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American Family Physician Jan 2019Migraines impose significant health and financial burdens. Approximately 38% of patients with episodic migraines would benefit from preventive therapy, but less than 13%...
Migraines impose significant health and financial burdens. Approximately 38% of patients with episodic migraines would benefit from preventive therapy, but less than 13% take prophylactic medications. Preventive medication therapy reduces migraine frequency, severity, and headache-related distress. Preventive therapy may also improve quality of life and prevent the progression to chronic migraines. Some indications for preventive therapy include four or more headaches a month, eight or more headache days a month, debilitating headaches, and medication-overuse headaches. Identifying and managing environmental, dietary, and behavioral triggers are useful strategies for preventing migraines. First-line medications established as effective based on clinical evidence include divalproex, topiramate, metoprolol, propranolol, and timolol. Medications such as amitriptyline, venlafaxine, atenolol, and nadolol are probably effective but should be second-line therapy. There is limited evidence for nebivolol, bisoprolol, pindolol, carbamazepine, gabapentin, fluoxetine, nicardipine, verapamil, nimodipine, nifedipine, lisinopril, and candesartan. Acebutolol, oxcarbazepine, lamotrigine, and telmisartan are ineffective. Newer agents target calcitonin gene-related peptide pain transmission in the migraine pain pathway and have recently received approval from the U.S. Food and Drug Administration; however, more studies of long-term effectiveness and adverse effects are needed. The complementary treatments petasites, feverfew, magnesium, and riboflavin are probably effective. Nonpharmacologic therapies such as relaxation training, thermal biofeedback combined with relaxation training, electromyographic feedback, and cognitive behavior therapy also have good evidence to support their use in migraine prevention.
Topics: Combined Modality Therapy; Humans; Migraine Disorders; Secondary Prevention
PubMed: 30600979
DOI: No ID Found -
European Journal of Internal Medicine Jun 2021β-blockers represent a mainstay in the pharmacological approach to patients affected by heart failure with reduced ejection fraction (HFrEF). However, underuse of this... (Review)
Review
β-blockers represent a mainstay in the pharmacological approach to patients affected by heart failure with reduced ejection fraction (HFrEF). However, underuse of this class of drugs is still reported, especially in the presence of cardiovascular and non-cardiovascular comorbidities, even if they are not contraindications for prescription of a β-blocker. The prognostic benefit of β-blockers is relevant in the presence of comorbidities, and achievement of the maximum tolerated dose is an important goal to increase their favorable prognostic role. The aim of the present review is to analyze the available evidence on the use of β-blockers in HFrEF patients with the most common comorbidities. In particular, we will discuss the role and most appropriate beta-blocker in patients with pulmonary disease (bisoprolol, metoprolol, nebivolol), diabetes (carvedilol and nebivolol), atrial fibrillation (all indicated for rate control, with metoprolol as the first choice followed by bisoprolol, nebivolol, and carvedilol), erectile dysfunction (bisoprolol and nebivolol), peripheral arterial disease (nebivolol), and other conditions, in order to clarify the correct use of this class of drugs in the clinical practice.
Topics: Adrenergic beta-Antagonists; Carbazoles; Heart Failure; Humans; Male; Propanolamines; Stroke Volume
PubMed: 33941435
DOI: 10.1016/j.ejim.2021.03.035 -
Cardiovascular Drugs and Therapy Oct 2022Bisoprolol and nebivolol are highly selective β-adrenoceptor antagonists, with clinical indications in many countries within the management of heart failure with... (Review)
Review
Therapeutic Properties of Highly Selective β-blockers With or Without Additional Vasodilator Properties: Focus on Bisoprolol and Nebivolol in Patients With Cardiovascular Disease.
Bisoprolol and nebivolol are highly selective β-adrenoceptor antagonists, with clinical indications in many countries within the management of heart failure with reduced left ventricular ejection fraction (HFrEF), ischaemic heart disease (IHD), and hypertension. Nebivolol has additional vasodilator actions, related to enhanced release of NO in the vascular wall. In principle, this additional mechanism compared with bisoprolol might lead to more potent vasodilatation, which in turn might influence the effectiveness of nebivolol in the management of HFrEF, IHD and hypertension. In this article, we review the therapeutic properties of bisoprolol and nebivolol, as representatives of "second generation" and "third generation" β-blockers, respectively. Although head-to-head trials are largely lacking, there is no clear indication from published studies of an additional effect of nebivolol on clinical outcomes in patients with HFrEF or the magnitude of reductions of BP in patients with hypertension.
Topics: Adrenergic beta-Antagonists; Benzopyrans; Bisoprolol; Cardiovascular Diseases; Ethanolamines; Heart Failure; Humans; Hypertension; Myocardial Ischemia; Nebivolol; Stroke Volume; Vasodilator Agents; Ventricular Function, Left
PubMed: 34106365
DOI: 10.1007/s10557-021-07205-y -
BMJ (Clinical Research Ed.) Jan 2013To clarify whether any particular β blocker is superior in patients with heart failure and reduced ejection fraction or whether the benefits of these agents are mainly... (Comparative Study)
Comparative Study Meta-Analysis Review
OBJECTIVE
To clarify whether any particular β blocker is superior in patients with heart failure and reduced ejection fraction or whether the benefits of these agents are mainly due to a class effect.
DESIGN
Systematic review and network meta-analysis of efficacy of different β blockers in heart failure.
DATA SOURCES
CINAHL(1982-2011), Cochrane Collaboration Central Register of Controlled Trials (-2011), Embase (1980-2011), Medline/PubMed (1966-2011), and Web of Science (1965-2011).
STUDY SELECTION
Randomized trials comparing β blockers with other β blockers or other treatments.
DATA EXTRACTION
The primary endpoint was all cause death at the longest available follow-up, assessed with odds ratios and Bayesian random effect 95% credible intervals, with independent extraction by observers.
RESULTS
21 trials were included, focusing on atenolol, bisoprolol, bucindolol, carvedilol, metoprolol, and nebivolol. As expected, in the overall analysis, β blockers provided credible mortality benefits in comparison with placebo or standard treatment after a median of 12 months (odds ratio 0.69, 0.56 to 0.80). However, no obvious differences were found when comparing the different β blockers head to head for the risk of death, sudden cardiac death, death due to pump failure, or drug discontinuation. Accordingly, improvements in left ventricular ejection fraction were also similar irrespective of the individual study drug.
CONCLUSION
The benefits of β blockers in patients with heart failure with reduced ejection fraction seem to be mainly due to a class effect, as no statistical evidence from current trials supports the superiority of any single agent over the others.
Topics: Adrenergic beta-Antagonists; Bayes Theorem; Heart Failure; Humans; Odds Ratio; Randomized Controlled Trials as Topic; Stroke Volume; Treatment Outcome
PubMed: 23325883
DOI: 10.1136/bmj.f55 -
Nature Communications Oct 2021Abnormal activation of epidermal growth factor receptor (EGFR) drives non-small cell lung cancer (NSCLC) development. EGFR mutations-mediated resistance to...
Abnormal activation of epidermal growth factor receptor (EGFR) drives non-small cell lung cancer (NSCLC) development. EGFR mutations-mediated resistance to tyrosine-kinase inhibitors (TKIs) is a major hurdle for NSCLC treatment. Here, we show that F-box protein FBXL2 targets EGFR and EGFR TKI-resistant mutants for proteasome-mediated degradation, resulting in suppression of EGFR-driven NSCLC growth. Reduced FBXL2 expression is associated with poor clinical outcomes of NSCLC patients. Furthermore, we show that glucose-regulated protein 94 (Grp94) protects EGFR from degradation via blockage of FBXL2 binding to EGFR. Moreover, we have identified nebivolol, a clinically used small molecule inhibitor, that can upregulate FBXL2 expression to inhibit EGFR-driven NSCLC growth. Nebivolol in combination with osimertinib or Grp94-inhibitor-1 exhibits strong inhibitory effects on osimertinib-resistant NSCLC. Together, this study demonstrates that the FBXL2-Grp94-EGFR axis plays a critical role in NSCLC development and suggests that targeting FBXL2-Grp94 to destabilize EGFR may represent a putative therapeutic strategy for TKI-resistant NSCLC.
Topics: Acrylamides; Aniline Compounds; Animals; Antineoplastic Agents; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Movement; Cell Proliferation; Drug Resistance, Neoplasm; Drug Synergism; ErbB Receptors; F-Box Proteins; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Membrane Glycoproteins; Mice; Mice, Nude; Nebivolol; Protein Kinase Inhibitors; Signal Transduction; Survival Analysis; Tumor Burden; Xenograft Model Antitumor Assays
PubMed: 34635651
DOI: 10.1038/s41467-021-26222-x -
Journal of Pharmacology &... 2015Adverse drug reactions play a substantial role in the etiology of gynecomastia. Gynecomastia as an adverse drug reaction, related to some cardiovascular drugs, has been...
Adverse drug reactions play a substantial role in the etiology of gynecomastia. Gynecomastia as an adverse drug reaction, related to some cardiovascular drugs, has been reported in literature. Nebivolol is a third generation beta-blocker, and gynecomastia as an adverse effect on the consumption of this drug has not been reported in any article yet. We herein present the case of a 42-year-old male, who developed bilateral gynecomastia following nebivolol use and complete regression after discontinuation of nebivolol. Other reasons causing gynecomastia were excluded. Discontinuation of the responsible drug is quite sufficient with regard to the treatment of drug-induced gynecomastia, without any pharmacological or surgical treatment.
PubMed: 26312003
DOI: 10.4103/0976-500X.162009