Pectovast MR Mechanism of Action

Pharmacology: Mechanism of Action: Trimetazidine Dihydrochloride inhibits mitochondrial long chain 3-KAT thus favoring glucose oxidation at the expense of fatty acid oxidation, which is impaired. Glucose and fatty acid metabolism in the heart after the formulation of acetyl-CoA, both processes follow a common pathway, whereas glucose is able to continue with glycolysis. Oxidation of fatty acids impairs pyruvate oxidation. Trimetazidine Dihydrochloride suppresses fatty acid oxidation via inhibition of enzyme 3-KAT, and enhances the process of glucose oxidation. The decrease in fatty acid oxidation and the stimulation of fatty acid oxidation provoked by Trimetazidine Dihydrochloride improve the coupling between glycolysis and carbohydrate oxidation. Accordingly, ATP production is achieved with consumption of less oxygen. Moreover, Trimetazidine Dihydrochloride stimulates membrane phospholipids turnover during ischemia, thus redirecting fatty acids towards phospholipids. Trimetazidine Dihydrochloride regulates ionic and extra cellular exchanges, correcting the abnormal flow of ions across the cell membrane caused by ischemia and preventing the cellular edema caused by anoxia. Thus it ensures the functioning of ion pumps and the sodium-potassium transmembrane flux and maintains the cellular homeostasis.
Pharmacodynamics: By preserving the energy metabolism in cells exposed to hypoxia or ischemia, Trimetazidine Dihydrochloride prevents a decrease in intracellular ATP levels, thereby ensuring the proper functioning of ionic pumps and transmembranous sodium-potassium flow whilst maintaining cellular homeostasis.
In man: controlled studies in angina patients have shown that Trimetazidine Dihydrochloride increases coronary flow reserve, thereby delaying the onset of ischemia associated with exercise, limits rapid swing blood pressure without any significant variations in heart rate, significantly decreases the frequency of angina attacks, leads to significant decrease in the use of nitrates.