https://orcid.org/0000-0002-2829-7198
Abstract
Myocardial bridging (MB) is considered a frequent and benign condition. However, some patients may experience symptoms. The recent ESC guidelines on sports participation provide guidance on the management of these symptomatic patients with MB but do not provide guidance in the presence of another cardiac pathology.
A 14-year-old-male was admitted for ongoing chest pain and palpitations. He practiced rowing at a competitive level and had an episode of exercise-induced paroxysmal atrial fibrillation (AF) a month ago. A 12-lead electrocardiogram and biomarkers orientated toward an acute coronary syndrome. Transthoracic echocardiography was normal. Cardiac magnetic resonance imaging ruled out the hypothesis of myocarditis and showed no ischemic scar. A coronary computed tomography scan showed a significant MB of the left anterior descending coronary artery. We introduced a beta-blocker and monitored the absence of inducible ischaemia with an exercise echocardiography. Our conclusion was a myocardial infarction with non-obstructive coronary arteries due to MB and adrenergic AF. Return to rowing practice including competitions was allowed under beta-blocker therapy. The 6-year follow-up showed no recurrence of AF under treatment. The patient kept on training and competing, though at a lower level.
This atypical case demonstrates that the so-called benign MB may become malignant, in particular in conjunction with rapid non-physiologic heart rate, and that dealing with this abnormality in athletes remains difficult despite the latest guidelines. Safe return-to-play and competition remain, however, possible under medical therapy if the patient is asymptomatic and has no inducible ischaemia.
Myocardial bridging is a common situation that may eventually be symptomatic in some patients.
In young athletes when there is no sign of stimulant or steroid abuse and no cardiomyopathy identified, genetic testing may help the physician by identifying variants at risk of atrial fibrillation.
Return-to-play and competition remain possible under medical therapy (preferentially beta-blocker) if the patient is asymptomatic and has no inducible ischaemia.
Background
Myocardial bridging (MB) is a congenital abnormality present in approximately 25% of patients.1 It is responsible for upstream-accelerated atherosclerosis while the segment included in the bridge is spared. The consequences are closely related to the degree of systolic compression (rather than the length or location of the bridge) and vary from no symptoms to angina pectoris and sudden death. Gated coronary computed tomography (CT) scan now allows for a non-invasive diagnosis with an increased sensitivity and safety compared with invasive coronary angiography. The management of symptomatic patients may, however, be challenging, in particular in athletes when other medical conditions occur.
Summary figure
Case summary
This case relates to a 14-year-old male with no personal/family history of cardiovascular disease, no treatment, and no drug use habits, including alcohol or tobacco. He reported no history of intake dietary supplements. He started rowing at the age of 8 and was in a study sports section, practicing 13 h per week with regular regional competitions.
He had been admitted for an episode of palpitations a month earlier related to paroxysmal atrial fibrillation (AF) with a ventricular rate of 160–180 beats/min (bpm). He was discharged without treatment, and a follow-up visit was scheduled with a cardiac rhythm specialist.
He was subsequently referred to our chest pain unit for constrictive chest pain with left arm radiation concomitant with an episode of palpitations that occurred after playing soccer. All symptoms stopped within 1 h after exercise discontinuation and before first medical contact.
Clinical examination upon admission showed normal blood pressure (112/63 mmHg), heart rate (88 bpm), and blood oxygen level (98%). No sign of cardiovascular disease was detected, as well as no sign of anabolic steroid abuse.
Admission 12-lead rest ECG (Figure 1) showed sinus rhythm, narrow QRS complexes, and ST-segment depression in inferior and leads V2 to V6 together with ST-segment elevation in aVR.
Twelve-lead rest electrocardiogram at admission in the chest pain unit.
Transthoracic echocardiography showed a normal left ventricle (dimensions and mass index), without wall motion abnormality. Left ventricular ejection fraction was 55%. The two coronary ostia were of normal origin, and no mitral and aortic valve disease was noted.
Standard blood tests were normal apart from cardiac biomarkers that were significantly increased, far beyond the 95th percentile [creatine kinase 754 international units (IU)/L, upper limit of normal (ULN) < 300 IU/L; cardiac troponin I 0.69 μg/L, ULN < 0.04 μg/L]. Thyroid-stimulating hormone level was 1.3 μIU/mL (normal range 0.5–3.4), serum potassium level was 3.9 mmol/L (normal range 3.2–5.1).
Considering the absence of cardiovascular risk factors, we performed a coronary CT scan (Figure 2) that confirmed the absence of abnormal coronary origin and showed a MB of the left anterior descending coronary artery (LAD) with an average depth of 2.3 mm and a length of 24 mm. This was confirmed by coronary angiography showing left coronary dominance and a significant systolic narrowing (>50%) of the LAD in its mid portion (Figure 3).
Coronary computed Tomography scan. The white arrows show the myocardial bridging on the left anterior descending coronary artery.
Coronary angiogram, caudal view. The black arrow shows the myocardial bridging on the left anterior descending coronary artery with a systolic compression of the lumen > 50%.
A cardiac magnetic resonance imaging was also performed in order to look for a potential acute myocarditis that could explain symptoms, ECG abnormalities, and biomarkers elevation. It reported normal left and right ventricular function (69% and 68%, respectively) without any ventricular dilatation. There was no myocardial hypertrophy, in particular in the apical portion, and no myocardial oedema. There was no pathological late gadolinium enhancement, confirming the absence of significant myocardial infarction or scar.
We finally concluded that the diagnosis was myocardial infarction with non-obstructive coronary arteries due to MB and adrenergic (exercise-induced) paroxysmal AF. The MB appeared symptomatic only during episodes of AF. We introduced a beta-blocker (atenolol 100 mg/day, reducing the resting heart rate from 67 to 59 bpm) and tested its efficacy after 48 h through an exercise echocardiography.
The stress test was performed up to exhaustion. The patient reached 270 Watts and 84% of his theoretical maximum heart rate. The test was normal, with no symptoms, no ischaemic ECG changes, and no regional wall motion abnormalities. No arrhythmia was documented during the hospital stay.
The patient was allowed to resume rowing training and competitions.
After 6 years of follow-up, he had only two recurrences of AF (without angina) after temporary suspension of the beta-blocker (by the family doctor at patient’s request), with no recurrence under treatment thereafter. He kept on training and competing, though at a lower level.
Discussion
Our case illustrates a rare consequence of MB in a young athlete. This condition, identified by coronary CT scan, may be efficiently treated with beta-blockers as a first-line therapy when symptomatic. The originality of this case of symptomatic MB leading to an acute coronary syndrome stands in the young age of our patient as opposed to the literature2–6 and to its concomitance with AF.
Schwartz et al.7 proposed a classification of MB, in order to guide treatment, which we adapted (Table 1). First-line medical treatment in symptomatic MB patients should include a beta-blocker or non-dihydropyridine calcium-channel blocker.1,8 The aim is to slow heart rate and extend the duration of diastole, thus optimizing coronary perfusion. However, use of beta blockers for MB has not been associated with reductions in mortality and morbidity in the literature.7 They may also have ergolytic effects, and this must be thoroughly discussed with the athletes as to educate them and reduce the risk of inobservance that may have severe consequences at the time of sports practice. Surgery may be considered on a case-to-case basis depending on symptoms persistence.1
Strategy proposed (and adapted) by Schwarz et al. for the therapeutic management of myocardial bridging
| Clinical symptoms | Signs of ischaemia | Initial treatment strategy | Secondary treatment if no improvement | |
|---|---|---|---|---|
| Type A | Yes | No | Reassurance, look for non-cardiac cause | — |
| Type B | Yes | Yes, by non-invasive stress testing | Beta-blockers, or if contraindicated non-dihydropyridine calcium-channel blockers. Target heart rate: 55–60 bpm at rest, consider ivabradine if not reached. | Intracoronary haemodynamic evaluation → surgery if abnormal |
| Type C | Yes | Yes, by altered intracoronary haemodynamics | Beta-blockers, or if contraindicated non-dihydropyridine calcium-channel blockers. Target heart rate: 55–60 bpm at rest, consider ivabradine if not reached. | Surgery |
| Clinical symptoms | Signs of ischaemia | Initial treatment strategy | Secondary treatment if no improvement | |
|---|---|---|---|---|
| Type A | Yes | No | Reassurance, look for non-cardiac cause | — |
| Type B | Yes | Yes, by non-invasive stress testing | Beta-blockers, or if contraindicated non-dihydropyridine calcium-channel blockers. Target heart rate: 55–60 bpm at rest, consider ivabradine if not reached. | Intracoronary haemodynamic evaluation → surgery if abnormal |
| Type C | Yes | Yes, by altered intracoronary haemodynamics | Beta-blockers, or if contraindicated non-dihydropyridine calcium-channel blockers. Target heart rate: 55–60 bpm at rest, consider ivabradine if not reached. | Surgery |
Strategy proposed (and adapted) by Schwarz et al. for the therapeutic management of myocardial bridging
| Clinical symptoms | Signs of ischaemia | Initial treatment strategy | Secondary treatment if no improvement | |
|---|---|---|---|---|
| Type A | Yes | No | Reassurance, look for non-cardiac cause | — |
| Type B | Yes | Yes, by non-invasive stress testing | Beta-blockers, or if contraindicated non-dihydropyridine calcium-channel blockers. Target heart rate: 55–60 bpm at rest, consider ivabradine if not reached. | Intracoronary haemodynamic evaluation → surgery if abnormal |
| Type C | Yes | Yes, by altered intracoronary haemodynamics | Beta-blockers, or if contraindicated non-dihydropyridine calcium-channel blockers. Target heart rate: 55–60 bpm at rest, consider ivabradine if not reached. | Surgery |
| Clinical symptoms | Signs of ischaemia | Initial treatment strategy | Secondary treatment if no improvement | |
|---|---|---|---|---|
| Type A | Yes | No | Reassurance, look for non-cardiac cause | — |
| Type B | Yes | Yes, by non-invasive stress testing | Beta-blockers, or if contraindicated non-dihydropyridine calcium-channel blockers. Target heart rate: 55–60 bpm at rest, consider ivabradine if not reached. | Intracoronary haemodynamic evaluation → surgery if abnormal |
| Type C | Yes | Yes, by altered intracoronary haemodynamics | Beta-blockers, or if contraindicated non-dihydropyridine calcium-channel blockers. Target heart rate: 55–60 bpm at rest, consider ivabradine if not reached. | Surgery |
Atrial fibrillation appears more common in endurance master athletes compared with non-athlete population.9,10 The potential mechanisms that may explain exercise-induced AF are increased vagal tone, typical in highly-trained athletes, but also inflammation, as intensive training sessions may have acute pro-inflammatory effect. Atrial fibrosis may also participate as a substrate for AF consecutive to chronic intensive training,11 but this may not be the case in such a young athlete. Importantly, the use of performance-enhancing substances should always be investigated.12 It is possible that genetic polymorphisms could explain why this young patient developed AF. Genetic testing may identify variants at risk of AF in young athletes when there is no sign of stimulant or steroid abuse and no cardiomyopathy identified, and should be added in the physician toolbox.13 Yet, no genetic testing was performed in this patient, and this hypothesis could not be verified. Thyroid-stimulating hormone and serum potassium levels were in the normal range. Unfortunately, data regarding serum magnesium level were not available.
Return-to-play (and competition) decision should be based on one hand on the underlying cardiac diagnosis, symptoms severity, type and need for treatment, persistence of arrhythmia in this case; and on the other hand, on the impact on athletic performance. The guidelines are substantial helping tools for physicians dealing with athletes; yet, cases of multiple combined cardiac abnormalities in athletes are uncommon and the correct management remains questionable. While the 2015 AHA/ACC guidelines suggest to restrict MB patients with prior myocardial infarction to sports with low-to-moderate dynamic and low-to-moderate static demands, the 2020 ESC guidelines do not mention prior myocardial infarction and open the way to competitive sports participation in asymptomatic MB patients without inducible ischaemia or ventricular arrhythmia during maximal exercise testing.14,15 Yet, our patient is out of the scope of the current guidelines because of this unusual association of cardiac conditions, i.e. symptomatic MB and adrenergic AF. Here, we demonstrate that the functional impact of a common MB can be dramatically increased when a rapid cardiac arrhythmia such as exercise-induced AF occurs. Medical treatment (with confirmed efficacy) and training resumption were safe and no further cardiac events occurred under medical therapy. These uncommon situations go beyond the scope of the most recent guidelines and should be reported to further increase our knowledge in sports physiology and improve athletes’ safety.
Lead author biography
Fabrice Ivanes is a cardiologist from Tours, France. Dr Ivanes received his medical degree from Lille University in 2008 and his Ph degree from Claude Bernard Lyon University in 2013. He completed a research fellowship in University College London in UK. He is now working in Tours University Hospital and has a position of Professor of Physiology in Tours University. He has clinical interest in the management of coronary artery disease, both invasive and non-invasive, and in sports cardiology.
Acknowledgements
We would like to acknowledge Professor Dominique Babuty for his guidance and counsels dealing with this case.
Consent: The authors confirm written consent for the submission and publication of this anonymized case report in line with Committee on Publication Ethics (COPE) guidelines.
Funding: None.
Data availability
The data underlying this article will be shared upon reasonable request to the corresponding author.
References
Author notes
Conflict of interest: None related to this clinical case.
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