Beta-adrenoreceptor blockers (beta-blockers) and selective serotonin reuptake inhibitors (SSRIs) are commonly used medications and often used together, such as for the treatment of anxiety. However, there is no recent review of any potential adverse events related to concomitant use of medicines from each group. This scoping review therefore aimed to provide this narrative synthesis. Key databases were searched for articles published in English from 1 January 1990 to 24 November 2025 reporting any adverse event due to the concomitant use of beta-blockers and SSRIs in people aged 18 or over. Any study design was permitted. From 2211 distinct records, 117 articles were eligible for full-text screening, and 48 articles were included. Eight of these were review articles referring to otherwise-included empirical studies. Most were interventional (n = 19, 36.9%) or case reports (n = 14, 29.2%). Bradycardia was the most frequently reported adverse event (n = 11) mostly in case reports involving metoprolol-fluoxetine, metoprolol-paroxetine, metoprolol-sertraline or propranolol-fluoxetine. Blood pressure changes (including hypotension) were observed in half of studies which explored them. Neurocognitive-related symptoms were heterogeneous and there were four case reports/series of self-poisoning suicide or self-harm. The adverse events discussed in this review could be signals for drug-drug interactions. Where mechanism was postulated, authors mostly proposed pharmacokinetically mediated effects via Cytochrome P450 2D6. Signals described in this review of potential adverse events should be examined in robust observational studies of specific beta-blocker-SSRI combinations. This will enable precise estimation of the magnitude of any associated risks and provide insight into the potential mechanism.

Children with congenital and acquired heart disease frequently require complex and prolonged pharmacotherapy, often involving off-label cardiovascular medications with narrow therapeutic ranges. Consequently, variability in drug response and medication-related adverse events remains a significant clinical challenge in pediatric cardiology. Pharmacogenetics provides a framework to individualize drug selection and dosing by incorporating genetic variability alongside established clinical and developmental factors. This review outlines the current clinical utility and emerging role of pharmacogenetics in pediatric cardiology, emphasizing applications most relevant to day-to-day patient care. Established pharmacogenetic associations with direct implications for pediatric cardiac practice include gene-drug pairs involving tacrolimus (CYP3A5), warfarin (CYP2C9, VKORC1, CYP4F2, rs12777823 within the CYP2C), clopidogrel (CYP2C19), flecainide (CYP2D6), metoprolol (CYP2D6), and statins (SLCO1B1, ABCG2, CYP2C9), many of which are supported by guideline-based recommendations from the Clinical Pharmacogenetics Implementation Consortium. This review also highlights pharmacogenetic considerations for commonly prescribed non-cardiac medications that may influence cardiovascular outcomes in children with heart disease, identifies emerging areas for research, and emphasizes that as pharmacogenetic testing becomes increasingly accessible, its thoughtful integration into pediatric cardiology practice may improve therapeutic precision, enhance safety, and reduce preventable adverse drug events.

A 70-year-old man from rural Colombia presented with new-onset atrial fibrillation, dyspnea, and palpitations. A peripheral blood smear revealed a Trypanosoma cruzi trypomastigote, which was confirmed by molecular testing. He reported ingesting armadillo blood 3 weeks earlier, identifying oral transmission as the likely route. Treatment with nifurtimox, oral metoprolol, and enoxaparin resulted in conversion to sinus rhythm and symptomatic improvement, although a parasitological cure could not be confirmed. Because the patient had several competing risk factors for atrial fibrillation-advanced age, long-standing hypertension, heavy smoking, and active small-cell lung carcinoma-a causal relationship with the infection could not be established. Acute Chagas disease was therefore proposed only as a possible, potentially reversible contributing factor. To our knowledge, this is among the few reported cases of acute oral Chagas disease presenting as reversible atrial fibrillation, highlighting an underrecognized cultural risk practice in non-endemic settings.

Peak integration is a major and often underestimated source of uncertainty in pharmaceutical LC-UV quality control (QC), particularly when minor impurity peaks appear as shoulders or rider peaks on the tails of overloaded active pharmaceutical ingredient (API) peaks. In routine QC, APIs are frequently injected at high concentrations to ensure sufficient sensitivity for impurity analysis, which can result in partial column overloading and pronounced peak tailing. Here, we systematically evaluated integration accuracy and analyst interaction for commonly used rule-based integration algorithms implemented in commercial chromatographic data systems (Agilent OpenLab and Waters Empower) and compared them with an in-house independent integration system (IIS). The assessment included synthetic chromatograms with known areas as well as experimental LC-UV data for metoprolol and six related impurities. For baseline-resolved symmetric peaks, relative integration errors remained within approximately ±1.5% across all systems. For partially overlapping symmetric peaks, integration errors depended on peak size, noise level, and the integration method applied. In several rider-peak scenarios, errors for the perpendicular drop method (PDM) exceeded 100%. Application of the exponential skim method (ESM) reduced errors considerably, typically to 10-30% and in some cases to below ±5%, although not consistently. In the selected complex cases, greater analyst interaction was required in the commercial systems, increasing the potential for user-dependent variability. Overall, in the investigated cases, integration accuracy was strongly dependent on peak shape and overlap, with larger errors observed in asymmetric, shoulder, and rider-peak scenarios. These findings highlight the importance of integration-method selection and standardized integration practice in pharmaceutical LC-UV impurity analysis.

Selective β1-blockers are fundamental in managing hypertension, coronary artery disease, and heart failure. Yet, despite their widespread use, practical guidance on safe and individualized prescribing remains limited. Existing evidence is largely derived from controlled clinical trials, which may not fully capture drug-specific adverse events, sex-related susceptibility, or early-onset risks observed in routine clinical practice. To generate real-world, evidence-based recommendations for the safe use of selective β1-blockers, we compared the adverse event profiles of metoprolol, bisoprolol, and atenolol using 2 large pharmacovigilance systems. Adverse drug events reported for the 3 agents between 2004 and Q2 2025 were retrieved from the US Food and Drug Administration Adverse Event Reporting System, a spontaneous-reporting system, and compared with reports from the Canadian Vigilance Adverse Reaction Online Database. Disproportionality analyses, preferred term mapping, exploratory sex-stratified comparisons, and time-to-onset modeling were conducted to characterize shared reporting patterns, drug-specific signals, and potential patient-level modifiers. Across all 3 agents, disproportionate reporting was observed for a common cardiovascular spectrum that included bradycardia, conduction abnormalities, heart failure, and blood pressure instability. Metoprolol showed prominent reporting signals for BRASH syndrome and neuropsychiatric and suicide-related events. Bisoprolol showed signals for bradyarrhythmia, hyperkalemia, and acute kidney injury. Atenolol showed reporting patterns involving blood pressure perturbations, electrolyte imbalance, and interaction-related events. Exploratory sex-stratified analyses identified differences in the reporting distributions of several PT = preferred terms for metoprolol and atenolol, whereas bisoprolol showed a more balanced distribution. All 3 agents displayed early-failure time-to-onset patterns, supporting closer monitoring after treatment initiation. This real-world pharmacovigilance assessment identifies drug-specific patterns of disproportionate reporting that may inform hypothesis generation and individualized monitoring. Because spontaneous-reporting data cannot establish incidence or causality, the findings should complement, rather than replace, clinical judgment and confirmation in controlled or longitudinal data sources.

Myocardial bridging (MB) is an anomaly in which a segment of a coronary artery takes an intramyocardial route. It can increase the risk of cardiovascular complications. Beta-blockers (BB) are usually the first line of treatment, and management may be challenging in patients with bradycardia. A 53-year-old male former smoker with hypertension and dyslipidemia presented to the emergency department complaining of retrosternal chest pain that awakened him from sleep and dyspnea. Upon evaluation, an electrocardiogram (ECG) revealed sinus bradycardia with T-wave inversions in leads II, III, aVF, and V3-V6. High-sensitivity troponin peaked at 335 pg/mL (4-79 pg/mL), and the patient was admitted with a diagnosis of non-ST-elevation myocardial infarction (NSTEMI). He was given 324 mg of aspirin, a heparin drip was started, and pain improved after sublingual nitroglycerin. Transthoracic echocardiogram (TTE) demonstrated a preserved left ventricular function without wall motion abnormalities. Coronary angiography identified a MB in the mid-left anterior descending coronary artery (LAD) without atherosclerotic disease. Coronary CT angiography described a 20 mm long and 7 mm deep MB with 90%-99% dynamic obstruction during end-systole. After a Heart Team meeting, the decision was to attempt medical management with metoprolol as tolerated. The patient remained angina-free and asymptomatic. A stress test prior to discharge was negative for ischemia or recurrent pain. After one-year follow-up, he has remained asymptomatic, with repeated unremarkable stress tests after reduction of BB dose. Severe MB may be associated with significant cardiovascular complications, including NSTEMI. Treatment poses a challenge in patients with bradycardia. This case illustrates that cautious beta-blocker therapy may be a feasible option in selected patients.

Beta-blockers are among the most widely prescribed drugs in the management of both supraventricular and ventricular arrhythmias, and they are frequently regarded as a homogeneous pharmacological class. They are not. The agents in current use differ substantially in beta1-receptor selectivity, lipophilicity, half-life, route of administration, intrinsic sympathomimetic activity, and ancillary properties, and arrhythmias themselves differ in mechanism, adrenergic dependence, anatomical origin, and structural substrate. This narrative review examines whether these pharmacological differences translate into clinically meaningful differences in efficacy and utility, asking not only whether a beta-blocker should be used but which one should be used. Evidence was drawn from a targeted search of PubMed, Web of Science, Scopus, Ovid, Embase, and the Cochrane Library, with priority given to randomized controlled trials, meta-analyses, large registries, and contemporary society guidelines, and was synthesized qualitatively by arrhythmia type. A class effect is apparent for many indications, particularly rate control in atrial fibrillation and atrial flutter, where metoprolol, bisoprolol, and carvedilol perform broadly similarly and the choice is driven mainly by comorbidity and tolerability. Drug-specific differences emerge in three settings. In adrenergically mediated inherited syndromes, namely catecholaminergic polymorphic ventricular tachycardia and long QT syndrome, nonselective agents and especially nadolol are clearly superior to beta1-selective agents, and the same principle appears to extend to ventricular electrical storm, in which propranolol has outperformed metoprolol in a randomized comparison. In acute care, pharmacokinetics dominate, and the ultra-short-acting agents esmolol and landiolol permit a degree of titration that longer-acting drugs cannot match. In patients with heart failure and reduced ejection fraction, carvedilol, metoprolol succinate, and bisoprolol should be preferred irrespective of arrhythmia subtype because of their established mortality benefit. Conversely, beta1-selective agents, including the highly selective agent nebivolol, improve tolerability in bronchospastic disease, although this reflects respiratory tolerability rather than any demonstrated antiarrhythmic advantage, and beta-blockers have little role in Brugada syndrome or in bradycardia-dependent acquired torsades de pointes. Beta-blockers should therefore not be treated as interchangeable. Selection should integrate arrhythmic mechanism, structural substrate, and patient characteristics, and head-to-head trials remain conspicuously scarce.

Pregnancy can trigger or exacerbate ventricular arrhythmias even in structurally normal hearts. A 41-year-old woman at 22 weeks' gestation developed symptomatic monomorphic premature ventricular contractions (PVCs) and frequent nonsustained ventricular tachycardia (NSVT), with 11% PVC burden and 313 NSVT episodes. Metoprolol reduced arrhythmic burden but not symptoms. Sotalol, introduced with serial QT monitoring, was followed by complete symptomatic and Holter suppression. One month postpartum, asymptomatic ventricular arrhythmia recurred off therapy, then resolved spontaneously by three months. Serial monitoring illustrates marked pregnancy-related variability and the potential dissociation between symptoms and arrhythmic burden.