Case Report
Myocardial Bridging in a Child With Hypertrophic Obstructive Cardiomyopathy
World Journal for Pediatric and Congenital Heart Surgery 2014, Vol. 5(4) 611-614 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/2150135114536901 pch.sagepub.com
Okan Yildiz, MD1, Firat H. Altin, MD1, Oyku Tosun, MD2, Muzeyyen Iyigun, MD3, and Ersin Erek, MD1
Abstract Myocardial bridging (MB) is a rare coronary anomaly in children which is typically associated with hypertrophic obstructive cardiomyopathy (HCM) or left ventricular hypertrophy. Hypertrophic obstructive cardiomyopathy is the leading cause of sudden cardiac death in young patients, and the association of myocardial ischemia with sudden death has been recognized in patients with HCM. In this report, we describe an 11-year-old boy presented with a history of exertional, nonspecific chest pain and palpitations. Cardiac catheterization revealed MB of the left anterior descending coronary artery with evidence of intramyocardial obstruction during systole. Surgical unroofing of the affected coronary artery segment resulted in complete recovery. Myocardial bridging should be included in the differential diagnosis of children presenting with signs of ischemia. Keywords myocardial bridging, coronary artery, hypertrophic cardiomyopathy, chest pain Submitted January 5, 2014; Accepted April 18, 2014.
Myocardial bridging (MB) occurs when a band of myocardial muscle overlies a segment of the coronary artery resulting in mechanical stenosis due to systolic compression.1 It is most commonly seen in the middle segment of the left anterior descending artery (LAD)2-6; however, there are reports about involvement of the right or circumflex coronary artery and their branches.4,6,7 Myocardial bridging is often an incidental finding in adults with the incidence of 0.5% to 1.6% in the general population. Its occurrence may increase up to 30% to 50% of adults who have hypertrophic obstructive cardiomyopathy (HCM), and MB in children is very rare, and the incidence in both normal children and those with HCM is unknown.3 Although clinical significance of isolated MB is controversial, it may be associated with a higher incidence of sudden cardiac death, ventricular tachycardia, and perfusion defects on thallium scintigraphy in adults with HCM.8 Myocardial bridging in children is almost always associated with HCM or with the conditions that cause left ventricular hypertrophy, such as aortic stenosis, but the reports are worrying about the significance of MB for the increased risk of adverse events in childhood.3,5 Here, we describe a symptomatic patient who had obstructive HCM with MB on the LAD and his surgical management.
over the left lower sternal border. Laboratory workup was normal. The electrocardiogram (ECG) on admission demonstrated normal sinus rhythm and left ventricular hypertrophy. There were nonspecific ST-T wave changes in the anterolateral leads. Transthoracic echocardiography showed HCM with severe obstruction of the left ventricular outflow tract and moderate mitral insufficiency with systolic anterior motion, normal fractional shortening. The peak gradient was 119 mm Hg, and the mean gradient was 59 mm Hg. The systolic muscular ventricular septum width was measured 30 mm. Due to the chest pain and suspected ischemic changes in ECG, thallium scintigraphy was performed. Thallium scintigraphy showed severe dipyridamole-induced ST-segment depression and reversible perfusion defects in the anterior wall. Based on these findings,
Case Report
Corresponding Author: Okan Yildiz, Department of Pediatric Cardiovascular Surgery, Istanbul Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, _Istasyon Mah. Turgut O ¨ zal Bulvarı No: 11 Ku¨c¸u¨kc¸ekmece, Istanbul 34303, Turkey. Email: [email protected]
An 11-year-old male presented with nonspecific chest pain, fatigue on exertion, and palpitations. Physical examination revealed a grade III/VI harsh long systolic murmur heard best
1 Department of Pediatric Cardiovascular Surgery, Istanbul Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Istanbul, Turkey 2 Department of Pediatric Cardiology, Istanbul Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Istanbul, Turkey 3 Department of Anesthesiology and Reanimation, Istanbul Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Istanbul, Turkey
612
World Journal for Pediatric and Congenital Heart Surgery 5(4)
Figure 1. A, Coronary angiography during diastole. B, Compression of the mid-left anterior descending artery during systole (arrow).
Abbreviations and Acronyms ECG HCM LAD LV MB QTc
electrocardiogram hypertrophic obstructive cardiomyopathy left anterior descending artery left ventricle Myocardial bridging corrected QT
the patient underwent cardiac catheterization, which demonstrated a gradient across the outflow tract of 103 mm Hg and revealed MB at the mid-segment of the LAD with a positive milking effect of approximately 95% systolic compression (Figure 1A, 1B). The patient underwent open heart operation under moderate hypothermia. After cardioplegic arrest with isothermic blood cardioplegia, aortotomy was done. Extensive myectomy was applied in addition to Morrow procedure (Figure 2). After closure of the aortotomy, distal end of the LAD was visualized. Myocardial bridging site was identified, and constricting muscle bundles were incised from distal to proximal segment of the LAD, until full visualization of the artery. The thickness of the muscular bridge was significantly greater than we had predicted from its angiographic appearance. Its length was approximately 4 cm, and its thickness was 8 mm (Figure 3). We performed suture fixation of the divided bridge edges on adjacent tissue to draw them back from the LAD. A small inadvertent entry into the right ventricle during surgical unroofing of the myocardial bridge occurred, and we repaired this with a single 7/0 polypropylene mattress suture with pericardial pledged. Cardiopulmonary bypass time and cross-clamp time were 152 and 101 minutes, respectively. The patient’s postoperative course was uneventful, and he was discharged from the hospital seven days after surgery. Control echocardiography in early postoperative period and two months later revealed normal left ventricular function and maximum 30 mm Hg gradient across
Figure 2. Intraoperative view reveals extensive myectomy material.
the left ventricle (LV) outflow tract. The patient remained symptom-free six months postoperatively.
Comment Myocardial bridging occurs when the epicardial coronary arteries are intramyocardial, resulting in systolic compression of a coronary artery on coronary angiography.4 Also reported is persistence of coronary artery compression through 50% of diastole in children.3 The high incidence of MB in patients with HCM is higher than normal population, but it is not certain
Yildiz et al
Figure 3. Intraoperative view reveals mid-left anterior descending artery after surgical unroofing (arrow).
whether the MB is congenital or acquired and what factors are linked to the development of bridging.8 Hypertrophic obstructive cardiomyopathy is the leading cause of sudden cardiac death in young patients, and the association of myocardial ischemia with sudden death has been recognized in patients with HCM.8 The cause of ischemia may be intramural abnormalities of the small vessels, abnormal myocellular architecture, or massive hypertrophy. The role of MB in ischemia is controversial. The prolongation of systolic compression by MB into diastole, when the largest proportion of coronary blood flow normally occurs, might be the cause of myocardial ischemia. This prolongation may have a greater effect in young children because the heart rate is faster and the diastolic filling time is shorter, especially during exercise.8 There is an ongoing debate whether hypertrophic cardiomyopathy-associated MB is an independent risk factor for ischemia and sudden cardiac death in children or simply an indicator of the severity of left ventricular hypertrophy.9 A study of 36 pediatric patients with HCM showed evidence that significant MB of the LAD is characterized by greater than 90% systolic compression of the middle third of the LAD with ongoing compression during a mean of 50% of diastole.3 A similar study reviewed the angiograms of 57 children with HCM for the presence of coronary artery compression. Their findings suggested that coronary compression did not make an important contribution to the myocardial ischemia in HCM; however, left ventricular hypertrophy and compression of intramural arteries might contribute significantly. Still, small series and case reports have offered compelling evidence for an association of MB and sudden death or myocardial infarction in children and young adults1,10,11 A study of five patients with MB has reported alleviation of cardiac ischemia and
613 symptoms through surgical relief of MB.12 Supracoronary myotomy may result in injury of the ventricular wall and coronary arteries and subsequent danger of opening the right ventricle and LV, ventricular aneurysm formation, or subsequent scar formation with recurrent extrinsic compression.13 Potential advantages of supra-arterial myotomy are increased coronary flow rate, which results in an increased myocardial perfusion, and a decreased rate of fatal arrhythmia incidence, especially when the response to medical therapy is suboptimal. Although some complications still exist, supra-arterial myotomy is the gold standard in the surgical treatment of MB. The challenges that we are facing are to determine whether the symptoms are caused by MB in symptomatic patients and to identify the patients who are at increased risk of complications. Usually, the diagnosis is established by chance in patients who are examined by coronary angiography or computerized tomography angiography for various reasons but not because they are suspected of having MB.8 Echocardiographic features are associated with the severity of the disease or with its complications but not with MB.3 On the other hand, LV wall thickness at the proximal interventricular septum, and the degree of asymmetrical septal hypertrophy are significantly greater in children with bridging. Furthermore, the association between LV outflow tract obstruction and bridging is further demonstrated by significantly higher LV systolic pressure in affected children.6 For all these reasons, indications for the visualization of the coronary arteries should be extensive, either by coronary angiography or by computerized tomography angiography. These should be performed for the patients with left ventricular outflow obstruction and symptoms like angina, syncope, and cardiac arrest and for the assessment of the children considered to be at high risk of sudden death (ventricular tachycardia, increased degree of corrected QT (QTc) dispersion on the ECG, or abnormal blood pressure response during exercise).3,6 We conclude that significant MB of the LAD may be an important and treatable cause of myocardial ischemia and sudden death in selected children with hypertrophic cardiomyopathy. Coronary angiography provides valuable information about children with hypertrophic cardiomyopathy who have angina, an abnormal blood pressure response during exercise, an increased degree of QTc dispersion on the ECG, ventricular tachycardia, or who have been resuscitated after cardiac arrest. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
References 1. Hillman ND, Mavroudis C, Backer CL, Duffy CE. Supraarterial decompression myotomy for myocardial bridging in a child [case reports]. Ann Thorac Surg. 1999;68(1): 244-246.
614 2. Kalaria VG, Koradia N, Breall JA. Myocardial bridge: a clinical review [review]. Catheter Cardiovasc Interv. 2002;57(4): 552-556. 3. Yetman AT, McCrindle BW, MacDonald C, Freedom RM, Gow R. Myocardial bridging in children with hypertrophic cardiomyopathy—a risk factor for sudden death. N Engl J Med. 1998; 339(17): 1201-1209. 4. Sorajja P, Ommen SR, Nishimura RA, Gersh BJ, Tajik AJ, Holmes DR. Myocardial bridging in adult patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 2003;42(5): 889-894. 5. Basso C, Thiene G, Mackey-Bojack S, Frigo AC, Corrado D, Maron BJ. Myocardial bridging, a frequent component of the hypertrophic cardiomyopathy phenotype, lacks systematic association with sudden cardiac death. Eur Heart J. 2009;30(13): 1627-1634. 6. Mohiddin SA, Begley D, Shih J, Fananapazir L. Myocardial bridging does not predict sudden death in children with hypertrophic cardiomyopathy but is associated with more severe cardiac disease. J Am Coll Cardiol. 2000;36(7): 2270-2278. 7. Vongpatanasin W, Willard JE, Hillis LD, Lange RA, Landau C. Acquired myocardial bridging [case report]. Am Heart J. 1997; 133(4): 463-465.
World Journal for Pediatric and Congenital Heart Surgery 5(4) 8. Bruschke AV, Veltman CE, de Graaf MA, Vliegen HW. Myocardial bridging: what have we learned in the past and will new diagnostic modalities provide new insights? Neth Heart J. 2013;21(1): 6-13. 9. Daana M, Wexler I, Milgalter E, Rein AJ, Perles Z. Symptomatic myocardial bridging in a child without hypertrophic cardiomyopathy [case report]. Pediatrics. 2006;117(2): e333-e335. 10. Morales AR, Romanelli R, Boucek RJ. The mural left anterior descending coronary artery, strenuous exercise and sudden death [case report]. Circulation. 1980;62(2): 230-237. 11. Basso C, Corrado D, Thiene G. Cardiovascular causes of sudden death in young individuals including athletes. Cardiol Rev. 1999; 7(3): 127-135. 12. Downar J, Williams WG, McDonald C, Wigle ED, McCrindle BW. Outcomes after ‘‘unroofing’’ of a myocardial bridge of the left anterior descending coronary artery in children with hypertrophic cardiomyopathy [case report]. Pediatr Cardiol. 2004; 25(4): 390-393. 13. Pratt JW, Michler RE, Pala J, Brown DA. Minimally invasive coronary artery bypass grafting for myocardial muscle bridging [case report]. Heart Surg Forum. 1999;2(3): 250-253.
Myocardial Bridging in a Child With Hypertrophic Obstructive Cardiomyopathy
World Journal for Pediatric and Congenital Heart Surgery 2014, Vol. 5(4) 611-614 ª The Author(s) 2014 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/2150135114536901 pch.sagepub.com
Okan Yildiz, MD1, Firat H. Altin, MD1, Oyku Tosun, MD2, Muzeyyen Iyigun, MD3, and Ersin Erek, MD1
Abstract Myocardial bridging (MB) is a rare coronary anomaly in children which is typically associated with hypertrophic obstructive cardiomyopathy (HCM) or left ventricular hypertrophy. Hypertrophic obstructive cardiomyopathy is the leading cause of sudden cardiac death in young patients, and the association of myocardial ischemia with sudden death has been recognized in patients with HCM. In this report, we describe an 11-year-old boy presented with a history of exertional, nonspecific chest pain and palpitations. Cardiac catheterization revealed MB of the left anterior descending coronary artery with evidence of intramyocardial obstruction during systole. Surgical unroofing of the affected coronary artery segment resulted in complete recovery. Myocardial bridging should be included in the differential diagnosis of children presenting with signs of ischemia. Keywords myocardial bridging, coronary artery, hypertrophic cardiomyopathy, chest pain Submitted January 5, 2014; Accepted April 18, 2014.
Myocardial bridging (MB) occurs when a band of myocardial muscle overlies a segment of the coronary artery resulting in mechanical stenosis due to systolic compression.1 It is most commonly seen in the middle segment of the left anterior descending artery (LAD)2-6; however, there are reports about involvement of the right or circumflex coronary artery and their branches.4,6,7 Myocardial bridging is often an incidental finding in adults with the incidence of 0.5% to 1.6% in the general population. Its occurrence may increase up to 30% to 50% of adults who have hypertrophic obstructive cardiomyopathy (HCM), and MB in children is very rare, and the incidence in both normal children and those with HCM is unknown.3 Although clinical significance of isolated MB is controversial, it may be associated with a higher incidence of sudden cardiac death, ventricular tachycardia, and perfusion defects on thallium scintigraphy in adults with HCM.8 Myocardial bridging in children is almost always associated with HCM or with the conditions that cause left ventricular hypertrophy, such as aortic stenosis, but the reports are worrying about the significance of MB for the increased risk of adverse events in childhood.3,5 Here, we describe a symptomatic patient who had obstructive HCM with MB on the LAD and his surgical management.
over the left lower sternal border. Laboratory workup was normal. The electrocardiogram (ECG) on admission demonstrated normal sinus rhythm and left ventricular hypertrophy. There were nonspecific ST-T wave changes in the anterolateral leads. Transthoracic echocardiography showed HCM with severe obstruction of the left ventricular outflow tract and moderate mitral insufficiency with systolic anterior motion, normal fractional shortening. The peak gradient was 119 mm Hg, and the mean gradient was 59 mm Hg. The systolic muscular ventricular septum width was measured 30 mm. Due to the chest pain and suspected ischemic changes in ECG, thallium scintigraphy was performed. Thallium scintigraphy showed severe dipyridamole-induced ST-segment depression and reversible perfusion defects in the anterior wall. Based on these findings,
Case Report
Corresponding Author: Okan Yildiz, Department of Pediatric Cardiovascular Surgery, Istanbul Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, _Istasyon Mah. Turgut O ¨ zal Bulvarı No: 11 Ku¨c¸u¨kc¸ekmece, Istanbul 34303, Turkey. Email: [email protected]
An 11-year-old male presented with nonspecific chest pain, fatigue on exertion, and palpitations. Physical examination revealed a grade III/VI harsh long systolic murmur heard best
1 Department of Pediatric Cardiovascular Surgery, Istanbul Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Istanbul, Turkey 2 Department of Pediatric Cardiology, Istanbul Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Istanbul, Turkey 3 Department of Anesthesiology and Reanimation, Istanbul Mehmet Akif Ersoy Thoracic & Cardiovascular Surgery Training and Research Hospital, Istanbul, Turkey
612
World Journal for Pediatric and Congenital Heart Surgery 5(4)
Figure 1. A, Coronary angiography during diastole. B, Compression of the mid-left anterior descending artery during systole (arrow).
Abbreviations and Acronyms ECG HCM LAD LV MB QTc
electrocardiogram hypertrophic obstructive cardiomyopathy left anterior descending artery left ventricle Myocardial bridging corrected QT
the patient underwent cardiac catheterization, which demonstrated a gradient across the outflow tract of 103 mm Hg and revealed MB at the mid-segment of the LAD with a positive milking effect of approximately 95% systolic compression (Figure 1A, 1B). The patient underwent open heart operation under moderate hypothermia. After cardioplegic arrest with isothermic blood cardioplegia, aortotomy was done. Extensive myectomy was applied in addition to Morrow procedure (Figure 2). After closure of the aortotomy, distal end of the LAD was visualized. Myocardial bridging site was identified, and constricting muscle bundles were incised from distal to proximal segment of the LAD, until full visualization of the artery. The thickness of the muscular bridge was significantly greater than we had predicted from its angiographic appearance. Its length was approximately 4 cm, and its thickness was 8 mm (Figure 3). We performed suture fixation of the divided bridge edges on adjacent tissue to draw them back from the LAD. A small inadvertent entry into the right ventricle during surgical unroofing of the myocardial bridge occurred, and we repaired this with a single 7/0 polypropylene mattress suture with pericardial pledged. Cardiopulmonary bypass time and cross-clamp time were 152 and 101 minutes, respectively. The patient’s postoperative course was uneventful, and he was discharged from the hospital seven days after surgery. Control echocardiography in early postoperative period and two months later revealed normal left ventricular function and maximum 30 mm Hg gradient across
Figure 2. Intraoperative view reveals extensive myectomy material.
the left ventricle (LV) outflow tract. The patient remained symptom-free six months postoperatively.
Comment Myocardial bridging occurs when the epicardial coronary arteries are intramyocardial, resulting in systolic compression of a coronary artery on coronary angiography.4 Also reported is persistence of coronary artery compression through 50% of diastole in children.3 The high incidence of MB in patients with HCM is higher than normal population, but it is not certain
Yildiz et al
Figure 3. Intraoperative view reveals mid-left anterior descending artery after surgical unroofing (arrow).
whether the MB is congenital or acquired and what factors are linked to the development of bridging.8 Hypertrophic obstructive cardiomyopathy is the leading cause of sudden cardiac death in young patients, and the association of myocardial ischemia with sudden death has been recognized in patients with HCM.8 The cause of ischemia may be intramural abnormalities of the small vessels, abnormal myocellular architecture, or massive hypertrophy. The role of MB in ischemia is controversial. The prolongation of systolic compression by MB into diastole, when the largest proportion of coronary blood flow normally occurs, might be the cause of myocardial ischemia. This prolongation may have a greater effect in young children because the heart rate is faster and the diastolic filling time is shorter, especially during exercise.8 There is an ongoing debate whether hypertrophic cardiomyopathy-associated MB is an independent risk factor for ischemia and sudden cardiac death in children or simply an indicator of the severity of left ventricular hypertrophy.9 A study of 36 pediatric patients with HCM showed evidence that significant MB of the LAD is characterized by greater than 90% systolic compression of the middle third of the LAD with ongoing compression during a mean of 50% of diastole.3 A similar study reviewed the angiograms of 57 children with HCM for the presence of coronary artery compression. Their findings suggested that coronary compression did not make an important contribution to the myocardial ischemia in HCM; however, left ventricular hypertrophy and compression of intramural arteries might contribute significantly. Still, small series and case reports have offered compelling evidence for an association of MB and sudden death or myocardial infarction in children and young adults1,10,11 A study of five patients with MB has reported alleviation of cardiac ischemia and
613 symptoms through surgical relief of MB.12 Supracoronary myotomy may result in injury of the ventricular wall and coronary arteries and subsequent danger of opening the right ventricle and LV, ventricular aneurysm formation, or subsequent scar formation with recurrent extrinsic compression.13 Potential advantages of supra-arterial myotomy are increased coronary flow rate, which results in an increased myocardial perfusion, and a decreased rate of fatal arrhythmia incidence, especially when the response to medical therapy is suboptimal. Although some complications still exist, supra-arterial myotomy is the gold standard in the surgical treatment of MB. The challenges that we are facing are to determine whether the symptoms are caused by MB in symptomatic patients and to identify the patients who are at increased risk of complications. Usually, the diagnosis is established by chance in patients who are examined by coronary angiography or computerized tomography angiography for various reasons but not because they are suspected of having MB.8 Echocardiographic features are associated with the severity of the disease or with its complications but not with MB.3 On the other hand, LV wall thickness at the proximal interventricular septum, and the degree of asymmetrical septal hypertrophy are significantly greater in children with bridging. Furthermore, the association between LV outflow tract obstruction and bridging is further demonstrated by significantly higher LV systolic pressure in affected children.6 For all these reasons, indications for the visualization of the coronary arteries should be extensive, either by coronary angiography or by computerized tomography angiography. These should be performed for the patients with left ventricular outflow obstruction and symptoms like angina, syncope, and cardiac arrest and for the assessment of the children considered to be at high risk of sudden death (ventricular tachycardia, increased degree of corrected QT (QTc) dispersion on the ECG, or abnormal blood pressure response during exercise).3,6 We conclude that significant MB of the LAD may be an important and treatable cause of myocardial ischemia and sudden death in selected children with hypertrophic cardiomyopathy. Coronary angiography provides valuable information about children with hypertrophic cardiomyopathy who have angina, an abnormal blood pressure response during exercise, an increased degree of QTc dispersion on the ECG, ventricular tachycardia, or who have been resuscitated after cardiac arrest. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
References 1. Hillman ND, Mavroudis C, Backer CL, Duffy CE. Supraarterial decompression myotomy for myocardial bridging in a child [case reports]. Ann Thorac Surg. 1999;68(1): 244-246.
614 2. Kalaria VG, Koradia N, Breall JA. Myocardial bridge: a clinical review [review]. Catheter Cardiovasc Interv. 2002;57(4): 552-556. 3. Yetman AT, McCrindle BW, MacDonald C, Freedom RM, Gow R. Myocardial bridging in children with hypertrophic cardiomyopathy—a risk factor for sudden death. N Engl J Med. 1998; 339(17): 1201-1209. 4. Sorajja P, Ommen SR, Nishimura RA, Gersh BJ, Tajik AJ, Holmes DR. Myocardial bridging in adult patients with hypertrophic cardiomyopathy. J Am Coll Cardiol. 2003;42(5): 889-894. 5. Basso C, Thiene G, Mackey-Bojack S, Frigo AC, Corrado D, Maron BJ. Myocardial bridging, a frequent component of the hypertrophic cardiomyopathy phenotype, lacks systematic association with sudden cardiac death. Eur Heart J. 2009;30(13): 1627-1634. 6. Mohiddin SA, Begley D, Shih J, Fananapazir L. Myocardial bridging does not predict sudden death in children with hypertrophic cardiomyopathy but is associated with more severe cardiac disease. J Am Coll Cardiol. 2000;36(7): 2270-2278. 7. Vongpatanasin W, Willard JE, Hillis LD, Lange RA, Landau C. Acquired myocardial bridging [case report]. Am Heart J. 1997; 133(4): 463-465.
World Journal for Pediatric and Congenital Heart Surgery 5(4) 8. Bruschke AV, Veltman CE, de Graaf MA, Vliegen HW. Myocardial bridging: what have we learned in the past and will new diagnostic modalities provide new insights? Neth Heart J. 2013;21(1): 6-13. 9. Daana M, Wexler I, Milgalter E, Rein AJ, Perles Z. Symptomatic myocardial bridging in a child without hypertrophic cardiomyopathy [case report]. Pediatrics. 2006;117(2): e333-e335. 10. Morales AR, Romanelli R, Boucek RJ. The mural left anterior descending coronary artery, strenuous exercise and sudden death [case report]. Circulation. 1980;62(2): 230-237. 11. Basso C, Corrado D, Thiene G. Cardiovascular causes of sudden death in young individuals including athletes. Cardiol Rev. 1999; 7(3): 127-135. 12. Downar J, Williams WG, McDonald C, Wigle ED, McCrindle BW. Outcomes after ‘‘unroofing’’ of a myocardial bridge of the left anterior descending coronary artery in children with hypertrophic cardiomyopathy [case report]. Pediatr Cardiol. 2004; 25(4): 390-393. 13. Pratt JW, Michler RE, Pala J, Brown DA. Minimally invasive coronary artery bypass grafting for myocardial muscle bridging [case report]. Heart Surg Forum. 1999;2(3): 250-253.
