Protecting Athletes From Sudden Cardiac Death

JAMA The Journal of the American Medical Association (Impact Factor: 35.29). 11/2006; 296(13):1648-50. DOI: 10.1001/jama.296.13.1648
Source: PubMed
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    • "This condition becomes progressively worse affecting the metabolic activity of the heart muscles. Over a period of time, the heart muscles become weak and may lead to heart failure and causing arrhythmias [4]. Even more, often the deposited plaques erode or rupture resulting into thrombus formation restricting the flow of blood to the heart muscles thereby increasing the risk of sudden cardiac death. "
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    ABSTRACT: Coronary artery disease (CAD) is the narrowing of coronary arteries leading to inadequate supply of nutrients and oxygen to the heart muscles. Over time, the condition can weaken the heart muscles and may lead to heart failure, arrhythmias and even sudden cardiac death. Hence, the early diagnosis of CAD can save life and prevent the risk of stroke. Electrocardiogram (ECG) depicts the state of the heart and can be used to detect the CAD. Small changes in the ECG signal indicate a particular disease. It is very difficult to decipher these minute changes in the ECG signal, as it is prone to artifacts and noise. Hence, we detect the R peaks from the ECG and use heart rate signals for our analysis. The manual inspection of the heart rate signals is time consuming, taxing and prone to errors due to fatigue. Hence, a decision support system independent of human intervention can yield accurate repeatable results. In this paper, we present a new method for diagnosis of CAD using tunable-Q wavelet transform (TQWT) based features extracted from heart rate signals. The heart rate signals are decomposed into various sub-bands using TQWT for better diagnostic feature extraction. The nonlinear feature called centered correntropy is computed on decomposed detail sub-band. Then the principal component analysis (PCA) is performed on these CC to transform the number of features. These clinically significant features are subjected to least squares support vector machine (LS-SVM) with different kernel functions for automated diagnosis. The experimental results demonstrate highest classification accuracy, sensitivity, specificity and Matthews correlation coefficient of for Q-factor =24 using Morlet wavelet kernel function with optimized kernel and regularization parameters. Also, we have developed a novel CAD Risk index using significant features to discriminate the two classes using a single number. Our proposed methodology is more suitable in classification of normal and CAD heart rate signals and can aid the clinicians while screening the CAD patients.
    Knowledge-Based Systems 07/2015; DOI:10.1016/j.knosys.2015.02.011 · 2.95 Impact Factor
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    • "Holter monitoring, indicated when necessary [28 ,29,46]. "
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    ABSTRACT: Electrocardiograms in elite endurance athletes sometimes show bizarre patterns suggestive of inherited channelopathies (Brugada syndrome, long QTc, catecholaminergic polymorphic ventricular tachycardia) and cardiomyopathies (arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy) responsible for unexpected sudden cardiac death. Among other methods, genetic analyses are required for correct diagnosis. To correlate 12-lead electrocardiographic patterns suggestive of inherited channelopathies and cardiomyopathies to specific genetic analyses. Prospective study (2004-2007) of screening 12-lead ECG tracings in standard position and higher intercostal spaces V1 to V3 precordial leads, performed in athletes and normal sedentary subjects aged match. Genetic analyses of subjects with ECG abnormalities suggested inherited channelopathies and cardiomyopathies. All cardiologic exams and electrocardiograms were performed at "Prof. Dr. C.C. Iliescu" National Institute of Cardiovascular Diseases (Bucharest, Romania). The genetic studies were done at "Mina Minovici" National Institute of Forensic Medicine (Bucharest, Romania). 347 elite endurance athletes (seniors--190, juniors--157), mean age of 20; 200 subjects mean age of 21, belonging to the control group of 505 normal sedentary population. Seniors. RSR' (V1 to V3) pattern, in 45 cases (23.68%), 5 of them with questionable Brugada sign (elevated J wave and "coved" ST segment, < 2 mm in one lead, V1. Typically, Brugada 1 sign was found in one case (0.52%) with no SCN5A abnormalities. One athlete (0.52%) had normal ECG and exon1 SCN5A duplication. MRI confirmed three arrhythmic right ventricular cardiomypathy epsilon waves (1.57%), in one case. ST-segment elevation myocardial injury like in V1-V3 precordial leads in 34 athletes (17.89%). Genetic analyses-no gene mutations. Juniors. Upright J wave was found in 43 cases (27.38%). Convex ST segment elevation in V1-V3/V4, in 39 cases (24.84%). Bifid T wave with two distinct peaks was found in 39 cases (24.84%), 5 of them with mild prolonged QTc (0.48"-0.56") and KCN genes mutations. Nine (5.73%) of the elevated ST segment juniors had questionable Brugada sign, two of which with KCN (n=1) and SCN5A (n=1) gene mutations. Ajmaline provocative test was negative in 4 and was refused by 5 subjects. Bizarre QRS, ST-T patterns suggestive of abnormal impulse conduction in the right ventricle, including the right outflow tract, associated with prolonged QTc interval in some cases were observed in highly trained endurance athletes. The genetic analyses, negative in most athletes, identified surprising mutations in SCN5A and KCN genes in some cases.
    11/2009; 2(4):361-72.
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    ABSTRACT: Habitual physical activity reduces coronary heart disease events, but vig- orous activity can also acutely and transiently increase the risk of sudden cardiac death and acute myocardial infarction in susceptible persons. This scientific statement discusses the potential cardiovascular complications of exercise, their pathological substrate, and their incidence and suggests strategies to reduce these complications. Exercise-associated acute cardiac events generally occur in individuals with structural cardiac disease. He- reditary or congenital cardiovascular abnormalities are predominantly responsible for cardiac events among young individuals, whereas athero- sclerotic disease is primarily responsible for these events in adults. The absolute rate of exercise-related sudden cardiac death varies with the prevalence of disease in the study population. The incidence of both acute myocardial infarction and sudden death is greatest in the habitually least physically active individuals. No strategies have been adequately studied to evaluate their ability to reduce exercise-related acute cardiovascular events. Maintaining physical fitness through regular physical activity may help to reduce events because a disproportionate number of events occur in least physically active subjects performing unaccustomed physical activity. Other strategies, such as screening patients before participation in exercise, excluding high-risk patients from certain activities, promptly evaluating possible prodromal symptoms, training fitness personnel for emergencies, and encouraging patients to avoid high-risk activities, appear prudent but have not been systematically evaluated.
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