Several studies have supported Dr Gideon Koren’s 1993 landmark article, “Medications Which Can Kill a Toddler with One Tablet or Teaspoonful.” Although each study has its own merits, most focus solely on pediatric overdoses, and few provide an exhaustive reference list for real-time evaluation of ingestions in children and adults. The following xenobiotics warrant special attention because of their potential to cause serious outcomes, even after exposure to small volumes. This list does not imply that all pediatric exposures to these agents result in fatality, and the absence of a xenobiotic from this list does not indicate that it is necessarily safe. α1-Adrenergic agonists and imidazoline receptor agonists: Clonidine, guanfacine, naphazoline, oxymetazoline, tetrahydrozoline, xylazine (veterinary). Sulfonylureas: Chlorpropamide, glyburide, glipizide, glimepiride. Calcium channel blockers: Verapamil, diltiazem, nifedipine, amlodipine, nicardipine, nimodipine; β-Blockers: Metoprolol, labetalol, propranolol, sotalol. Tricyclic antidepressants: Imipramine, desipramine, amitriptyline, nortriptyline. Opioids: Codeine, hydrocodone, methadone, morphine, heroin. Antidiarrheals: Diphenoxylate plus atropine, loperamide. Salicylates and methyl salicylate: Oil of wintergreen, bismuth subsalicylate, mentholated balms, paramao or lawang root oil . Antipsychotics: Loxapine, thioridazine, chlorpromazine. Antimalarials: Chloroquine, hydroxychloroquine, quinine, primaquine. Antiarrhythmics: Quinidine, disopyramide, procainamide, flecainide, amiodarone. Camphor: A terpenoid used as an analgesic, antipruritic agent, and component of cooling gels, ointments, balms, mothballs, household fragrances, and essential oils. Oral camphor use occurs in some regions for religious ceremonies, traditional remedies, aphrodisiacs, or lactation suppression. Nonalkaloid toxic lignan: Podophyllin, podofilox. Unique plant toxins: Colchicine. Oral acetylcholinesterase inhibitors: Rivastigmine, donepezil, galantamine, carbamate pesticides. Methylxanthines: Theophylline, 1,3-dimethylxanthine, caffeine. Other opioids: Buprenorphine, fentanyl. Toxic alcohols: Methanol, ethylene glycol, diethylene glycol. Caustics and other household products: Acidic or alkaline household products, hydrofluoric acid, selenious acid, acetonitrile, methylene chloride. Accidental overdoses continue to occur regularly despite the implementation of various safety measures, including widespread public education, the use of childproof containers, and easy access to poison control centers. In the US, poison control centers receive more than 2.4 million calls annually, with more than 50% involving children younger than 6 years. Most pediatric accidental ingestions involve household cleaning products and analgesics, followed by cosmetics, foreign objects, and dietary supplements. Adult overdoses may be unintentional but often involve larger total doses or high-risk medications, including opioids and sedative-hypnotics. America's Poison Centers identify the 5 most common substance classes as analgesics, household cleaners, antidepressants, cosmetic or personal care items, and cardiovascular drugs. The number of ingestions involving cleaning products increased sharply during the COVID-19 pandemic but has since declined.

Swallow syncope is a rare situational syncope caused by an exaggerated vagal reflex and may result in bradyarrhythmia or atrioventricular block.

Hypertrophic cardiomyopathy (HCM) is a genetically determined myocardial disease in which symptoms are driven not simply by ventricular hypertrophy, but by a combination of dynamic left ventricular outflow tract obstruction (LVOTO), impaired diastolic filling and other factors.The therapy for HCM differs fundamentally from routine heart failure management and must be mechanism based. In obstructive HCM, the pharmacologic objective is to blunt hypercontractility, lengthen diastole, preserve loading conditions, and reduce the LVOT gradient. In non-obstructive HCM, management is focused on symptom control, heart-rate moderation, careful volume management, and treatment of arrhythmias and congestion. Non-vasodilating beta-blockers, non-dihydropyridine calcium-channel blockers, and disopyramide have constituted the foundation of medical therapy. The contemporary era has added sarcomere-directed treatment with cardiac myosin inhibitors, particularly mavacamten and aficamten, The present review provides a pragmatic algorithm for publication-level clinical use in contemporary practice.

Background/Objectives: Guidelines for obstructive hypertrophic cardiomyopathy (HCM) recommend treatment with disopyramide as an add-on to beta-blockers or calcium-channel blockers when symptoms persist. Data pertaining to effective disopyramide use in practice beyond single-center experience are very limited. This study aimed to quantify disopyramide use in patients with obstructive HCM in England, France and Germany, before the availability of cardiac myosin inhibitors. Methods: This retrospective study used nationally representative databases from England (Clinical Practice Research Datalink and Hospital Episode Statistics, 2010-2019), France (National Healthcare Data System, 2012-2019) and Germany (German statutory health insurance, 2011-2019). Adults (18+) with obstructive HCM were included, based on diagnostic codes for obstructive HCM or any HCM with septal reduction therapy. Disopyramide usage was defined as ≥1 prescription for a patient in a calendar year. Results: Overall, 3730, 6823 and 1141 patients diagnosed with obstructive HCM were identified in the English, French and German databases, respectively. In England, disopyramide use ranged from 4.7% to 5.6% per year with use generally stable over time. The equivalent usage for France was 1.7% to 2.6% per year. As expected, no recorded reimbursed use was reported in Germany during the study period. Conclusions: Disopyramide use is very low in patients with obstructive HCM, possibly due to treatment-related issues, availability or lack of reimbursement. These barriers may drive the uptake of alternative guideline recommended therapies for obstructive HCM treatment.

Hypertrophic cardiomyopathy (HCM) stands as the most common monogenic cardiac disease, with an estimated prevalence historically reported as 1:500, but likely closer to 1:200 based on contemporary population studies in the general population. The past decade has marked a fundamental shift in therapeutic strategy: from symptomatic relief toward interventions directly targeting pathological sarcomeric hypercontractility. Conventional therapy relies on beta-blockers and non-dihydropyridine calcium channel antagonists, which provide symptomatic benefits through negative inotropic effects. For refractory left ventricular outflow tract obstruction, disopyramide constitutes an effective third-line option, although its anticholinergic profile requires cautious administration. Cardiac myosin inhibitors, mavacamten and aficamten, have introduced a novel therapeutic paradigm through direct modulation of actin-myosin cross-bridge formation. Pivotal clinical trials have demonstrated significant improvements in exercise capacity, reduction in obstruction severity, and enhancement of functional status, validating for the first time a therapeutic strategy that directly targets the underlying sarcomeric mechanism of hypercontractility. The therapeutic horizon includes next-generation myosin modulators, metabolic pathway interventions, and gene-based strategies. Current challenges involve accessibility to these therapies, substantial costs, and the requirement for mandatory regular echocardiographic monitoring. Future perspectives are oriented toward precision personalized medicine, integrating molecular therapeutics with genetic profiling to enable increasingly individualized risk stratification and therapeutic decision making.

Hypertrophic obstructive cardiomyopathy (HOCM) is characterized by dynamic left ventricular outflow tract (LVOT) obstruction and impaired quality of life. Mavacamten, a first-in-class myosin inhibitor, offers a novel therapeutic approach for HOCM, which improves clinical symptoms and exercise capacity while leading to reduction of LVOT gradient and favourable cardiac remodelling in echocardiography and cardiovascular magnetic resonance (CMR). However, data on CMR-derived treatment effects remain limited to short follow-up studies.

Anti-arrhythmic drugs (AADs) have been a mainstay of dysrhythmia control for over a century. Even in the current era of evolving ablation use and technology, AADs remain therapeutically important. Nonetheless, the effectiveness of AADs may be incomplete and/or adverse effects may limit their use despite efficacy. Ideally, to maximize the clinical profile of AADs, clinicians should be aware of the full array of their complexities and selection options. However, commonly, some of them seem to be frequently underappreciated. Among others, these include dosing intricacies, targeting therapy to the arrhythmia trigger, avoiding habitual choices of AAD selection, consideration of AAD combinations, and more. These factors are discussed in this paper as a means of improving AAD use by clinicians and tolerance by patients. Notably, it is only these issues that are the focus of this paper, which is not meant as a review of the pharmacologic profile of each of our AADs.

Hypertrophic cardiomyopathy (HCM) is the most prevalent genetic cardiac disease and a leading cause of heart failure, arrhythmia, and sudden cardiac death in both young and older adults. This consensus document was developed by a multidisciplinary panel of European and U.S. experts in HCM, imaging, electrophysiology, genetics, and heart failure. While it aligns with the 2023 ESC and 2024 AHA/ACC guidelines on HCM, the paper addresses areas where clinicians might require further guidance. Key sections include phenotypic classification, diagnostic strategies incorporating multimodal imaging and genetic testing, and risk stratification for sudden cardiac death. The document outlines therapeutic pathways for pharmacologic treatment, including beta-blockers, calcium channel blockers, disopyramide, and cardiac myosin inhibitors such as mavacamten and aficamten, as well as indications for septal reduction therapies. Management of atrial fibrillation, hypertension, coronary artery disease, pregnancy, paediatric HCM, and comorbidities is discussed in detail. Importantly, the consensus addresses current controversies including optimal risk stratification models, the care of genotype-positive/phenotype-negative individuals, and exercise recommendations. Finally, the manuscript highlights future directions such as gene therapy, precision medicine approaches, use of artificial intelligence and novel biomarkers for screening and diagnosis.

Hypertrophic cardiomyopathy (HCM) represents the most common inherited cardiac disease and a leading cause of heart failure, arrhythmias, and sudden cardiac death in young individuals. For decades, management of HCM has relied on symptom control with β-blockers, calcium channel blockers, disopyramide, or invasive septal reduction in advanced cases. The identification of pathogenic sarcomere variants and the recognition of hypercontractility as a central disease mechanism have paved the way for cardiac myosin inhibitors (CMIs), the first truly disease-specific pharmacological therapy for HCM. Indeed, CMIs represent a revolutionary therapeutic paradigm that redefines the standard of care by translating molecular discovery into clinical application. This review provides a guide to the mechanistic basis of sarcomere modulation, summarizes the clinical evidence for mavacamten and aficamten, and critically evaluates the evolving roles of both medications in obstructive and non-obstructive HCM.

Left ventricular outflow tract obstruction (LVOTO) commonly occurs in patients with hypertrophic cardiomyopathy (HCM). Management options include drugs-beta-blockers, disopyramide, and myosin inhibitors like mavacamten and aficamten. Septal reduction therapy should be considered for patients who remain symptomatic despite medical therapy. Surgical myectomy is considered the gold standard. However, alcohol septal ablation and surgical myectomy have good and comparable long-term outcomes. Surgical myectomy has a lower incidence of heart block and a lower residual gradient. Surgical myectomy may be preferred in the presence of intrinsic mitral valve disease, papillary muscle abnormalities, markedly thickened septum, multiple levels of obstruction, long length of mid-cavity obstruction, and absence of a suitable septal artery. Alcohol septal ablation should be preferred in individuals who are at high surgical risk. In most other patients, both procedures may be considered, and the choice should be based on available resources and patient preferences.