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Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Metoprolol is a cardioselective competitive β1-adrenergic receptor antagonist with antihypertensive properties. This agent antagonizes β1-adrenergic receptors in the myocardium, thereby reducing the rate and force of myocardial contraction, leading to a reduction in cardiac output. Metoprolol is indicated for the treatment of angina, heart failure, myocardial infarction, atrial fibrillation, atrial flutter and hypertension. Off-label uses of metoprolol include supraventricular tachycardia and thyroid storm. In pharmaceutical products, metoprolol is most often employed as metoprolol succinate (CAS number 98418-47-4, EC number not available, molecular formula C34H56N2O10) or as metoprolol tartrate (CAS number 56392-17-7, EC number 260-148-9, molecular formula C34H56N2O12) (1).
Genetically Determined Ventricular Arrhythmias
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Houman Khakpour, Jason S. Bradfield
Among symptomatic patients, nadolol and propranolol performed better than metoprolol. The risk of cardiac events was 3.9-fold greater when patients were treated with metoprolol.29 However, in another recent large retrospective study assessing the efficacy of the 4 most commonly prescribed β-blockers (atenolol, metoprolol, nadolol, and propranolol) in 1530 patients, all β-blockers were equally effective in reducing the risk of a first cardiac event. In the subcohort of patients with LQT1 (n = 379), no β-blocker was superior, whereas in LQT2 (n = 406), nadolol was slightly more effective than other β-blockers. In patients with at least one cardiac event while taking β-blockers, propranolol appeared to be the least effective drug.30 The data from the retrospective studies clearly underline the beneficial effect of β-blocker therapy in LQTS but caution should be exercised before drawing conclusions about their relative efficacy. There is agreement that nadolol is probably one of the more effective drugs for this condition.31 Abrupt discontinuation of beta-blockers should be avoided.
Drug therapy in the cardiac catheterisation laboratory: A guide to commonly used drugs
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
John Edward Boland, Fuyue Jiang, Andrew Fenning
Cardioselective β1 blockers (e.g. metoprolol, atenolol) that act specifically on β1 receptors are available. Metoprolol is a selective beta blocker that stimulates cardiac contraction and reduces heart rate and blood pressure. Hence it is useful as a rate control agent in patients with atrial fibrillation and heart disease. A potential unwanted side effect is hypotension.
Multi-modality management of hypertrophic cardiomyopathy
Published in Hospital Practice, 2023
Shiavax J. Rao, Shaikh B. Iqbal, Arjun S. Kanwal, Wilbert S. Aronow, Srihari S. Naidu
Beta-blockers (specifically non-vasodilating agents) are among the first-line pharmacotherapeutic options for relief of LVOTO, and should be titrated to maximally tolerated doses, while focusing on symptoms [6]. The first study involving beta-blockers demonstrated reduction of LVOTO gradient and associated symptoms through propranolol therapy [7]. Most typically in contemporary practice, metoprolol is utilized in long-acting twice-daily formulation. Another agent, nadolol (a nonselective beta-blocker), which exhibits a good antiarrhythmic profile and is generally well tolerated by patients, is an increasingly used pharmacotherapy for patients with LVOTO [6,8]. Beta-blockers are particularly effective in reducing LV-gradient-induced symptoms of LVOTO during exercise. If there is evidence of a significant LV-gradient at rest, the latest guidelines recommend association with disopyramide [1,2]. Furthermore, owing to their negative inotropic and chronotropic effects, beta-blockers are also recommended in symptomatic patients with non-obstructive HCM, to improve symptoms of dyspnea and angina, precipitated by diastolic dysfunction, microvascular ischemia and elevated cardiac filling pressures [1,2,6].
Massive suicidal ingestion of caffeine: a case report with investigation of the cardiovascular effect/concentration relationships
Published in Clinical Toxicology, 2021
Vincent Grémain, Lucie Chevillard, Elodie Saussereau, Guillaume Schnell, Bruno Mégarbane
Various strategies have been used to manage caffeine poisoning in addition to supportive care, provided to our patient according to the guidelines [9]. Benzodiazepines are useful to treat agitation, hypertension and sinus tachycardia. Dexmedetomidine, a sedative agent with α2-agonist properties, was also used successfully in this purpose [10]. Reported in theophylline-poisoned patients to slow paroxysmal supraventricular tachycardia [11], adenosine is unlikely to be effective or may only show transient efficacy due to the adenosine antagonism. The most logical therapy combines a short-acting β-blocker such as esmolol that antagonizes β1-stimulation to reverse tachycardia and improve diastolic filling and norepinephrine that provides α1-stimulation to counteract β2-induced peripheral vasodilation. Metoprolol has been proposed as an alternative to treat supraventricular tachycardia [12]. Phenylephrine is a suitable potent α-agonist with useful reflex bradycardic effects [13]. Other anti-arrhythmic drugs including procainamide (class Ia), lidocaine (class Ib), propranolol (class II) and amiodarone (class III) have been used; however, physicians should be aware of the risk of conduction impairment when using high doses of class I and II agents. Lipid emulsion [14] and extracorporeal membrane oxygenation [15] have been successfully used to manage circulatory compromise with refractory ventricular arrhythmia.
Effect of naringenin on the pharmacokinetics of metoprolol succinate in rats
Published in Xenobiotica, 2021
Ravindra Babu Pingili, Sridhar Vemulapalli, Vijaya R. Dirisala, Surya Sandeep Mullapudi, Yamini Gullapalli, Naveen Babu Kilaru
Globally, hypertension is the single most important risk factor for mortality and the third highest cause of morbidity (Ezzati et al. 2002). Hypertension is a major risk factor for coronary heart disease and stroke in the Indian population (Gupta et al. 2008). Metoprolol, a β1-selective (cardioselective) adrenoceptor antagonist, is widely used in the treatment of mild to moderate hypertension and angina pectoris. Blockade of the β1 receptor reduces heart rate, myocardial contractility, and cardiac output. It also reduces plasma renin activity (Benfield et al. 1986; Kendall et al. 1991). Intestinal absorption of metoprolol is rapid and almost complete and a significant beta-blockade effect occurs within 60 min of administration. However, due to extensive first-pass metabolism, the bioavailability of metoprolol is only approximately 50%. It is metabolized predominantly by CYP2D6 but that CYP3A4, CYP2B6, and CYP2C9 are also involved in the three major pathways of metoprolol metabolism. CYP3A4, 2B6, and 2C9 catalyse α-hydroxylation, O-demethylation, and N-dealkylation of metoprolol metabolism, respectively (Benjamin et al. 2018). These enzymes can be inhibited by several drugs or compounds. Therefore, concomitant use of CYP3A4, CYP2B6, CYP2C9, and CYP2D6 inhibitors will increase blood levels of metoprolol several-folds.