Rare Cause of Syncope in Young Athletes | Chapter 9 | Current Innovations in Disease and Health Research Vol. 4

 This member reports about a rare cause of blackout in young athletes. Syncope is a common occurrence in which skilled is a transient misfortune of consciousness and postural attitude. Although syncope is generally a mild event in young women (less than 35 age of age) and, in many cases, never reaches the consideration of a physician, exercise-related blackout can signal sudden death. This affliction causes parasympathetic failure happening in cardiac failure, arrhythmogenic, cardiomyopathy, unexplained death, mega esophagus and monumental colon.  A 36-year-granny emigrated from Mexico to America when she was 15 years traditional and currently lies in Australia. She is an intensive care nurse, married from a ship and has a boy and a lady aged 12 and 15 age old. The ailment could be reactivated in immunosuppressed patients. Infection and chronicity of the ailments is mainly CD4 intervened and colonel populate CD8. Reactivation in immunocompromised patient is not exceptional, and can present with cardiac syncope.

Author(s) Details:

Adel Ekladious,
Faculty of Health and Medical Sciences, Internal Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.

Please see the link here: https://stm.bookpi.org/CIDHR-V4/article/view/11452

A Case Report on Hypomethylating Agent-Induced Cardiomyopathy | Chapter 5 | Highlights on Medicine and Medical Science Vol. 4

 In Myelodysplastic syndrome, hypomethylating agents, 5-azacytidine and 5-aza-2'-deoxycytidine (decitabine), which work by inhibiting DNA methyltransferase, have been approved (MDS). Cytopenias, nausea, pain, and local reactions in injection sites are the most common side effects of hypomethylating agents. Toxicity associated with other organ functions is extremely uncommon. As the fourth case in the literature, our paper reported a case in which a decrease in left ventricular ejection fraction (EF) was observed as a result of Decitabine treatment due to no response to Azacitidine. In the literature, three cases of cardiac toxicity and function loss have been reported. Because our case did not have an ECHO before beginning Decitabine treatment after Azacitidine, it is unclear whether cardiac toxicity occurred with 10 cycles of Azacitidine or 1 cycle of Decitabine treatment. To understand the etiology and pathophysiology of this side effect, large patient series in randomized controlled trials are required.

Author (S) Details

Mehmet Can Ugur
Department of Hematology, Health Sciences University, Bozyaka Education and Training Hospital, Turkey.

Cansu Atmaca Mutlu
Hematology, Democracy University, Buca Seyfi Demirsoy Education and Training Hospital, Turkey.

Prof. Dr. Oktay Bilgir
Department of Hematology, Health Sciences University, Bozyaka Education and Training Hospital, Turkey.

View Book :- https://stm.bookpi.org/HMMS-V4/article/view/1688

 Background information: The current study looked at the potential cardioprotective benefits of GLP1 and SGLT2i against diabetic cardiomyopathy (DCM) in type 2 diabetic rats, as well as the mechanisms behind them. The existence of heart failure in the absence of coronary artery disease is referred to as DCM.

 Methods: Forty-two male Sprague Dawley rats were randomized into four equal groups at random; a) DM+ GLP1, as DM group with GLP1 analogue (liraglutide) at a dose of 75 g/kg for 4 weeks, and DM+ SGLT2i: as DM group with SGLT2 inhibitor (dapagliflozin) at a dose of 1 mg/kg for 4 weeks. Serum blood glucose, HOMA-IR, insulin, and cardiac enzymes (LDH, CK-MB) were all tested at the end of the four-week treatment.

Myocardial oxidative stress markers (MDA, GSH, and CAT) as well as norepinephrine (NE), myocardial fibrosis, and the expression of caspase-3, TGF-, TNF-, and tyrosine hydroxylase (TH) in myocardial tissues were all assessed. As a result, T2DM resulted in a considerable increase in blood sugar levels. (p 0.05) serum glucose, HOMA-IR, serum CK-MB, and LDH In addition, DM resulted in severe myocardial damage and fibrosis, as well as an increase in myocardial MDA, NE, and upregulation of myocardial caspase-3, TNF, TGF, and TH, as well as a substantial drop in serum insulin, myocardial GSH, and CAT (p0.05). All examined indicators improved significantly (p 0.05) after administration of either GLP1 analog or SGLT2i. Conclusion: We found that both GLP1 and SGLT2i had cardioprotective effects against DCM in T2DM, with SGLT2i having the upper hand. This could be related to fibrosis, oxidative stress, apoptosis (caspase-3), sympathetic nerve activity, and other factors.

Author (s) Details

Prof. Dr. Abdelaziz M. Hussein
Department of Medical Physiology, Mansoura Faculty of Medicine, Mansoura, Egypt

Elsayed A. Eid
Department of Internal Medicine and Endocrinology, Delta University for Science and Technology, Gamasa, Egypt

Medhat Taha
Department of Anatomy, Mansoura Faculty of Medicine, Mansoura, Egypt.

Rami M. Elshazli
Department of Biochemistry, Faculty of Physical Therapy, Horus University-Egypt, New Damietta, Egypt.

Raouf Fekry Bedir
Department of Anatomy, Mansoura Faculty of Medicine, Mansoura, Egypt.


Lashin Saad Lashin
Department of Medical Physiology, Mansoura Faculty of Medicine, Mansoura, Egypt and Department of Medical Physiology, Horus University, Damietta, Egypt.

View Book :- https://stm.bookpi.org/HMMR-V9/article/view/1021