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. 2006 Jul;209(1):43–50. doi: 10.1111/j.1469-7580.2006.00590.x

The relationship of myocardial bridges to coronary artery dominance in the adult human heart

Marios Loukas 1,2, Brian Curry 1, Maggi Bowers 1, Robert G Louis Jr 3, Artur Bartczak 4, Miroslaw Kiedrowski 4, Michal Kamionek 4, Martin Fudalej 5, Teresa Wagner 4
PMCID: PMC2100301  PMID: 16822268

Abstract

Myocardial bridging is recognized as an anatomical variation of the human coronary circulation in which an epicardial artery lies in the myocardium for part of its course. Thus, the vessel is ‘bridged’ by myocardium. The anterior interventricular branch of the left coronary artery has been reported as the most common site of myocardial bridges but other locations have been reported. The purpose of this study was to provide more definitive information on the vessels with myocardial bridges, the length and depth of the bridged segment, and the relationship between the presence of bridges and coronary dominance. Two hundred formalin-fixed human hearts were examined. Myocardial bridges were found in 69 (34.5%) of the hearts with a total of 81 bridges. One bridge was found in 59 of these hearts and multiple bridges were observed in ten (eight with double bridges and two with triple bridges). Bridges were most often found over the anterior interventricular artery (35 hearts). Bridges were also found over the diagonal branch of the left coronary artery (14), over the left marginal branch (five) and over the inferior interventricular branch of the left coronary artery (six). Bridges were also found over the right coronary artery (15 hearts), over the right marginal branch (four) and over the inferior interventricular branch of the right coronary artery (two). The presence of bridges appeared to be related to coronary dominance, especially in the left coronary circulation. Forty-six (66.6%) of the hearts with bridges were left dominant. Forty-two of these had bridges over the left coronary circulation and four over the right coronary circulation. Seventeen hearts (24.6%) were right dominant. Eleven of these had bridges over the right coronary circulation and six over the left coronary circulation. The remaining six hearts were co-dominant with four having bridges over the left coronary circulation and two over the right coronary circulation. The mean length of the bridges was 31 mm and the mean depth was 12 mm. The possible clinical implications of myocardial bridging may vary from protection against atherosclerosis to systolic vessel compression and resultant myocardial ischaemia.

Keywords: anterior interventricular artery, coronary artery dominance, left coronary artery, myocardial bridges, right coronary artery

Introduction

A segment of an epicardial artery that has an intramural course within the myocardium (Geiringer, 1951; Noble et al. 1976; Ishimori et al. 1977; Ge et al. 1994), or a segment of an epicardial artery that is surrounded by muscular fibres or a band of myocardial tissue (Tangkawattana et al. 1997; Ozbag & Hatipoglu, 2002), is variously described as a myocardial bridge, an intramural coronary artery, a mural coronary artery and a tunnelled artery (Angelini et al. 1983, 1999; Bourasa et al. 2003). Myocardial bridges were first described by Rayman (1737) and then by Black (1805). The first post-mortem examination of myocardial bridges was performed by Geiringer (1951) and was followed by the first radiological description by Portman & Ingrid (1960).

During the last century, many investigators reported myocardial bridges in the adult human heart. The frequency of myocardial bridging varies widely. It has been reported in 15–85% of hearts (Edwards et al. 1956; Polacek, 1961; Ferreira et al. 1991; Ge et al. 1994) as found on autopsy and in 0.5–2.5% of hearts (Noble et al. 1976; Ishimori et al. 1977; Ge et al. 1994) as demonstrated by radiography.

Descriptions of myocardial bridges have discussed the length of the intramural segment, the coronary artery involved and the possible clinical consequences of the bridges (Lee & Ting, 1972; Bezerra et al. 1987; Kosinski & Grzybiak, 2001). The anterior interventricular branch of the left coronary artery has been the vessel most commonly bridged (Ishii & Hosoda, 1986; Vidal et al. 1988; Bezerra et al. 1989; Ferreira et al. 1991; Morales et al. 1993). However, the relationship of coronary dominance to myocardial bridges has not yet been fully investigated.

The clinical significance of myocardial bridges is uncertain and many patients are asymptomatic (Kramer et al. 1982; Juilliere et al. 1995; Bourassa et al. 2003). It has been suggested that myocardial bridges may be a contributing factor in the development of myocardial ischaemia, circulatory problems, angina, myocardial infarction, sudden cardiac death, systolic compression and other cardiac disturbances that may require surgical intervention (Visscher et al. 1983; Vidal et al. 1988; Bezerra et al. 1989; Kuhn et al. 1991; Baptista & DiDio, 1992). Conversely, it has been proposed that myocardial bridges offer a ‘protective effect’ from atherosclerosis within the coronary artery that is bridged when compared with non-bridged vessels of the same heart (Ishii & Hosoda, 1986; Laifer & Weiner, 1991; Kosinski & Grzybiak, 2001). However, Laifer & Weiner (1991) reported a case in which angioplasty was used specifically for stenosis of the anterior interventricular artery within a myocardial bridge.

At present, the mechanisms by which myocardial bridges induce clinical symptoms are not known. In addition, methods for identification and treatment of significant myocardial bridging have not been widely established (Smith et al. 1997; Angelini, 2003; Bourassa et al. 2003). The focus of this study was therefore to offer a more complete description of the location of myocardial bridges in the adult human heart and the relationship between bridges and coronary artery dominance.

Materials and methods

Two hundred adult human hearts, collected from autopsies performed at the Department of Pathology at the Institute of Rheumatology, Warsaw, and at the Department of Forensic Medicine at Warsaw Medical University, during the period 1999–2003, were used. The hearts were from 82 females and 118 males who had died from non-cardiovascular causes. The mean age at death was 63 years (range 21–76 years). The specimens had been fixed in 4% formalin PBS solution. Following preliminary examination, the perivascular fatty tissue was carefully removed, where necessary, to visualize the epicardial course of the coronary arteries.

Images from the dissected specimens were recorded with a Sony Cyber-Shot DSC-f717 digital camera and studied using a computer-assisted image analysis system [all measurements were carried out with the Lucia program (1998 edition for Windows), developed by Nikon (Laboratory Imaging Ltd, Precoptic Co., Medical and Optical Instruments, Poland)]. The digital camera was connected to an image processor (Nvidia Riva TNT model 64) that was linked to a mainframe computer. Digitized images of the coronary arteries, as well as the surrounding myocardial segment of the myocardial bridges, were stored in the Lucia program (1152 × 864 pixels) and converted to intensity grey levels from 0 (darkest) to 32 bit (lightest). After applying a standard 1-mm scale to all images, the program was able to calculate pixel differences between two selected points. The software allowed accurate translation of pixel differences into metric measurements as previously described (Loukas et al. 2005).

Once a myocardial bridge had been identified, it was removed en block from the specimen and photographed with the Sony digital camera. The length of the bridge and the depth to which the coronary artery penetrated the myocardium was measured. All measurements were carried out with the Lucia program. The nomenclature for the coronary arteries used in this study is that proposed by Anderson et al. (2004). The reason for this is the need for cardiac anatomists to follow the ‘rules’ of anatomy, and describe the heart as it lies in the body, not in ‘Valentine’ fashion.

Results

A total of 81 myocardial bridges were found in 69 (34.5%) of the 200 examined hearts. Myocardial bridges were found more frequently in male (59, 85.5%) than in female (ten, 14.5%) hearts. In addition, the coronary dominance of the 69 hearts with bridges, as well as the intramural course, was examined. Based on the findings, a classification system was developed to define the results based upon the artery bridged, the prevalence of myocardial bridges over that artery, the coronary dominance and the degree of myocardial bridge thickening (Tables 1 and 2).

Table 1.

Classification of myocardial bridges according to location and the relationship to gender, thickness and length of myocardial bridge segment

Location No. of myocardial bridges % Male/Female Mean thickness of myocardial bridge (depth, mm) Mean length of myocardial bridge (mm)
Anterior descending artery (ADA) 35 43.2 29/6 12 32
Diagonal branch of (LCA) 14 17.2 11/3 11 30
Marginal branch of LCA 6 7.4  6/0 12 31
Inferior descending artery of LCA 5 6.1  5/0 10 29
Right coronary artery (RCA) 15 18.5 13/2 13 33
Acute marginal branch of RCA 4 4.9  3/1 12 32
Inferior descending artery of RCA 2 2.4  2/0 12 32
Total 81 100% 69/12 12 31
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Table 2.

Summary of the percentages and number of specimens with regard to coronary dominance in myocardial bridged coronary arteries (n = 69)

No. of specimens with: Bridged left coronary arterial circulation Bridged right coronary arterial circulation
Right coronary dominance 17 (24.6%)  6 (8.6%) 11 (15.9%)
Left coronary dominance 46 (66.6%) 42 (60.8%)  4 (5.8%)
Co-dominance  6 (8.7%)  4 (5.7)  2 (2.9%)
Total 69 (100%) 52 (75.3%) 17 (24.6%)
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The most common location of myocardial bridges was over the anterior interventricular branch of the left coronary artery, found in 35 (43.2%) of the hearts (Figs 1 and 2). Bridges were found over the diagonal branch of the left coronary artery (Fig. 3) in 14 hearts (17.2%), over the left marginal branch in six hearts (7.4%) and over the inferior interventricular (posterior interventricular) branch of the left coronary artery in five hearts (6.1%). Bridging was also observed over the right coronary artery in 15 hearts (18.5%) (Fig. 4), over the right marginal branch in four hearts (4.9%) and over the inferior interventricular branch of the right coronary artery in two hearts (2.4%) (Fig. 5).

Fig. 1.

Fig. 1

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A myocardial bridge covering a large portion of the distal left anterior descending artery of the left coronary artery (LCA).

Fig. 2.

Fig. 2

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A myocardial bridge covering a small portion of the proximal left anterior descending artery of the left coronary artery (LCA).

Fig. 3.

Fig. 3

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Two different myocardial bridges over the diagonal artery illustrating variations in the depth of bridging.

Fig. 4.

Fig. 4

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A myocardial bridge over the right coronary artery (RA, right atrium; RV, right ventricle).

Fig. 5.

Fig. 5

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A myocardial bridge covering a large portion of the inferior interventricular coronary artery. In this case the inferior interventricular artery is a branch of the right coronary artery revealing right coronary heart dominance (LV, left ventricle; RV, right ventricle).

The presence of only one myocardial bridge was noted in 59 (85.5%) hearts but multiple bridges were observed in ten (14.5%). Of these ten specimens there were eight with two bridges, two with three bridges, and two or more bridges were found over the same vessel in six of these hearts (four double and two triple). The vessel that most often had multiple bridges was the anterior interventricular branch of the left coronary artery.

The coronary dominance of all of the hearts in the study was as follows: 110 (55%) were right dominant, 66 (33%) left dominant and 24 (12%) co-dominant. Forty-six (66.6%) of the hearts with bridges were left dominant. Forty-two of these hearts had myocardial bridges over the left coronary circulation and four had bridges over the right coronary circulation. Seventeen hearts (24.6%) exhibited right dominance. Eleven of these hearts had bridges over the right coronary circulation and six over the left coronary circulation. Of the co-dominant hearts (6, 8.6%), four had bridges over the left coronary circulation and two over the right coronary circulation. Table 2 summarizes our findings for coronary dominance in association with myocardial bridges.

The length of the myocardial bridges ranged from 12 to 49.5 mm, with a mean of 31 mm. The thickness of the bridges ranged from 5 to 27 mm, with a mean of 12 mm (Table 1). Seventy-four of the coronary arteries (91.3%) exhibited an intramural course within the myocardium and were classified as deep myocardial bridges. However, in seven (8.6%) of the specimens the coronary arteries did not exhibit an intramural course; rather, the myocardial tissue extended over the coronary artery and was thus classified as superficial. All of the superficial myocardial bridges were found to be located over the anterior interventricular branch of the left coronary artery. No differences in prevalence, length, thickness or location were observed with regard to age or ethnicity.

Discussion

Interest in myocardial bridges began to emerge when their presence was observed in a large number of cases and theories were developed on the potential protective, or detrimental, effect that these bridges might have on various cardiac conditions. The results of the current study show that myocardial bridges occur most frequently over the anterior interventricular branch of the left coronary artery, in agreement with the results of the majority of earlier studies (Ishii & Hosoda, 1986; Bezerra et al. 1987; Ferreira et al. 1991; Morales et al. 1993; Virmani & Farb, 1993) (Table 3).

Table 3.

Summary of percentages of the single type myocardial bridge locations of past studies

Type of single myocardial bridge (location)
Author/date/Total no. of specimens Anterior descending artery Diagonal branch of left coronary artery (LCA) Marginal branch of LCA Inferior descending artery of LCA Right coronary artery (RCA) Acute marginal branch of RCA Inferior descending artery of RCA
Baptista/1992/82 35.4 3.6 7.3 – – – 6.1
Bezzera/1987/50 52.0 8.0 14.0 2.0 12.0 2.0 2.0
Bezzera/1989/90 – – – – – 1.1 –
Ciampricotti/1988/1 100.0 – – – – – –
Ferreira/1991/90 38.8 – – – – – –
Ishii/1986/642 642 – – – – – –
Kosinski/2001/100 33.0 5.0 3.0 – – 1.0 4.0
Kuhn/1991/2 100.0 – – – – – –
Laifer/1991/1 100.0 – – – – – –
Morales/1993/39 100.0 – – – – – –
Vidal/1988/12 100.0 – – – – – –
Virmani/1993/690 1.3 – – – – – –
Visscher/1983/1 100.0 – – – – – –
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The current study found that the next most common sites of myocardial bridges were over the right coronary artery (18.5%), the diagonal branch of the left coronary artery (17.2%), the left marginal branch (7.4%) and the inferior interventricular branch of the left coronary artery (6.1%). However, whereas Kosinski & Grzybiak (2001) reported the anterior interventricular branch as the most common site for bridges in a study of 100 specimens, he also reported that the diagonal branch of the left coronary artery was the second most common site and the inferior interventricular branch of the right coronary artery the third most common.

A comprehensive study was performed by Morales et al. (1993) on 39 human hearts that all had myocardial bridges over the anterior interventricular artery. Bridging was also reported over the inferior interventricular branch of 33%, and over the first diagonal branch of the left coronary artery of 18%, of the hearts. These findings are similar to those of Baptista & DiDio (1992) who, in 82 specimens, found myocardial bridges over the anterior interventricular artery in 35.4% of the specimens and over the inferior interventricular branch in 6.1% of the specimens. These results are similar to those of the current study. However, none of the authors explored the relationship of coronary artery dominance to myocardial bridges.

Multiple myocardial bridges occurring in a single heart have been observed in a number of studies. Kosinski & Grzybiak (2001) reported one myocardial bridge in 24% of cases, two bridges over the same vessel in 4% of cases and two myocardial bridges over different vessels in 2% of cases. These findings are similar to the results of the current study.

An interesting finding was the occurrence of myocardial bridging over vessels of the left coronary circulation in hearts with left coronary dominance. Despite the fact that the overall pattern of coronary dominance in the 200 hearts examined was very similar to that reported in previous studies (James & Burch, 1958; James, 1960; Effler et al. 1967), the hearts with bridges expressed a very different pattern. Forty-six of the 70 hearts with bridges had left dominance and 42 of these had bridges over the left coronary circulation. Only 17 of the hearts with bridges were right dominant and, although 11 of these hearts had bridges over the right coronary circulation, six had bridges over the left circulation. Of the co-dominant hearts, five had bridges over the left, and two over the right, coronary circulation. According to these results, the location of myocardial bridges is closely associated with coronary dominance. This association is suggestive of a developmental pattern between left coronary dominance and myocardial bridges over the left coronary circulation.

It is important to note that one-third of the specimens examined had left coronary arterial dominance. This is rather unusual; it is generally considered that only one-tenth of the population has left coronary arterial dominance. Clinically, this may suggest that bridges could be less frequent in populations with the more usual spread of arterial dominance.

There is still debate concerning symptomatic vs. non-symptomatic myocardial bridges (Endo et al. 1978; Feldman et al. 1978; Morales et al. 1993; Kramer et al. 1982; Angelini et al. 1983; Bestetti et al. 1989; Ramos et al. 1993; Juilliere et al. 1995). It remains to be determined whether the superficial (non-intramural) or the deep (intramural) segment of a bridged artery is responsible for clinical signs. According to Ferreira et al. (1991), the location and orientation of the muscle fibre bundles over the embedded artery may affect systolic compression. It has been hypothesized that the superficial variant may not constrict the bridged artery during systole; however, the deep variant, because of its relation with the anterior interventricular branch of the left coronary artery, could twist the artery, thus compromising its diastolic flow and producing ischaemia.

Left ventricular hypertrophy, hypertrophic cardiomyopathy and aortic stenosis have been shown to be associated with symptomatic myocardial bridges. The clinical symptoms may be explained by a progressive increase in left ventricular wall tension and compression of the affected artery (Noble et al. 1976; Morales et al. 1993; Bestetti et al. 1989). The correlation between a patient, whether symptomatic or asymptomatic, and the presence of myocardial bridging over the left coronary circulation in conjunction with left coronary dominance has yet to be established.

Some reports attribute the clinical symptoms of myocardial bridges to their extensive length (Kramer et al. 1982; Angelini et al. 1983; Juilliere et al. 1995). Both angiography and autopsy reports have shown that the length of myocardial bridges varies widely from 4 to 40 mm, which is similar to the current findings (Polacek, 1961; Hansen, 1982; Ishii & Hosoda, 1986; Ferreira et al. 1991). It has been shown experimentally that the length of coronary arterial narrowing markedly influences coronary haemodynamics (Feldman et al. 1978). This may explain why relatively long bridges are observed in symptomatic patients (Bourasa et al. 2003).

Perhaps the most intriguing aspect of myocardial bridges concerns the positive or negative clinical correlation with regard to the degree of atherosclerosis. Do myocardial bridges offer a ‘protective effect’ upon the particular cardiac vessel covered by the muscle fibres or are they actually a contributing factor in the development of cardiac disorders? Many researchers believe that the presence of a myocardial bridge over a particular coronary artery will result in decreased atherosclerotic thickening of the tunica intima of that vessel (Geiringer, 1951; Angelini et al. 1983; Ishii & Hosoda, 1986; Ferreira et al. 1991). Recent studies have confirmed the absence of atherosclerotic changes in the bridged segment of the artery and in the segment distal to the bridge (Angelini et al. 1983; Geiringer, 1951; Ishii & Hosoda, 1986; Ferreira et al. 1991). However, the mechanisms responsible for this selective protection are unknown.

In contrast to the above reports supporting the protective effect of myocardial bridges, a number of studies have related the presence of myocardial bridges to the development of atherosclerosis (Angelini et al. 2002; Angelini, 2003). The suggested mechanisms for the development of atherosclerosis, as well as myocardial ischaemia, largely stem from recent available techniques in cardiac catheterization such as intravascular ultrasound and intracoronary Doppler (Bourasa et al. 2003). The bridged artery is characterized by phasic systolic compression, persistent diastolic lumen diameter reduction, increased blood flow velocities, retrograde systolic flow and reduced coronary flow reserve (Bourasa et al. 2003). It remains to be proved experimentally whether these factors result from myocardial bridging rather than being an associated effect.

However, it has been proposed that systolic compression may increase the trauma sustained by the intima proximal to the bridge (Polacek, 1961; Ishii & Hosoda, 1986; Ge et al. 1994). Two studies using intravascular ultrasound reported that the segments proximal to the bridge were atherosclerotic in 86% of the patients (Ge et al. 1994), while significant stenosis was observed in 17.3% of the patients who were subsequently treated with percutaneous coronary intervention (Ge et al. 1999).

Similarly, suggested theories for the aggressive development of atherosclerosis are vasospastic coronary compression and endothelial damage. Both factors are postulated to stimulate a cascade reaction, which eventually will lead to platelet aggregation and coronary vasospasm (Kuhn et al. 1991). The clinical relevance of myocardial bridges in this situation clearly depends on the degree and location of coronary artery occlusion. Obstructing blood flow to the first septal perforating artery, which is responsible for the supply of the AV node and bundle of His, or to the AV nodal artery, could prove fatal. There have been reports in the literature of sudden cardiac death and the coexistence of myocardial bridges over the anterior interventricular artery, as well as the right coronary artery (Yetman et al. 1998; Akdemir et al. 2002; Arjomand et al. 2002).

Symptomatic myocardial bridges are treated with coronary stent placement. However, a study by Haagen et al. (2000) reported that the placement of stents in patients with myocardial bridges leads to restenosis in 46% of the cases, as shown by angiography 7 weeks after the procedure. Angelini et al. (2002) suggested that the mechanism responsible for re-stenosis is intimal fibrocellular growth in addition to phasically active collapsing forces generated by the myocardial bridges.

Myocardial bridging is an attractive and intriguing area of research and should remain the focus for future studies. It is hoped that this study will contribute to the existing body of knowledge of myocardial bridges and their role in the pathophysiology of atherosclerosis.

Acknowledgments

We would like to thank Professor Anderson for his constructive criticism and invaluable comments. His help and expertise were crucial to the publication of this study.

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