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Noninvasive Cardiovascular Evaluation of the Competitive Athlete

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Presentation on theme: "Noninvasive Cardiovascular Evaluation of the Competitive Athlete"— Presentation transcript:

1 Noninvasive Cardiovascular Evaluation of the Competitive Athlete
Gregory Piazza, M.D. Beth Israel Deaconess Medical Center March 19, 2008

2 Death on the Soccer Field
Antonio Puerta, a midfielder for Sevilla FC, collapsed during a game on August 25, 2007. He regained consciousness and was walked to the locker room where he collapsed again. He was resuscitated and brought to the ICU of a nearby hospital. He suffered multiple prolonged cardiac arrests over the next several hours resulting in anoxic brain injury and multisystem organ failure. He died 3 days after his initial collapse at age 22. Work-up revealed arrhythmogenic right ventricular cardiomyopathy (ARVC). Antonio Puerta (November 26, 1984 – August 28, 2007)

3 Overview Although rare, sudden cardiac deaths (SCD) among young competitive athletes have substantial emotional and social impact upon the lay public and medical community. Because competitive athletes are often thought to exemplify health and invulnerability, their sudden deaths seem counterintuitive. N Engl J Med 2003;349:11

4 Overview Even with widespread availability of portable automated defibrillators at sporting events, the mortality for athletes after syncope or cardiac arrest remains high. An improved understanding of conditions that predispose to SCD among trained athletes has lead to a great interest in pre-participation screening. N Engl J Med 2003;349:11

5 Objectives Describe the physiological adaptations of the cardiovascular system to athletic training Highlight the epidemiology and causes of SCD in competitive athletes Discuss the role of noninvasive testing in the evaluation of competitive athletes Review the recommendations for pre-participation screening

6 The Physiological Adaptations in the Trained Athlete
Athletic training for competitive endurance (aerobic) or isometric (static or power) sports results in characteristic changes in cardiac structure and function. This physiological form of left ventricular (LV) hypertrophy is known as the “athlete’s heart” and must be distinguished from pathological conditions that may predispose to SCD. Depending on the nature of the exercise training benign increases in LV mass, wall thickness, and cavity size as well as left atrial volume may be observed in healthy athletes. N Engl J Med 2003;349:11

7 The Physiological Adaptations in the Trained Athlete
Endurance Training Isometric Training Increase in LV cavity size Minimal increase in LV wall thickness Increase in LV wall thickness out of proportion to increase in cavity size Circulation 2000;101:336

8 The Athlete’s Heart The major difference is that the athlete’s heart will regress to normal after short periods of deconditioning while the pathologically hypertrophied heart will not. Gray area of overlap between the “athlete’s heart” and cardiomyopathies. N Engl J Med 2003;349:11

9 The Athlete’s Heart The physiological changes of the athlete’s heart have been evaluated by cardiac MRI and 3-D echo. In a study of 30 patients, members of a men’s professional rowing team were compared with sedentary untrained male subjects. Each patient underwent evaluation with 3-D echo and cardiac MRI. While 2-D echo significantly underestimated measurements, 3-D echo demonstrated good agreement with cardiac MRI. Compared with sedentary subjects, athletes had significantly increased LVEDV, LVESV, and LV mass. There were no differences in LVEF or the ratio of LV mass to LVEDV (LV remodeling index). Heart 2006;92:975

10 The Athlete’s Heart In another study, 23 male and 20 female endurance athletes were compared with age-matched controls using cardiac MRI. Male and female athletes demonstrated similar increases in LV and RV volumes and mass indices compared with controls. No gender-specific differences in the effect of training on LV and RV volumes, mass indices, ejection fractions, and LV to RV ratios of volume and mass indices were noted. J Magn Reson Imaging 2006;24:297

11 Competitive Sports This classification is based on peak static and dynamic components achieved during competition. It should be noted, however, that higher values may be reached during training. The increasing dynamic component is defined in terms of the estimated percent of maximal oxygen uptake (MaxO2) achieved and results in an increasing cardiac output. The increasing static component is related to the estimated percent of maximal voluntary contraction (MVC) reached and results in an increasing blood pressure load. The lowest total cardiovascular demands (cardiac output and blood pressure) are shown in green and the highest in red. Blue, yellow, and orange depict low moderate, moderate, and high moderate total cardiovascular demands. Classification of sports based on peak static and dynamic components achieved during competition.

12 Extrinsic Risk Factors for SCD
The risk of SCD in competitive sports increases with “burst” exertion (rapid acceleration and deceleration; common in basketball, tennis, and soccer). Extreme environmental conditions (temperature, humidity, and altitude) that affect blood volume and electrolyte balance also contribute to the risk. Progressive and systematic training to achieve higher levels of conditioning and performance may further increase the risk by resulting in a total cardiovascular demand that often exceeds that of competition. Circulation 2004;109:2807 J Am Coll Cardiol 2005;45:1364

13 Other Extrinsic Risk Factors for SCD
Cocaine abuse Amphetamine abuse Performance enhancing drugs (anabolic steroids) Dietary and nutritional supplements (including ephedra-containing products) Potentially arrhythmogenic N Engl J Med 2001;345:351 J Am Coll Cardiol 2002;39:1083

14 Epidemiology of Sudden Cardiac Death
Although likely underestimated, the incidence of SCD among competitive athletes appears to be low, ranging from 1 per 50,000 to 1 per 300,000. In a study of Minnesota high school athletes, the incidence of SCD was 1 in 200,000. In a study of nearly 220,000 marathon runners, SCD occurred in 4 individuals. None had any prior cardiac symptoms 2 had competed in several previous marathons 3 had coronary disease on autopsy JAMA 1996;276:1999 J Am Coll Cardiol 1998;32:1881 J Am Coll Cardiol 1996;28:428

15 Causes of Sudden Cardiac Death
Causes of SCD in athletes vary by age and geographic location. Among young competitive athletes (< 35 years old) in the U.S., inherited or congenital heart conditions (such as hypertrophic cardiomyopathy) are the most common etiologies. Among “masters” athletes (> 35 years old), coronary artery disease (CAD) appears to be the predominant cause of SCD. J Am Coll Cardiol 2003;41:974 Am J Cardiol 1980;45:1292

16 Causes of Sudden Cardiac Death in Young Athletes
In a U.S. registry of 236 young competitive athletes with SCD and structural heart disease on autopsy, the following conditions were reported: Hypertrophic cardiomyopathy (HCM)(36%) Anomalous coronary artery (13%) Myocarditis (7%) Ruptured aortic aneurysm (4%) ARVC (4%) Myocardial bridging (4%) Aortic stenosis (3%) CAD (3%) Idiopathic dilated cardiomyopathy (3%) Mitral valve prolapse (MVP)(3%) In other countries J Am Coll Cardiol 2003;41:974

17 Causes of Sudden Cardiac Death in Young Athletes
More recent Distribution of causes of SCD in 1435 young competitive athletes. From the Minneapolis Heart Institute Foundation Registry, 1980 to 2005. Circulation 2007;115:1643

18 Causes of Sudden Cardiac Death in Young Athletes
In an analysis of data from over 6 million U.S. military recruits ≤ 35 years old, 64 exercise-related deaths were due to an identifiable structural abnormality: Anomalous coronary artery (33%) Myocarditis (20%) CAD (16%) HCM (13%) Ann Intern Med 2004;141:829

19 Causes of Sudden Cardiac Death in Young Athletes
In contrast, a series of 49 young athletes with SCD from Northern Italy demonstrated the following distribution: ARVC (22%) CAD (18%) Anomalous coronary artery (12%) MVP (10%) Myocarditis (6%) HCM (2%) In other countries N Engl J Med 1998;339:364

20 Hypertrophic Cardiomyopathy
Incidence is approximately 1 in 500. It is a heterogeneous genetic disorder resulting in LV hypertrophy and fibrosis. Sudden death is most likely due to reentrant ventricular tachyarrhythmias. Most patients have an abnormal ECG. May be diagnosed by echo and cardiac MRI. Marked septal hypertrophy with SAM Late gadolinium enhancement consistent with myocardial fibrosis JAMA 2002;287:1308

21 Anomalous Coronary Anatomy
Incidence is likely underestimated. In SCD, most common anomaly is a left main coronary artery originating from the right sinus of Valsalva. May be suggested by chest pain or syncope with exercise but often SCD is the first symptom. Mechanism of ischemia is likely kinking or compression of the anomalous artery between the aorta and pulmonary trunk. ECG and echo are often normal. Best diagnosed by cardiac MRI, CT, or catheterization. Two patients with left main coronary arteries originating from right sinus of Valsalva J Am Coll Cardiol 2000;35:1493

22 Myocarditis May be preceded by a viral illness.
Clinical findings may include chest pain and heart failure symptoms in an otherwise healthy young person. ECG often demonstrates diffuse repolarization changes. SCD is likely due to ventricular arrhythmias or atrioventricular conduction disease. May be suggested by LV systolic dysfunction (as detected by echo, cardiac MRI, or cath) in the absence of CAD. Cardiac MRI may demonstrate focally increased T2-signal consistent with myocardial inflammation and late gadolinium enhancement suggestive of fibrosis. Inferolateral and lateral hypokinesis in a young patient with myocarditis Late gadolinium enhancement of the inferolateral and lateral wall in the same patient

23 Aortic Aneurysm and Dissection
In young athletes, aortic aneurysm and dissection is most often associated with aortopathy. Closely linked with inherited connective tissue disorders (Marfan’s syndrome). Marfan’s is inherited in an autosomal dominant fashion with an incidence of 1 in 10,000 to 20,000. Characteristic morphological findings (arachnodactyly, hyperflexible joints) may be noted on examination. SCD occurs due to aortic aneurysm rupture or dissection. Diagnosed on basis of clinical criteria. Echo is recommended to evaluate for aortic disease (including AR). Cardiac MRI and CT also detect aortic pathology. J Am Coll Cardiol 2005;45:1340

24 Arrhythmogenic Right Ventricular Cardiomyopathy
Characterized by fibrofatty infiltration of the RV free wall (may affect the LV). Symptoms include exercise induced palpitations, presyncope, or syncope. SCD is due to catecholamine-sensitive ventricular arrhythmias. ECG findings include increased QRS duration, epsilon waves in V1-2, and T wave inversions in the right precordium. Imaging may demonstrate RV dilatation and aneurysms. Echo and cardiac MRI are the most widely used noninvasive tests for ARVC. Epsilon waves In inexperienced hands, CMR is prone to false positives. Increased signal on T1-weighted imaging in the RV free wall (left) and decreased signal on fat suppressed imaging (right) J Am Coll Cardiol 2001;38:1773

25 Myocardial Bridging Myocardial bridging occurs when a portion of an epicardial coronary artery “tunnels” into the myocardium. Systolic vessel compression and delayed diastolic relaxation impair coronary blood flow in the intramyocardial segment. Although usually of little clinical consequence, myocardial bridging may infrequently result in exertional angina, infarction, and SCD. Myocardial bridging may be diagnosed on cardiac CT, MRI, or catheterization. Contrast-enhanced EBCT image revealing an intramyocardial segment of the LAD N Engl J Med 2003;349:1047

26 Aortic Stenosis Aortic stenosis (AS) in young athletes is most often due to congenital abnormalities of the aortic valve. Most common abnormality is a bicuspid aortic valve. More unusual etiologies include subvalvar and supravalvar aortic stenoses. Nearly all adult patients with SCD and congenital AS experience preceding symptoms. The majority of children may not have symptoms before SCD. Echo is the test of choice (although cardiac CT or MRI may be required to assess for concomitant aortic pathology). Circulation 1993;87:I16

27 Premature Coronary Artery Disease
CAD in young patients is frequently asymptomatic. Therefore, its incidence is likely underestimated. In an autopsy study, advanced coronary stenoses were noted in 20% of men and 8% of women aged years. 19% and 8% of men and women aged years, respectively, had ≥ 40% stenosis of the LAD. Coronary artery disease is the most common cause of SCD among “masters” athletes (> 35 years old). Circulation 2000;102:374

28 Idiopathic Dilated Cardiomyopathy
Idiopathic cardiomyopathy is a relatively uncommon cause of SCD in young competitive athletes (3%). The mechanism of SCD is most often reentrant ventricular tachyarrhythmia originating from areas of abnormal myocardium. Bradyarrhythmia or asystole may lead to SCD if cardiomyopathic process involves the conduction system. Late gadolinium enhancement in a patient with cardiomyopathy and normal coronary arteries

29 Mitral Valve Prolapse Although its relationship to tachyarrhythmia has been controversial, MVP is associated with an increased risk of SCD. However, the increased risk of SCD seems to correlate with the degree of mitral valve pathology and MR. In one study, the annual SCD mortality was significantly increased (from 0.9% to 1.9%) in patients with advanced mitral valve pathology compared with patients with isolated MVP (no MR) or the general population. Late gadolinium enhancement of the papillary muscles may be noted in some patients with MVP suggesting the presence of scarring or fibrosis. Late gadolinium enhancement of the anterolateral papillary muscle in a patient with MVP Am Heart J 1987;113:1298

30 Other Congenital Heart Disease
In addition to arrhythmic causes, cyanosis during exercise in the setting of adult congenital heart disease with right-to-left shunt may lead to syncope and SCD. Cardiac arrest is an unusual first presentation of adult congenital heart disease as most are symptomatic and therefore diagnosed before SCD. Adult congenital heart disease may be diagnosed by echo, cardiac CT, or MRI. Cardiac MRI currently offers the best definition of the complex anatomy of repaired and unrepaired congenital heart disease. Top caval baffle bringing blood to the LV (pulmonary) and bottom is the PV baffle into RV (systemic)

31 Sudden Cardiac Death in the Absence of Structural Heart Disease
SCD in competitive athletes may also occur in the absence of structural heart disease. Causes of SCD in structurally “normal” hearts include inherited arrhythmia syndromes such as: Long QT syndrome Brugada syndrome Catecholaminergic polymorphic VT Wolf-Parkinson-White syndrome Congenital short QT syndrome In addition, idiopathic VF and commotio cordis may result in SCD among competitive athletes.

32 Long QT Syndromes Often acquired, long QT syndrome can be inherited.
Long QT syndromes may result in polymorphic VT (torsade de pointes) and SCD. Among inherited long QT syndromes, precipitants and prognosis vary. Examples of long QT syndromes N Engl J Med 2008;113:1298

33 Brugada Syndrome Autosomal dominant disorder resulting in increased risk of SCD. Multiple mutations in the cardiac sodium channel SCN5A have been described. Characterized by RBBB and ST segment elevations in V1-V3 on ECG. Typical ECG pattern for Brugada Syndrome

34 Catecholaminergic Polymorphic VT
Also known as familial polymorphic VT, catecholaminergic polymorphic VT typically manifests itself in childhood or adolescence. SCD may occur in the setting of emotional or physical stress. Like LQT1, SCD while swimming has been described. Several mutations have been described including in the cardiac ryanodine receptor and calsequestrin 2 genes. Circulation 2002;106:69

35 Wolf-Parkinson-White
WPW syndrome has been associated with an increased risk of SCD. The mechanism of SCD is most often atrial fibrillation or AVNRT that degenerates to VF. In up to 25% of patients with SCD due to WPW, pre-excitation and arrhythmias have been previously undiagnosed. Typical pre-excitation pattern for WPW J Am Coll Cardiol 1991;18:1711

36 Congenital Short QT Syndrome
Congenital short QT syndrome is a rare autosomal dominant disorder associated with SCD due to VF. Multiple genetic abnormalities have been described including gain-of-function mutations in potassium channel genes. Short QT is defined as a corrected QT interval (QTc) ≤ 340 msec. Patients often develop atrial fibrillation at a young age . Not all patients with short QTc carry an increased risk of SCD. Circulation 2003;108:965

37 Idiopathic VF Also called “primary electrical disease,” idiopathic VF is diagnosed when SCD occurs in a structurally normal heart and other arrhythmic disorders are excluded. May account for up to 5% of SCD cases. Idiopathic VF is more common in men and has a mean onset of 36 years. A history of syncope precedes SCD in up to 25% of patients. Am Heart J 1990;120:661

38 Commotio Cordis Commotio cordis describes SCD that occurs following precordial trauma. A registry analysis revealed that 62% of cases occurred during organized or recreational sporting activities (baseball, hockey). In an animal model, low-energy impact to the chest wall just before the peak of the T wave produced VF, while impact during the QRS complex produced complete heart block. Frequency of VF was related to the hardness of the projectile and velocity of impact. In one series, only 16% of individuals survived an arrhythmic event in the setting of commotio cordis. JAMA 2002;287:1142 N Engl J Med 1998; 338:1805

39 Commotio Cordis Fatal commotio cordis in a 14-year-old boy during a karate match. N Engl J Med 2003;349:11

40 Syncope in Competitive Athletes
Syncope in competitive athletes without known structural heart disease is most often due to neurocardiogenic, or vasovagal, mechanisms. However, the diagnosis of neurocardiogenic syncope in this patient population is a diagnosis of exclusion. Careful evaluation warrants a detailed history, physical examination, and ECG. Echocardiography, exercise treadmill testing, cardiac MRI, and electrophysiological testing may be required to exclude structural and dysrhythmia-related causes of syncope.

41 Cardiovascular Events in Spectators
The emotional stress of watching competitive sports may increase the risk of cardiovascular events. A recent study demonstrated an increased incidence of cardiac emergencies among German men and women on days that the German team was playing a 2006 World Cup match compared to non-match days (incidence ratio 2.66, 95% CI ; p<0.001. The incidence of STEMI, NSTEMI, and arrhythmia increased by a factor of 2.5, 2.6, and 3.1, respectively, during match days. Daily cardiovascular events from May 1 to July 31 in 2003, 2005, and 2006. Numbers 1-7 correspond to German soccer matches during the 2006 World Cup (8 = Final, Italy v. France). N Engl J Med 2008;358:475

42 Screening Due to the devastating nature of SCD and the potential to prevent such deaths by diagnosing associated disorders noninvasively, clinicians have a strong incentive to screen athletes. However, the following obstacles prevent widespread screening with noninvasive testing: Large number of competitive athletes (8 million in the U.S., including high school, collegiate, professional) Low prevalence of underlying congenital heart disease Number of disorders to consider, each with different optimal testing modalities Impact of false-positive studies (substantial when screening for rare diseases; possible medicolegal implications) No randomized trials evaluating the impact of pre-participation screening on the incidence of SCD Young, masters, rec N Engl J Med 2003;349:11

43 Screening In an observational series from Italy, a mandatory screening program including ECG was associated with a decrease in the annual incidence of SCD in athletes from 3.6 to 0.4 per 100,000 person-years from 1980 to 2004. AHA guidelines differ from those of the European Society of Cardiology (ESC) and the International Olympic Committee (IOC) such that routine noninvasive testing (including ECG) is not recommended. Young, masters, rec JAMA 2006;296:1593 Circulation 2007;115:1643

44 AHA Screening Recommendations
Younger competitive athletes (<35) Complete personal/family history and physical exam Performed by physicians or certified non-physicians q2 years for high school and yearly for college/pro Masters athletes (>35) Exercise testing for moderate-to-high risk patients (men >40, women >50 with one or more CAD risk factors; symptoms suggestive of CAD; ≥65 regardless of risk factors/symptoms) Recreational athletes No explicit AHA guidelines; exercise testing recommended in patients at high risk for CAD Circulation 2007;115:1643

45 12-Element AHA Pre-Participation Screening Recommendations
Personal history (confirmed by parent if minor) Exertional chest discomfort Unexplained syncope/presyncope Excessive exertional fatigue/dyspnea Prior heart murmur Elevated blood pressure Family history (confirmed by parent if minor) Premature death due to heart disease before age 50 Disability due to heart disease in relative <50 Specific knowledge of certain cardiac conditions (HCM, other CM, ion channelopathy, Marfan’s, arrhythmias) Physical examination Cardiac exam (supine and standing) Femoral pulses Physical stigmata of Marfan’s Bilateral blood pressure readings *Positive finding of any 1 element warrants referral to cardiovascular specialist +/- further testing Circulation 2007;115:1643

46 Activity Restriction Recommendations
The 26th Bethesda Conference guidelines have established clear recommendations for the athletic eligibility and restriction of athletes with conditions associated with SCD. The decision to remove athletes from eligibility may be associated with complex social and medicolegal ramifications. A U.S. appellate court has ruled that the Bethesda Conference report can be used by clinicians to determine an athlete’s eligibility. Guidelines such as the Bethesda Conference report have been endorsed as a means for resolving medicolegal disputes involving the eligibility of young athletes. N Engl J Med 2003;349:11

47 Conclusions SCD in competitive athletes may result from a variety of disorders that may be detected by noninvasive testing. Noninvasive testing must be interpreted carefully in order to distinguish the physiological effects of exercise training from pathology. AHA guidelines do not endorse routine pre-participation screening with noninvasive testing. However, noninvasive testing plays a critical role in the evaluation of competitive athletes with positive findings on screening history and physical examination.

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