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<strong>Thursday</strong>, May 30, 2013<br />

S342 Vol. 45 No. 5 Supplement<br />

D-59 Clinical Case Slide - Cardiovascular<br />

May 30, 2013, 3:15 PM - 5:15 PM<br />

Room: 103<br />

1768 Chair: Aaron L. Baggish. Massachusetts General Hospital,<br />

Boston, MA.<br />

(No relationships reported)<br />

1769 discussant: Sandra J. Hoffmann, FACSM. Idaho State University,<br />

Pocatello, ID.<br />

(No relationships reported)<br />

1770 discussant: Warren B. Howe, FACSM. Bellingham, WA.<br />

(No relationships reported)<br />

1771 May 30, 3:15 PM - 3:35 PM<br />

sudden Cardiac death--running<br />

Kenneth Leclerc, James Watts, Mark Peele, Kevin Steel, Michael<br />

Rose. San Antonio Military Medical Center, Fort Sam Houston, TX.<br />

(No relationships reported)<br />

hIsTOry: A 51-year-old male had sudden loss of consciousness while running on<br />

a treadmill at the gym. He had been evaluated 4 months prior for a neurocardiogenic<br />

syncopal event following a colonoscopy. Patient found to be without a pulse.<br />

Bystander CPR was performed and the use of an automated external defibrillator<br />

(AED) with successful restoration of a regular pulse. Interrogation of the AED<br />

revealed ventricular fibrillation appropriately defibrillated to normal sinus rhythm.<br />

PhysICaL EXaMINaTION: Heart rate 60, Blood pressure 130/81, Respiratory<br />

rate 12. His breath sounds were clear to auscultation. His heart was regular in rate and<br />

rhythm, normal S1 and S2 without murmur. He had no elevation in his jugular venous<br />

pulsation and was without lower extremity edema.<br />

PhysICaL EXaMINaTION:<br />

1. Acute coronary syndrome<br />

2. Arrhythmogenic right ventricular cardiomyopathy<br />

3. Catecholaminergic polymorphic ventricular tachycardia<br />

4. Brugada syndrome<br />

5. Long QT syndrome<br />

6. Torsades de Pointe<br />

TEsT aNd rEsuLTs:<br />

EKG<br />

--Normal sinus rhythm, right axis deviation, and right bundle branch block<br />

Echocardiogram<br />

--Normal left ventricular size, wall thickness and function with moderate dilation of<br />

the right ventricle and right atrium.<br />

Coronary Angiography<br />

--Luminal irregularities<br />

Cardiac MRI<br />

--Mildly dilated right ventricle with a mildly low right ventricular ejection fraction of<br />

46.4% without other evidence for arrhythmogenic right ventricular dysplasia<br />

Electrophysiology Study<br />

--No accessory pathway found, no evidence of dual AV node physiology, and<br />

normal corrected QT interval after epinephrine infusion. A monomorphic ventricular<br />

tachycardia occurred after high dose (20mcg/min) isoproterenol infusion<br />

Genetic Testing<br />

--4 novel gene mutations coding for sarcomeric proteins (actinin, myosin, and titin).<br />

FINaL WOrKING dIaGNOsIs:<br />

Catecholamine sensitive ventricular tachycardia with aborted sudden death secondary<br />

to apparent RV cardiomyopathy<br />

TrEaTMENT aNd OuTCOMEs:<br />

1. AICD placed for secondary prevention of sudden cardiac death<br />

2. Suppressive long-acting beta-blocker therapy<br />

3. Cardiac rehabilitation without recurrence of symptoms<br />

4. Genetic counseling for the patient and first degree relatives<br />

5. Further evaluation as to the role that the genetic variants may play into malignant<br />

arrhythmias<br />

1772 May 30, 3:35 PM - 3:55 PM<br />

syncope and abnormal Electrocardiogram in an adolescent<br />

Basketball Player<br />

Jodi L. Zilinski, Miranda E. Contursi, Patricia A. Lowry, Caitlin<br />

H. O’Callaghan, Michael A. Fifer, Gregory D. Lewis, Aaron L.<br />

Baggish. Massachusetts General Hospital, Boston, MA.<br />

(No relationships reported)<br />

hIsTOry: A 17 year old Caucasian male basketball player presented following a<br />

syncopal episode, which occurred during basketball practice. He had just completed<br />

MEDICINE & SCIENCE IN SPORTS & EXERCISE ®<br />

sprinting drills and was walking to the bench when he felt lightheaded and lost<br />

consciousness for approximately 30 seconds. He sustained no injuries. He had recently<br />

completed a course of azithromycin for an upper respiratory tract illness. He denied<br />

antecedent chest pain, palpitations, and prior syncope.<br />

PhysICaL EXaMINaTION:<br />

Vital signs: Ht 1.78 meters, Wt 68.0 kg, Heart rate 50 bpm, Blood Pressure 112/62<br />

mmHg<br />

Healthy appearing. Lungs clear. Bradycardic regular rate, normal S1 and S2 without<br />

murmur or gallop. Nonfocal neurologic examination.<br />

PhysICaL EXaMINaTION:<br />

Neurally mediated syncope<br />

Cardiac arrhythmia<br />

Anomalous origin of coronary artery<br />

Structural heart disease (HCM, ARVC)<br />

Athletic remodeling<br />

Myocarditis<br />

TEsT aNd rEsuLTs:<br />

ECG: (Fig. a)<br />

- Sinus bradycardia<br />

- QTc 428 ms<br />

- Increased precordial voltage<br />

- Diffuse repolarization abnormalities<br />

Echocardiogram:<br />

- LV- asymmetric hypertrophy (LV mass 107 g/m 2 , wall measurements: interventricular<br />

septum 9 mm, posterior wall thickness 12 mm)<br />

- RV- normal structure and function<br />

- Coronary Arteries- well visualized, normal coronary origins and proximal courses<br />

Cardiac MRI: (Fig. B)<br />

-LV mass 115 g/m 2<br />

- Asymmetric LV hypertrophy (max wall thickness = 15 mm in inferior region)<br />

- No T2 weighted edema, early or late gadolinium enhancement<br />

- No RV hypertrophy<br />

Cardiopulmonary Exercise Test (CPET):<br />

- Exercise time: 12:54 min<br />

- Peak workload 196 Watts<br />

- Maximal oxygen uptake (VO2) 33.4 ml·kg -1 ·min -1 (75% predicted)<br />

- Decreased peak O2 pulse consistent with abnormal stroke volume augmentation<br />

- No arrhythmias<br />

WOrKING dIaGNOsEs:<br />

Hypertrophic cardiomyopathy vs. Athletic remodeling with neurally mediated syncope<br />

TrEaTMENT aNd OuTCOMEs:<br />

1. Prescribed detraining x 6 months<br />

2. Repeat EKG (Fig. C): Persistent although less marked repolarization abnormalities<br />

3. Repeat Cardiac MRI (Fig. d): Marked regression of LV wall thickness (max = 10<br />

mm in inferolateral region) and LV mass 79 g/m 2 (Δ = -36 g/m 2 , % Δ = -31%)<br />

Discussion with patient and family regarding prognostic uncertainties surrounding<br />

“bizarre” ECG patterns in the absence of structural heart disease. Ultimately cleared<br />

for participation with close follow-up.<br />

1773 May 30, 3:55 PM - 4:15 PM<br />

decreased Ejection Fraction - Baseball<br />

Peter H. Seidenberg, Wayne J. Sebastianelli. Penn State<br />

University, State College, PA. (Sponsor: Francis G. O’Connor,<br />

FACSM)<br />

(No relationships reported)<br />

hIsTOry: A 19 year old freshman baseball catcher underwent routine screening<br />

2D echocardiography as part of his initial preparticipation evaluation. He reports no<br />

history of chest pain, syncope, dizziness, palpitations, or shortness of breath. His past<br />

medical history is unremarkable. There is no history of recent illness. There is a history<br />

of a severe flu-like illness 2-3 years ago, for which he did not seek medical attention.<br />

There is no significant family medical history. He has no current or prior history of<br />

smoking, alcohol use, drug use, or anabolic steroid use.<br />

ACSM May 28 - June 1, 2013 Indianapolis, Indiana

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