Discussion

Coronary arteries and their major branches lie on the surface of the heart. When a band of myocardial muscle fibres overlies a segment of the coronary artery, which results in mechanical stenosis secondary to systolic compression, a condition termed as myocardial bridging occurs. The incidence of myocardial bridging in the general population is between <5% and 86% in different series, according to the method used to determine the bridging.Reference Mohlenkamp, Hort Wge and Erbel ⁵ Such a wide discrepancy suggests that only a minority of patients with myocardial bridging are in fact at risk of clinical symptoms and cardiac events.

Myocardial bridging is usually seen in the setting of hypertrophic cardiomyopathy or left ventricular hypertrophy and is rarely reported in an otherwise structurally normal heart. The incidence of myocardial bridging among children with hypertrophic cardiomyopathy on coronary angiography varies between 28% and 40%.Reference Yetman, McCrindle, McDonald, Freedom and Gow ^{1 ,} Reference Mohiddin, Begley, Shih and Fananapazir ⁶ As selective coronary angiography is not a routine procedure for children, the exact incidence of myocardial bridging among healthy children and patients, other than those having hypertrophic cardiomyopathy, is not known. Yet, symptomatic myocardial bridging probably occurs in a small subgroup of children, in whom ischaemic symptoms can be linked directly to their myocardial bridging. Sharma reported symptomatic myocardial bridgings in children. All patients included his study had significant symptoms of chest pain or syncope with exertion or cardiac arrest, supported by the evidence of coronary ischaemia linked to myocardial bridging, which ultimately resolved after mechanical decompression in short-term follow-up. Further, all his patients had hypertrophic cardiomyopathy or left ventricle hypertrophy, in contradistinction to our patient.Reference Sharma, Hellenbrand, Kleinman and Mosca ⁷

Myocardial bridgings are most commonly located over the middle segment of the left anterior descending coronary artery and may occasionally involve the diagonal branches, the posterior descending right coronary artery, and the marginal branch of the circumflex artery.Reference Bourassa, Butriaru, Lesperance and Tardif ³ In our patient, two different parts of the left anterior descending artery followed an intramural course, causing a 70–80% and 100% narrowing during systole, respectively. Over 90% systolic compression of the tunnelled coronary segment with an ongoing diastolic compression of at least 50% characterises a significant myocardial bridging, as was seen in our case.Reference Mohlenkamp, Hort Wge and Erbel ⁵ It is surprising that our patient never displayed symptoms, even during tremendous exercise.

Discrete subaortic stenosis can be seen in different members of the same family. The genetic basis of this disease is still indefinite. Some authors propose an autosomal recessive condition, whereas others propose an autosomal dominant inheritance pattern.Reference Petsas, Anastassiades, Constantinou and Antonopoulos ⁸ A multi-factorial model of inheritance, in association with environmental factors, may be involved in the pathogenesis. A familial incidence of discrete subaortic stenosis, although very rare, signifies the screening of family members.Reference Fatimi, Ahman, Javed, Shamim and Ahmad ⁹ In our case, three members of the same family had mild subaortic stenosis.

Myocardial bridging is usually a benign condition with a long-term survival but can also cause myocardial ischaemia, myocardial infarction, exercise-induced tachycardia, conduction disturbances, and sudden death. Our patient was symptom-free in her daily life but had ischaemic findings during the exercise stress test. We estimate that her brother who died suddenly during exercise also had myocardial bridging with discrete subaortic stenosis. Therefore, we recommended her elderly brother to undergo coronary angiography, although he is asymptomatic.

In patients with myocardial bridging, medical or surgical management remains controversial. To date, however, there is no convincing evidence that surgery improves morbidity or mortality in patients with bridging.Reference Downar, Williams, McDonald, Wigle and McCrindle ¹⁰ Nitrates, β-blockers, and calcium channel blockers could be used for symptomatic relief. Surgery could be the choice for severe cases. Although our patient was asymptomatic but had a myocardial bridging segment of 100% narrowing, surgical decompression was performed. After surgery, she remained asymptomatic, and the signs of ischaemia on the exercise test resolved.

Our case is different from those reported in the literature, as our patient had neither left ventricular hypertrophy nor hypertrophic cardiomyopathy on echocardiography but had severe myocardial bridging on angiography. This case is also unique as the myocardial bridging was concomitant with familial subaortic stenosis.