A. Sh. Akhadova
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
A. Sh. Akhadova has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Alesya A. Klimenko
Pirogov Russian National Research Medical University
1 shared publication - Alina Yu. Chernyaeva
N.I. Pirogov Russian National Research Medical University, Ministry of Health of Russia
1 shared publication - Anaida A. Muradyants
N.I. Pirogov Russian National Research Medical University, Ministry of Health of Russia
1 shared publication - Angelina V. Aksionova
N.I. Pirogov Russian National Research Medical University, Ministry of Health of Russia
1 shared publication - Natalya G. Pravdyuk
N.I. Pirogov Russian National Research Medical University, Ministry of Health of Russia
1 shared publication - V. A. Zargaryan-Smurova
N.I. Pirogov Russian National Research Medical University, Ministry of Health of Russia
1 shared publication
Latest Publications
- Open Access
- 17 March 2026
- Published by Publishing House ABV Press in The Clinician
- Vol. 19 (4) , 75-86
Clinical case of a young patient with generalized sarcoidosis and heart disease
Aim. To demonstrate a multidisciplinary approach in management of a patient with generalized sarcoidosis, heart disease and a life-threatening complication in the form of cerebral infarction which required selection of treatment tactics. Material and methods. Patient A., 41, presented with sarcoidosis and Löfgren’s syndrome onset at the age of 23 and developed clinically manifested cardiac disease over the next three years. Cardiac sarcoidosis was characterized by complex life-threatening arrhythmias, progression of chronic heart failure, and infarction-like changes in electrocardiograms and echocardiograms necessitating differential diagnosis. Results. Uncontrolled intermittent use of prednisolone, lack of regular standard therapy for sarcoidosis, and lack of antiarrhythmic therapy largely predetermined the unfavorable course of events, including development of an ischemic stroke at a young age. The development of the cerebral infarction was due to a combination of factors: arrhythmia, newly diagnosed congenital heart defect (patent foramen ovale), hyperhomocysteinemia, and the presence of polymorphisms in the folate cycle genes (MTHFR, MTR). Conclusion. The diversity of clinical manifestations often leads to diagnostic difficulties and errors. In the absence of adequate therapy, the disease progresses and has an unfavorable prognosis. This article presents a clinical observation of a young patient with generalized sarcoidosis with progressive heart disease, hereditary thrombophilia, patent foramen ovale complicated by the development of a stroke.
- 17 March 2026
- Published by Publishing House ABV Press in The Clinician
- Vol. 19 (4) , 75-86
Open AccessClinical case of a young patient with generalized sarcoidosis and heart disease
Aim. To demonstrate a multidisciplinary approach in management of a patient with generalized sarcoidosis, heart disease and a life-threatening complication in the form of cerebral infarction which required selection of treatment tactics. Material and methods. Patient A., 41, presented with sarcoidosis and Löfgren’s syndrome onset at the age of 23 and developed clinically manifested cardiac disease over the next three years. Cardiac sarcoidosis was characterized by complex life-threatening arrhythmias, progression of chronic heart failure, and infarction-like changes in electrocardiograms and echocardiograms necessitating differential diagnosis. Results. Uncontrolled intermittent use of prednisolone, lack of regular standard therapy for sarcoidosis, and lack of antiarrhythmic therapy largely predetermined the unfavorable course of events, including development of an ischemic stroke at a young age. The development of the cerebral infarction was due to a combination of factors: arrhythmia, newly diagnosed congenital heart defect (patent foramen ovale), hyperhomocysteinemia, and the presence of polymorphisms in the folate cycle genes (MTHFR, MTR). Conclusion. The diversity of clinical manifestations often leads to diagnostic difficulties and errors. In the absence of adequate therapy, the disease progresses and has an unfavorable prognosis. This article presents a clinical observation of a young patient with generalized sarcoidosis with progressive heart disease, hereditary thrombophilia, patent foramen ovale complicated by the development of a stroke.