Heart and Athlete

Sudden Cardiac Death in Young Athletes

Assessment of the 12-lead ECG as a screening test for detection of cardiovascular disease in healthy general populations of young people (12-25 Years of Age): a scientific statement from the American Heart Association and the American College of Cardiology.

Clinical profile of congenital coronary artery anomalies with origin from the wrong aortic sinus leading to sudden death in young competitive athletes

/n summer 2012 I had the opportunity to death in athletes. In 1993, Dr. Maron brought the work as a research intern at the MinneapNational Registry of Sudden Death in Young olis Heart Institute Foundation (MHIF). Athletes to MHIF. The Registry is an autopsy MHIF is a nonprofit organization with the based database that records athlete deaths meeting mission of improving cardiovascular health five criteria: the athlete must have been related to through research and education. The internship the USA in some capacity, such as an American they offer is an effective extension of this athlete or a foreign athlete on American soil; a mission: future physicians (the interns) are victim of sports-related sudden death-, under the educated about healthcare through a collection age Qfforty, working towards improvement and of diverse experiences, and in return the interns excellence in their sport; and they must have died work with physicians to advance clinical in 1980 or later (Maron et al., 2009). The research projects. The internship program at database currently holds about 2300 cases of MHIF is primarily designed for pre-medical athlete deaths, and an additional 225 cases of students in the latter stages of undergraduate aborted death, which is defined as a sudden education (juniors, seniors, and graduated cardiac arrest that would have resulted in death if students). In existence since 2002, the program nQt for cardiopUlmonaiy resuscitation (CPR) or has three main purposes for participating automated external defibrillator (AED) use. Since interns: to gain experience with clinical rethere is no mandatory reporting of athlete deaths search, to learn more about cardiovascular h the USA, the Registiy is responsible for many healthcare, and to develop an accurate understatistics ()n ^ |ssue of sudden aftlete deaths and standing of medicine as a career (Willenbring et . r . , r , 1 20081 1S ore an imPortant resource for physicians, administrators, and public health officials. The most recent statistical analysis of the Clinical research Registry was published in 2009, and this analysis is still considered accurate (the per The most valuable part of the internship was centages do not change much over time). This gaining exposure to clinical research. I was analysis offers many useful figures conceming assigned to work under Dr. Bany J. Maron, who the demographics of sudden death in athletes, holds a special interest in researching sudden For example% the most recent years of the database suggest a sudden death incidence rate in athletes of 99 deaths per year (Maron et al., Correspondence to: cjmurphy2@students.nwc.edu 2009). The age of these athletes at death was

Asthma-related sudden death in athletes: a retrospective analysis of the US NCCSIR database (1982-2018).

Sudden cardiac death is the second most common cause of athletic mortality in both elite human and equine athletes. Racehorses perform at extremely high exercise intensities with maximal heart rates and aerobic capacities exceeding those of human athletes. A predisposition to life-threatening arrhythmias unmasked by athletic activity, is suspected to underlie sudden cardiac death in both species and predicting risk is critical for the health and safety of athletes. Cardiac restitution ratio (CRR) is used as a measure of arrhythmia risk at rest in humans and represents the ability of cardiomyocytes to recover between successive action potentials. CRR can be calculated as QT/TQ on an electrocardiogram (ECG) and has never been investigated during high intensity exercise. The objectives are to characterize changes in the QT interval and CRR in normal racehorses to establish a risk threshold and to identify unique ion channels in the equine myocardium that may be involved in accommodation of the cardiac action potential to changes in heart rate. It is hypothesized that CRR will be highest during exercise periods when sudden cardiac death most frequently occurs, and that the horse will exhibit differences in myocardial ion channel expression. Over 3800 cardiac cycles obtained from ECGs of 42 racehorses were analysed using custom software to calculate RR interval, QT interval, and CRR. Instantaneous heart rate ranged from 26 beats per minute at rest to 293 during racing. Interquartile ranges (median) of QT interval and CRR during maximal effort were 176-198 ms (186 ms) and 2.1-3.3 (2.5), respectively. CRR was highest during race exercise; the first 30 seconds of cardiac deceleration following the race; and sporadically during non-race exercise, corresponding to periods when sudden death most frequently occurs. Preliminary multivariable regression analyses revealed numerous significant associations for both QT interval and CRR, including with exercise period, RR interval, racing gait, sex, and age. Apparently healthy horses during exercise routinely displayed CRRs exceeding the described arrhythmogenic threshold of 1, established in humans. Left ventricular free wall myocardium was obtained from horses of typical racing breeds. A combined proteomic approach using mass spectrometry and immunoblotting revealed presence of several ion channels not known or not known to be significant to the ventricular action potential in humans, including Kv1.5 and Kir6.2, and different primary isoforms of sodium and calcium channels. These findings identify unique aspects of myocardial electrophysiology in horses with potential implications for sudden cardiac death in human athletes. Funding graciously provided by Equine Guelph. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Physical activity is an invaluable tool to fight cardiovascular disease, but physical activity may trigger sudden death (SD) in athletes, especially if they are unknown with an underlying condition. Although the incidence of SD remains rather low in athletes (estimated at 0.5–2 events per 100,000 participants), some data suggest that the overall SD risk is higher in athletes than in sedentary individuals. Most athletes who die suddenly present with a silent cardiac condition, most commonly hypertrophic cardiomyopathy in American series or arrhythmogenic right ventricular cardiomyopathy in European data sets. Other causes of SD include coronary congenital abnormalities, valve disease, channelopathies, or commotio cordis. Based on these data, efforts have been undertaken to reduce the impact of SD in athletes. First, preparticipation screening programmes, including a clinical history, physical examination, and an electrocardiogram (ECG), interpreted through standardized criteria, aim at an early detection of cardiac conditions predisposing to SD. Second, a quick response to a cardiac arrest may save lives; training sports personnel in cardiac resuscitation, readily available automated external defibrillators, and sport medical action plans may critically influence outcomes.

To review available evidence establishing the validity of the preparticipation evaluation (PPE) as a method for screening health risk prior to participation in exercise and sport. Specific emphasis was placed on reviewing original research evaluating methods to screen participants for risk of sudden cardiovascular death. Literature on the current state of the PPE as a screening tool for athletic participation was examined. Electronic databases were searched for articles relating to mass screening for sports participation and sudden cardiac death in athletes published up to January 2004. Databases searched included Medline (OVID Web, 1966-2004), PubMed (1966-2004), Sport Discuss (1975-2004), Current Contents, CISTI Source (1993-2004), Cochrane Database of Systematic Reviews, and EBM Reviews. Additional references from the bibliographies of retrieved articles were also reviewed. All study designs were retrieved, but only those studying athletes and/or student-athletes under age 36 years were reviewed. Of the original research retrieved, the majority of the articles sought to establish incidence or prevalence of cardiovascular causes of sudden death in athletes or the validity of various screening tools. Original research articles seeking to establish the current use of the PPE in all its various forms were also reviewed. All of the articles selected for review consisted of type II, population-based data. The initial literature search identified 639 papers. Of these, 310 articles that met the selection criteria were reviewed, and 25 articles were identified as original research directly relating to the PPE. All of these contained type II evidence-population-based clinical studies. The majority of the literature on the PPE consists of type III evidence-case-based opinion papers and position papers from respected authors and sports medicine societies and reports of expert committees. This literature was also reviewed, but only original research relevant to the PPE is reported in this article. The majority of these studies examined cardiovascular diseases and screening procedures. The 5 studies that assessed the format or effectiveness of the PPE concluded that it was inadequate. The format of the PPE is not standardized and does not consistently address the American Heart Association recommendations for cardiovascular screening history and physical exams. A variety of health care professionals, some without proper training, administer the PPE. The 12 original studies that looked at specific cardiovascular screening techniques were divided on the effectiveness of history, physical examination, electrocardiogram, and echocardiography for detecting cardiovascular risks for sudden death in athletes. A PPE is required by most sport organizations in America, but research as to its effectiveness is very limited. PPEs have been mandatory in Italy for many years, and we can draw on some the data recorded over this time. Otherwise, very few studies in America or elsewhere have been performed on the PPE process. The research available indicates that the PPE is not implemented adequately or uniformly. An opportunity exists to create a standardized, validated PPE that meets medical standards for quality and provides sensitive, specific screening of potential participants in sport and exercise.

Sudden death in athletes

Sudden cardiac death in athletes is one of the most tragic health events seen both in our country and all over the world. In some of those athletes, there is no obvious structural abnormality. Dynamic changes in intracardiac hemodynamics during exercise may be a cause for sudden death in these athletes, the impact of exercise on intracardiac gradient and cardiac hemodynamic parameters in athletes was compared with healthy controls. A total of 21 professional male athletes and 21 healthy male controls were included in the study. Transthoracic echocardiography was performed in all participants both at rest and maximal exercise level to assess the intraventricular gradient (IVG) and cardiac systolic and diastolic functions. Abnormal IVG was defined as gradient of >30 mm Hg at peak exercise level. Both groups reached the level of predicted maximum exercise. There was no exercise limiting symptom among participants during exercise test. The athletes revealed a higher maximum peak systolic IVG at baseline and after exercise in comparison with the control group. None of the participants showed an abnormal IVG level. Our results showed that there was no dynamic intraventricular obstruction with aerobic exercise in subjects with a structurally normal heart.

Sudden death (SD) in athletes represents a cardiac ‘earthquake’ affecting apparently healthy and highly trained individuals. This is not due to excessive demands on a normal heart, as occurred to...

For centuries it was a mystery why cardiac arrest should occur in young vigorous athletes, who had previously achieved extraordinary exercise performance without complaining of any symptoms. The cause was generally ascribed to myocardial infarction, even though evidence of regional ischemic myocyte necrosis had rarely been reported. It is now clear that the usual mechanism is an abrupt arrhythmia, that a wide spectrum of cardiovascular abnormalities may cause sudden death in young athletes and that even minor lesions may be life-threatening by jeopardizing the electrical order of the heart during effort (1–16). The culprit diseases are clinically covert and unlikely to be diagnosed or suspected. Early identification might reduce the risk and incidence of sudden death and systematic preparticipation screening for qualification of individuals embarking in competitive sports is now carried out in some countries such as Italy. However, the efficacy and cost-effectiveness of this screening is the subject of debate.

Chronicle of a death foretold. It is time for echocardiographic screening in young athletes

Long‐lasting athletic training induces an overload on the heart that leads to structural, functional, and electrical adaptive changes known as the “athlete's heart.” The amount of this heart remodeling has been traditionally considered balanced between the left and the right heart chambers. However, during intense exercise, the right heart is exposed to a disproportional afterload and wall stress which over a long period of time could lead to more pronounced exercise‐induced changes. Highly trained athletes, especially those involved in endurance sport disciplines, can develop marked right ventricular (RV) remodeling that could raise the suspicion of an underlying RV pathology including arrhythmogenic cardiomyopathy (ACM). The distinction between physiological and pathological RV remodeling is essential as ACM is a common cause of sudden cardiac death in athletes, and high‐intensity exercise training has demonstrated to accelerate its phenotypic expression and worsen its prognosis. The distinction between physiological and pathological RV remodeling is essential since ACM is a common cause of sudden cardiac death in athletes, and high‐intensity exercise training has demonstrated to accelerate the phenotypic expression and worsen the prognosis. This article outlines the physiological adaptation of the RV to acute exercise, the subsequent physiological structural and functional changes induced by athletic training and provides useful tips of how to differentiate between physiological RV remodeling and a cardiomyopathy phenotype.

Mandating Cardiac Screening for Athletes