China
Africa
Explore chapters and articles related to this topic
Angina pectoris in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Wilbert S. Aronow, William H. Frishman
Trimetazidine is an antianginal drug which improves myocardial glucose utilization through inhibition of fatty acid metabolism. A meta-analysis of 13 randomized clinical trials showed that trimetazidine was efficacious in the treatment of patients with stable angina pectoris and reduced the number of weekly anginal episodes, reduced the weekly nitroglycerin use, caused a longer time to 1 mm of ischemic ST-segment depression, increased total work, and caused a longer exercise duration at peak exercise (129).
Pleural disease induced by drugs
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Only mild adverse events, including rash and diarrhoea, have been reported with vitamin B5. There is an isolated report of a 76-year-old woman who was hospitalized with chest pain and dyspnoea.55 She had no history of atopic disease. She had been taking trimetazidine for 6 years, vitamin H (10 mg daily) and vitamin B5 (300 mg daily) for 2 months for the treatment of alopecia. Chest radiograph showed cardiac enlargement and a pleural effusion. Clinical examination and echocardiogram revealed cardiac tamponade. The absolute pleural fluid eosinophil count ranged from 1200 to 1500/μL. At pericardiectomy the fluid was a sterile exudate with protein 6.7 g/dL with 1500 eosinophils/μL. Histology showed an eosinophilic infiltrate. The pleural fluid also confirmed eosinophilia. Despite multiple thoracenteses the pleural effusion recurred, leading to thoracotomy. All studies for rheumatological disorders, infection and occult malignancy were negative. Vitamins B5 and H were discontinued, and 1 week later the patient improved dramatically with resolution of blood eosinophilia. Trimetazidine was also discontinued but readministered a few months later without symptoms or an increase in eosinophilia. The patient was symptom-free without relapse at a 2-year follow-up visit.
Antinociceptive effect of ranolazine and trimetazidine
Published in Expert Review of Cardiovascular Therapy, 2021
Trimetazidine can be preferred with its low side effect profile in the treatment of patients with persistent angina who are not suitable for percutaneous and surgical revascularization. Trimetazidine (1-2,3,4-trimethoxybenzyl piperazine dihydrochloride), a member of the 3-ketoacyl coenzyme A class of thiolase inhibitors, is a metabolic modulator. It inhibits the β-oxidation of fatty acids; increases myocardial glucose utilization, prevents a decrease in ATP and phosphocreatine levels in response to hypoxia or ischemia; It minimizes free radical production and protects against intracellular calcium overload and acidosis. The most common side effects of trimetazidine are nausea, vomiting, tiredness, dizziness and muscle pain. The drug may increase extrapyramidal stiffness, bradykinesia, and tremor by inducing Parkinson’s symptoms. Although the mechanism responsible for these reactions is unknown, it is thought that trimetazidine is a piperazine derivative and causes such side effects because it causes blockage of central D2 dopamine receptors [16].
Advances in small-molecule therapy for managing angina pectoris in the elderly
Published in Expert Opinion on Pharmacotherapy, 2019
Nida Waheed, Ahmad Mahmoud, Cecil A. Rambarat, Carl J. Pepine
Trimetazidine is an antianginal whose use has been readily adopted in Europe, although it was never submitted for FDA approval in the US. This small molecule works by decreasing myocardial oxygen demand in low flow states through inhibition of free fatty acid oxidation, leading to an increased metabolism of glucose to reduce myocardial oxygen consumption [79]. In a meta-analysis examining trimetazidine in patients with angina, trimetazidine was shown to decrease angina frequency and increase exercise capacity while not significantly affecting hemodynamics [80]. In another study, it was shown that elderly patients (mean age 78 years) receiving trimetazidine had improvement in the number of angina episodes per week (−2.3 ± 1, p = 0.023) and QOL [81]. The Task Force on the Management of Stable Angina Pectoris of the ESC has given this small molecule a class IIB indication as an adjunct or substitute for treatment of angina when conventional therapy is not tolerated [82]. There are currently three trials further examining the effects of trimetazidine for angina, one of which is being performed in patients with angina and suspected CMD [83–85].
Psychocardiological disorder and brain serotonin after comorbid myocardial infarction and depression: an experimental study
Published in Neurological Research, 2018
Li-Jun Zhang, Mei-Yan Liu, Radhika Rastogi, Jessie N. Ding
Trimetazidine has been used as a metabolic agent for the myocardium protection for more than 40 years. One meta-analysis on the adjuvant effect of trimetazidine on acute myocardial infarction demonstrated that trimetazidine reduced significant adverse cardiac events in patients with myocardial infarction [15]. Another meta-analysis of trimetazidine-related studies suggests that preoperative administration of trimetazidine has a positive protective effect on the myocardium of patients undergoing coronary artery bypass grafting [16]. It has long been suggested that the mechanism of trimetazidine is to inhibit the fatty acid oxidation by inhibiting 3-ketoacyl CoA thiolase (3-KATase), increasing glucose oxidation, and increasing intracellular ATP levels to protect ischemic cardiomyocytes and the intracellular–environmental balance [17]. Kay et al. [18] and Dehina et al. [19] suggested that trimetazidine protects the heart by protecting mitochondrial structure and function. With an established role in myocardial protection, trimetazidine also has a potential role in comorbid CHD and depression via 5-HT related mechanisms as well.