Heart Failure and Its Treatment with Trimetazidine | Chapter 7 | Advanced Concepts in Pharmaceutical Research Vol. 6

This review summarizes the basic pathological changes in the myocardium, with an emphasis on the alteration of cardiac metabolism in the development of heart failure. Trimetazidine was shown to directly improve myocardial metabolism by modulating beta oxidation, rather than by indirectly improving the hemodynamics. Heart failure can be attributed to various pathogenic reasons and is a systemic syndrome. The results of current therapy are not satisfactory. Trimetazidine has been shown in several fundamental investigations to have a heart-protective action that involves reducing inflammation, autophagy, fibrosis, and myocardial apoptosis in addition to altering metabolism. Clinical studies have consistently indicated that trimetazidine acts as an adjunct to conventional treatments and improves the symptoms of heart failure. The clinical application of trimetazidine in heart failure and the mechanism of its protective effects on the myocardium are carefully discussed, as well as its main adverse effects. Non-ischemic heart failure has a variety of causes, including diabetes and hypertension; therefore, specific treatments targeting the causes may provide more promising outcomes than simply relieving the symptoms of heart failure. The intention of this review is to highlight this treatment as an effective alternative against heart failure and provide additional perspectives for future studies.

Author(s) Details:

Hongyang Shu,
Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China and Hubei Key Laboratory of Genetics and Molecular Mechanism of Cardiologic Disorders, Huazhong University of Science and Technology, Wuhan, China.

Yizhong Peng,
Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Weijian Hang,
Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China and Hubei Key Laboratory of Genetics and Molecular Mechanism of Cardiologic Disorders, Huazhong University of Science and Technology, Wuhan, China.

Ning Zhou,
Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China and Hubei Key Laboratory of Genetics and Molecular Mechanism of Cardiologic Disorders, Huazhong University of Science and Technology, Wuhan, China.

Daowen Wang,
Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China and Hubei Key Laboratory of Genetics and Molecular Mechanism of Cardiologic Disorders, Huazhong University of Science and Technology, Wuhan, China.

Please see the link here: https://stm.bookpi.org/ACPR-V6/article/view/13465