VOLUME 16 | ISSUE 5 | SEPTEMBER 1996

Original Article Font size:

Myocardial Bridges: Their Clinical Implications and Prognostic Signs

Ibrahim Wasfy, MD, PhD; Mohamed S. Nouh, MSc Cardio, MD; Mohamed Foda, FRCS; Mostafa Alshemairi, MRCP; Ahmed Al-Seddeeki, FRCS

From King Saud University, King Khalid University Hospital, Riyadh.

How to cite this article:

I Wasfy, MS. Nouh, M Foda, M Alshemairi, A Al-Seddeeki, Myocardial Bridges: Their Clinical Implications and Prognostic Signs. 1996; 16(5): 505-508

DOI: 10.5144/0256-4947.1996.505

Abstract

Among 980 consecutive selective coronary angiograms performed, nine patients had myocardial bridges of the left anterior descending (LAD) coronary artery. The overall prevalence of myocardial bridges was 0.92%. Among these patients, three patients had coronary artery disease, while six cases were isolated myocardial muscle bridges. With respect to functional abnormality, three had grade III milking effect, three had grade II and three had grade I milking effect. The indications for coronary angiograms were typical chest pain in seven cases and atypical pain in two cases. Their clinical and laboratory investigations are presented with literature review.

Ann Saudi Med 1996;16(5):505-508.

Myocardial bridges are sections of a coronary artery, almost all the left anterior descending and/or one of its diagonal branches, which run under a strip of left ventricular muscle and dip below the epicardial surface under small areas of the myocardium: During systole, the segment of the artery surrounded by myocardium is narrowed and appears as localized stenosis. This systolic compression is defined as the "milking" effect. The key to recognizing these myocardial bridges is that the apparent localized stenosis returns to normal during diastole.¹ In 1976, Noble et al. stated that myocardial bridges with a milking effect on the proximal third of the left anterior descending artery could represent a new type of ischemic heart disease.² In 1977, Grondin et al. classified the milking effect as grade I when less than 50% of arterial narrowing occurs, grade II when it is between 50% and 75%, and grade III when it is greater than 75%.³ As early as 1951, Geiringer reported the etiology of this anatomical variant to be congenital, explaining that most of the coronary arteries have an intramyocardial course during fetal life.⁴

As suggested by Binet et al. in 1975, muscle bridges might explain some cases of sudden death occurring during strenuous exercises among athletes in whom no coronary arterial lesions are demonstrated at postmortem examination.⁵ In 1993, on an experimental basis, Campbell et al. studied similarities between dynamic elastance responsible for the left ventricular chamber and the papillary muscle of a rabbit heart. They concluded that the dynamic elements responsible for myofiber stiffness were also responsible for left ventricle chamber elastance. Furthermore, it was possible to describe and interpret dynamic chamber elastance and muscle stiffness with a common model based on the muscle-bridge theory. This model did a reasonable job of reproducing all the important features of experimentally observed left ventricular chamber elastance and muscle stiffness. Thus, dynamic homologies between chamber and muscle were established in experimental data and, in fact, this single interpretive model served equally well for both chamber elastance and muscle stiffness.^5,6

The aim of this study is to assess the prevalence of myocardial bridging of the left anterior descending coronary artery in a population of patients referred for diagnostic coronary angiography and to throw some light on the pathophysiology, clinical implications and prognosis of this disorder.

Methods

Material and Methods

Nine males, between the ages of 31 and 68 years, with a mean of 48.1 years, were studied. Seven cases suffered from typical anginal pain for a minimum of two years prior to admission, while two cases complained of atypical chest pain. All patients had been performing heavy manual work before the onset of their symptoms. Each case was admitted to the coronary care unit where chest pain relief was given, the patients were monitored and proper investigations were requested, including cardiac enzymes, which were reported to be normal in several serial estimations. Coronary angiography and left ventriculography were performed and the results were reviewed by two experienced observers.

Table 1. Milking effects of left anterior descending coronary artery.

		Angina-like chest pain		E.C.G.
Case no.	Age	Character	Duration	Baseline	Stress	Angiographic	Grading
1	37	Typical	7 years	Ant. lateral isch.	+ ve	Large muscle bridge compressing LAD (mid)	(III) 80%
2	37	Atypical	3 years	Abn. repolarization, no ischemic changes	− ve	Small muscle bridge LAD (mid)	(II) 50%
3	54	Typical	4 years	Old ant. sept. M.I.	+ ve	Muscle bridge ant. basal proximal LAD. No other abnormality	(II) 60%
4	48	Typical	2 years	Old ant. sept. M.I.	+ ve	Muscle bridge (proximal LAD)	(III) 55%
5	48	Typical	One year	Infer. lateral isch.	+ ve	Large significant muscle bridgez (LAD)	(III) 80%
6	31	Typical	4 months	Older inferior M.I.	not done	Small muscle bridge (first diagonal) 100% occlusion RCA 90% in circumflex	(II) 60%
7	31	Typical	6 months	Non-specific ST&T changes	− ve	Muscle bridge across mid-LAD	(I) 40%
8	68	Typical	5 years	1st degree AV block ST elevation (septal leads)	− ve	Small muscle bridge across mid LAD	(I) 30%
9	61	Atypical	3 months	ST changes	not done	Minor muscle bridge distal to first diagnonal	(I) 15%

Grade III milking efect (>75%), 2 cases; grade II milking effect (50%-75%), 4 cases; grade I milking effect (<50 %), 3 cases; typical angina chest pain, 7 cases; atypical chest pain, 2 cases; LAD=left anterior descending.

Results

Table 1 represents the milking effects of the left anterior descending coronary artery and its grading, clinical, ECG changes and angiographic abnormalities in the nine presented cases. Grade III milking effect (> 75%) was reported in two cases, grade II milking effect (50% to 75%) in four cases, and grade I milking effect (< 50%) was reported in three cases. Atherosclerotic coronary artery disease was diagnosed in five cases with variable risk factors, including heavy smoking in two cases, high low density lipoproteins in two cases, and in one case, the patient was treated for high uncontrolled blood pressure.

Angiographic Features

There was some variation among the individual patients in coronary angiography. These variations were related to the degree of milking effect of the LAD coronary artery, where measurement of the degree of constriction in the narrowed segment was done by visual assessment. A coronary angiogram revealed 80% systolic constriction of the LAD at the junction of the proximal and middle third in two patients with large muscle bridges (Figures 1A, B, 2A, B). Grade II systolic narrowing was seen in four cases, in two of which the narrowing occured after the first and the second diagonal branches respectively.

Grade I systolic constriction occurred due to small bridges in two cases. Other atherosclerotic changes included complete occlusion of the right coronary artery with 90% occlusion in the circumflex coronary artery in one patient. The left ventricular function was within normal limits in all cases.

Hospital Course

Patients number 1, 2, 7, 8 and 9 were taken to the operating room for routine cardiopulmonary bypass, where the muscle bridges were identified and divided. These patients had an uneventful postoperative course, while the other four cases were treated medically according to individual needs.

Discussion

The intramyocardial course of a segment of the left anterior descending coronary artery was first described in 1922 by Craincianu.⁷ This anomaly is well known to pathologists, with a 23% rate being observed at autopsy by Geiringer.⁴ Portsmann and Iwig were the first to report a radiological description of transient occlusion in a segment of LAD during systole.⁸ The importance of differentiating myocardial bridging, with its transient nature of coronary arterial narrowing, from fixed atherosclerotic stenosis was emphasized by Amplatz and Anderson in 1968.⁹ The origin of this arterial anomaly is probably congenital in light of the intramural location of the left anterior descending coronary artery during embryonic life.⁴ This congenital anomaly is important⁹ to recognize because it can be associated with ischemic symptoms. In some cases, cardiac catheterization fails to demonstrate the expected finding of coronary atherosclerosis, as muscle bridges may prevent a normal increase in coronary blood flow during tachycardia, when both systolic and diastolic coronary flow may be important.

The prevalence of myocardial bridging in the angiographic population varies from 0.5% to 1.6%.³ These percentages are confirmed by our study concerning a large series of consecutive patients undergoing selective coronary angiography, where our incidence is 0.92%. The milking effect in intramyocardial portions of LAD could be explained by the depth and length of the embedded press, by a peculiar cellular orientation of myocardial fibers or by concentric pathological hypertrophy of the surrounding muscles.^10,11 We suggest that biopsy studies taken intraoperatively during the process of dividing muscular bridges may explain the process of milking. In the presenting cases, the manifestations started to appear and develop after middle age. Noble and associates attributed manifestation delay to an increase in systolic wall tension and the acquisition of the milking effect might be secondary to gradual growth of the heart muscles, a secondary phenomenon in left ventricular hypertrophy, a localized or diffuse cardiomyopathy, or the onset of arteriosclerotic deterioration of the coronary arterial tree.^2,3

In 1985, Risse and Weiler¹² studied muscle bridges and their relation to coronary artery diseases, and found intimal thickness of 406.6 microns in the coronary artery, situated proximal to the muscle bridge, while in the region of the bridge, the intimal thickness was 66.3 microns. They concluded that the stenosis proximal to the bridge was almost completely of eccentric kind and was potentially dynamic stenosis.¹² In 1988, Voelker et al. reported a case of anterior wall infarction, and were able to demonstrate a myocardial bridge over the LAD coronary. This was the only abnormal finding in selective coronary angiography and the investigators suggested a causal relationship,¹³whereas sudden death was attributed to physical overload and strenuous exercises.^14,15

Clinical Implications and Prognostic Signs

Patients with grade III milking effect can experience severe myocardial ischemia, especially during bouts of tachycardia. The pathophysiological explanation is probably due to a shortening of the diastolic filling when the heart rate is increased above a given level.² Advising the patient to avoid strenuous exercise should be sufficient to prevent pain episodes. Beta adrenergic blocking agents could attenuate the effect of tachycardia and contractility of these patients. Two patients with grade III milking effect were sent for surgical intervention to release systolic compression facing the left anterior descending coronary artery. In 1950, Geiringer stated that when symptoms are refractory to medical therapy and when inducible ischemia has been equivocally demonstrated, coronary bypass grafting or simple unroofing of the bridged coronary artery segment resulted in normalization of myocardial perfusion and metabolism.⁴ The long-term prognosis of isolated myocardial bridges appears to be excellent, irrespective of the degree of systolic reduction of internal luminal diameter. Finally, it seems important to consider surgical dislodgment of the embedded segment of the left anterior descending coronary artery in some patients with severe symptoms, particularly when they are obliged to perform heavy work. Therefore, surgical relief may lead to subjective and objective improvement in selected patients.

References

1. Paim DS, Harrison DC. Muscle bridges. In: The Heart, 4th ed. J. D. Hurst, editor. 1982.

2. Noble J, Bourassa MG, Petitclerc R, et al. Myocardial bridging and milking effect of the LAD coronary artery: normal variant or obstruction? Am J Cardiol 1976;37:993.

3. Grondin P, Bourassa MG, Noble J, et al. Successful course after supra-arterial myotomy for myocardial bridging and milking effect of the left anterior descending artery. Ann Thorac Surg 1977;24:422-9.

4. Geiringer E. The mural coronary. Am Heart J 1951;41:259.

5. Binet JP, Piot C, Planche C, et al. Pont myocardique compriment l'artère intraventriculaire antérieure: a propos d'un cas opéré avec succès. Arch Mal Coeur 1975;68:87.

6. Campbell KB, Taheri H, Kirpatrick RD, et al. Similarities between dynamic elastance of left ventricular chamber and papillary muscle of rabbit heart. Am J Physiol 1993;254:926-41.

7. Craincianu A. Anatomische Studien über die coronararterien und experientelle untersuchungen über ihre Durchgangigkeit. Virchow's Arch Path Anat 1922;238:1-8.

8. Portsmann W, Iwig J. Die intermurale koronarie in Angiogram. Fortschr Rantgenstr 1960;92:129-32.

9. Amplatz K, Anderson R. Angiographic appearance of myocardial bridging of the coronary artery. Invest, Radiol 1968;3:213-5.

10. Razavi M. Unusual forms of coronary artery disease. Cardiovascular Clin 1975;7:25.

11. Levin DC, Fellows KE, Abrams HL. Hemodynamically significant primary anomalies of the coronary arteries, angiographic aspects. Circulation 1979;58:25.

12. Risse M, Weiler G. Coronary muscle bridge and its relation to local coronary sclerosis, regional myocardial ischemia and coronary spasm. A morphometric study. Z Kardiol 1985;74:700-5.

13. Voelker W, Ickrath O, Mauser M, et al. Anterior wall infarct in an angiographically demonstrated muscle bridge of the ramus interventricularis anterior. Dysch-Med-Wochenschr 1988;113:551-4.

14. Liasauskaite VV. A case of sudden death from a muscle bridge spanning the anterior interventricular branch of the left coronary artery. Arkh-Patol 1988;50:67-9.

15. Chiappa E, Vineis C. Sudden death during a game of soccer in a young adolescent with a myocardial muscle bridge. G-Ital-Cardiol 1993;23:473-7.