Case Reports of the Athletic Heart

In this educational section for CA ACC Sports and Exercise Health Committee, test your knowledge with clinical case reports and multiple choice questions. Further information and references provided in the discussion sections.

Athletes with Coronary Artery Calcifications: A Case Report

Authors: Deepak Ravi, MD; Timothy Canan, MD, Division of Cardiology, Department of Medicine, University of California, Los Angeles

A 58-year-old male with history of prostate adenocarcinoma, treated with robotic prostatectomy without the need for androgen deprivation therapy, was referred to cardiology for evaluation of coronary artery calcifications that were noted incidentally during staging computed tomography (CT) imaging. He has otherwise been healthy and takes only vitamins regularly. His parents both smoked and died of lung cancer and has no family history of early coronary artery disease. He stopped eating fast food as a teenager, gave up red meat, and has now been following a plant-based diet for many years. He has exercised his entire adult life, including weightlifting, running, high-intensity circuit training, and has now switched mainly to cycling due to knee arthritis. His current exercise routine includes 60-minute rides on a stationary bike with high-intensity power intervals six days per week. He denies any chest pain, pressure, dyspnea, or drops in exercise capacity or power output recently. He does endorse some palpitations during early recovery that last less than 10 seconds without lightheadedness or syncope. His blood pressure in clinic is 121/60 mmHg, BMI 25.7 kg/m2, with no abnormalities on physical exam. Labs show a total cholesterol of 244 mg/dL, HDL 91 mg/dL, LDL 137 mg/dL, and triglycerides 80 mg/dL. Resting electrocardiogram shows sinus bradycardia at 50 bpm without ectopy, ST or T wave abnormalities.

Question 1 of 2 What would you do next?

  • A. Lifestyle modifications of diet and exercise
  • B. Medical management with aspirin, low dose statin, and beta blocker
  • C. Further risk stratification needed
  • D. Invasive coronary angiography
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Question: What would you do next? Answer: C

Further risk stratification needed The patient has already optimized his lifestyle and is exceeding current physical activity guidelines.1 He is asymptomatic without clear evidence of ischemia or acute coronary syndrome, so jumping to invasive coronary angiography for his coronary artery calcifications would not be appropriate at this time. Medical management may be indicated, so his 10-year ASCVD Risk is calculated and found to be borderline at 5.1%. Initiation of a low dose aspirin and a moderate intensity statin therapy are both IIb recommendations and can be considered if other risk-enhancing factors are present.2 He is therefore sent for labs and studies for further risk stratification. Lipoprotein (a) is elevated at 198 nmol/L, high sensitivity CRP <0.2 mg/L, and hemoglobin A1c is 5.3%. A two-week external rhythm monitor to assess his symptomatic palpitations demonstrated sinus rhythm ranging from 37 bpm to 162 bpm with an average rate of 56 bpm. Patient triggered events on the monitor during episodes of post-exercise palpitations showed brief runs of an irregular supraventricular tachycardia with a maximum rate of 200 bpm and the longest run lasting 14 beats at average rate of 94 bpm. There are rare premature ventricular contractions seen but no ventricular runs. A CT coronary calcium score reveals a total Agatston score of 2085, placing him in the 99th percentile. The distribution shows no calcium in the left main, 461 in the left anterior descending, 347 in the left circumflex, and 1278 in the right coronary artery.

Question 2 of 2 What is the next appropriate step?

  • A. Medical management with aspirin, low dose statin, and beta blocker
  • B. Exercise stress testing
  • C. CT coronary angiogram
  • D. Invasive coronary angiography
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What is the next appropriate step? Answer: B

Exercise stress testing Given his significant coronary calcium burden in the 99th percentile, a high dose statin is more appropriate. A beta blocker is certainly reasonable but requires an informed discussion with athletes as it can be tolerated poorly with a reduction in exercise heart rate and capacity. CT coronary angiography could be useful to evaluate plaque morphology, but can be challenging in the setting of a high calcium burden with reduced sensitivity and positive predictive value due to extensive blooming artifact. Invasive angiography would be preferred if the patient had chest pain, decreased systolic function, ischemia on stress testing, or ventricular arrhythmias, which have not been demonstrated in this patient. He agreed to start taking aspirin 81 mg daily and high intensity statin therapy with rosuvastatin 20 mg daily. He then underwent cardiopulmonary exercise testing with stress echocardiography imaging. He exercised on a recumbent bicycle with ramp protocol, reaching a peak work rate of 262 W, heart rate of 163 bpm (101%MPHR), and a VO 2 Max of 41.1 ml/kg/min (141% predicted). Anaerobic threshold was calculated at 206 W using the V-slope method and occurred at a heart rate of 146 bpm. He experienced no symptoms or arrhythmias during or after peak exercise and had no evidence of ischemia by electrocardiogram or echocardiography. Repeat lipid panel on statin therapy showed a reduction in total cholesterol to 168 mg/dL, HDL 88 mg/dL, LDL 69 mg/dL, and triglycerides 56 mg/dL. He is cleared to continue his current level of exercise, predominantly in the aerobic range based on his CPET test results. He is given instructions on symptoms to monitor for during exercise, as well as precautions for when to seek emergency care. He has done well so far with no statin-induced myopathy symptoms, ischemic symptoms or events.

Athletes with COVID-19: A Case Report

Authors: Christine P. Shen, MD; Sandeep R. Mehta, MD, Division of Cardiology, Scripps Clinic

A 29-year-old female tested positive for coronavirus disease 2019 (COVID-19) after presenting to outpatient COVID testing with cough, chills, and body aches. Her course was complicated by left-sided numbness, and MRI brain showed left frontal and parietal lobe abnormal hyperintense signals. She was treated with a course of prednisone for presumed viral leukoencephalopathy. Prior to her infection, she was a competitive athlete in weightlifting and performed high-intensity workouts 2-3 hours per day, 5-6 days per week. She had no prior medical history. Family history was significant for myocardial infarction in two first-degree relatives. Within 3 weeks of being diagnosed with COVID-19, she developed severe exertional intolerance. Upon standing or walking for a few minutes, she experienced lightheadedness, shortness of breath, and tachycardia with heart rates of 120s-150s as measured on a consumer-grade wearable device. Her heart rate decreased to the 70s, her usual resting heart rate, upon lying down. She reported generalized fatigue and difficulty concentrating. She presented for cardiologist consultation three months after her initial COVID-19 diagnosis. At that time her blood pressure was 122/78 and her heart rate was 90 while sitting. She did not have orthostatic hypotension. On physical exam, she did not have any abnormalities. Her most recent lipid panel showed LDL 57 mg/dL, HDL 62 mg/dL, triglycerides 53 mg/dL, and total cholesterol 130 mg/dL. BMP, CBC, and TSH were normal. EKG showed sinus rhythm with sinus arrhythmia. Resting echocardiogram showed normal ejection fraction of 65%, normal wall thickness, normal diastolic function, and normal valvular function. CT angiography of the chest showed no evidence of pulmonary embolus.

Question 1 of 2 Which of the following tests will most likely show the cause of her symptoms?

  • A. Exercise treadmill stress test
  • B. CT coronary cardiac
  • C. Tilt table testing
  • D. Cardiac MRI
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Question: Which of the following tests will most likely show the cause of her symptoms? Answer: C

Tilt table testing The patient’s symptoms are concerning for autonomic dysfunction after a viral infection. She has atypical features not concerning for angina, so a stress test or cardiac CT would not likely show ischemia. A cardiac MRI could be useful in showing inflammation but would not likely explain her symptoms. She was therefore sent for autonomic reflex testing. Valsalva maneuver also reproduced symptoms, but beat-to-beat blood pressure response was normal. Tilt table testing showed severe symptomatic orthostatic intolerance with lightheadedness, blurry vision, chest tightness, and shortness of breath with head-up tilt at 70º. End-tidal CO2 was reduced after 3 minutes in head-up tilt. She remained in regular sinus rhythm. Her heart rate increased from 61 to 116 bpm, and her blood pressure rose inappropriately, from 106/68 to 110/76 mmHg. She had reduced mean cerebral blood flow velocity in the right middle cerebral artery as much as 35% during head up tilt at 70 degrees compared with baseline, consistent with postural orthostatic tachycardia syndrome (POTS).

Authors: Christine P. Shen, MD; Sandeep R. Mehta, MD, Division of Cardiology, Scripps Clinic

Question 2 of 2 What is the next appropriate step for this patient?

  • A. Lifestyle management with salt and fluid loading, compression stockings, and graded exercise.
  • B. Beta-blocker
  • C. Fludrocortisone
  • D. Midodrine
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Question: What is the next appropriate step for this patient? Answer: A

Lifestyle management with salt and fluid loading, compression stockings, and graded exercise. POTS is best treated initially with lifestyle management with salt and fluid loading, compression stockings, and graded exercise. Patients should drink 2-3 L of water per day, consume salt 10-12 g/day, and wear compression stockings. Patients should start a graded, structured, and supervised exercise program. Propranolol at a low-dose can help with sinus tachycardia and palpitations. Fludrocortisone and Midodrine have been used if symptoms persist after lifestyle management. Authors: Christine P. Shen, MD; Sandeep R. Mehta, MD, Division of Cardiology, Scripps Clinic

Deciding Return to Play in the Grey Area of Guidelines

Neal M. Dixit MD1, Ali Nsair MD1,2, Jeffrey J. Hsu MD, PhD1,2 1Department of Medicine, 2Division of Cardiology David Geffen School of Medicine at UCLA Los Angeles, California 90095

Case Presentation

A 20-year-old male presents to the office seeking a third opinion regarding his risk of playing competitive American-style football. He was a star athlete in high school and excelled in his first year of college football last year. Prior to his sophomore year, electrocardiogram (ECG) screening was implemented at his university, and his ECG revealed T-wave abnormalities that prompted further workup. Echocardiogram by report showed normal left and right ventricular (RV) ejection fraction, wall thickness, and size. An exercise treadmill test and coronary angiogram revealed no abnormalities. The patient had no exercise induced symptoms or ectopy and achieved 16 metabolic equivalents. He was allowed to resume participation in football activities and a two-week ambulatory electrocardiographic monitor was placed as a precaution.

However, the ambulatory monitor showed 3 episodes of non-sustained ventricular tachycardia (NSVT), all of which occurred at night without symptoms and lasted 5 beats or less. The total PVC burden was less than 1%. He was referred for a second opinion, and subsequently underwent further testing with cardiac magnetic resonance imaging (MRI) (Figure 1), which revealed left ventricular (LV) apical wall hypokinesis with associated wall thinning characterized by fatty metaplasia, mid-myocardial delayed gadolinium enhancement, and a normal RV. The left ventricle was mildly enlarged (LV end-diastolic dimension = 126.4 ml/m^2, LV end-systolic dimension = 60.3 ml/m^2, LV ejection fraction = 52%) and the RV was normal in size (RV end-diastolic dimension = 93.9 ml/m^2, RV end-systolic dimension = 38.1 ml/m^2, RV ejection fraction = 59%). 

He was advised that participation in high intensity competitive athletics would put him at increased risk of ventricular arrhythmia and sudden cardiac death and subsequently stopped football activities. He now comes seeking a third opinion regarding participation in the upcoming football season.

His past medical history is only notable for a pre-mature birth at 27 weeks due to placental insufficiency. He takes no medications. He has no family history of cardiomyopathy or sudden death. He drinks alcohol only occasionally and has never smoked or used drugs.

His cardiac exam reveals a regular, bradycardic rhythm, normal S1/S2, and a I/VI systolic murmur along the left sternal border. Jugular venous pressure is estimated at 7cm of water. He was not noted to have any hair or skin abnormalities. The remainder of the exam is normal.

Electrocardiogram (Figure 2) shows sinus bradycardia at 45 beats per minute, biphasic T-waves in leads V1-V5,, inferolateral ST segment depressions, no axis deviation or interval prolongation, no evidence of chamber enlargement, and a QRS duration of 108ms. Prior imaging is described as above.

Question 1 of 2 How should you counsel him on whether he should play in the upcoming football season?

  • A. Advise against resuming high intensity competitive athletics and recommend placement of an implantable cardiac defibrillator (ICD)
  • B. Discuss the risk of continued high intensity competitive athletics and come to a shared-decision 
  • C. Advise to sit out the season with symptom follow up and repeat cardiac imaging in 1 year
  • D. Allow continued participation of competitive athletics under close cardiology follow up
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Question 1 of 2 How should you counsel him on whether he should play in the upcoming football season? Answer is B

Given the features that raise significant concern for ACM, the patient should be advised that participation in high intensity competitive athletics increases his risk of ventricular arrhythmia and sudden death (2,3). ICD may be reasonable for some patients with ACM and a history of sudden cardiac arrest, sustained ventricular tachycardia, LV ejection fraction <45%, and those with multiple major and minor disease criteria (2). In patients without an ICD, beta blockers are a reasonable therapeutic option to reduce the risk of arrhythmia (Class IIa, Level of Evidence: C).

Question 2 of 2 Which of the following may be helpful in establishing a formal diagnosis?

  • A. Identification of a second-degree relative with confirmed ACM
  • B. Identification of the morphology of ventricular ectopy
  • C. Identification of a likely pathogenic mutation for ACM by genetic testing
  • D. None of the above 
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Question 2 of 2 Which of the following may be helpful in establishing a formal diagnosis? Answer is C

The patient meets several of the 2020 Padua criteria for LV variant of ACM (known as ALVC) (4). However, in patients with normal RV findings, it is suggested that ACM not be diagnosed solely off LV phenotypic criteria due to overlap with conditions such as dilated cardiomyopathy, hypertrophic cardiomyopathy, and cardiac sarcoidosis. In this patient with several clinical findings suggestive of arrhythmogenic cardiomyopathy (ACM), identification of a pathogenic mutation association with ACM would allow for the diagnosis of ALVC by Padua criteria. Identification of first and second degree relatives with confirmed ACM consist of major and minor Padua criteria, respectively, however, they are insufficient to confirm diagnosis of ALVC. A right bundle branch block pattern of ventricular tachycardia is a minor Padua criteria, insufficient to confirm diagnosis of ALVC.  

In our patient, genetic testing of the Arrhythmia and Cardiomyopathy Comprehensive Panel (Invitae) of 67 inherited genes did not reveal any mutations associated with ACM or other cardiomyopathy. Thus, a formal diagnosis of ALVC was not able to be made by Padua criteria.