This executive summary of the hypertrophic cardiomyopathy clinical practice guideline provides recommendations and algorithms for clinicians to diagnose and manage hypertrophic cardiomyopathy in ...adult and pediatric patients as well as supporting documentation to encourage their use.
A comprehensive literature search was conducted from January 1, 2010, to April 30, 2020, encompassing studies, reviews, and other evidence conducted on human subjects that were published in English from PubMed, EMBASE, the Cochrane Collaboration, Agency for Healthcare Research and Quality reports, and other relevant databases.
Many recommendations from the earlier hypertrophic cardiomyopathy guidelines have been updated with new evidence or a better understanding of earlier evidence. This summary operationalizes the recommendations from the full guideline and presents a combination of diagnostic work-up, genetic and family screening, risk stratification approaches, lifestyle modifications, surgical and catheter interventions, and medications that constitute components of guideline directed medical therapy. For both guideline-directed medical therapy and other recommended drug treatment regimens, the reader is advised to follow dosing, contraindications and drug-drug interactions based on product insert materials.
Current guidelines recommend that patients with hypertrophic cardiomyopathy (HCM) not partake in high-intensity exercise due to the increased risk of sudden cardiac death. But individuals with ...genetic cardiomyopathies are not immune from cardiometabolic diseases, and inactivity is common in patients with HCM, likely due to fear of exercise-induced adverse events. The RESET-HCM trial (Study of Exercise Training in Hypertrophic Cardiomyopathy) illustrated that although moderate-intensity exercise may be safe in this population, the increase in cardiorespiratory fitness achieved with this training paradigm is modest. High-intensity exercise is an efficacious stimulus for increasing cardiorespiratory fitness in chronic disease populations. Such increases in fitness are associated with substantial reductions in cardiovascular mortality and may outweigh the theoretical risks associated with exercise in patients with HCM. The goal of this review is to examine the evidence supporting the safety and efficacy of different intensities of exercise training in HCM, and consider novel strategies to improve fitness.
Commotio cordis, sudden cardiac death (SCD) caused by relatively innocent impact to the chest, is one of the leading causes of SCD in sports. Commercial chest protectors have not been demonstrated to ...mitigate the risk of these SCDs.
To develop a standard to assess chest protectors, 4 phases occurred. A physiological commotio cordis model was utilized to assess variables that predicted for SCD. Next, a surrogate model was developed based on data from the physiological model, and the attenuation in risk was assessed. In the third phase, this model was calibrated and validated. Finally, National Operating Committee on Standards for Athletic Equipment adopted the standard and had an open review process with revision of the standard over 3 years.
Of all variables, impact force was the most robust at predicting SCD. Chest wall protectors which could reduce the force of impact to under thresholds were predicted to reduce the risk of SCD. The correlation between the experimental model and the mechanical surrogate ranged from 0.783 with a lacrosse ball at 30 mph to 0.898 with a baseball at 50 mph. The standard was licensed to National Operating Committee on Standards for Athletic Equipment which initially adopted the standard in January 2018, and finalized in July 2021.
An effective mechanical surrogate based on physiological data from a well-established model of commotio cordis predicts the reduction in SCD with chest protectors. A greater reduction in force provides a great degree of protection from commotio cordis. This new National Operating Committee on Standards for Athletic Equipment standard for chest protectors should result in a significant reduction in the risk of commotio cordis on the playing field.
Don't Forget Commotio Cordis Maron, Barry J.; Link, Mark S.
The American journal of cardiology,
10/2021, Letnik:
156
Journal Article
Recenzirano
Non-penetrating chest blows can occasionally trigger fatal ventricular tachyarrhythmias and sudden death (commotio cordis). Such events were initially reported in association with sporting activities ...and projectiles such as baseball/lacrosse balls. However, similar potentially fatal chest blows, seemingly incapable of causing death, can occur during a variety of other circumstances such as when delivered during a fight (by a fist) such as in the accompanying paper. Notably, commotio cordis events can be reversed by resuscitation and defibrillation.
Sudden cardiac death (SCD) accounts for 230,000 to 350,000 deaths per year in the United States. While many who suffer SCD possess underlying structural heart disease, inherited arrhythmia syndromes ...are also important contributors to SCD. In patients without structural heart disease, inherited arrhythmia syndromes are identified in >50% of the remaining patients. In this review, we will focus on the presentation and management of three major inherited syndromes that lead to SCD in patients without structural heart disease: long QT syndrome (LQTS), Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia (CPVT). All these syndromes can present in patients who are asymptomatic or, at the other extreme, with syncope and even SCD. LQTS syndrome and Brugada are the most common inherited arrhythmogenic syndromes, while CPVT is much rarer. Determining which patients need pharmacologic treatment and those who would benefit from more aggressive treatment such as sympathectomies and implantable defibrillators is not always clear.
Atrial fibrillation (AF) is the most common arrhythmia encountered by cardiologists and is a major cause of morbidity and mortality. Risk factors for AF include age, male sex, genetic predisposition, ...hypertension, diabetes mellitus, sleep apnea, obesity, excessive alcohol, smoking, hyperthyroidism, pulmonary disease, air pollution, heart failure, and possibly excessive exercise. The management of AF involves decisions about rate versus rhythm control. Asymptomatic patients are generally managed with rate control and anticoagulation. Symptomatic patients will desire rhythm control. Rhythm control options are either antiarrhythmic agents or ablation, with each having its own risks and benefits. Ablation of AF has evolved from a rare and complex procedure to a common electrophysiological technique. Selection of patients to undergo ablation is an important aspect of AF care. Patients with the highest success rates of ablation are those with normal structural hearts and paroxysmal AF, although those with congestive heart failure have the greatest potential benefit of the procedure. Although pulmonary vein isolation of any means/energy source is the approach generally agreed on for those with paroxysmal AF, optimal techniques for the ablation of nonparoxysmal AF are not yet clear. Anticoagulation reduces thromboembolic complications; the newer anticoagulants have eased management for both the patient and the cardiologist. Aggressive management of modifiable risk factors (hypertension, diabetes mellitus, sleep apnea, obesity, excessive alcohol, smoking, hyperthyroidism, pulmonary disease, air pollution, and possibly excessive exercise) after ablation reduces the odds of recurrent AF and is an important element of care.
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