The doses of metoprolol succinate and tartrate are slightly different due to the difference in weight of the two salts, but they are therapeutically equivalent, e. It is important, however, not to confuse the different formulations of metoprolol when they are prescribed. A mg modified-release form of metoprolol tartrate, taken once daily, is available fully subsidised in New Zealand.
All beta-blockers produce competitive antagonism of beta-adrenoceptors in the autonomic nervous system. Research is ongoing into the complex ways in which these properties translate into treatment effects for patients. Beta-blockers are classified according to their adrenoceptor binding affinities Table 1 , the degree of which varies within each class. Some beta-blockers, e. Non-selective beta-blockers , e. Cardioselective beta-blockers , e. Bisoprolol is reported to be more cardioselective than metoprolol and atenolol.
Vasodilating beta-blockers , e. Celiprolol and pindolol have intrinsic sympathomimetic activity ISA and therefore simultaneously block and stimulate beta-adrenoceptors causing less bradycardia and peripheral vasoconstriction. Water-soluble beta-blockers, e. Bisoprolol is processed by both the liver and kidneys therefore does not require dose adjustments for patients with either renal or liver dysfunction, 6 and is also less likely to interact with other medicines.
All beta-blockers can potentiate bradycardia, hypotension and cardiac effects caused by other medicines, e. Beta-blockers that are metabolised by hepatic enzymes may also interact with medicines that are metabolised via the same pathway.
The NZF interactions checker provides details on medicine interactions, including their clinical significance, available from: www. The indications for beta-blockers have shifted over the years.
Originally widely prescribed for hypertension and contraindicated for the treatment of heart failure, beta-blockers now have a limited role in the treatment of hypertension and are routinely prescribed to patients with heart failure. The benefits of beta-blockers post-myocardial infarction are also no longer as clear as they once were. Beta-blockers or calcium channel blockers are recommended as the first-line anti-anginal medicines.
A cardioselective beta-blocker such as bisoprolol or metoprolol succinate will provide the maximum effect with the minimum amount of adverse effects.
Beta-blockers that reduce resting heart rate less than others due to ISA tend not to be used for angina, e. Information on the management of stable angina is available from: bpac. Beta-blockers are the first-line treatment for long-term symptomatic rate control in patients with a range of cardiac arrhythmias, including atrial fibrillation and ventricular tachycardia. Bisoprolol is preferred as it is more cardioselective than metoprolol and may cause more bradycardia.
Sotalol should not be used for rate control in atrial fibrillation due to its pro-arrhythmic action. Sotalol is used exclusively for rhythm control in patients with supraventricular and ventricular arrhythmias, but use has declined since the SWORD survival with oral d-sotalol study in the s was discontinued when it was found that sotalol was associated with a higher rate of sudden death when administered to patients after myocardial infarction. Information on the management of atrial fibrillation is available from: bpac.
Bisoprolol, carvedilol or metoprolol succinate are generally prescribed for heart failure in New Zealand; there is no strong evidence of effectiveness for one over another. Any of these three choices are appropriate if heart failure is associated with ischaemic heart disease, but it is important that the beta-blocker is slowly titrated to maximum tolerated dose. Patients with heart failure with preserved ejection fraction HF-PEF may also be prescribed a beta-blocker if they have other cardiovascular co-morbidities, such as atrial fibrillation or hypertension.
Information on the management of heart failure is available from: bpac. For patients with uncomplicated hypertension beta-blockers are generally a fourth-line option as angiotensin converting enzyme ACE inhibitors, angiotensin II receptor blockers ARBs , diuretics or calcium channel blockers are associated with better outcomes.
There is no evidence that one beta-blocker is superior to any other for the management of hypertension. Information on the management of hypertension is available from: bpac. Beta-blockers are given acutely as first-line treatment post-myocardial infarction to decrease infarct size, increase the threshold for ventricular arrhythmias, and in the long-term, to prevent dysfunctional ventricular remodelling and heart failure.
At 6—months post-myocardial infarction prescribers are encouraged to consider withdrawing beta-blockers from patients without atrial fibrillation or heart failure, if re-vascularisation occurred while they were being treated for their myocardial infarction.
If re-vascularisation did not occur the beta-blocker is likely to be required long term to prevent angina or if there is poor ventricular function. This is an evolving area of research and increasingly the evidence appears to support the withdrawal of beta-blockers from patients without other indications for treatment, e. Information on the management of acute coronary syndromes is available from: bpac.
There are two reasons why the optimal duration of beta-blocker treatment post-myocardial infarction is uncertain: A systematic review of sixty trials that divided studies into either the reperfusion era or the pre-reperfusion era, found that beta-blockers reduced mortality in patients post-myocardial infarction in the pre-reperfusion era, but not the reperfusion era.
Guidelines support the use of a beta-blocker for one to three years post-myocardial infarction, 18, 19 but in practice they are now being stopped earlier in patients who are otherwise well, with no signs of angina or heart failure. The adverse effect profile varies between beta-blockers according to their properties Table 1.
Tolerance to treatment may be improved with a slow upward titration of the beta-blocker until the maintenance dose is established. Actually, nebivolol appears to be the drug with the highest beta1-selectivity8. However, this has been questioned by other authors. In addition, plasma concentrations of Nebivolol do not increase during exercise ,14 thus indicating that nebivolol is not taken up into, stored in and released from adrenergic cells during exercise together with noradrenaline, a common feature of most other beta-blockers so far investigated15, which might explain why these beta-blockers may still be effective after withdrawal of therapy even when they are no longer detectable in plasma.
Furthermore, carvedilol does not reduce nocturnal melatonin release ,13 a finding unique to carvedilol and nebivolol among all beta-blockers so far investigated on this issue. Carvedilol shows an additional feature, namely an increase in heart rate in healthy subjects with the administration of increasing doses of the drug, thus being a unique finding in the class of beta-blockers that increasing doses may cause increasing heart rates Figure.
Sotalol is a non-selective, hydrophilic beta-blocker that prolongs cardiac repolarisation independent of its antiadrenergic action, thus representing class III antiarrhythmic effects. Thus, antiarrhythmic class III properties may be useful in order to provide the antiarrhythmic effects of sotalol. However, beta-blockade effected exclusively by the l-enantiomer appears to play a major role in the efficacy and safety of sotalol. Propranolol is a non-selective, lipophilic beta-blocker with two additional features: On the one hand, only the non-beta-blocking d-enantiomer inhibits the conversion of thyroxin to triiodothyronin, whereas only the l-enantiomer shows beta-blocking effects.
This effect on thyroid hormones is well achieved with generally recommended doses of propranolol in humans. On the other hand, propranolol has been shown to exert antiarrhythmic class I effects residing equally in both the d- and l-enantiomers.
Thus, the c linical relevance of its antiarrhythmic class I effect is questionnable. Taken together, some beta-blockers exert further interesting features in addition to their well-known effects on beta-adrenoceptors. Table 1 : The three generations of beta-blockers 1st generation. Cruickshank JM. Are we misunderstanding beta-blockers? Int J Cardiol ; 2. Atenolol in hypertension : is it a wise choice? Lancet ; Should Beta-blockers remain first choice in the treatment of arterial hypertension?
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What is blood pressure? Can having vitamin D deficiency cause high blood pressure? Weightlifting: Bad for your blood pressure? What are opioids and why are they dangerous? What's your high blood pressure risk? White coat hypertension Wrist blood pressure monitors: Are they accurate? Effectively managing chronic kidney disease Show more related content. Recent studies, however, have suggested that the use of a nonselective beta blocker may be desirable to antagonize some betamediated metabolic effects, such as hypokalemia, induced by epinephrine.
Pindolol is the only beta-receptor antagonist available in the United States with intrinsic sympathomimetic, or partial agonist, activity. Such drugs, because of their partial agonist activity, cause some sympathetic stimulation under conditions of low endogenous sympathetic tone, such as while subjects are at rest in the supine position.
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