Metoprolol succinate and metoprolol tartrate(comparison)

On the basis of the pharmacologic actions of metoprolol, employ the following measures. There is very limited experience with the use of hemodialysis to remove metoprolol, however metoprolol is not highly protein bound.

Evaluate the need for atropine, adrenergic-stimulating drugs or pacemaker to treat bradycardia and conduction disorders. Consider intravenous vasopressor infusion, such as dopamine or norepinephrine. Heart failure and shock: Can usually be reversed by bronchodilators. Metoprolol Succinate Description Metoprolol Succinate, is a beta1-selective cardioselective adrenoceptor blocking agent, for oral administration, available as extended-release tablets.

Metoprolol Succinate extended-release tablets, USP have been formulated to provide a controlled and predictable release of metoprolol for once-daily administration. The tablets comprise a multiple unit system containing Metoprolol Succinate in a multitude of controlled release pellets. Each pellet acts as a separate drug delivery unit and is designed to deliver metoprolol continuously over the dosage interval.

The tablets contain Its structural formula is: Metoprolol Succinate, USP is a white crystalline powder with a molecular weight of It is freely soluble in water; soluble in methanol; sparingly soluble in ethanol; slightly soluble in dichloromethane and 2-propanol; practically insoluble in ethyl-acetate, acetone, diethylether and heptane. The mechanism of the antihypertensive effects of beta-blocking agents has not been elucidated.

However, several possible mechanisms have been proposed: The precise mechanism for the beneficial effects of beta-blockers in heart failure has not been elucidated.

Pharmacodynamics Clinical pharmacology studies have confirmed the beta-blocking activity of metoprolol in man, as shown by 1 reduction in heart rate and cardiac output at rest and upon exercise, 2 reduction of systolic blood pressure upon exercise, 3 inhibition of isoproterenol-induced tachycardia, and 4 reduction of reflex orthostatic tachycardia. Metoprolol is a beta1-selective cardioselective adrenergic receptor blocking agent.

This preferential effect is not absolute, however, and at higher plasma concentrations, metoprolol also inhibits beta2-adrenoreceptors, chiefly located in the bronchial and vascular musculature. Metoprolol has no intrinsic sympathomimetic activity, and membrane-stabilizing activity is detectable only at plasma concentrations much greater than required for beta-blockade. Animal and human experiments indicate that metoprolol slows the sinus rate and decreases AV nodal conduction. The relative beta1-selectivity of metoprolol has been confirmed by the following: This contrasts with the effect of nonselective beta-blockers, which completely reverse the vasodilating effects of epinephrine.

The relationship between plasma metoprolol levels and reduction in exercise heart rate is independent of the pharmaceutical formulation. Although beta-adrenergic receptor blockade is useful in the treatment of angina, hypertension, and heart failure there are situations in which sympathetic stimulation is vital. In patients with severely damaged hearts, adequate ventricular function may depend on sympathetic drive.

In the presence of AV block, beta-blockade may prevent the necessary facilitating effect of sympathetic activity on conduction. Beta2-adrenergic blockade results in passive bronchial constriction by interfering with endogenous adrenergic bronchodilator activity in patients subject to bronchospasm and may also interfere with exogenous bronchodilators in such patients.

In other studies, treatment with Metoprolol Succinate extended-release tablets produced an improvement in left ventricular ejection fraction.

Metoprolol Succinate extended-release tablets was also shown to delay the increase in left ventricular end-systolic and end-diastolic volumes after 6 months of treatment. In man, absorption of metoprolol is rapid and complete. Plasma levels achieved are highly variable after oral administration. When administered orally, it exhibits stereoselective metabolism that is dependent on oxidation phenotype. Elimination is mainly by biotransformation in the liver, and the plasma half-life ranges from approximately 3 to 7 hours.

The systemic availability and half-life of metoprolol in patients with renal failure do not differ to a clinically significant degree from those in normal subjects. Consequently, no reduction in Metoprolol Succinate dosage is usually needed in patients with chronic renal failure. CYP2D6 can be inhibited by a number of drugs. Poor metabolizers and extensive metabolizers who concomitantly use CYP2D6 inhibiting drugs will have increased several-fold metoprolol blood levels, decreasing metoprolol's cardioselectivity [see Drug Interactions 7.

In comparison to conventional metoprolol, the plasma metoprolol levels following administration of Metoprolol Succinate extended-release tablets are characterized by lower peaks, longer time to peak and significantly lower peak to trough variation.

The peak plasma levels following once-daily administration of Metoprolol Succinate extended-release tablets average one-fourth to one-half the peak plasma levels obtained following a corresponding dose of conventional metoprolol, administered once daily or in divided doses. The bioavailability of metoprolol shows a dose-related, although not directly proportional, increase with dose and is not significantly affected by food following Metoprolol Succinate extended-release tablets administration.

Metoprolol succinate extended-release tablets have been formulated to provide a controlled and predictable release of metoprolol for once daily oral administration.

The tablets comprise a multiple unit system containing metoprolol succinate in a multitude of controlled-release pellets. Each pellet acts as a separate drug delivery unit and is designed to deliver metoprolol continuously over the dosage interval. The tablets contain Its structural formula is: Metoprolol succinate is a white crystalline powder with a molecular weight of It is freely soluble in water; soluble in methanol; sparingly soluble in ethanol; slightly soluble in dichloromethane and 2-propanol; practically insoluble in ethyl-acetate, acetone, diethylether and heptane.

Animal and human experiments indicate that metoprolol slows the sinus rate and decreases AV nodal conduction. Clinical pharmacology studies have confirmed the beta-blocking activity of metoprolol in man, as shown by 1 reduction in heart rate and cardiac output at rest and upon exercise, 2 reduction of systolic blood pressure upon exercise, 3 inhibition of isoproterenol-induced tachycardia, and 4 reduction of reflex orthostatic tachycardia. The relative beta1-selectivity of metoprolol has been confirmed by the following: This contrasts with the effect of nonselective beta-blockers, which completely reverse the vasodilating effects of epinephrine.

In five controlled studies in normal healthy subjects, the same daily doses of metoprolol succinate extended-release tablets and immediate-release metoprolol were compared in terms of the extent and duration of beta 1-blockade produced.

Both formulations were given in a dose range equivalent to to mg of immediate release metoprolol per day. In these studies, metoprolol succinate extended-release tablets were administered once a day and immediate-release metoprolol was administered once to four times a day. A sixth controlled study compared the beta1- blocking effects of a 50 mg daily dose of the two formulations.

In each study, beta1-blockade was expressed as the percent change from baseline in exercise heart rate following standardized submaximal exercise tolerance tests at steady state.

Metoprolol succinate extended-release tablets administered once a day, and immediate-release metoprolol administered once to four times a day, provided comparable total beta1-blockade over 24 hours area under the beta1-blockade versus time curve in the dose range to mg. At a dosage of 50 mg once daily, metoprolol succinate extended-release tablets produced significantly higher total beta1-blockade over 24 hours than immediate-release metoprolol.

For metoprolol succinate extended-release tablets, the percent reduction in exercise heart rate was relatively stable throughout the entire dosage interval and the level of beta1-blockade increased with increasing doses from 50 to mg daily. In contrast to metoprolol succinate extended-release tablets, immediate-release metoprolol given at a dose of 50 to mg once a day produced a significantly larger peak effect on exercise tachycardia, but the effect was not evident at 24 hours.

To match the peak to trough ratio obtained with metoprolol succinate extended-release tablets over the dosing range of to mg, a t.

The risk of the secondary outcome of cardiovascular mortality was not significantly different between carvedilol and metoprolol users aHR, 1. Among these patients, the risk of mortality was not significantly different between carvedilol and metoprolol users aHR, 0.

Third, we estimated a risk score for mortality and included this as an adjustment variable instead of propensity score.

The C statistic for the risk score model was between 0. Adjustment for risk score yielded an estimate that was very similar to that in the primary analysis aHR, 0. Fifth and finally, 1: The hazard ratios for all-cause and cardiovascular mortality in the propensity score—matched cohort were 0. Discussion In this large contemporary national cohort study of patients with HF with reduced LVEF, we found no significant difference in all-cause mortality between carvedilol and metoprolol succinate users.

The primary findings were consistent through various analyses, including the secondary outcome of cardiovascular mortality, key subgroups, and robustness analyses. This suggests that any difference between carvedilol and metoprolol succinate, if it exists, is unlikely to be clinically meaningful. We designed this study to investigate whether carvedilol is associated with improved survival compared with metoprolol succinate, a hypothesis based on the different adrenergic receptor profiles of the 2 drugs, other mechanistic differences, and results of the COMET trial and a recent network meta-analysis.

Given the required size and associated cost, it is unlikely that a randomized trial that resolves this issue will be conducted in the near future. Therefore, we did a cohort study of real-world patients in clinical practice.

Our results are consistent with the notion that no clinically relevant differences between carvedilol and metoprolol succinate exist. To our knowledge, no directly comparable studies have been published. A few observational comparative effectiveness studies have been conducted, but these only included metoprolol tartrate and did not have data on LVEF and NYHA class 29 , 30 or were conducted at a single center with a limited number of adjustment variables.

Our study has strengths and limitations. Treatment was not randomly assigned and could therefore have been influenced by unmeasured factors that, if also associated with the outcome, could have introduced confounding.

To reduce this possibility, we took into account a range of potential confounders through the use of a comprehensive propensity score model. Of note, although some baseline differences between the treatment groups were present, such as higher prevalence of ischemic heart disease among metoprolol users, potentially introducing a certain level of heterogeneity that might not have been captured by adjustment for propensity score, the main results were replicated in a 1: Despite this, our findings should be interpreted considering the observational design of the study and need replication in an independent population.

Furthermore, a study of clinical effectiveness in real-world patients should be seen as complementary rather than comparable to a trial. The use of total population registers allowed detailed characterization of included patients, minimal loss to follow-up, and exact assessment of outcomes throughout the study period.

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