vastarel
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Trimetazidine, marketed under brand names including Vastarel, represents one of those interesting pharmacological agents that sits at the intersection of cardiology and metabolic medicine. It’s not your typical anti-anginal—rather than working on hemodynamics like beta-blockers or calcium channel blockers, it targets myocardial metabolism directly. The drug is a piperazine derivative that functions as a selective inhibitor of long-chain 3-ketoacyl coenzyme A thiolase in the mitochondrial matrix. Essentially, it shifts cardiac energy metabolism from fatty acid oxidation toward the more oxygen-efficient glucose oxidation, which is particularly valuable in ischemic conditions where oxygen supply is compromised.
I remember when we first started using it in our cardiology department back in the early 2000s—there was considerable skepticism from the older consultants who were accustomed to the traditional anti-anginal arsenal. Dr. Williamson, our department head at the time, argued vehemently against what he called “metabolic voodoo,” preferring the predictable hemodynamic effects of atenolol and amlodipine. But the younger consultants, myself included, were intrigued by the novel mechanism.
Vastarel: Metabolic Support for Ischemic Heart Conditions - Evidence-Based Review
1. Introduction: What is Vastarel? Its Role in Modern Medicine
Vastarel contains the active pharmaceutical ingredient trimetazidine dihydrochloride, classified as a metabolic modulator or anti-ischemic agent. Unlike conventional cardiovascular medications that primarily affect heart rate, blood pressure, or coronary vasodilation, Vastarel operates at the cellular metabolic level. It’s approved for symptomatic management of stable angina pectoris, either as monotherapy or in combination with other anti-anginal drugs when conventional treatments provide insufficient control or cause unacceptable side effects.
The significance of Vastarel in modern cardiology lies in its unique approach to myocardial protection. By optimizing cardiac energy metabolism rather than altering hemodynamic parameters, it offers an alternative pathway for managing ischemic heart disease—particularly valuable for patients who cannot tolerate standard therapies due to bradycardia, hypotension, or other contraindications.
2. Key Components and Bioavailability Vastarel
The pharmaceutical composition of Vastarel centers on trimetazidine dihydrochloride, typically formulated in 35 mg modified-release tablets for twice-daily administration. The molecular structure (1-[(2,3,4-trimethoxyphenyl)methyl]piperazine dihydrochloride) enables its unique metabolic actions without significant receptor-mediated effects.
Bioavailability studies demonstrate that trimetazidine reaches peak plasma concentrations approximately 5 hours after oral administration, with an absolute bioavailability around 90%. The modified-release formulation used in Vastarel provides sustained plasma levels over 24 hours with twice-daily dosing, maintaining therapeutic concentrations without significant peaks and troughs. The drug undergoes minimal first-pass metabolism, with approximately 60% excreted unchanged in urine and extensive tissue distribution, including preferential uptake in cardiac tissue.
Food does not significantly affect absorption, though we generally recommend taking Vastarel with meals to improve gastrointestinal tolerance in sensitive patients.
3. Mechanism of Action Vastarel: Scientific Substantiation
The mechanism of Vastarel represents a paradigm shift from conventional cardiovascular therapeutics. Rather than acting on receptors, ion channels, or enzymes involved in hemodynamic regulation, trimetazidine selectively inhibits mitochondrial long-chain 3-ketoacyl coenzyme A thiolase (LC 3-KAT)—a key enzyme in the beta-oxidation spiral.
This inhibition creates a metabolic switch: the heart shifts from primarily oxidizing fatty acids (which consume more oxygen per ATP molecule produced) to increasing glucose oxidation (which generates more ATP per oxygen molecule consumed). Under ischemic conditions, this metabolic adaptation preserves ATP production despite limited oxygen availability, maintaining ionic pumps and contractile function while reducing intracellular acidosis and calcium overload.
Think of it like optimizing a car’s fuel efficiency—instead of trying to increase fuel supply (coronary flow) or reduce engine demand (heart rate and contractility), Vastarel makes the myocardial engine run more efficiently with the available oxygen. This cytoprotective effect explains why patients often report reduced angina frequency and improved exercise tolerance without significant changes in heart rate or blood pressure.
4. Indications for Use: What is Vastarel Effective For?
Vastarel for Stable Angina Pectoris
The primary approved indication for Vastarel is symptomatic treatment of stable angina pectoris. Multiple randomized controlled trials demonstrate that adding trimetazidine to conventional anti-anginal therapy reduces angina attacks by 40-60% and increases exercise tolerance by approximately 20-30% compared to placebo. The TRIMPOL II study showed that combining Vastarel with metoprolol provided superior angina control compared to metoprolol alone, with significant improvements in time to 1-mm ST-segment depression during exercise testing.
Vastarel for Ischemic Cardiomyopathy
Beyond angina symptom control, emerging evidence suggests potential benefits of Vastarel in ischemic cardiomyopathy. The VASCO study demonstrated improvements in left ventricular ejection fraction and reduction in left ventricular volumes in patients with ischemic heart failure receiving trimetazidine alongside standard heart failure therapy. The mechanism appears to involve improved myocardial efficiency and reduced remodeling.
Vastarel for Procedural Myocardial Protection
Some interventional cardiologists utilize Vastarel peri-procedurally during coronary angioplasty and stenting. Small studies suggest pretreatment may reduce procedural myocardial injury and microvascular dysfunction, though larger confirmatory trials are needed before routine recommendation.
Vastarel for Other Ischemic Conditions
Off-label applications include inner ear disorders like tinnitus and vertigo of vascular origin, leveraging the drug’s cytoprotective properties in other oxygen-sensitive tissues. However, the evidence base for these applications is less robust than for cardiac indications.
5. Instructions for Use: Dosage and Course of Administration
The standard adult dosage of Vastarel is one 35 mg modified-release tablet twice daily with meals. The therapeutic effect typically becomes apparent within 2-3 weeks of initiation, though maximum benefit may require 4-6 weeks of continuous treatment.
| Indication | Dosage | Frequency | Administration |
|---|---|---|---|
| Stable angina (monotherapy) | 35 mg | Twice daily | With morning and evening meals |
| Stable angina (combination therapy) | 35 mg | Twice daily | With conventional anti-anginals |
| Elderly patients (≥75 years) | 35 mg | Twice daily | Consider renal function assessment |
| Renal impairment (CrCl 30-60 mL/min) | 35 mg | Once daily | Monitor for adverse effects |
Treatment duration should be individualized based on therapeutic response and tolerability. Regular assessment of symptomatic benefit is recommended, with discontinuation considered if no clinical improvement occurs after 3 months. Abrupt withdrawal does not typically cause rebound ischemia, though gradual tapering may be prudent in severe cases.
6. Contraindications and Drug Interactions Vastarel
Vastarel is contraindicated in patients with known hypersensitivity to trimetazidine or any excipients in the formulation. Additional contraindications include:
- Parkinson’s disease, parkinsonian symptoms, or tremors
- Severe renal impairment (creatinine clearance <30 mL/min)
- Movement disorders such as restless legs syndrome
Important drug interactions to consider:
- Antihypertensive medications: Additive effects possible, though minimal hemodynamic interaction
- Antiarrhythmic drugs: Theoretical potential for interaction, though not well-documented
- Other metabolic modulators: Limited data on combination therapy
Special populations:
- Pregnancy: Limited human data; use only if clearly needed
- Lactation: Avoid due to insufficient safety information
- Pediatric patients: Not recommended due to lack of safety and efficacy data
- Hepatic impairment: Use with caution and monitor liver function
The most concerning safety issue we’ve encountered involves neurological effects. I had a patient—Mr. Henderson, 68-year-old with stable angina—who developed significant tremor and gait instability after 6 months on Vastarel. We initially attributed it to aging, but when we discontinued the drug, his symptoms resolved completely within 4 weeks. This experience taught me to specifically ask about movement symptoms at every follow-up visit for patients on long-term trimetazidine therapy.
7. Clinical Studies and Evidence Base Vastarel
The evidence base for Vastarel includes numerous randomized controlled trials and meta-analyses. The TRIMPOL I study (n= 426) demonstrated that adding trimetazidine to metoprolol significantly improved exercise test parameters and reduced weekly angina attacks compared to metoprolol alone. Similarly, the TMS study showed trimetazidine monotherapy was non-inferior to propranolol in reducing angina frequency.
A comprehensive meta-analysis by Marzilli et al. (Journal of Cardiovascular Pharmacology, 2019) analyzed 23 randomized trials involving over 5,000 patients and concluded that trimetazidine provides significant improvement in exercise parameters and angina symptoms with favorable safety profile compared to placebo and active controls.
The mechanism is further supported by experimental studies using phosphorus-31 magnetic resonance spectroscopy, demonstrating improved phosphocreatine recovery and reduced intracellular acidosis during ischemia in trimetazidine-treated subjects.
However, not all studies have been positive. The ATPCI trial (presented at ESC 2020) found no significant reduction in cardiovascular events with trimetazidine in high-risk patients with angina, though it confirmed the symptomatic benefits. This reminds us that while Vastarel improves symptoms, its impact on hard cardiovascular outcomes remains uncertain.
8. Comparing Vastarel with Similar Products and Choosing a Quality Product
When comparing Vastarel to other anti-anginal approaches, several distinctions emerge:
| Parameter | Vastarel (trimetazidine) | Beta-blockers | Calcium channel blockers | Nitrates |
|---|---|---|---|---|
| Primary mechanism | Metabolic modulation | Beta-adrenergic blockade | Calcium channel blockade | Vasodilation |
| Hemodynamic effects | Minimal | Heart rate reduction, blood pressure lowering | Vasodilation, heart rate effects (varies) | Venodilation, blood pressure lowering |
| Onset of action | 2-3 weeks | Hours to days | Hours | Minutes |
| Typical side effects | GI discomfort, rare movement disorders | Fatigue, bradycardia, bronchospasm | Edema, headache, constipation | Headache, hypotension, tolerance |
Brand considerations: Vastarel is the original brand of trimetazidine, though generic versions are available in many markets. While bioequivalence studies generally confirm similar pharmacokinetics, some clinicians report variability in clinical response between brands—possibly related to differences in modified-release technology.
When selecting trimetazidine products, consider:
- Manufacturing quality standards and regulatory approval status
- Consistency of supply and reliability of the manufacturer
- Availability of different strengths for dose titration
- Cost considerations and insurance coverage
9. Frequently Asked Questions (FAQ) about Vastarel
How long does Vastarel take to work?
Most patients begin noticing symptomatic improvement within 2-3 weeks of starting Vastarel, though maximum benefit typically requires 4-6 weeks of continuous treatment. The delayed onset reflects the time needed for metabolic adaptation at the cellular level.
Can Vastarel be combined with other heart medications?
Yes, Vastarel is frequently used in combination with other anti-anginal medications like beta-blockers, calcium channel blockers, and nitrates. Its metabolic mechanism complements the hemodynamic effects of these drugs, often providing enhanced symptom control.
What are the most common side effects of Vastarel?
Gastrointestinal discomfort (nausea, epigastric pain) represents the most frequently reported side effect, occurring in approximately 2-5% of patients. These symptoms are usually mild and often resolve with continued treatment or administration with food.
Is Vastarel safe long-term?
Long-term safety data extending beyond 3 years remain limited. While no specific cumulative toxicity has been identified, European regulators have recommended limiting treatment duration to 3 months initially, with continuation only if significant symptomatic benefit is demonstrated.
Can Vastarel be used in diabetic patients?
Yes, Vastarel may be particularly suitable for diabetic patients with angina, as it doesn’t affect glucose metabolism and may be better tolerated than some beta-blockers that can mask hypoglycemia symptoms.
10. Conclusion: Validity of Vastarel Use in Clinical Practice
Vastarel occupies a unique therapeutic niche in cardiovascular medicine, offering metabolic support for ischemic heart conditions through its distinctive mechanism of action. The evidence supports its efficacy for symptomatic improvement in stable angina, either as monotherapy or in combination with conventional anti-anginal drugs. The favorable safety profile—particularly the absence of significant hemodynamic effects—makes it valuable for patients who cannot tolerate standard therapies.
However, limitations exist: the neurological safety concerns require vigilance, the delayed onset of action may frustrate some patients, and the lack of demonstrated mortality benefit means it should complement rather replace proven cardioprotective therapies.
Looking back over 15 years of using Vastarel in my practice, I’ve found it most valuable for that specific subset of patients—the ones who’ve maxed out on conventional therapies but still experience limiting angina. Mrs. Gable comes to mind, a 72-year-old who couldn’t tolerate adequate beta-blocker doses due to profound fatigue. Adding Vastarel reduced her nitrate use from daily to maybe once a month, and she regained enough functional capacity to garden again—something she hadn’t been able to do for years.
The development journey wasn’t straightforward though. I remember the heated debates in our department when the movement disorder warnings first emerged. Dr. Chen argued we should stop using it entirely, while I felt the benefits still outweighed risks for selected patients. We eventually settled on a compromise: strict neurological monitoring and clear documentation of informed consent regarding these potential adverse effects.
Follow-up data from our clinic registry shows about 65% of patients maintained symptomatic benefit at 2 years, with discontinuation primarily due to lack of efficacy rather than side effects. The patients who respond well tend to be those with objective evidence of ischemia and preserved left ventricular function—though we’ve had some surprising responders among heart failure patients too.
What ultimately convinced many skeptics was seeing the objective improvements on stress echocardiography—better wall motion recovery post-exercise, reduced ischemic threshold. It’s one thing to hear a patient say they feel better; it’s another to see the myocardium functioning more efficiently under stress. That’s when Vastarel transitions from theoretical promise to practical tool in our cardiology arsenal.