Pediatr Cardiol 11:186-190, 1990
Pediatric Cardiology 9 Springer-Verlag New York Inc. 1990
Morphometric Analysis of Myocardial Bridges in Children with Ventricular Hypertrophy J. R e i g , I C. Ruiz de M i g u e l , 2 and A. Moragas L2 mDepartment of Morphological Sciences, School of Medicine, Autonomous University of Bareclona, Bellaterra (Barcelona); and 2Department of Pathology, "Vall d'Hebrrn" Hospital and Docent Unit, Barcelona, Spain
SUMMARY. The nuclear cross-sectional area of the muscular fibers from a series of myocardial bridges was analyzed and compared to both the adjacent and underlying myocardial fibers. The series came from 12 hearts of children, ranging in age from 24 h to 2 years, with diverse forms of congenital heart disease, which caused left ventricular hypertrophy and had a myocardial bridge in the path of the anterior interventricular coronary artery. The cross-sectional areas of myocardial nuclei were measured for the bridging myocardial fibers, the adjacent myocardium, and the myocardial fibers underlying the bridged coronary artery. A significant statistical difference between the bridging muscular fibers and those underlying the submerged artery was observed, as well as between the bridging fibers and its adjacent ones. This finding suggests that myocardial bridges not only represent an anatomical abnormality, but probably imply different functional behavior as well. KEY WORDS: Myocardial bridge - - Cardiac ventricular hypertrophy - - Children's hearts
The main coronary arteries show a subepicardial course that occasionally is intramyocardial (Fig. 1). This arrangement has been described with various terms, including mural coronary artery [6], submerged coronary artery [7], or, more frequently, myocardial bridges [16]. Both the frequency of myocardial bridges and their functional significance have been the object of considerable controversy in the literature, because, independently of the technique of study, the quoted frequency of myocardial bridges is notably variable [171. The interpretations of their physiopathological significance are contradictory and may in part depend on the frequency of observation. Thus, if one concedes to Pol~tcek [16], that bridges are found in 87.5% of the hearts, it could be concluded that the anomaly is not the presence of the bridges but rather their absence. The question has been proAddress offprint requests to: Dr. J. Reig, Departamento de Cien-
cias Morfol6gicas, Facultad de Medicina, Universidad Aut6noma de Barcelona, E-08193-Bellaterra (Barcelona), Spain.
Fig. 1. Myocardial bridge located above the middle third of the anterior interventricular artery (arrows).
Reig et al.: Cardiac Hypertrophy and Myocardial Bridges
187
Table 1. Characteristics of the cases in the present study Case
Sex
Age
Weight
Heart weight
% Ventricular hypertrophy
Cardiac defects
Location of the bridge
1 2 3 4 5 6 7 8 9 l0 II 12
M M M F M M M M M M F M
10 m 4d 36 d l0 d 2.5 m 1y 3m 2y 2m 10 d 35 d 24 h
9860 3600 2530 2600 3250 4650 2850
85 g 36 g 45 g 25 g 50 g 80 g 32 g 86 g 45 g 30 g 50 g 20 g
73 50 49 24 54 45 28 35 43 37 69 l0
PA, dextroposition of aorta, VSD TGV Taussig-Bing, TGV AVSD, CoA CoA, Bernheim AVSD AVSD, MA, CoA SV L-TGV, VSD CoA PA AVSD
AIV AIV AIV AIV AIV AIV PIV AIV AIV AIV AIV AIV
g g g g g g g
2500 g 1680 g 2100 g 1890 g
AIV, Anterior interventricular artery; AVSD, atrioventricular septal defect; CoA, coarctacion of the aorta; MA, mitral atresia; PA, pulmonary atresia; PIV, posterior interventricular artery; SV, single ventricle; TGV, transposition of the great vessels; VSD, ventricular septal defect; m, month; d, day; y, year.
Table 2. Means (M) and standard deviations (SD) of the nuclear areas of the myocardial fibers (p.m2) in the three measured zones Case
1 2 3 4 5 6 7 8 9 10 11 12
Zone B
Zone U
Zone L
M
SD
M
SD
M
SD
25.62 36.51 30.77 24.59 41.24 35.72 38.12 21.77 36.75 60.64 32.64 34.23
9.72 8.79 9.63 9.02 15.39 8.88 10.67 7.05 9.08 18.15 7.47 5.82
41.83 47.23 36.79 41.85 62.73 55.19 36.27 35.25 46.48 69.11 40.84 40.68
14.85 10.86 11.50 11.24 33.81 19.42 8.14 9.76 11.33 21.28 10.60 7.10
42.63 41.83 46.24 42.69 36.35 48.37 38.66 27.96 39.56 61.03 32.21 40.38
20.14 9.09 16.59 11.50 28.59 11.82 10.34 6.61 8.96 19.25 7.07 6.82
Zone B, "fibers of the myocardial bridge; zone U, fibers of myocardium underlying the submerged artery; zone L, fibers of myocardium lateral to the bridge.
posed as to what extent the presence of myocardial bridges could protect or obversely favor coronary atherosclerosis [2, 6, 7] and consequently the development of ischemia and myocardial infarction [4, 14, 15]. It is over this last point that there is a major controversy between the proponents of the socalled milking effect [15], as the cause of myocardial ischemia, and its opponents [1]. The significance of myocardial bridges in patients with ventricular hypertrophy is certainly confused. Thus, Ishimori et al. [10] found the frequency of myocardial bridges to be higher in cases of left ventricular hypertrophy. Kitazume et al. [12]
Fig. 2. Myocardial bridge above the anterior interventricular artery (transverse section). The three zones from which the samples were taken: B, zone of myocardial bridge; U, underlying myocardial zone; L, lateral zone to the bridge. Verhoff-Van Gieson stain; original magnification, • 12.
pointed out that the systolic compression due to the myocardial fibers of the bridge was more severe in patients with ventricular hypertrophy. However, survival curves do not appear to indicate an adverse effect of this feature. In the present study, we have considered myocardial bridges in relation to ventricular hypertrophy, about which there is no reference in the literature. To what extent do the morphometric characteristics of the myocardial fibers of the bridge differ from those of adjacent fibers and from those
188
Pediatric Cardiology Vol. 11, No. 4, 1990
70
2
T
3
i
I
I
B
U
L
MYOCAHUtAL
SAMPLES
Fig. 3. Nuclear areas of the myocardial fibers (B, zone of the myocardial bridge; U, underlying myocardial zone; L, lateral zone to the bridge).
Fig. 4. Light micrograph of ventricular myocardium. (A) hypertrophic heart (zone B); (B) hypertrophic heart (zone U); (C) normal heart. Hematoxylin-eosin stain; original magnification, x800.
underlying the bridged coronary artery? If we accept the common assumption that there is a relationship between the cross-sectional nuclear area of muscle fibers and the response to mechanical stress [5, 18], then the finding of significant statistical differences between the nuclei of bridging myocardial fibers and the nuclei of adjacent myocardial fibers could lead one to assume a different functional activity for the myocardial bridge and the adjacent myocardium. Materials and Methods Twelve hearts of children ranging in age from 24 h to 2 years were studied; the hearts had various types of congenital defects causing myocardial hypertrophy. All showed a myocardial bridge in the course of some of their main coronary arteries (Table 1). In each case, three blocks of myocardial tissue were selected from the bridge (zone B), the zone under the bridged artery (zone U), and the zone lateral to the bridge (zone L) (Fig. 2). The samples were routinely embedded in paraffin and stained with hematoxylin-eosin and Gomori's trichrome. For
each myocardial zone, 100 cross-sectional nuclear areas were measured by means of a TAS-Leitz Image Analyzer on line with a Digital 350 PC (Table 2). Thus, the data obtained were stastistically processed by the nonparametric Friedman test (two-way analysis of variance by ranks).
Results
In all cases but one the myocardial bridge was found above the anterior interventricular artery. In the remaining case, the bridge was located above the posterior interventricular artery. In this case, the myocardial bridge was very thin. Figure 3 gives the mean values of the nuclear cross-sectional area of the myocardial fibers, expressed in square micrometers and corresponding for each case to the bridge zone, the underlying zone, and the lateral zone to the bridge, respectively. One case presented notably higher values in the three zones than the rest of the series. They were from a premature infant who died at 35 days with marked ventricular hypertrophy of 50 g (normal weight for age, 15 g). The Friedman test showed a significant statistical difference (p = 0.004) among the muscular fibers of the bridge, the adjacent subepicardial fibers, and those underlying the coronary artery. It is evident from Figs. 3 and 4 that the nuclei in the bridges are always the smallest, irrespective of the degree of hypertrophy. In only one case were the values practically the same for the three zones examined. This was in
Reig et al.: Cardiac Hypertrophy and Myocardial Bridges
case 7, in which there was a simple band of myocardial fibers located above the posterior interventricular artery. Nonetheless, this case was included in our series for comparison.
Discussion The various interpretations of the functional significance of myocardial bridges are conjectural and mainly concern the dependence of coronary flow on myocardial contraction. It is recognized that coronary blood flow is not uniform but depends on the cycle of systolic contraction and on the diastolic relaxation of the myocardium [20], especially at the level of the type B arteries [3] which cross the ventricular wall before branching. It has been shown that the coronary transport arteries, or the epicardial arteries, are subjected to a relatively low pressure during the systolic phase, so that in them the blood flow would be more homogeneous in the two phases of the myocardial cycle [11]. In the case of myocardial bridges above a "transport artery," a "milking" or squeezing effect on the artery by the overlying myocardial fibers has been suggested [15], with possibly a low systolic flow in its branching territory. On the other hand, Mays et al. [13] proposed, on the basis of experimental data, an ancillary mechanism for ischemia in the presence of myocardial bridges. In their view the bridge would produce, in addition to a systolic constriction, a delay in diastolic relaxation of the involved artery, resulting in an important reduction of the cross-sectional area during the systolic phase and one of 25-50% during the diastolic phase. This effect, described in some cases of myocardial bridges [8], has also been observed in the intramural or type B arteries but without any functional or clinical consequences
[1]. Our results indicate that the nuclei of the muscular fibers of the bridge are significantly different from those of the fibers underlying the coronary artery and the adjacent subepicardial fibers. The nuclei in the bridges were always the smallest, irrespective of the degree of hypertrophy. These findings suggest that the mechanical response of the muscular fibers of the bridge are significantly distinct from that of the adjoining myocardial fibers and the underlying ones, and also lend support to the view that the mechanical tensions to which the myocardial fibers are subjected, or their stretching overload, are not homogeneous within the whole myocardium but depend, in part, on structural factors or on the disposition and interrelation of the muscular fibers. In the case of myocardial bridges,
189
their isolation from deeper zones and their continuity with only its own lateral muscular cells would be enough to determine, at least in the abnormal conditions of our series, a reduced response to mechanical overloads as evidenced by the presence of significantly smaller nuclei, on the assumption that the size of the nucleus and the functional activity of the muscular cells are correlated [5, 18]. Thus, myocardial bridges in cases with ventricular hypertrophy do not appear to produce a strong systolic compression. This is independent of their angiographic appearance, which is related to several factors [9, 19]. In summary, our observations support the view that the myocardial bridges represent not only an anomaly or a peculiar anatomical disposition but also signify a functional difference of the fibers of the bridge in relation to their adjoining myocardium, irrespective of any influence on coronary flow and thus perfusion of the corresponding myocardial territory.
References 1. Angelini P, Trivellato M, Donis J, Leachman RD (1983) Myocardial bridges: A review. Progr Cardiovasc Dis 36:7588 2. Edwards JC, Burnsides C, Swarm RL, Lansing AI (1956) Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 13:235241 3. Estes EH, Entman ML, Dixon HB, Hackel DB (1966) The vascular supply of the left ventricular wall. Anatomic observations, plus a hypothesis regarding acute events in coronary artery disease. Am Heart J 71:58-65 4. Faruqui AMA, Maloy WC, Felner JM, Schlant RC, Logan WD, Symbas P (1978) Symptomatic myocardial bridging of coronary artery. Am J Cardiol 41 : 1305-1310 5. Ferrans VJ, Morrow AG, Roberts WC (1972) Myocardial ultrastructure in idiopathic hypertrophyc subaortic stenosis. Circulation 45:769-792 6. Geiringer E (1951) The mural coronary. Am Heart J 41:359368 7. Hadziselimovic H (1982) Blood vessels o f the human heart. VEB Georg Thieme, Leipzig, pp 38-50 8. Hill RC, Chitwood WR, Bashore TM, Sink JD, Cox JL, Wechsler AS (1981) Coronary flow and regional function before and after supraarterial myotomy for myocardial bridging. Ann Thorac Surg 31:176-181 9. Hutchins GM, Bulkley BH, Ridolfi RL, Griffith LSC, Lohr FT, Piasio MA (1977) Correlation of coronary arteriograms and left ventriculograms with postmortem studies. Circulation 56:32-37 10. Ishimori T, Raizner AE, Chahine RA, Awdeh M, Luchi RJ (1977) Myocardial bridges in man: Angiographic accentuation with nitroglycerine. Cathet Cardiovasc Diagn 3:59-65 11. Kirk ES, Honing CR (1964) Nonuniform distribution of blood flow and gradients of oxygen tension within the heart. Am J Physiol 207:351-358 12. Kitazume H, Kramer JR, Krauthamer D, El Tobgi S, Proud-
190
13.
14.
15.
16.
Pediatric Cardiology Vol. 11, No. 4, 1990
fit WL, Mason Sones F (1983) Myocardial bridges in obstructive hypertrophic cardiomyopathy. A m Heart J 106: 131-135 Mays AE, McHale PA, Greenfield JC (1981) Transmural myocardial blood flow in a canine model of coronary artery bridging. Circ Res 49:726-732 Morales AR, Romanelli R, Boucek RJ (1980) The mural left anterior descending coronary artery, strenuous exercise and sudden death. Circulation 62:230-237 Noble J, Bourassa MG, Petitclerc R, Dyrda I (1976) Myocardial bridging and milking effect of the left anterior descending coronary artery: Normal variant or obstruction? Am J Cardiol 37:993 -999 Pol~.cek P (1961) Relation of myocardial bridges and loops on
17.
18. 19.
20.
the coronary arteries to coronary occlusions. Am Heart J 61:44-52 Reig J, Loncfin MP, Martin S, Binia M, Petit M, Domenech JM (1986) Ponts myocardiques--Incidence et relation avec certaines variables coronariennes. Arch Anat Histol Embryol 69:101-110 Sandritter W, Thomas C (1978) Histopathologie, 7th edn. F.K. Schattauer Verlag, Stuttgart, pp 36-42 White CW, Wright CB, Doty DB, Hiratza LF, Eastham CL, Harrison DG, Marcus ML (1984) Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? N Engl J Med 310:819-824 Wiggers C J, Cotton FS (1933) The coronary pressure pulses and their interpretation. Am J Physiol 106:9-17
Pediatric Cardiology 9 Springer-Verlag New York Inc. 1990
Morphometric Analysis of Myocardial Bridges in Children with Ventricular Hypertrophy J. R e i g , I C. Ruiz de M i g u e l , 2 and A. Moragas L2 mDepartment of Morphological Sciences, School of Medicine, Autonomous University of Bareclona, Bellaterra (Barcelona); and 2Department of Pathology, "Vall d'Hebrrn" Hospital and Docent Unit, Barcelona, Spain
SUMMARY. The nuclear cross-sectional area of the muscular fibers from a series of myocardial bridges was analyzed and compared to both the adjacent and underlying myocardial fibers. The series came from 12 hearts of children, ranging in age from 24 h to 2 years, with diverse forms of congenital heart disease, which caused left ventricular hypertrophy and had a myocardial bridge in the path of the anterior interventricular coronary artery. The cross-sectional areas of myocardial nuclei were measured for the bridging myocardial fibers, the adjacent myocardium, and the myocardial fibers underlying the bridged coronary artery. A significant statistical difference between the bridging muscular fibers and those underlying the submerged artery was observed, as well as between the bridging fibers and its adjacent ones. This finding suggests that myocardial bridges not only represent an anatomical abnormality, but probably imply different functional behavior as well. KEY WORDS: Myocardial bridge - - Cardiac ventricular hypertrophy - - Children's hearts
The main coronary arteries show a subepicardial course that occasionally is intramyocardial (Fig. 1). This arrangement has been described with various terms, including mural coronary artery [6], submerged coronary artery [7], or, more frequently, myocardial bridges [16]. Both the frequency of myocardial bridges and their functional significance have been the object of considerable controversy in the literature, because, independently of the technique of study, the quoted frequency of myocardial bridges is notably variable [171. The interpretations of their physiopathological significance are contradictory and may in part depend on the frequency of observation. Thus, if one concedes to Pol~tcek [16], that bridges are found in 87.5% of the hearts, it could be concluded that the anomaly is not the presence of the bridges but rather their absence. The question has been proAddress offprint requests to: Dr. J. Reig, Departamento de Cien-
cias Morfol6gicas, Facultad de Medicina, Universidad Aut6noma de Barcelona, E-08193-Bellaterra (Barcelona), Spain.
Fig. 1. Myocardial bridge located above the middle third of the anterior interventricular artery (arrows).
Reig et al.: Cardiac Hypertrophy and Myocardial Bridges
187
Table 1. Characteristics of the cases in the present study Case
Sex
Age
Weight
Heart weight
% Ventricular hypertrophy
Cardiac defects
Location of the bridge
1 2 3 4 5 6 7 8 9 l0 II 12
M M M F M M M M M M F M
10 m 4d 36 d l0 d 2.5 m 1y 3m 2y 2m 10 d 35 d 24 h
9860 3600 2530 2600 3250 4650 2850
85 g 36 g 45 g 25 g 50 g 80 g 32 g 86 g 45 g 30 g 50 g 20 g
73 50 49 24 54 45 28 35 43 37 69 l0
PA, dextroposition of aorta, VSD TGV Taussig-Bing, TGV AVSD, CoA CoA, Bernheim AVSD AVSD, MA, CoA SV L-TGV, VSD CoA PA AVSD
AIV AIV AIV AIV AIV AIV PIV AIV AIV AIV AIV AIV
g g g g g g g
2500 g 1680 g 2100 g 1890 g
AIV, Anterior interventricular artery; AVSD, atrioventricular septal defect; CoA, coarctacion of the aorta; MA, mitral atresia; PA, pulmonary atresia; PIV, posterior interventricular artery; SV, single ventricle; TGV, transposition of the great vessels; VSD, ventricular septal defect; m, month; d, day; y, year.
Table 2. Means (M) and standard deviations (SD) of the nuclear areas of the myocardial fibers (p.m2) in the three measured zones Case
1 2 3 4 5 6 7 8 9 10 11 12
Zone B
Zone U
Zone L
M
SD
M
SD
M
SD
25.62 36.51 30.77 24.59 41.24 35.72 38.12 21.77 36.75 60.64 32.64 34.23
9.72 8.79 9.63 9.02 15.39 8.88 10.67 7.05 9.08 18.15 7.47 5.82
41.83 47.23 36.79 41.85 62.73 55.19 36.27 35.25 46.48 69.11 40.84 40.68
14.85 10.86 11.50 11.24 33.81 19.42 8.14 9.76 11.33 21.28 10.60 7.10
42.63 41.83 46.24 42.69 36.35 48.37 38.66 27.96 39.56 61.03 32.21 40.38
20.14 9.09 16.59 11.50 28.59 11.82 10.34 6.61 8.96 19.25 7.07 6.82
Zone B, "fibers of the myocardial bridge; zone U, fibers of myocardium underlying the submerged artery; zone L, fibers of myocardium lateral to the bridge.
posed as to what extent the presence of myocardial bridges could protect or obversely favor coronary atherosclerosis [2, 6, 7] and consequently the development of ischemia and myocardial infarction [4, 14, 15]. It is over this last point that there is a major controversy between the proponents of the socalled milking effect [15], as the cause of myocardial ischemia, and its opponents [1]. The significance of myocardial bridges in patients with ventricular hypertrophy is certainly confused. Thus, Ishimori et al. [10] found the frequency of myocardial bridges to be higher in cases of left ventricular hypertrophy. Kitazume et al. [12]
Fig. 2. Myocardial bridge above the anterior interventricular artery (transverse section). The three zones from which the samples were taken: B, zone of myocardial bridge; U, underlying myocardial zone; L, lateral zone to the bridge. Verhoff-Van Gieson stain; original magnification, • 12.
pointed out that the systolic compression due to the myocardial fibers of the bridge was more severe in patients with ventricular hypertrophy. However, survival curves do not appear to indicate an adverse effect of this feature. In the present study, we have considered myocardial bridges in relation to ventricular hypertrophy, about which there is no reference in the literature. To what extent do the morphometric characteristics of the myocardial fibers of the bridge differ from those of adjacent fibers and from those
188
Pediatric Cardiology Vol. 11, No. 4, 1990
70
2
T
3
i
I
I
B
U
L
MYOCAHUtAL
SAMPLES
Fig. 3. Nuclear areas of the myocardial fibers (B, zone of the myocardial bridge; U, underlying myocardial zone; L, lateral zone to the bridge).
Fig. 4. Light micrograph of ventricular myocardium. (A) hypertrophic heart (zone B); (B) hypertrophic heart (zone U); (C) normal heart. Hematoxylin-eosin stain; original magnification, x800.
underlying the bridged coronary artery? If we accept the common assumption that there is a relationship between the cross-sectional nuclear area of muscle fibers and the response to mechanical stress [5, 18], then the finding of significant statistical differences between the nuclei of bridging myocardial fibers and the nuclei of adjacent myocardial fibers could lead one to assume a different functional activity for the myocardial bridge and the adjacent myocardium. Materials and Methods Twelve hearts of children ranging in age from 24 h to 2 years were studied; the hearts had various types of congenital defects causing myocardial hypertrophy. All showed a myocardial bridge in the course of some of their main coronary arteries (Table 1). In each case, three blocks of myocardial tissue were selected from the bridge (zone B), the zone under the bridged artery (zone U), and the zone lateral to the bridge (zone L) (Fig. 2). The samples were routinely embedded in paraffin and stained with hematoxylin-eosin and Gomori's trichrome. For
each myocardial zone, 100 cross-sectional nuclear areas were measured by means of a TAS-Leitz Image Analyzer on line with a Digital 350 PC (Table 2). Thus, the data obtained were stastistically processed by the nonparametric Friedman test (two-way analysis of variance by ranks).
Results
In all cases but one the myocardial bridge was found above the anterior interventricular artery. In the remaining case, the bridge was located above the posterior interventricular artery. In this case, the myocardial bridge was very thin. Figure 3 gives the mean values of the nuclear cross-sectional area of the myocardial fibers, expressed in square micrometers and corresponding for each case to the bridge zone, the underlying zone, and the lateral zone to the bridge, respectively. One case presented notably higher values in the three zones than the rest of the series. They were from a premature infant who died at 35 days with marked ventricular hypertrophy of 50 g (normal weight for age, 15 g). The Friedman test showed a significant statistical difference (p = 0.004) among the muscular fibers of the bridge, the adjacent subepicardial fibers, and those underlying the coronary artery. It is evident from Figs. 3 and 4 that the nuclei in the bridges are always the smallest, irrespective of the degree of hypertrophy. In only one case were the values practically the same for the three zones examined. This was in
Reig et al.: Cardiac Hypertrophy and Myocardial Bridges
case 7, in which there was a simple band of myocardial fibers located above the posterior interventricular artery. Nonetheless, this case was included in our series for comparison.
Discussion The various interpretations of the functional significance of myocardial bridges are conjectural and mainly concern the dependence of coronary flow on myocardial contraction. It is recognized that coronary blood flow is not uniform but depends on the cycle of systolic contraction and on the diastolic relaxation of the myocardium [20], especially at the level of the type B arteries [3] which cross the ventricular wall before branching. It has been shown that the coronary transport arteries, or the epicardial arteries, are subjected to a relatively low pressure during the systolic phase, so that in them the blood flow would be more homogeneous in the two phases of the myocardial cycle [11]. In the case of myocardial bridges above a "transport artery," a "milking" or squeezing effect on the artery by the overlying myocardial fibers has been suggested [15], with possibly a low systolic flow in its branching territory. On the other hand, Mays et al. [13] proposed, on the basis of experimental data, an ancillary mechanism for ischemia in the presence of myocardial bridges. In their view the bridge would produce, in addition to a systolic constriction, a delay in diastolic relaxation of the involved artery, resulting in an important reduction of the cross-sectional area during the systolic phase and one of 25-50% during the diastolic phase. This effect, described in some cases of myocardial bridges [8], has also been observed in the intramural or type B arteries but without any functional or clinical consequences
[1]. Our results indicate that the nuclei of the muscular fibers of the bridge are significantly different from those of the fibers underlying the coronary artery and the adjacent subepicardial fibers. The nuclei in the bridges were always the smallest, irrespective of the degree of hypertrophy. These findings suggest that the mechanical response of the muscular fibers of the bridge are significantly distinct from that of the adjoining myocardial fibers and the underlying ones, and also lend support to the view that the mechanical tensions to which the myocardial fibers are subjected, or their stretching overload, are not homogeneous within the whole myocardium but depend, in part, on structural factors or on the disposition and interrelation of the muscular fibers. In the case of myocardial bridges,
189
their isolation from deeper zones and their continuity with only its own lateral muscular cells would be enough to determine, at least in the abnormal conditions of our series, a reduced response to mechanical overloads as evidenced by the presence of significantly smaller nuclei, on the assumption that the size of the nucleus and the functional activity of the muscular cells are correlated [5, 18]. Thus, myocardial bridges in cases with ventricular hypertrophy do not appear to produce a strong systolic compression. This is independent of their angiographic appearance, which is related to several factors [9, 19]. In summary, our observations support the view that the myocardial bridges represent not only an anomaly or a peculiar anatomical disposition but also signify a functional difference of the fibers of the bridge in relation to their adjoining myocardium, irrespective of any influence on coronary flow and thus perfusion of the corresponding myocardial territory.
References 1. Angelini P, Trivellato M, Donis J, Leachman RD (1983) Myocardial bridges: A review. Progr Cardiovasc Dis 36:7588 2. Edwards JC, Burnsides C, Swarm RL, Lansing AI (1956) Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 13:235241 3. Estes EH, Entman ML, Dixon HB, Hackel DB (1966) The vascular supply of the left ventricular wall. Anatomic observations, plus a hypothesis regarding acute events in coronary artery disease. Am Heart J 71:58-65 4. Faruqui AMA, Maloy WC, Felner JM, Schlant RC, Logan WD, Symbas P (1978) Symptomatic myocardial bridging of coronary artery. Am J Cardiol 41 : 1305-1310 5. Ferrans VJ, Morrow AG, Roberts WC (1972) Myocardial ultrastructure in idiopathic hypertrophyc subaortic stenosis. Circulation 45:769-792 6. Geiringer E (1951) The mural coronary. Am Heart J 41:359368 7. Hadziselimovic H (1982) Blood vessels o f the human heart. VEB Georg Thieme, Leipzig, pp 38-50 8. Hill RC, Chitwood WR, Bashore TM, Sink JD, Cox JL, Wechsler AS (1981) Coronary flow and regional function before and after supraarterial myotomy for myocardial bridging. Ann Thorac Surg 31:176-181 9. Hutchins GM, Bulkley BH, Ridolfi RL, Griffith LSC, Lohr FT, Piasio MA (1977) Correlation of coronary arteriograms and left ventriculograms with postmortem studies. Circulation 56:32-37 10. Ishimori T, Raizner AE, Chahine RA, Awdeh M, Luchi RJ (1977) Myocardial bridges in man: Angiographic accentuation with nitroglycerine. Cathet Cardiovasc Diagn 3:59-65 11. Kirk ES, Honing CR (1964) Nonuniform distribution of blood flow and gradients of oxygen tension within the heart. Am J Physiol 207:351-358 12. Kitazume H, Kramer JR, Krauthamer D, El Tobgi S, Proud-
190
13.
14.
15.
16.
Pediatric Cardiology Vol. 11, No. 4, 1990
fit WL, Mason Sones F (1983) Myocardial bridges in obstructive hypertrophic cardiomyopathy. A m Heart J 106: 131-135 Mays AE, McHale PA, Greenfield JC (1981) Transmural myocardial blood flow in a canine model of coronary artery bridging. Circ Res 49:726-732 Morales AR, Romanelli R, Boucek RJ (1980) The mural left anterior descending coronary artery, strenuous exercise and sudden death. Circulation 62:230-237 Noble J, Bourassa MG, Petitclerc R, Dyrda I (1976) Myocardial bridging and milking effect of the left anterior descending coronary artery: Normal variant or obstruction? Am J Cardiol 37:993 -999 Pol~.cek P (1961) Relation of myocardial bridges and loops on
17.
18. 19.
20.
the coronary arteries to coronary occlusions. Am Heart J 61:44-52 Reig J, Loncfin MP, Martin S, Binia M, Petit M, Domenech JM (1986) Ponts myocardiques--Incidence et relation avec certaines variables coronariennes. Arch Anat Histol Embryol 69:101-110 Sandritter W, Thomas C (1978) Histopathologie, 7th edn. F.K. Schattauer Verlag, Stuttgart, pp 36-42 White CW, Wright CB, Doty DB, Hiratza LF, Eastham CL, Harrison DG, Marcus ML (1984) Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? N Engl J Med 310:819-824 Wiggers C J, Cotton FS (1933) The coronary pressure pulses and their interpretation. Am J Physiol 106:9-17
