarrhythmic agent: Carvedilol 6,25 mg twice a day and also a neurotrophic treatment with Actovegin 2 tb twice a day, with a slow improvement. He will return for a new course of neuromotor therapy in 2 months.
Conclusions: Cardiotoxicity is an important complication of the chemotherapy, that may appear whenever during the treatment or after completing it, the manifestations depending on the agent and also on it’s cumulative dose. The association of the post-chemotherapy dilated cardiomyopathy and the genetic predisposition to hypercoagulability determined the ischemic stroke in an young patient, 10 years after the oncological treatment.