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Clinical significance of isolated coronary bridges: Benign and frequent condition involving the left anterior descending artery
Clinical significance of isolated coronary bridges: Benign and frequent condition involving the left anterior descending artery John R. Kramer, M.D., Hidemasa Kitazume, F. Mason Sones, Jr., M.D. Cleveland, Ohio
M.D., William
Review of 658 normal cineangiograms performed in the cardiac laboratory of the Cleveland Clinic during 1974 revealed myocardial bridging in 81 patients (12 % ). Maximal systolic compression was measured and compared to diastolic dimension above and below the obstruction by means of a programmable digital caliper. Systolic bridging involved the left anterior descending coronary artery in all cases and was mild in 26 patients, moderate in 55 patients, and severe in 11 patients. Seventy per cent of the patients were men and 30% were women. The majority had atypical symptoms although 15 patients were thought to have angina pectoris. Fiveyear survival rate was 97.5 % . No survivor had acute myocardial infarction during this follow-up period of 5 years. In the patient with normal coronary arteries and normal left ventricular function, myocardial bridging is benign. Myocardial bridging of coronary arteries was recognized and described by Black’ in 1796. If specifically sought at autopsy, such bridges are found in 5 % to 86% of hearts examined.2-4 These bridges also can be recognized arteriographically as a systolic compression of the vessel involved. A prevalence of 0.5% to 1.6% has been reported.5p6 It has been suggested that myocardial bridges, by reducing myocardial blood flow in systole, are responsible for cardiac ischemia,5*7 acute myocardial infarction (AMI),7-g ventricular fibrillation,‘O and sudden death.” Furthermore, it has been implied that myocardial bridging may have the same significant clinical morbidity and mortality as coronary atherosclerosis.12
From the Department of Cardiology, The Cleveland Clinic Foundation. Received for publication Sept. 18, 1981; accepted Sept. 25, 1981. Reprint requests: John R. Kramer, M.D., The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44106.
0002~8703/82/020283
+ 06$00.60/O
@ 1982 The
C. V. Moshy
Co.
L. Proudfit,
M.D., and
PATIENTSEVALUATEDANDVARIABLESANALYZED
During 1974, a total of 5955 cardiac catheterizations were performed at the Cleveland Clinic. Included were 5878 selective coronary cineangiographic studies by the Sones technique.13 Of these, 658 cases were identified through the Cardiovascular Information Registry as “normal”; that is, no fixed coronary artery obstruction with normal valvular and left ventricular function. Cineangiograms of all 658 “normal” patients were reviewed and 81 (12%) were found to have myocardial bridging. Arteriographic quantification of systolic lumen compression. These 81 cases were again reviewed by the
authors separately using a programmable digital caliper (A2D Prodical) to measure the systolic lumen diameter reduction and the length as follows: (1) % lumen diameter reduction = 100 - [2m/ (D, + D2) X 1001, where m = minimal lumen diameter in systole, D, = diastolic diameter proximal to the obstruction, and Dz = diastolic diameter distal to the obstruction; and (2) actual length of systolic obstruction (mm) = 2.64/C X L,, where C = mea: sured diameter of the catheter on tine, 2.64 = actual diameter of the No. 8 French catheter, and L, = the measured length of the systolic obstruction. If a discrepancy of more than 20% occurred between viewers in either category, the films were again reviewed together until a concensus was obtained. Patients were divided into three groups on the basis of the degree of systolic compression: group I (1% to 30% systolic compression, 26 patients); group II (31% to 50% systolic compression, 44 patients); and group 111 (51% to 100% systolic compression, 11 patients). Associated symptomatology, exercise testing, chronic follow-up. Angina pectoris was defined
and
as a discomfort other than dyspnea located in the upper half of the body precipitated by walking and relieved by rest in less than 15 minutes. Stress
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Kramer et al.
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m
GROUP I
u
GROUP II
lieart
1982 Journal
@i?ii GROUP Ill
DURATION
OF SYMPTOMS (mods)
Fig. 1. Duration of symptoms prior to catheterization related to severity of systolic obstructions.
Table
1. Referring diagnosisin patients with isolated myocardial bridging Diagnosis
group
Anginapectoris Questionable history of MI Syncope History of abnormal rhythm Pericarditis
I
group
22 0 2 2 0
II
group
35 1 1 6 1
III
11 0 0 0 0
Total
68 [84O<] 1 [I?< 1 3 [4C<.] 8 [lo?] 1 [lC, 1
Majority of patients were referred with diagnosis of angina pectoris. MI = myocardial infarction.
testing was performed at several referring institutions and at the Cleveland Clinic. All tests were reviewed and designated positive if downsloping ST segments of 1.5 mm or greater were seen or if significant ventricular arrhythmias occurred. Clinical information for each group was obtained by chart review, and follow-up information was obtained by telephone interview of the patient, a relative living with the patient, or the patient’s family physician. All patients were followed for 5 years or until death. Statistical analysis was by the nonpaired t test where appropriate with p < 0.05 considered significant. Correlation coefficients were determined by linear regression analysis and survival was computed by the actuarial method.14 CLINICAL CHARACTERlSTlCS IN MYOCARDlAL BFUDGlNG Clinical features myocrrdkaal bridges.
AND PROGNOSIS
and ECG finding
in patients
with
Of 658 normal studies reviewed, 81 (12 % ) were found to have myocardial bridging. Fifty-seven (70% ) of these patients were men and 24 (30 % ) were women; their ages ranged from 20 to 70
years (mean 46 & 11 years). Sixty-eight patients (84%) were referred for catheterization with the diagnosis of angina pectoris (Table I). Thirty-five (43%) had been hospitalized at least once prior to referral with a cardiac diagnosis. The majority of patients (58%) had been symptomatic for less than one year (Fig. 1). On the basis of historic information obtained before catheterization, most patients had symptoms thought to be atypical for coronary artery disease (CAD). Fifteen patients (19%), however, were thought to have typical angina pectoris (Fig. 2). The ECG was normal in 58 patients (72% ) and showed nonspecific ST-T changes in 13 (16%). Conduction abnormalities were noted in ten patients (incomplete right bundle branch block in two patients, complete right bundle branch block in three patients, left anterior hemiblock in two patients, Wolff-Parkinson-White syndrome in two patients, and third degree atrioventricular block in one patient). Coronary myeeaMal
arterkr~ephic absecratieno . Ci~i~a~y
in pM8nts
wtth
revealed systolic compression of the left anterior descending coronary art&y (LAD) in all patients. Compression
Volume
103
Number
2
Benign
consequence
of
isolated
coronary
myocardial
bridges
285
60
SYMPTOMS
m
GROUP
I
0
GROUP
II
6$?%$d
GROUP
III
AT CATHETERIZATION
Fig. 2. Clinical diagnosisat catheterization in relation to severity of systolic obstruction.
II. Mean percentage and length of systolic stenosis due to myocardial bridging Table
Mean stenosis (%)
Mean length (mm)
I (l-30%) II (31-50%;1) III (51-100%)
23.5 -t 4.5 40.0 t 5.4 61.0 +_ 9.8
11.5 + 5.6 13.0 2 6.9 11.5 +- 6.1
Total
37.5 + 13.3
12.5 f 6.4
Group
.
l .
. . . . .
:
Mean percentage of systolic stenosis (compression) and mean length of systolic stenosis (compression) in 81 patients with systolic myocardial bridging. The greater length noted in group II was not statistically significant.
of the right coronary or circumflex artery was not seen and the left ventriculogram was normal in all cases. Systolic compression ranged from 18% to 37% (mean 37.5 -t 13.3%). The length of systolic obstruction varied from 3 to 33 mm (Table II) and could not be correlated with the severity of obstruction (Fig. 3). Group I (1% to 30%) systolic compression. Seventeen men and nine women had mild systolic LAD compression. Patient age range was 20 to 70 years (mean 43 + 12 years). Of these 26,22 patients were referred with a diagnosis of angina pectoris, two with a history of syncope, and two patients with a history of rhythm abnormalities. At initial examination, 17 patients (65 % ) had atypical symptoms, five had
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PERCENT SYSTOUC OBSTRUCTION 3. Relation of the length of systolic obstruction to percentageof systolic obstruction (F = 0.067). Fig.
symptoms suggestive of angina pectoris, and four were asymptomatic. Patients had been symptomatic from 1 to 48 months (median 5.5 months) and 12 had been hospitalized with the same symptoms. ECGs were normal in 22 patients. Ten patients had
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February, 1982 Heart Journal
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Fig. 4. Percentageof systolic obstruction in relation to cardiac cycle. Two cardiac cycles from a patient in group III are shown. Systolic compressionL 50% occurred for approximately 167 msecor 20% of each entire cycle, 40% of each systole. The left anterior descendingartery wasnot significantly obstructed for the majority of each cardiac cycle.
III. Results of stresstesting on myocardial bridg-
Table
ing Group
I II III Total
Positive
-
Negative
0
10
2
1
10 2
3
22
The three positive patients developed downsloping ST segments S- 1.5 mm with exercise; one patient in group II was thought to have angina pectoris and the other two patients had atypical symptoms.
undergone stress testing with all results being negq-
tive (Table III). At catheterization, all patients demonstrated systolic compression of the LAD ranging from 13% to 30% reduction in lumen diameter (mean 23.5 + 4.5%). These obstructions were from 3 to 29 mm long (mean 11.5 f 5.6). There was no relation between length and degree of obstruction (r = 0.11). Group II (31% to 50%) systolic compression. Thirtyone men and 13 women had moderate systolic LAD compression. Patients were 25 to 69 years old (mean 47 -+ 10 years). Thirty-five (89%) were referred with a diagnosis of angina pectoris, and 18 (41%) had been hospitalized at least once previously with a diagnosis of heart disease. Symptoms had been present from 1 to 240 months (median 14 months). On initial examination, six patients were thought to have angina, 31 (70% ) had atypical symptoms, and seven were aaymptomatie. ECGs were normal in 28 patients but showed nonspecific ST-T segment
changes in eight and conduction abnormalities in
eight. Results of stress tests in the 12 patients so studied were positive in two and negative in ten. Systolic compression of the LAD was noted in all cases and the lumen was narrowed by 31% to 50% (mean 40 +- 5.4%) over a length of 3 to 37 mm (mean 13 rf: 6.9 mm). Although this length was greater than that in group I or III, the difference was not statistically significant. Within this group there was no relation between length and degree of obstruction (r = 0.026). Group Ill (> so%) systetic compressioa. Nine men and two women were found to have significant systolic LAD compression. Their age range was 24 to 58 years (mean 49 k 12 years). All 11 were referred with a diagnosis of angina pectoris and five had been hospitalized previously with this diagnosis. Symptoms had been present for two to 60 months (median 20 months). At initial examination, seven patients had atypical symptoms, and four had a diagnosis of angina pectoris. ECGs were normal in eight patients but showed nonspecific ST segment changes in two and a conduction abnormality in one. Stress testing had been performed in three patients with one positive result. At cathetkxation, systolic compression involved the LAD, reducing the systolic lumen by52% to8’7% (mean61 +- 9.8%)overalengthof4 to 27 mm (11.5 k 6.1 mm), There was no relation between O.CMWf% of systole and lasted for leas than 100 msec. Significant stenosis (L 50% reduction in lumen diameter)
Volume Number
103 2
was present for less than half of systole and did not extend into diastole. Release of compression occurred abruptly with the onset of isovolumetric relaxation (Fig. 4). Patient survival and chronic AMI incidence. Overall patient survival rate at 5 years for the entire group was 97.5% (Fig. 5). Two deaths occurred during the follow-up period. One patient in group I died of accidental trauma 23 months after catheterization. One patient in Group II died 26 months after catheterization at age 71 in a coronary care unit while being treated for AMI. Autopsy revealed DeBakey type I acute aortic dissection with extension into the coronary arteries. There were no deaths in group III. None of the survivors had an AMI. The majority are working or leading active lives in retirement. Only three of the patients originally thought to have angina pectoris were still symptomatic with exertional chest discomfort. Of the 79 surviving patients, four (5% ) were receiving disability compensation for “heart disease.” Three of these had atypical symptoms. COMMENTS
CONCERNING
MYOCARDIAL
of myocardial
too
95
that angina and ischemia can occur in patients with myocardial bridges during tachycardia.5*7 On the basis of such observations, an association between myocardial bridges and cardiac morbidity and mortality has been made:-I1 and in some cases surgical alleviation of the obstructive bridge has been undertaken.1Q*20 There has been conflicting evidence, however, suggesting that the bridge may be benign. Greenspan et al.2l were unable to demonstrate
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bridges.
Absence of objective evidence of myocardial ischemia with myocardial bridges. It has been suggested
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BRIDGES
It is disconcerting to think that myocardial bridges may behave as fixed atherosclerotic obstructional where morbidity and mortality are known to be severe.15 First, bridges are a relatively frequent incidental finding at autopsy and second, many patients with myocardial bridges found at the time of an otherwise normal catheterization have been reassured and expect a favorable long-term prognosis.16* l7 There are significant problems if one considers the myocardial bridge to be pathologic. The anomaly is present from birth and yet symptoms, morbidity, or mortality in children have not been reported. In addition, significant maximal stenosis occurs for only a short portion of each systole. During this period, compressive resistance in the entire intramyocardial vascular bed is known to be high and little antegrade flow is expected to occur in any event.18 How could systolic squeeze produce ischemia under these conditions? Physiology
287
Benign consequence of isolated coronary myocardial bridges
o-o o---o @.-.-.a
MB (81) NORMAL OR MILD MODERATE (63)
o-o
SVD
(III)
l . . .. . . . . . . . ..
LA,,
(28)
0
0 l
(458)
I
I
I
I
I
I
2
3
4
5
YEARS Fig. 5. Total survival rate in patients with myocardial
bridging compared with survival rate in patients with fixed atherosclerotic obstructions of varying severity. MB = myocardial bridge; normal or mild = no coronary obstruction of L 30’Sz4;moderate = patients with 30% to 50% coronary obsttuctiorP’; SVD = operative candidates with 2 50% obstruction of one coronary artery+; LAD = operative candidates with L 50% obstruction of the left anterior descendingartery.15
ischemia in seven patients with significant myocardial bridges by means of exercise thallium-201 scintigraphy. It is of note that all seven patients had normal coronary arteries and normal left ventricular function. Voss et al.= also failed to demonstrate ischemia with stress in 21 patients with myocardial bridging. Lack of relation systolic coronary
of mortality/morbidity to degree of obstruction. If myocardial bridges
are important clinically, one should. be able to demonstrate significant symptoms, morbidity, and mortality related to the degree of systolic obstruction in patients free of other significant cardiac pathology.23 Our patients were specifically selected
February,
288
Kramer et al.
American
to exclude left ventricular hypertrophy, cardiomyopathy, and atherosclerotic CAD. Analysis of our present series suggests that myocardial bridges, as an isolated finding, are benign. When all degrees of coronary obstruction were taken into account, bridges were detected with a surprisingly high frequency (12%) compared with that in previous repork5*” The majority of patients had mild to moderate obstruction. Only 11 of 658 patients (1.7%) demonstrated systolic narrowing of more than 50% (comparable to that reported by Ishimori et al6 using the same criteria in 313 consecutive unselected coronary angiograms, where many patients had coexistent CAD or myocardial disease). Atypical angina/normal ECG with myocardial bridg ing. Clinically, our patients resembled previously
reported normal or nearly normal patients in whom myocardial bridging was absentz4 Most of our patients were suspected of having CAD and many had been hospitalized for “angina” prior to referral. At initial evaluation, however, 68% had atypical symptoms and 13% were asymptomatic. Only 15 patients had exertional symptoms suggestive of angina pectoris. ECGs were normal in 72% and showed nonspecific ST-T changes in 16%. No patient had ECG evidence of remote myocardial infarction. High frequency of myocardial LAD involvement/benign chronic
bridges/consistent clinical course.
At catheterization all patients had varying degrees of systolic obstruction of the LAD, the equivalent of “single-vessel disease.” The prognosis, however, appears to be significantly better for these patients than for those with fixed atherosclerotic obstruction. No cardiac deaths or AMI occurred during the &year follow-up period. The overall survival rate in our patients was similar to that previously reported for patients with normal or nearly normal coronary arteries.24 Myocardial bridging as an isolated finding is benign and should not be considered an indication for coronary surgery. We thank Carol Slivka for programming assistance, Jo Rolph for manuscript preparation, and M. Rita Feran for editorial suggeetions. REFERENCES
1. Black S: A case of angina pectoris of the Medical Society of London
2. Geiringer 1951.
E: The mural
with a dissection. 6:41, 1805. coronary. AM HEART
Memoirs
J 41:359,
3. Edwards JC, Burnsides C, Swarm RL, Lansing AI: Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 13:235, 1956.
Heart
1982 Journal
4. Polacek P: Relation of myocardial bridges and loops on the coronary arteries to coronary occlusions. AM HEART ,J 61:44, 1961.
5. Noble d, Bourassa MG, Petitclerc R, Dyrda I: Myocardial bridging and milking effect of the left anterior descending coronary artery: Normal variant, or obstruction? Am J Cardiol 37:933, 1976. 6. Ishimori T. Raizner AE, Chahine RA. Awdeh M, Luchi RJ: Myocardial bridges in man: Clinical correlations and angiographic accentuation with nitroglycerine. Cathet Cardiovasc Diagn 3:59, 1977. 7. Ishimori T, Raizner AE, Verani MS, Miller RR Documentation of ischemic manifestations in patients with myocardial bridges. Clin Res 27:176A, 1979. 8. Endo M, Lee YW, Hayashi H, Wada J: Angiographic evidence of myocardial squeezing accompanying tachyarrhythmia as a possible cause of myocardial infarction. Chest 73:431, 1978. 9. Raizner AE, Chahine RA: Myocardial infarction with normal coronary arteries. in Hurst JW, editor: The heart, Update I. New York, 1979, McGraw-Hill, Book Company, Inc. p 157. 10. Farugui AMA, Maloy WC, Felner JM, Schlant RC, Logan WD, Symbas P: Symptomatic myocardial bridging of coronary artery. Am J Cardiol 41:1305, 1978. 11. Morales AR, Romanelli R, Boucek RJ: The mural left anterior descending coronary artery, strenuous exercise and sudden death. Circulation 623230, 1980. 12. Ishimori T: Myocardial bridges: A new horizon in the evaluation of ischemic heart disease. Cathet Cardiovasc Diagn 6:355, 1980. 13. Sones FM Jr, Shirey EK: Cine coronary arteriography. Mod Conceots Cardiovasc Dis 31:735. 1962. 14. Anderson RP, Bonchek LI, Gruhkemeier GL, Lambert LE, Starr A: The analysis and presentation of surgical results by actuarial methods. J Surg kes 16:224, 1974. 15. Proudfit WL. Bruschke AVG. Sones FM Natural historv of obstructive coronary artery disease: Ten-year study of -601 nonsurgical cases. Prog Cardiovasc Dis 21:53, 1978. anatomy of the coronary 16. Gensini GG: The pathological arteries of man. in Coronary arteriography. Mt. Kisco, NY, 1975, Futura, pp 299 & 462. 17. Sones FM: The current status of coronary arteriography and myocardial revascularization by surgical techniques. Jpn Circ tJ 38 (suppl):61, 1974. 18. Klocke FJ: Coronary blood flow in man. Prog Cardiovasc Dis l&117, 1976. 19. Grondin I’, Bourassa MG, Noble JN, Petitclerc R, Dydra I: Successful course after supra-arterial myotomy for myocardial bridging and milking effect of the left anterior descending artery. Ann Thorac Surg 24:422, 1977. 20. Raizner AE, Ishimori T, Verani MS, Spencer WH, Guinn G, Chahine RA, Howell JF, Miller RR: Surgical relief of myocardial ischemia due to mvocardial bridges. Am J Cardiol 45:417, 1980. 21. Greenspan M, Iskandrian AS, Catherwood E, Kimbiris D, Bemis CE. Seeal BL: Mvocardial brideine of the left anterior descending artery: Evaluation using-exercise thallium-201 myocardial scintipaphy. Cathet Cardiovasc Diagn 6:173, 1980. 22. Voss H, Kupper W, Hanrath P, Mathey D, Montz R, Bucking J: Clinical correlations, lactate extraction, coronary venous blood flow and thallium-201 myocardial imaging in patients with isolated left anterior descending muscle bridges: Normal variant or obstruction? Z Kardiol 66r347, 1980. 23. Cheitlin MD: The intramural coronary artery: Another cause for sudden death with exercise? Circulation 62:238,1980. 24. Proudfit WL, Bruschke AVG, Sones FM: Clinical course of patients with normal or slightly or moderately abnormal coronary arteriograms: lo-year follow-up of 521 patients. Circulation 62:712, 1980.
M.D., William
Review of 658 normal cineangiograms performed in the cardiac laboratory of the Cleveland Clinic during 1974 revealed myocardial bridging in 81 patients (12 % ). Maximal systolic compression was measured and compared to diastolic dimension above and below the obstruction by means of a programmable digital caliper. Systolic bridging involved the left anterior descending coronary artery in all cases and was mild in 26 patients, moderate in 55 patients, and severe in 11 patients. Seventy per cent of the patients were men and 30% were women. The majority had atypical symptoms although 15 patients were thought to have angina pectoris. Fiveyear survival rate was 97.5 % . No survivor had acute myocardial infarction during this follow-up period of 5 years. In the patient with normal coronary arteries and normal left ventricular function, myocardial bridging is benign. Myocardial bridging of coronary arteries was recognized and described by Black’ in 1796. If specifically sought at autopsy, such bridges are found in 5 % to 86% of hearts examined.2-4 These bridges also can be recognized arteriographically as a systolic compression of the vessel involved. A prevalence of 0.5% to 1.6% has been reported.5p6 It has been suggested that myocardial bridges, by reducing myocardial blood flow in systole, are responsible for cardiac ischemia,5*7 acute myocardial infarction (AMI),7-g ventricular fibrillation,‘O and sudden death.” Furthermore, it has been implied that myocardial bridging may have the same significant clinical morbidity and mortality as coronary atherosclerosis.12
From the Department of Cardiology, The Cleveland Clinic Foundation. Received for publication Sept. 18, 1981; accepted Sept. 25, 1981. Reprint requests: John R. Kramer, M.D., The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44106.
0002~8703/82/020283
+ 06$00.60/O
@ 1982 The
C. V. Moshy
Co.
L. Proudfit,
M.D., and
PATIENTSEVALUATEDANDVARIABLESANALYZED
During 1974, a total of 5955 cardiac catheterizations were performed at the Cleveland Clinic. Included were 5878 selective coronary cineangiographic studies by the Sones technique.13 Of these, 658 cases were identified through the Cardiovascular Information Registry as “normal”; that is, no fixed coronary artery obstruction with normal valvular and left ventricular function. Cineangiograms of all 658 “normal” patients were reviewed and 81 (12%) were found to have myocardial bridging. Arteriographic quantification of systolic lumen compression. These 81 cases were again reviewed by the
authors separately using a programmable digital caliper (A2D Prodical) to measure the systolic lumen diameter reduction and the length as follows: (1) % lumen diameter reduction = 100 - [2m/ (D, + D2) X 1001, where m = minimal lumen diameter in systole, D, = diastolic diameter proximal to the obstruction, and Dz = diastolic diameter distal to the obstruction; and (2) actual length of systolic obstruction (mm) = 2.64/C X L,, where C = mea: sured diameter of the catheter on tine, 2.64 = actual diameter of the No. 8 French catheter, and L, = the measured length of the systolic obstruction. If a discrepancy of more than 20% occurred between viewers in either category, the films were again reviewed together until a concensus was obtained. Patients were divided into three groups on the basis of the degree of systolic compression: group I (1% to 30% systolic compression, 26 patients); group II (31% to 50% systolic compression, 44 patients); and group 111 (51% to 100% systolic compression, 11 patients). Associated symptomatology, exercise testing, chronic follow-up. Angina pectoris was defined
and
as a discomfort other than dyspnea located in the upper half of the body precipitated by walking and relieved by rest in less than 15 minutes. Stress
283
February,
284
Kramer et al.
American
m
GROUP I
u
GROUP II
lieart
1982 Journal
@i?ii GROUP Ill
DURATION
OF SYMPTOMS (mods)
Fig. 1. Duration of symptoms prior to catheterization related to severity of systolic obstructions.
Table
1. Referring diagnosisin patients with isolated myocardial bridging Diagnosis
group
Anginapectoris Questionable history of MI Syncope History of abnormal rhythm Pericarditis
I
group
22 0 2 2 0
II
group
35 1 1 6 1
III
11 0 0 0 0
Total
68 [84O<] 1 [I?< 1 3 [4C<.] 8 [lo?] 1 [lC, 1
Majority of patients were referred with diagnosis of angina pectoris. MI = myocardial infarction.
testing was performed at several referring institutions and at the Cleveland Clinic. All tests were reviewed and designated positive if downsloping ST segments of 1.5 mm or greater were seen or if significant ventricular arrhythmias occurred. Clinical information for each group was obtained by chart review, and follow-up information was obtained by telephone interview of the patient, a relative living with the patient, or the patient’s family physician. All patients were followed for 5 years or until death. Statistical analysis was by the nonpaired t test where appropriate with p < 0.05 considered significant. Correlation coefficients were determined by linear regression analysis and survival was computed by the actuarial method.14 CLINICAL CHARACTERlSTlCS IN MYOCARDlAL BFUDGlNG Clinical features myocrrdkaal bridges.
AND PROGNOSIS
and ECG finding
in patients
with
Of 658 normal studies reviewed, 81 (12 % ) were found to have myocardial bridging. Fifty-seven (70% ) of these patients were men and 24 (30 % ) were women; their ages ranged from 20 to 70
years (mean 46 & 11 years). Sixty-eight patients (84%) were referred for catheterization with the diagnosis of angina pectoris (Table I). Thirty-five (43%) had been hospitalized at least once prior to referral with a cardiac diagnosis. The majority of patients (58%) had been symptomatic for less than one year (Fig. 1). On the basis of historic information obtained before catheterization, most patients had symptoms thought to be atypical for coronary artery disease (CAD). Fifteen patients (19%), however, were thought to have typical angina pectoris (Fig. 2). The ECG was normal in 58 patients (72% ) and showed nonspecific ST-T changes in 13 (16%). Conduction abnormalities were noted in ten patients (incomplete right bundle branch block in two patients, complete right bundle branch block in three patients, left anterior hemiblock in two patients, Wolff-Parkinson-White syndrome in two patients, and third degree atrioventricular block in one patient). Coronary myeeaMal
arterkr~ephic absecratieno . Ci~i~a~y
in pM8nts
wtth
revealed systolic compression of the left anterior descending coronary art&y (LAD) in all patients. Compression
Volume
103
Number
2
Benign
consequence
of
isolated
coronary
myocardial
bridges
285
60
SYMPTOMS
m
GROUP
I
0
GROUP
II
6$?%$d
GROUP
III
AT CATHETERIZATION
Fig. 2. Clinical diagnosisat catheterization in relation to severity of systolic obstruction.
II. Mean percentage and length of systolic stenosis due to myocardial bridging Table
Mean stenosis (%)
Mean length (mm)
I (l-30%) II (31-50%;1) III (51-100%)
23.5 -t 4.5 40.0 t 5.4 61.0 +_ 9.8
11.5 + 5.6 13.0 2 6.9 11.5 +- 6.1
Total
37.5 + 13.3
12.5 f 6.4
Group
.
l .
. . . . .
:
Mean percentage of systolic stenosis (compression) and mean length of systolic stenosis (compression) in 81 patients with systolic myocardial bridging. The greater length noted in group II was not statistically significant.
of the right coronary or circumflex artery was not seen and the left ventriculogram was normal in all cases. Systolic compression ranged from 18% to 37% (mean 37.5 -t 13.3%). The length of systolic obstruction varied from 3 to 33 mm (Table II) and could not be correlated with the severity of obstruction (Fig. 3). Group I (1% to 30%) systolic compression. Seventeen men and nine women had mild systolic LAD compression. Patient age range was 20 to 70 years (mean 43 + 12 years). Of these 26,22 patients were referred with a diagnosis of angina pectoris, two with a history of syncope, and two patients with a history of rhythm abnormalities. At initial examination, 17 patients (65 % ) had atypical symptoms, five had
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000
50
100
PERCENT SYSTOUC OBSTRUCTION 3. Relation of the length of systolic obstruction to percentageof systolic obstruction (F = 0.067). Fig.
symptoms suggestive of angina pectoris, and four were asymptomatic. Patients had been symptomatic from 1 to 48 months (median 5.5 months) and 12 had been hospitalized with the same symptoms. ECGs were normal in 22 patients. Ten patients had
286
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February, 1982 Heart Journal
16b3
Fig. 4. Percentageof systolic obstruction in relation to cardiac cycle. Two cardiac cycles from a patient in group III are shown. Systolic compressionL 50% occurred for approximately 167 msecor 20% of each entire cycle, 40% of each systole. The left anterior descendingartery wasnot significantly obstructed for the majority of each cardiac cycle.
III. Results of stresstesting on myocardial bridg-
Table
ing Group
I II III Total
Positive
-
Negative
0
10
2
1
10 2
3
22
The three positive patients developed downsloping ST segments S- 1.5 mm with exercise; one patient in group II was thought to have angina pectoris and the other two patients had atypical symptoms.
undergone stress testing with all results being negq-
tive (Table III). At catheterization, all patients demonstrated systolic compression of the LAD ranging from 13% to 30% reduction in lumen diameter (mean 23.5 + 4.5%). These obstructions were from 3 to 29 mm long (mean 11.5 f 5.6). There was no relation between length and degree of obstruction (r = 0.11). Group II (31% to 50%) systolic compression. Thirtyone men and 13 women had moderate systolic LAD compression. Patients were 25 to 69 years old (mean 47 -+ 10 years). Thirty-five (89%) were referred with a diagnosis of angina pectoris, and 18 (41%) had been hospitalized at least once previously with a diagnosis of heart disease. Symptoms had been present from 1 to 240 months (median 14 months). On initial examination, six patients were thought to have angina, 31 (70% ) had atypical symptoms, and seven were aaymptomatie. ECGs were normal in 28 patients but showed nonspecific ST-T segment
changes in eight and conduction abnormalities in
eight. Results of stress tests in the 12 patients so studied were positive in two and negative in ten. Systolic compression of the LAD was noted in all cases and the lumen was narrowed by 31% to 50% (mean 40 +- 5.4%) over a length of 3 to 37 mm (mean 13 rf: 6.9 mm). Although this length was greater than that in group I or III, the difference was not statistically significant. Within this group there was no relation between length and degree of obstruction (r = 0.026). Group Ill (> so%) systetic compressioa. Nine men and two women were found to have significant systolic LAD compression. Their age range was 24 to 58 years (mean 49 k 12 years). All 11 were referred with a diagnosis of angina pectoris and five had been hospitalized previously with this diagnosis. Symptoms had been present for two to 60 months (median 20 months). At initial examination, seven patients had atypical symptoms, and four had a diagnosis of angina pectoris. ECGs were normal in eight patients but showed nonspecific ST segment changes in two and a conduction abnormality in one. Stress testing had been performed in three patients with one positive result. At cathetkxation, systolic compression involved the LAD, reducing the systolic lumen by52% to8’7% (mean61 +- 9.8%)overalengthof4 to 27 mm (11.5 k 6.1 mm), There was no relation between O.CMWf% of systole and lasted for leas than 100 msec. Significant stenosis (L 50% reduction in lumen diameter)
Volume Number
103 2
was present for less than half of systole and did not extend into diastole. Release of compression occurred abruptly with the onset of isovolumetric relaxation (Fig. 4). Patient survival and chronic AMI incidence. Overall patient survival rate at 5 years for the entire group was 97.5% (Fig. 5). Two deaths occurred during the follow-up period. One patient in group I died of accidental trauma 23 months after catheterization. One patient in Group II died 26 months after catheterization at age 71 in a coronary care unit while being treated for AMI. Autopsy revealed DeBakey type I acute aortic dissection with extension into the coronary arteries. There were no deaths in group III. None of the survivors had an AMI. The majority are working or leading active lives in retirement. Only three of the patients originally thought to have angina pectoris were still symptomatic with exertional chest discomfort. Of the 79 surviving patients, four (5% ) were receiving disability compensation for “heart disease.” Three of these had atypical symptoms. COMMENTS
CONCERNING
MYOCARDIAL
of myocardial
too
95
that angina and ischemia can occur in patients with myocardial bridges during tachycardia.5*7 On the basis of such observations, an association between myocardial bridges and cardiac morbidity and mortality has been made:-I1 and in some cases surgical alleviation of the obstructive bridge has been undertaken.1Q*20 There has been conflicting evidence, however, suggesting that the bridge may be benign. Greenspan et al.2l were unable to demonstrate
l\
‘\
..
‘\
‘\
.... 0 *.. ‘@-*-*?e :. 1 .-.-..
. ‘4*.
*. : \
bridges.
Absence of objective evidence of myocardial ischemia with myocardial bridges. It has been suggested
q8-o--..----* -p,‘\.~o.~o~<, ‘+ ..>I, .‘\..‘\.........-..‘:. \ \ -0.. .. ..\
BRIDGES
It is disconcerting to think that myocardial bridges may behave as fixed atherosclerotic obstructional where morbidity and mortality are known to be severe.15 First, bridges are a relatively frequent incidental finding at autopsy and second, many patients with myocardial bridges found at the time of an otherwise normal catheterization have been reassured and expect a favorable long-term prognosis.16* l7 There are significant problems if one considers the myocardial bridge to be pathologic. The anomaly is present from birth and yet symptoms, morbidity, or mortality in children have not been reported. In addition, significant maximal stenosis occurs for only a short portion of each systole. During this period, compressive resistance in the entire intramyocardial vascular bed is known to be high and little antegrade flow is expected to occur in any event.18 How could systolic squeeze produce ischemia under these conditions? Physiology
287
Benign consequence of isolated coronary myocardial bridges
o-o o---o @.-.-.a
MB (81) NORMAL OR MILD MODERATE (63)
o-o
SVD
(III)
l . . .. . . . . . . . ..
LA,,
(28)
0
0 l
(458)
I
I
I
I
I
I
2
3
4
5
YEARS Fig. 5. Total survival rate in patients with myocardial
bridging compared with survival rate in patients with fixed atherosclerotic obstructions of varying severity. MB = myocardial bridge; normal or mild = no coronary obstruction of L 30’Sz4;moderate = patients with 30% to 50% coronary obsttuctiorP’; SVD = operative candidates with 2 50% obstruction of one coronary artery+; LAD = operative candidates with L 50% obstruction of the left anterior descendingartery.15
ischemia in seven patients with significant myocardial bridges by means of exercise thallium-201 scintigraphy. It is of note that all seven patients had normal coronary arteries and normal left ventricular function. Voss et al.= also failed to demonstrate ischemia with stress in 21 patients with myocardial bridging. Lack of relation systolic coronary
of mortality/morbidity to degree of obstruction. If myocardial bridges
are important clinically, one should. be able to demonstrate significant symptoms, morbidity, and mortality related to the degree of systolic obstruction in patients free of other significant cardiac pathology.23 Our patients were specifically selected
February,
288
Kramer et al.
American
to exclude left ventricular hypertrophy, cardiomyopathy, and atherosclerotic CAD. Analysis of our present series suggests that myocardial bridges, as an isolated finding, are benign. When all degrees of coronary obstruction were taken into account, bridges were detected with a surprisingly high frequency (12%) compared with that in previous repork5*” The majority of patients had mild to moderate obstruction. Only 11 of 658 patients (1.7%) demonstrated systolic narrowing of more than 50% (comparable to that reported by Ishimori et al6 using the same criteria in 313 consecutive unselected coronary angiograms, where many patients had coexistent CAD or myocardial disease). Atypical angina/normal ECG with myocardial bridg ing. Clinically, our patients resembled previously
reported normal or nearly normal patients in whom myocardial bridging was absentz4 Most of our patients were suspected of having CAD and many had been hospitalized for “angina” prior to referral. At initial evaluation, however, 68% had atypical symptoms and 13% were asymptomatic. Only 15 patients had exertional symptoms suggestive of angina pectoris. ECGs were normal in 72% and showed nonspecific ST-T changes in 16%. No patient had ECG evidence of remote myocardial infarction. High frequency of myocardial LAD involvement/benign chronic
bridges/consistent clinical course.
At catheterization all patients had varying degrees of systolic obstruction of the LAD, the equivalent of “single-vessel disease.” The prognosis, however, appears to be significantly better for these patients than for those with fixed atherosclerotic obstruction. No cardiac deaths or AMI occurred during the &year follow-up period. The overall survival rate in our patients was similar to that previously reported for patients with normal or nearly normal coronary arteries.24 Myocardial bridging as an isolated finding is benign and should not be considered an indication for coronary surgery. We thank Carol Slivka for programming assistance, Jo Rolph for manuscript preparation, and M. Rita Feran for editorial suggeetions. REFERENCES
1. Black S: A case of angina pectoris of the Medical Society of London
2. Geiringer 1951.
E: The mural
with a dissection. 6:41, 1805. coronary. AM HEART
Memoirs
J 41:359,
3. Edwards JC, Burnsides C, Swarm RL, Lansing AI: Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 13:235, 1956.
Heart
1982 Journal
4. Polacek P: Relation of myocardial bridges and loops on the coronary arteries to coronary occlusions. AM HEART ,J 61:44, 1961.
5. Noble d, Bourassa MG, Petitclerc R, Dyrda I: Myocardial bridging and milking effect of the left anterior descending coronary artery: Normal variant, or obstruction? Am J Cardiol 37:933, 1976. 6. Ishimori T. Raizner AE, Chahine RA. Awdeh M, Luchi RJ: Myocardial bridges in man: Clinical correlations and angiographic accentuation with nitroglycerine. Cathet Cardiovasc Diagn 3:59, 1977. 7. Ishimori T, Raizner AE, Verani MS, Miller RR Documentation of ischemic manifestations in patients with myocardial bridges. Clin Res 27:176A, 1979. 8. Endo M, Lee YW, Hayashi H, Wada J: Angiographic evidence of myocardial squeezing accompanying tachyarrhythmia as a possible cause of myocardial infarction. Chest 73:431, 1978. 9. Raizner AE, Chahine RA: Myocardial infarction with normal coronary arteries. in Hurst JW, editor: The heart, Update I. New York, 1979, McGraw-Hill, Book Company, Inc. p 157. 10. Farugui AMA, Maloy WC, Felner JM, Schlant RC, Logan WD, Symbas P: Symptomatic myocardial bridging of coronary artery. Am J Cardiol 41:1305, 1978. 11. Morales AR, Romanelli R, Boucek RJ: The mural left anterior descending coronary artery, strenuous exercise and sudden death. Circulation 623230, 1980. 12. Ishimori T: Myocardial bridges: A new horizon in the evaluation of ischemic heart disease. Cathet Cardiovasc Diagn 6:355, 1980. 13. Sones FM Jr, Shirey EK: Cine coronary arteriography. Mod Conceots Cardiovasc Dis 31:735. 1962. 14. Anderson RP, Bonchek LI, Gruhkemeier GL, Lambert LE, Starr A: The analysis and presentation of surgical results by actuarial methods. J Surg kes 16:224, 1974. 15. Proudfit WL. Bruschke AVG. Sones FM Natural historv of obstructive coronary artery disease: Ten-year study of -601 nonsurgical cases. Prog Cardiovasc Dis 21:53, 1978. anatomy of the coronary 16. Gensini GG: The pathological arteries of man. in Coronary arteriography. Mt. Kisco, NY, 1975, Futura, pp 299 & 462. 17. Sones FM: The current status of coronary arteriography and myocardial revascularization by surgical techniques. Jpn Circ tJ 38 (suppl):61, 1974. 18. Klocke FJ: Coronary blood flow in man. Prog Cardiovasc Dis l&117, 1976. 19. Grondin I’, Bourassa MG, Noble JN, Petitclerc R, Dydra I: Successful course after supra-arterial myotomy for myocardial bridging and milking effect of the left anterior descending artery. Ann Thorac Surg 24:422, 1977. 20. Raizner AE, Ishimori T, Verani MS, Spencer WH, Guinn G, Chahine RA, Howell JF, Miller RR: Surgical relief of myocardial ischemia due to mvocardial bridges. Am J Cardiol 45:417, 1980. 21. Greenspan M, Iskandrian AS, Catherwood E, Kimbiris D, Bemis CE. Seeal BL: Mvocardial brideine of the left anterior descending artery: Evaluation using-exercise thallium-201 myocardial scintipaphy. Cathet Cardiovasc Diagn 6:173, 1980. 22. Voss H, Kupper W, Hanrath P, Mathey D, Montz R, Bucking J: Clinical correlations, lactate extraction, coronary venous blood flow and thallium-201 myocardial imaging in patients with isolated left anterior descending muscle bridges: Normal variant or obstruction? Z Kardiol 66r347, 1980. 23. Cheitlin MD: The intramural coronary artery: Another cause for sudden death with exercise? Circulation 62:238,1980. 24. Proudfit WL, Bruschke AVG, Sones FM: Clinical course of patients with normal or slightly or moderately abnormal coronary arteriograms: lo-year follow-up of 521 patients. Circulation 62:712, 1980.