Bridge of the left anterior descending artery revealed by syncope: a case report

The myocardial bridge is a congenital coronary anomaly defined as the presence of a region of myocardium overlying an epicardial coronary artery. This is a 51-year-old patient, diabetic for 4 years on oral hypoglycemic, has had stress angina for 4 years, neglected by the patient. The current history goes back to 2 months by the installation of an episode of syncope occurring with the effort, then of a second episode the day of its admission. Electrocardiogram on admission showed complete atrioventricular block with an heart rate of 32 beats per minute, the patient spontaneously recovered sinus rhythm with a heart rate of 88 beats per minute and a PR interval of 200 ms, coronary angiography was performed showing coronary arteries without stenosis with an intramyocardial bridge of the left anterior descending artery. During exercise and in the presence of a myocardial bridge on the left anterior descending artery, systolic compression leads to a decrease in flow to the septal branches, which is responsible for an alteration of the vascularization of the sub-nodal tissue with paroxysmal conduction disorders leading to syncope. Conduction disorders of ischemic origin are not always associated with atherosclerotic or thromboembolic lesions, but may also be secondary to myocardial bridges.


Introduction
The myocardial bridge is a congenital anomaly first described by Reyman in 1737, defined by the presence of an area of myocardium overlying an epicardial coronary artery.
Patients with myocardial bridges are usually asymptomatic, but this congenital anomaly may be associated with acute or chronic coronary syndromes, rhythm or conduction disorders, syncope, or even sudden death.
Treatment consists of medical, interventional, or surgical management.
This case report has been reported in line with the Surgical Case REport (SCARE 2020) criteria [1] .

Case report
A 51 years old man, diabetic for 4 years on oral hypoglycemic, without a medical history, and without a particular family history, has had stress angina for 4 years, neglected by the patient. Current history goes back 2 months by the installation of an episode of syncope occurring with the effort, then a second episode the day of its admission. The clinical examination on admission finds a conscious patient, blood pressure at 130/ 70 mmHg, bradycardia with a heart rate (HR) at 32 beats per minute, the oxygen saturation was at 96% in room air, and cardiac and pulmonary examinations were normal. A 18-leads resting electrocardiogram shows complete atrioventricular (AV) block with a HR of 32 beats per minute, (Fig. 1). The patient spontaneously recovered sinus rhythm with a HR of 88 beats per minute and a PR interval of 200 ms, without rhythm or conduction disturbances (Fig. 2). Transthoracic echocardiography was performed, showing normal global and segmental left ventricular systolic function (ejection fraction at 69%), no mitroaortic valvuloplathy, a right ventricle of normal size and systolic function (tricuspid annular plane systolic excursion: 18 mm; S wave: 0,11 m/s) with a dry pericardium. The biological checkup has shown a correct renal function with a creatinine level at HIGHLIGHTS • The myocardial bridge is a congenital coronary anomaly.
• The left anterior descending artery represents the coronary branch most prone to this anomaly. • The treatment consists of medical, interventional, or surgical management.
6 mg/l, kalemia at 3.7 mmol/l, a normal thyroid check-up with TSH us at 1.5 mUI /l, a negative troponin, a CRP at 6 mg. Other results are summarized in (Table 1). Coronary angiography was performed showing coronary arteries without stenosis (Figs. 3 and 4) with an intramyocardial bridge of the left anterior descending artery (LAD). (Fig. 5). The patient was put on a calcium channel blocker with a good evolution without recurrence of syncope over a follow-up period of 10 months. Holter electrocardiogram of control was realized objectifying a sinusal rhythm without rhythm or conduction disorder.

Discussion
The first radiological description of myocardial bridges was given by Portsmann and Iwig in 1960. Before that, Geiringer gave an autopsy description in 1951, and Reyman gave the first anatomic description in 1737 [2] . Its prevalence varies between series. It is less than 5% in angiographic series and 5-86% in autopsy series [3][4][5] . Myocardial bridges have a higher incidence in obstructive hypertrophic cardiomyopathy [4] , and are often multiple and severe. Corban et al. [5] reported that 67-98% of myocardial bridges were located in the LAD.
The myocardial bridge is a congenital coronary anomaly defined by the presence of a region of myocardium overlying the epicardial coronary arteries such that the coronary arteries have an intramyocardial pathway [6] . Contraction of the myocardium during systole results in compression of the epicardial arteries, in most cases, this systolic compression is silent [7] because coronary perfusion is diastolic. In its symptomatic form, it is manifested by acute or chronic coronary syndromes [8] , ventricular or supraventricular arrhythmias, conduction disorders suggestive of ischemic mechanisms, syncope, or even sudden death [9] .
The vascularization of the sinus node is ensured by the sinus node artery, which originates from the right coronary artery in 64% of cases, and from the left coronary artery in 36% of cases (most often from the circumflex artery) in patients with left coronary dominance [10] . The vascularization of the AV node is ensured by the AV node artery, a branch of the right coronary artery in 90% of cases, of the left coronary artery in 10% of cases [11] . Ischemic conduction disturbances are mainly seen in acute lower territory myocardial infarction, where the right coronary artery is often the culprit artery, high-grade AV block described in up to 17% of cases [12] , the majority of these cases are transient, while about 9% require a permanent pacemaker due to permanent nodal tissue damage [13] . Coronary angiography in our patient identified a coronary network without significant stenosis, which excluded atherosclerotic or thrombotic causes of the observed conduction disturbances.  Arterial vascularization of the sub-nodal conduction system is provided almost entirely by the septal branches of the LAD [14] . In the presence of a myocardial bridge over the LAD, systolic compression results in decreased flow to the septal branches, which are responsible for impaired vascularization of the subnodal tissue resulting in secondary conduction disorders.
During exercise, tachycardia shortens the diastolic filling time, increases myocardial contractility, which increases the degree of compression and prolongs the obstructive effect of the tunneled segment, resulting in reduced cardiac output on the one hand and impaired vascularization of the sub-nodal tissue on the other. This results in low cerebral blood flow and paroxysmal conduction disorders, leading to syncope on exertion [15] .
The treatment of myocardial bridging consists of medical, interventional, or surgical management. For patients with symptomatic myocardial bridges, beta-blockers are the first-line treatment in the absence of contraindications. They lower the HR and promote an increase in ventricular diastolic time and a decrease in systolic compression [16] . Calcium channel blockers are used when beta-blockers are contraindicated or when vasospasm is suspected. Percutaneous coronary intervention with stenting can be considered for symptomatic improvement, but results in a high rate of restenosis and other complications. Myotomy or coronary artery bypass grafting may be the treatment of choice in patients with symptomatic myocardial bridges resistant to medical therapy [17] .

Conclusion
Myocardial bridging is a congenital coronary anomaly characterized by an intramyocardial course of an epicardial coronary artery.
The LAD represents the coronary branch most prone to this anomaly.
Usually asymptomatic, but clinical and electrical signals reflecting disturbances of myocardial perfusion, rhythm, or conduction may occur.
Conduction disorders of ischemic origin are not always associated with atherosclerotic or thromboembolic lesions, but may also be secondary to myocardial bridges.

Ethical approval
NA.

Consent
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request

Sources of funding
No funding was received for this work. Conflicts of interest disclosure