05/09/2010 (Público.es)
Un estudio español propone añadir resonancias magnéticas y pruebas genéticas.
No siempre basta con el electrocardiograma estándar. Un estudio español presentado en el Congreso de la Sociedad Europea de Cardiología, celebrado en Estocolmo la pasada semana, demuestra que los chequeos a futbolistas jóvenes deben ajustarse al deporte que practican y, en algunos casos, incluir también pruebas de imagen como la resonancia magnética y análisis genéticos.
Poco después de cumplirse tres años del fallecimiento del sevillista Puerta, el estudio aporta datos que ayudarían a prevenir muertes súbitas en futbolistas con anomalías cardiacas. Los especialistas, dirigidos por el jefe de Cardiología de la Clínica Quirón de Madrid, José Ángel Cabrera, explicaron en Estocolmo que el chequeo que se recomienda para identificar el riesgo de cardiomiopatía hipertrófica (causa más común de muerte súbita en futbolistas profesionales) incluye un examen físico, historia médica y un procedimiento diagnóstico llamado electrocardiograma de 12 derivaciones. Sin embargo, los parámetros para someterse a esta última prueba no están separados por modalidad deportiva. Así, ante un resultado en el electrocardiograma, las pruebas complementarias a realizar son las mismas, con los protocolos actuales, para un futbolista que para un corredor de maratón.
Según los resultados de su trabajo, el 30% de los 30 futbolistas analizados (del Cádiz y del Xerez) presentaba irregularidades en el electrocardiograma. Sin embargo, el porcentaje disminuyó a cero cuando les fue practicada la resonancia y, en algunos casos, los análisis genéticos.
Cabrera explicó a Público que "no se trata de hacer tests genéticos a todo el mundo", pero sí de "ajustar las pruebas a la intensidad de cada deporte". El cardiólogo desconoce si estas pruebas hubieran salvado al jugador sevillista, pero lo ve como una posibilidad.
European Society of Cardiology
http://www.escardio.org/about/press/press-releases/esc10-stockholm/Pages/Cabrera-screening-athletes.aspx
Topics: Genetics
Stockholm, Sweden, 29 August: The screening process for young footballers at risk of heart disease needs to be re-evaluated. That is the conclusion of a recent study, which has shown that the common criteria used for assessment does not take into account the type and intensity of the exercise performed. The single most common cause of sudden death in competitive footballers is hypertrophic cardiomyopathy (HCM) – a disease that thickens the heart muscle without any obvious cause.
The recommended screening process to identify risk of HCM, which is particularly common in young athletes, involves physical examination, an assessment of medical history and a process called 12-lead ECG. However, this ECG screening process does not take into account the type and intensity of the exercise performed, so there is a question over its validity. A joint team from the Hospital Quiron at the Universidad Europa de Madrid; the Institute of Molecular Pathology and Immunology of the University of Porto; DADISA in Cadiz; and the University of Extramadura in Badajoz undertook a study into the correlation of all aspects of the screening process.
Doctor José Angel Cabrera is Head of Cardiology at Hospital Quiron and co-author of the study report. He explains: “The aim of the study was to assess the capacity of different cardiovascular tests to identify the risk from sudden death due to Hypertrophic Cardiomyopathy, Arrhythmogenic Right Ventricle Dysplasia and Dilated Cardiomyopathy. In particular, we wanted to understand the relationship between ECG results and actual cardiovascular risk to assess the accuracy and efficiency of the screening process for HCM.”
Two professional football teams were selected for the study, with a total of 30 males participating. They had an average age of 31, and all were healthy with a high dynamic (isotonic) component training history. They underwent a complete cardiovascular examination and HCM screening procedures that included a physical examination, a study of their personal and family history, a 12-lead ECG, an MRI study and a genetic analysis. The results showed ECG abnormalities in just over half of the subjects (56 percent), which -according to the current criteria- should have required them to undergo further evaluation for the diagnosis of cardiovascular disease.
Based on their MRI results alone, not one of the subjects showed clinical evidence of HCM. They all displayed normal left ventricular wall thickness, no systolic anterior motion of the mitral valve and no left ventricular outflow obstruction. Furthermore, genetic analysis showed no evidence of mutations in the genes that could lead to heart disease. So while over half of the subjects would have required further evaluation based on their ECG test results, the MRI and genetic tests showed a complete absence of heart disease.
These finding would suggest that ECG-based screening needs to be reviewed, and the criteria for further evaluation should be recalculated according to the type and intensity of the exercise performed.
Contributors: E. Gonzalez, JA. Cabrera, JC. Machado, A. Luna, P. Caro, B. Fuertes, D. Sanchez-Quintana
September 13, 2010 | Sue Hughes
http://www.theheart.org/article/1121345.do
Stockholm, Sweden - The European ECG-based screening process for hypertrophic cardiomyopathy (HCM) in young athletes needs to be reviewed, and the criteria for further evaluation should be recalculated according to the type and intensity of the exercise performed, a new study suggests.
"Training-related changes on the ECG are different for individuals participating in different sports. We should not be using the same screening criteria for a whole range of sports. As well as the type and intensity of sport, other factors that can influence ECG changes are gender and race. Therefore, we need a whole set of different individual guidelines for each group," study author Dr José Angel Cabrera (Hospital Quiron, Madrid, Spain) told heartwire.
Cabrera explained that the European ECG screening criteria for young athletes are associated with a very high rate of false positives, meaning that many individuals are referred on unnecessarily for further tests. "The guidelines have changed recently, and the situation has improved. We used to see a rate of about 70% false positives, but this has now been reduced to about 50%. But we can improve the ECG criteria even more if we factor in type of sport, race, and gender. We can then really refine what we are looking for as a sign of structural heart disease." Several groups are working on producing such guidelines, he added.
Guidelines for screening athletes for cardiovascular disease vary widely worldwide. The American College of Cardiology and the American Heart Association, for example, limit screening to a physical examination and medical history, while the European Society of Cardiology and International Olympic Committee recommend resting 12-lead ECG to detect cardiac abnormalities. Italy has adopted its own rules and has made it a law that all competitive athletes under the age of 35 have to have an annual ECG.
Cabrera presented results of his study in young footballers at the recent European Society of Cardiology (ESC) 2010 Congress. The aim of the study was to assess the capacity of different cardiovascular tests to identify the risk from sudden death due to HCM, arrhythmogenic right ventricle dysplasia, and dilated cardiomyopathy, with the aim of understanding the relationship between ECG results and actual cardiovascular risk to assess the accuracy and efficiency of the screening process for HCM.
The study involved 30 males (average age 31 years) from two professional football teams. All were healthy, with a high dynamic (isotonic) component training history. They underwent a complete cardiovascular examination and HCM screening procedures that included a physical examination, a study of their personal and family history, a 12-lead ECG, an MRI study, and a genetic analysis. The results showed ECG abnormalities in 56%, which should have required them to undergo further evaluation for the diagnosis of cardiovascular disease. However, based on their MRI results alone, not one of the subjects showed clinical evidence of HCM, and they all displayed normal left ventricular wall thickness, no systolic anterior motion of the mitral valve, and no left ventricular outflow obstruction. Furthermore, genetic analysis showed no evidence of mutations in the genes that could lead to heart disease.
"Many of the ECG changes classified as abnormal are actually normal for these young football players who, because of their training, have physiological changes to their hearts. And people who engage in different types of training regimens will show different physiological changes. We need to do more work to distinguish these physiological changes, which are not harmful, from changes that signify structural heart disease," Cabrera said.
By John Gever, Senior Editor, MedPage Today
Published: August 27, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
http://www.medpagetoday.com/MeetingCoverage/ESCCongress/21911
STOCKHOLM -- While hypertrophic cardiomyopathy is the most common cause of sudden death in competitive soccer players, when pro players were screened for the problem with electrocardiography (ECG), the positive results all turned out to be false positives, according to a small study.
The study of 30 pro soccer players who underwent 12-lead ECG screening showed that nearly 60% displayed abnormalities suggestive of cardiac hypertrophy -- but none were confirmed with MRI scans, according to Jose Angel Cabrera, MD, of Hospital Quiron in Madrid, Spain, and colleagues.
In an abstract scheduled for presentation here at the European Society of Cardiology (ESC) annual meeting, the researchers indicated that recommendations for routine ECG-based screening of athletes "should be reevaluated."
Some earlier studies, particularly from Italy, had indicated that 12-lead ECG screening could identify athletes with hypertrophic cardiomyopathy, putting them at risk for sudden cardiac death. Making such screening routine in Italy was said to reduce cardiac arrests among athletes by 90%.
However, the new Spanish study suggests that instituting such screening may also involve a great deal of waste -- since positive findings typically result in expensive follow-up evaluations.
Cabrera and colleagues reported on their experience with 30 professional soccer players, mean age 31 (SD 4), who underwent 12-lead ECG screening conducted and interpreted according to proposed ESC guidelines.
The participants also underwent MRI cardiac scans and genotyping for mutations in nine genes known to be associated with various types of heart disease.
ECG results in 17 of the players showed abnormalities that, under the guidelines, were indicative of cardiac hypertrophy warranting follow-up.
But the MRI results in all 17 showed normal left ventricular wall thickness and no signs of systolic anterior mitral valve motion or left ventricular outflow obstruction.
On the other hand, the evaluations failed to identify minor pericardial effusion in two players and persistent ductus arteriosus in another.
None of the participants had risk-associated genotype findings.
Alfred Bove, MD, of Temple University in Philadelphia and past president of the American College of Cardiology, told MedPage Today in an interview that the findings are plausible but at the same time pose a conundrum for clinical practice.
"It's a tough call," he said. "How do you find these kids [with serious cardiac abnormalities]? It's very small numbers, one in 100,000 or something like that. How many do you screen with expensive tests to find the one kid -- it becomes a big issue."
He noted that ECG screening is relatively cheap and easy to perform, and there is nothing else available for mass use that would not cost substantially more.
But Bove agreed that relying on ECG causes problems, particularly in the U.S. where rates of actual cardiac abnormalities are much lower than in northern Italy, where the research underlying the current recommendations was conducted.
"The Italians have convinced the world that everybody should have an electrocardiogram," he quipped.
Bove, who said he sometimes helps evaluate young athletes with suspected heart problems, indicated that, as a result, it's common to see one athlete "with a very bizarre-looking electrocardiogram -- perfectly normal kid, playing excellent sports, no history of anything ... and everybody gets all upset."
He said these athletes can get "million-dollar workups" that, most times, show nothing abnormal other than the "weird" ECG.
No external funding for the study was reported.
Cabrera had no conflict of interest disclosures.
Bove said he had no relationships with commercial entities relevant to the research.
Primary source: European Society of Cardiology
Source reference:
Gonzalez E, et al "Are the consensus screening criteria for a positive 12-lead ECG valid in competitive professional football (soccer) players? A genetic analysis and magnetic resonance imaging correlations" ESC 2010; Abstract P3980.

Title: |
Signs of subclinical myocarditis in a cohort of professional football players: a magnetic resonance imaging and genetic test study |
E. Gonzalez-Caballero1, G. Pizarro1, B. Fuertes1, S. Bayona1, JC. Machado2, A. Luna3, P. Caro3, D. Sanchez-Quintana4, JA. Cabrera1 - (1) Hospital Quiron-Madrid. Universidad Europea de Madrid, Madrid, Spain (2) IPATIMUP. GENETEST, Oporto, Portugal (3) DADISA, Cadiz, Spain (4) University of Extremadura, Department of Anatomy and Cell Biology, Badajoz, Spain |
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Introduction: Athletes possess greater relative risk of sudden death due to cardiovascular causes, where autopsies reveal myocardial fibrosis. Although hypertrophic cardiomyopathy (HCM) has been consistently reported to be the single most common cause of cardiovascular death, myocarditis can also be an important entity in this population. |
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LV lateral wall delayed enhancement |
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Title: |
Are the consensus screening criteria for a positive 12-lead ECG valid in competitive professional football (soccer) players? A genetic analysis and magnetic resonance imaging correlations |
E. Gonzalez1, JA. Cabrera1, JC. Machado2, A. Luna3, P. Caro3, B. Fuertes1, G. Pizarro1, S. Bayona1, D. Sanchez-Quintana4 - (1) Hospital Quiron-Madrid. Universidad Europea de Madrid, Madrid, Spain (2) IPATIMUP. GENETEST, Oporto, Portugal (3) DADISA, Cadiz, Spain (4) University of Extremadura, Department of Anatomy and Cell Biology, Badajoz, Spain |
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Introduction: Hipertrophyc cardiomyopathy (HCM) is the single most common cause of sudden death in competitive football players. Twelve lead-ECG ( in addition to history and physical examination) is the recommended pre-participation screening for identification of HCM and preventing sudden death. However none of the criteria for a positive 12-lead ECG included in the screening consensus protocol differentiated the type and intensity of exercise performed. |
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The left atrium extra-appendicular pectinate muscles of the mitral isthmus detected by multislice computed tomography: Implications for the safety of atrial fibrillation catheter ablation |
G. Pizarro1, D. Sanchez-Quintana2, M. Murillo2, E. Gonzalez-Caballero1, B. Fuertes1, S. Bayona1, V. Martinez1, JA. Cabrera1 - (1) Hospital Quiron-Madrid. Universidad Europea de Madrid, Madrid, Spain (2) University of Extremadura, Department of Anatomy and Cell Biology, Badajoz, Spain |
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Purpose: Previous anatomical studies in human hearts have demonstrated muscular trabeculations and remnants of extra-appendicular pectinate muscles (PM) at the area of the left mitral isthmus (LMI), between the ostium of the left inferior pulmonary vein and the mitral valve annulus. The areas in between the muscular trabeculas at this region of the LMI are large enough to trap an ablation catheter leading to excessive tissue heating and eventual tamponade due to a pop phenomenon. |
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Extra-appendicular pectinate muscles |
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The artery of the left atrial lateral ridge detected by multidetector computed tomography: a potential cause of atrial fibrillation recurrence after pulmonary vein catheter isolation |
G. Pizarro1, D. Sanchez-Quintana2, M. Murillo2, E. Gonzalez-Caballero1, B. Fuertes1, S. Bayona1, V. Martinez1, JA. Cabrera1 - (1) Hospital Quiron-Madrid. Universidad Europea de Madrid, Madrid, Spain (2) University of Extremadura, Department of Anatomy and Cell Biology, Badajoz, Spain |
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Purpose: Recovery of the left atrium-pulmonary vein conduction is the major cause of atrial fibrillation (AF) recurrence after catheter ablation. As previously reported by anatomical studies, the lateral ridge (LR) is located between the left atrial appendage (LAA) and the left superior pulmonary vein (LSPV). Occasionally, there is an artery following the course of the LR, which can be a cause of unablated gaps due to flow-mediated convective tissue cooling. |
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Left atrium lateral ridge artery |
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Epicardial catheter ablation of left ventricular tachycardias: the anatomic risk of inducing left phrenic nerve injury |
M. Murillo1, D. Sanchez-Quintana1, G. Pizarro2, E. Gonzalez2, B. Fuertes2, S. Bayona2, V. Climent1, JA. Cabrera2 - (1) University of Extremadura, Department of Anatomy and Cell Biology, Badajoz, Spain (2) Hospital Quiron-Madrid. Universidad Europea de Madrid, Madrid, Spain |
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Purpose: Epicardial catheter ablation is an increasingly important technique in the treatment of left ventricular tachycardia. The left phrenic nerve (LPN) is a structure especially at risk when procedures are carried out at the vicinity of the high left ventricular wall (HLVW). Detailed information of the anatomic relations between the LPN and the HLVW may be useful to perform the ablation procedures more safely. |
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Left Phrenic Nerve and Ventricular Wall |
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Accessory pathways in perinatal hearts with Ebstein malformation. Implications for surgical or transcatheter procedures. |
B. Picazo-Angelin1, JA. Cabrera2, M. Murillo3, G. Pizarro2, B. Fuertes2, E. Gonzalez2, S. Bayona2, V. Climent3, D. Sanchez-Quintana3 - (1) Hospital Costa del Sol, Marbella, Spain (2) Hospital Quiron-Madrid. Universidad Europea de Madrid, Madrid, Spain (3) University of Extremadura, Department of Anatomy and Cell Biology, Badajoz, Spain |
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Introduction: Advances in catheter ablation procedures in children have created the need for a better understanding of the anatomic bases involving abnormal pathways. Some congenital heart diseases, such as Ebstein malformation (EM), show a high incidence of associated arrhythmias. We have performed histological studies in perinatal hearts with EM and describe the associated accessory pathways found. |
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Transmural crossover of myocardial fibers underneath the pulmonary valve: implication for ablation of idiopathic ventricular outflow tract tachycardias |
M. Murillo1, JA. Cabrera2, G. Pizarro2, B. Fuertes2, E. Gonzalez1, S. Bayona2, V. Climent1, D. Sanchez-Quintana2 - (1) University of Extremadura, Department of Anatomy and Cell Biology, Badajoz, Spain (2) Hospital Quiron-Madrid. Universidad Europea de Madrid, Madrid, Spain |
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Most right ventricular outflow tracts (RVOT) tachycardias originate in perivalvular tissue, which may be anatomically predisposed to fiber disruption. Structural discontinuities and heterogeneous fibers orientation in the infundibulum of the RV has not been previously described |
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Myocardial fibers of the RVOT |
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The architecture of the infundibulum: more than a simple tubular structure with relevance for ablation of idiopathic tachycardia of the right ventricular outflow tract |
D. Sanchez Quintana1, M. Murillo1, G. Pizarro2, E. Gonzalez2, B. Fuertes2, S. Bayona2, V. Climent1, JA. Cabrera2 - (1) University of Extremadura, Department of Anatomy and Cell Biology, Badajoz, Spain (2) Hospital Quiron-Madrid. Universidad Europea de Madrid, Madrid, Spain |
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The most common site of origin for right ventricular outflow tract (RVOT) tachycardias is the left septal side of the infundibulum just underneath the pulmonary valve (PV). Detailed anatomic information of this ventricular structure may be useful to perform the ablation techniques more efficiently and safely. |
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The Right Ventricular Outflow Tract |
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