topeeng.gif (8383 bytes)

[ Scientific Activity - Actividad Científica ] [ Brief Communications - Temas Libres ]

Coronary  muscular bridges: incidence and clinic association

Vázquez Roberto M.D.; Muratore Ivana M.D.; Abdala Gabriel M.D.; Guglieri German M.D.; Sosa Osvaldo M.D.; Colque Roberto M.D.; Jiménez Kockar Marcelo M.D.; Velarde Mariscal José Luis M.D.; Villegas Alberto M.D.; Pieroni Mario Daniel M.D.

Instituto de Cardiología - Hospital Italiano - Córdoba - Argentina

Material and Methods

Introduction:coronary artery bypass (CAB), constitute a reduced group of patients (pts.) in coronary heart disease, and its clinical correlation with presence of myocardial ischemia is variable.
Objectives: observing incidence of CAB, and correlating the presence of symptoms that caused the mentioned study in the population of pts. that underwent coronary angiography (CAG). As a secondary objective, the presence of ischemia in myocardial ischemia was studied in pts. with CAB.
Material and Methods: since January, 1997, to October, 1998, 561 CAG were carried out in pts. that consulted due to symptoms and/or suspicious signs of coronary arterial disease. The presence of ischemia was assessed with myocardial perfusion with Tc99 Sestamibi radioisotopes both in rest and in stress, with S.P.E.C.T. scanning.
Results: out of the 561 pts., twelve (2.1%) presented CAB. The mean age was 51 (range 36-76), a 58% being males. Out of the 12 pts., six (50%) presented as main symptom, Typical Angina (Group I), and the rest (50%), Atypical Angina (Group II). The latter (GII) were studied to present factors of coronary risk associated to alterations in ECG. Out of the pts. of GI, a 50% displayed significant coronary heart disease associated, while none (0%) of GII was associated to heart disease (p.0.182). The CAG presented deficit of perfusion in 5 pts. (83.3%) in GI, and only in one (16.6%) of Group II (p.0.084). In GI, a 100% were males vs. a 16.6% of GII (p.0.019).
Discussion: this work shows a correlation between muscular bypasses and deficit of coronary perfusion (ischemia) by scanning, and as more transcending, the relation between muscular bypasses, and coronary atherosclerotic pathology.
Conclusions: incidence of CAB was low in our series. In the pts. with symptoms of Typical Angina, male sex prevailed, and presented a greater association to heart disease and myocardial ischemia.



Myocardial bridges or coronary arterial bridge (CAB), was described first by Black in 1796, a necropsy finding.These bridges consist of the introduction of little segments of the epicardic coronary arteries in the myocardium for a variable distance, which involves in most of the instances to the Anterior Descending Artery. Male prevalence was observed. The reported incidence is between 5 and 12 %of the population. This anatomical disposition is responsible that for each systolic contraction a narrowing of the artery is produced which might alter the hemodinamics of the coronary circulation, in a low percentage of the cases.
The CAB represent a complex hemodynamics and functional entity of the coronary vasculature. The traditional concept is that the ischemia sustains in the "Milking effect", that is, outer vascular compression of the coronary artery in sistole by the myocardial bridging contraction, reducing the coronary systolic flow. Thereafter it deduces the severity of the isquemia depends upon the degree of systolic narrowing of the involved vessel. However the coronary perfusion in the left ventricle occur during the diastole. Authors as Dr. Schwarz and Dr. Klues performed studies through the C.C.G. And velocimetry measurements of flow by Intracoronary Eco-Doppler with the purpose of elucidating the hemodynamics alterations determining of the ischemia in the CAB.They observed a typical pattern with a rapid acceleration of the velocity peak of the diastolic flow in protodiastole, with a rapid mesodiastolic deceleration and a mesotelediastolic plateau, which means an important reduction of the coronary reserve. It was proved a persistent reduction of the mesodiastolic diameter non less than 30% of the vascular lumen, different of the distal and proximal portions to the muscular bridge. This flow reduction it is increased during spontaneous or induced stress, (rapid auricular pacemake) due to the shortening of the diastolic period, during which the coronaryperfusion is developed.
It may interpret that these coronary hemodynamics alterations that induce a deficit in the coronary flow and therefore a myocardial ischemia (detectable by Gamma Chamber), with clinical significance (typical angina, dyspnea, arrhythmia and even I.A.M.), are localize principally in the proto and mesodiastole (persistent reduction of the diastolic vascular gauge), generating the hypoperfusion at the time the myocardium demand it. This fisiopathologic profile of the CAB is depending upon offer upon and demand factors, common these latter with the atheroesclerotic coronary failure: cardiac rate, contractil candition and peripheric vascular resistance.
A total of the 12 patiens are analyzed with C.A.B angiographically shown and its clinical correlation in the total of patiens angiographically studied dring 1998



a- Observe the incidence of coronary muscular bridge (C.A.B) in our Institute.
b- Analize the asociation with the symptoms that motivated the cinecoronariography (C.C.G.).
c- Aim the presence ischemia in the myocardial perfusion with stress related to the area with C.A.B.

Material and Methods:

Since january 1997 until october 1998, 561 cinecoronariographies were performed. These patients revealed sings and suspicious symptoms of arterial coronary disease. Twelve of them (2,1%) showed C.A.B.
The patients were divided in two groupsaccordings the following symptoms: A) Typica Angina considered as the oppressive precordial pain thet appears with stress and subsides with rest or nitrites, o B) Atypical Angina (other forms of presentation), plusthe presence of both groupsof risk factors, Hypertension, dislipemia, diabetes, smoking and unespecific changes of the ST-T in the electrocardiogram (E.C.G).In all the patients ECG of 12 leads were obtained and the presence of ischemia with myocardial perfusion, (Tc 99 sestamibii), rest and stress, with Gamma Chamber S.P.E.C.T. was assessed. In every instance the cardiovascular medication was suspended at least 48 hours before the test.
The images were processed in an equipment Elscint Sp4 and assessed by two independent observers (specialized physicians), who ignored the result of the cinecoronariography, by the quantitative method.
The cinecoronariography was performed by the Judkins technique with 6 and 7 French catheters. The quantification of the systolic compression of the vessel lumen was performedwith caliper.
The statistic analysis was undertaken with test T (student) of the percentages and was considered significant with p< 0, 05.



From the 561cinecoronarographies performed from January 1997 until October of 1998, twelvw patiens (2,1%) were found with coronary arterial bridge (see figure I), in the half third of the Anterior Descending Artery whit a percentege of systolic obstruction between 30-90%. Thesewere divided in two groups according the mode of clinical presentation (see figure2): 6 patients (50%) were studied because they revealed tipical angina, representing the GI, the remainder (6 patients, 50%) because they revealed Atipical Angina, GII.
The mean age was 51 years (range 36 to 76 years), 7 patients (58%) were males and 5 patients (42%) were females, from which 6 males represent the GI and 5 women the GII and a man (P <0.001).(see figuireIII)
All patients of the group CAB showed ST segment and T wave alterations in the electrocardiogram. BIRDHH was associated in one patient of the GI and HBAI associated.regardingthe risk factorsn all the patients presented at least two, for coronary arterial disease, beingmore frequent the hypertension, dislipemia, and smoking, only one patient of the GII was a non- insulin dependent diabetic patient.
In the analysis of the coronary lesions associated to C.A.B, Three patients (50%) of the GI, presented coronary atheroesclerotic obstruction significant in the cinecoronariography (higher than 70%). we did not find such association in any patient of the GII (P<0,05).(See figure IV).
A deficit of myocardial perfusion was observed whit Tc99 sestamibi in five patients of the GI(83,3%) and in one patient (16, 6%) of the G II (p<0,02).(See figure V). From the three patients of the GI with significant coronary lesions (LOAS) the ischemic area corresponds to the ill vessel, in the remainder where they did not have LOAS, the perfusion deficit was correlated with the coronary muscular bridge, similr to the patien belonging the G II.

fig1i.jpg (24038 bytes)


fig2i.jpg (23199 bytes)


fig3i.jpg (31283 bytes)


fig4i.jpg (30434 bytes)


fig5i.jpg (28385 bytes)



For most of the world bibliography and general medical consensus, the muscular bridges represent a benign coronary pathology, or a normalanatomical variant. As was explained above (see introduction) it as been proved in cinecoronariography and Eco-Doppler intracoronary (flow velocity measures), the correlation that exists between the muscular bridges and the induction of myocardial ischemia (detectable by Gamma Chamber), mainly in patients with symptoms of typical angina, sustained in the hemodynamically significative changes that these produce during the diastole in the cardiac cycle.
In our analysis we show the correlation between C.A.B and the deficit of coronary perfusion (ischemia) by Gamma Chamber and the association between muscular bridges with coronary atheroesclerotic pathology. The mariced difference in the incidence of C.A.B as a finding in cinecoronariographies(C.C.G.) betwen our study (2,1%) regarding the consulted bibliography, (5-12%) derives from the fact that our population is composed by patients whit and without significant lesions, whereas the populations of such publications arise from findings in normal subjects (without LOAS). Coincidentally with the published data we found statistically significant. The fact that most of the patients with C.A.B with confirmed ischemia and concomitant atherosclerotic pathology were men.
Another challenge before the diagnosis of C.A.B is the therapeutic behavior to follow. The used option for a long time, and even todayin most of the patients are the B-Blockers. Its effect is basd on its negative inotropic and cronotropic action, that decrease the coronary vascular resistance, increasing the diastolic coronary perfusion by diminishing of the myocardial contractil tone, and hence of the muscular bridge. Also reducing the cardiac rate, the diastolic period is prolonged whit the same effect previouslymentioned. It has been proved with similar studies those of Klues the complete normalization of the physiopathologic hemodynamic alterations induced by the C.A.B and the disappearance of clinic of angor and ischemia by Gamma Chamber after administration of B-Blockers.



A -The incidence of the CAB in the analyzed sample was lower than the averages in the bibliography.

B - In the patients with typical angina there was a male predominace.

C - The patients with typical angina (GI), revealed a higher association with an atherosclerotic coronary arterial disease, and coincidentally the presence of ischemia in the myocardial perfusión was higher in this group.


1. Levin D.C, Gardiner G.: Puentes Miocárdicos.Branwald, Tratado de Cardiología, Edit. Interamericana, Boston, 4ta Edición. 1993, p.p. (280)
2. Kramer J.R., Kitazune H., Proudfit W.L, Mason Sones F.: Clinical significance of isolated coronary bridges: Benign and frequent condiction involving the left anterior descending artery. AM Heart J. 103: 283 – 288, 1982.
3. Schwarz E.R., Klues H.G., Dohl J., Klein I., Krels W., Hanrath P.: Funtionall characteristics of myocardial bridging: A combined angiographic and intracoronary Doppler flow study. EUR Heart J. 18: 434 – 442, 1997.
4. Klues H. G., Schwarz E.R., Dohl J., Reffelmann T., Helmut R., Pottbast K, Schmitz C., Minortz J., Krels W, Hanrath P.: disturbed Intracoronary Hemodinamics in myocardial Bridging: Early Normalization by Intracoronary Stent Placement. Circulation 96: 2095 – 2912, 1997.
5. Clariá Olmedo R.: Angor pectoris, en corazón, exploración semiológica. Edit. Multieditora. Córdoba, 2da edición. 1983, p.p. 112-113.
6. Agirbasli M, Martín G.S., Stout J.B., Jennings H.S., Dixon J.H.: Myocardial bridge as a cause of thrombus formation and myocardial infarction in a young athlete, clin cardial 20: 1032-6, 1997.
7. Agirbasli M., Hillegass W.B., Chapman G.D., Brott B.C.: Stent procedure complicated by thrombus formation distal to the lesion within a muscle bridge. Cathet cardiovasc diagn. 43: 73-6, 1998.
8. Kodama K., Morioka N., Hara Y., Shigematsu Y., Hamada M., Hiwada K: Coronary vasospasm at the site of myocardial bridge. Report of two cases.. Angiology. 49: 659-63, 1998.
9. Black, S.: a case of angina pectoris with a disection. Memoris of the Medicall Society of London. 6: 41, 1805.
10. Pittaluga, J., Marchena E., Posada, J.D., Romanelli, R., Morales A.: Left anterior descending coronary artery bridge. A cause of early death after cardiac transplantion. Chest 111: 511-3, 1997.
11. Schwarz E.R., Klues H.G., Dohl J., Klein I., Krels W, Hanrath P.: funtionall angiographic and intracoronary doppler flow characteristics in syntomatic patients with myocardial bridging: effecto of short-terme intravenous beta-blocker medication. J. Am Coll Cardial, 27: 1637-45, 1996.
12. Ishii T., Asuwa N., Masuda S., Ihikawa Y.: The effects of a myocardial bridge on coronary atherosclerosis and ischemia. J. Pathol. 185: 4-9, 1998.
13. Winter, R, J., Kok W.E., Piek J.J.: Coronary atheroesclerosis Withim a myocardial bridge, not a bening condition. Heart. 80: 91-3, 1998.
14. Podbielski F.J., Chaer R., Massad M.G., Chami Y.G., Nawas S., Leary P., Benedetti, E.: What makes a coronary myocardial bridge sintomatic?. Minerva Cardioangiol. 46: 127-30, 1998.
15. Takeuchi M., Himevo E.: Coronary Angioplasty of a severe coronary stenosis at the site of a myocardial bridge. Cathet cardiovasc diagn. 41: 416-20, 1997.
16. Smith S.C,., Taber M.T., Robiolio P.A.; Lasala J.M.: Acute myocardial infarction caused by a myocardial bridge treated with intracoronary stenting. Cathet cardiovas diagn. 42: 209-12, 1997.


Questions, contributions and commentaries to the Authors: send an e-mail message (up to 15 lines, without attachments) to , written either in English, Spanish, or Portuguese.



This company contributed to the Congress:

agilent.gif (2552 bytes)