Myocardial Bridging Robert E

CASE STUDY

Myocardial Bridging Robert E. Frank, Jr, MD

Human myocardial bridging is a normal anatomic variation in Address: Nationwide Insurance En- which a coronary artery is bridged by a short segment of myocar- terprise, Columbus, Ohio. dium. It can cause variable degrees of systolic obstruction. The ma- Correspondence: Robert E. Frank, jority of patients are asymptomatic. A wide variety of syndromes Jr, MD, Nationwide Insurance En- can occur, including myocardial infarction and sudden death. All terprise, Life Insurance Medical Ser- patients with myocardial bridges have systolic artery compression, vices, One Nationwide Plaza 1-24- but it is postulated that ischemia develops only in those who have 04, Columbus, OH 43215-2220; tele- a concomitant decrease in diastolic coronary artery blood flow. Sur- phone (614) 249-4033; fax (614) 249- gical removal of the myocardial bridge can be curative, and various 1089; e-mail other treatments can alleviate symptoms. The overall prognosis is frankr 1@nationwide. com. good. Key words: Myocardial bridge, cardiac ischemia without coronary atherosclerosis. Received: February 8, 1999. Accepted: February 22, 1999.

CASE REPORT ongoing low back pain with intermittent rad- iculopathy. The statement included documen- In 1997, a 68-year-old man applied for a tation of degenerative disk disease of the modified single-premium variable life insur- lumbar spine and intermittent treatment with ance policy. The single premium payable was various types of nonsteroidal anti-inflamma- $65,000, with a net amount at risk of approx- tory drugs. The proposed insured’s weight imately $50,000. The history admitted on the was 157 lb. In August 1987 it was noted that application was that of a possible myocardial he had a positive thallium stress test with no infarction in 1990. At that time, the proposed chest pain during the test. There was no in- insured admitted to a catheterization with a dication of why the test was performed, but finding of myocardial bridging. He was treat- it may be presumed that he was experiencing ed with atenolo125 mg/d, and since that time chest pain. He was prescribed diltiazem daily he had no further symptoms. The only other and nitroglycerin as required. The remainder admitted history was that of remote surgery of the notation states that the patient would on his left knee. be followed clinically, and if further chest Because of the admitted history, an Attend- pain occurred, angiography would be per- ing Physician’s Statement was obtained. The formed. The proposed insured did well for information was quite interesting. There were the next 3 years without any apparent chest numerous visits during 1985-1997 because of pain. In 1990, a resting electrocardiogram

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(ECG) showed the development of ST de- the cholesterol to be 196 mg/dL, high-density pression and T wave changes. Because of the lipoprotein 42 mg/dL, low-density lipopro- changed ECG and his previous history, a re- tein 132 mg/dL, and triglycerides 112 mg/ peated thallium treadmill stress test was per- dL. Thyroid function studies were also nor- formed. This test showed ECG changes of mal at this time. ischemia (amount of ST depression not noted), as well as reversible areas on the thallium CASE DISCUSSION scan in the septal area plus a fixed defect in the inferior wall consistent with an old scan Typically, the coronary arteries are epicar- After this, cardiac catheterization was per- dial in location, running on the surface of the formed. The catheterization showed the pro- myocardium. Myocardial bridging describes posed insured to have a left dominant sys- an anatomic variation in which a portion of tem, with the inferior left ventricle suppliedthe coronary artery lies within the myocar- by a branch from the left coronary artery. The dium itself and is no longer epicardial in lo- right coronary artery was clear. The proximal cation. The myocardial bridge (MB) usually left anterior descending artery showed mini- consists of a short segment of a superficial mal plaque formation. The middle left ante- muscular band that runs across a coronary rior descending artery was described as hav- artery, thus forming a "bridge." ing an area of severe bridging with 75% to Myocardial bridging was first described in 95% narrowing. In the circumflex artery, the 1737, when Reyman noted this particular proximal marginal branch was also described anatomy in human hearts.1 In 1961, Polacek as having an area of severe bridging, with was the first person to use the term myocardial 75% to 95% narrowing. The chamber sizes bridge.2 With the development and increasing were all normal as was the ejection fraction. frequency of coronary angiography, an in- The recommendation was to treat the patient creasing interest in this entity developed. with a p-blocker, and atenolol 50 mg/d was There has been a great deal of debate regard- started. The proposed insured continued on ing whether MB is related to a true myocar- atenolol without apparent chest pain. In Feb- dial abnormality or a normal variant of cor- ruary 1995, a resting ECG showed the new onary anatomy. Animals have been divided development of a complete right bundle into 3 groups depending on the location of branch block (RBBB). Because of this, a re- their coronary arteries.3 In type A, the coro- peated thallium treadmill stress test was per- nary arteries are entirely within the myocar- formed. The proposed insured exercised for dium (eg, squirrels, rabbits). In type B, the 9 minutes, achieving a maximum heart ratecoronary arteries are predominantly epicar- of 154 beats per minute with a normal blood dial but frequent MBs are found (eg, sheep, pressure response. The thallium scan showed dogs). In type C, the coronary arteries are reversible areas of ischemia in the anterior completely epicardial (eg, horses, cows). Hu- and apical portions, but the previously de- mans are type B. Most researchers now con- scribed fixed inferior defect was not present. sider MB to be a normal variation of human The recommendation was to continue ateno- coronary anatomy. lol and diltiazem. The subject continued to MB findings are frequent. The occurrence do well with no further notations of any has been estimated from 15% to 66%.4 An av- chest pain. The only other data in the Attend- erage of 25% seems reasonable on the basis ing Physician’s Statement were lipid measure- of prevalence studies. The length of MBs has ments. In 1990, the subject’s cholesterol was been reported to range from 3 to 69 mm, and 221 mg/dL, high-density lipoprotein was 42 they occur predominantly in the proximal left mg/dL, low-density lipoprotein was 160 anterior descending artery and rarely in the mg/dL, and triglycerides were 75 mg/dL. In right coronary artery,s Interestingly, the MB 1995, repeated lipid measurements showed muscle is different from other myocardial

32 FRANK--MYOCARDIAL BRIDGING muscle, with a distinctive spatial arrange- onary arteries, as described. It is reasonable ment and the myofibers separated by an in- to assume that myocardial ischemia could re- creased amount of connective tissue com- sult in a setting in which there are .decreases pared with normal muscle. MBs cause re- in both systolic and diastolic flow. tardation of coronary artery systolic blood Another interesting finding has been that flow by way of compression, and this com- the intima of the coronary arteries is thinner pression can be of variable degree. Noble et at the site of the MB but is often accompanied al classified this obstruction (called the milk- by hyperplasia of the intima in the coronary ing effect on angiography) into 3 grades: artery just proximal (and occasionally distal) grade 1 with K50% obstruction, grade 2 with to the MB.8 Hansen postulated that this hy- 50% to 75% obstruction, and grade 3 with perplastic area is more likely to develop ath- >75% obstruction.6 The degree of obstruction erosclerotic narrowing, thus leading to occlu- is important because most clinical syndromes sion and infarct.9 Actual atherosclerotic nar- associated with MB are found in the grade 3 rowing in the area of the MB itself occurs in- classification. However, patients who have the frequently, perhaps related to the thinning of same degree of obstruction do not manifest the intima, which may be protective. Various any common clinical presentations, which forms of therapy may be tried in sympto- can range from no symptoms to serious life- matic patients with MB. Bourassa et al first threatening consequences. The clinical syn- suggested surgical removal in 1975.l° Patients dromes associated with MB include chest with classic angina pectoris have shown relief pain, typical angina pectoris, myocardial of their symptoms with either removal of the ischemia as documented by objective testing MB or bypass grafting to the coronary artery (such as thallium testing), myocardial infarc- distal to the lesion. ~-Blockers have been used tion, atherosclerosis of coronary arteries, ven- to alleviate symptoms by slowing the heart tricular arrhythmias, and sudden death. The rate, thus allowing increased flow during the vast majority of persons with MBs are longer diastolic perfusion phase. Calcium asymptomatic. channel blockers have also been used. Ni- Investigators have attempted to define the trates have been shown to increase the sys- differences between symptomatic and tolic obstruction from MB and actually wors- asymptomatic patients who appear to have en symptoms. the same degree of systolic artery compres- To summarize, MB is a fairly common and sion. Current research has focused on the use normal variation in human coronary artery of intracoronary Doppler flow studies to anatomy. It has been associated with a vari- measure actual decreases in flow seen on an- ety of clinical syndromes, but overall this is giography.7 All grades of MB milking effect quite uncommon. When it is associated with cause a decrease in coronary artery blood ischemia, the systolic compression is usually flow during systole. This is more pronounced severe, and ischemia probably results from a when tachycardia is present. Normally, after reduction in diastolic coronary flow. Systolic the systolic compression of the coronary ar- compression alone does not cause ischemia tery, there is a fairly quick return of the di- under baseline conditions. ameter beginning in early diastole concomi- How can we apply this information to our tant with an increase in blood flow. Early di- proposed insured? Ten years before the ap- astolic diameter increase has been shown to plication he had a positive thallium stress be delayed and accompanied by a decrease in test, apparently performed because of chest mean coronary blood flow reserve distal to pain. Three years later, he had repeated thal- the MB. In the 42 symptomatic patients stud- lium testing because of a resting ECG abnor- ied by Schwartz et al, all had grade 2 or 3 mality. Catheterization at this time showed a narrowing.7 All patients also had a delayed myocardial bridge described as a class 3 nar- increase in the diastolic diameter of the cor- rowing of 75% to 95%. There were no other

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significant atherosclerotic lesions to explainwould suggest a reasonable prognosis in the his chest pain. The long-term use of nonster- near future. oidal anti-inflammatory drugs could cause In underwriting MB, one needs to know gastrointestinal symptomatology that could the degree of coronary obstruction occurring mimic cardiac pain. The thallium stress test during systole. Additionally, one needs objec- of 1990 suggested an old inferior infarction, tive data that could suggest true ischemia but this was not apparent at the time of an- (which would correlate with the delay in di- giography and also was not present on a re- astolic filling postulated to be the mechanism peated thallium treadmill in 1995. When the for ischemia in these patients). It is necessary patient developed a new complete RBBB in to correlate this with the clinical presentation, 1995, he was able to exercise for 9 minutes if an)~ and it is advisable to know whether with a normal blood pressure response and any of these clinical events were life threat- no chest pain. He continued to be asympto- ening. Finally, one should take into consid- matic on atenolol and diltiazem dai- eration the treatment administered. ly. Because the patient’s MB was severe, he belongs to the category in which clinical syn- REFERENCES dromes could develop. He had reversible ar- 1. Reyman HC. Dissertatio de vasis cordis propriis. Hailer Biblioth Anat. 1737;2:366. eas of ischemia on thallium stress tests in2. Polacek P. Relation of myocardial bridge and loops 1987, 1990, and 1995. Despite this, he re- on the coronary arteries to coronary occlusion. Am mained asymptomatic with no chest pain. He Heart J. 1961;61:44-52. did develop RBBB. It is interesting to specu- 3. Polacek P, Zechmeister A. The Occurrence and Sig- nificance of Myocardial Bridges and Loops on Coronary late on the significance of this RBBB. In 80% Arteries. Brno, Czech: University ]E Purkyne; 1968: to 90% of human hearts, the right coronary 134. artery has a large first posterior interventri- 4. Chen JN, Rei L. A study of the myocardial bridges cular artery that supplies the atrioventricular on the coronary arteries in the Chinese. Acta Anat node and the proximal right bundle. In our Sin. 1965;8:106-112. 5. Yamaguchi M, Tangkawattana P, Hamlin RL. Myo- patient, the right coronary artery was clear on cardial bridging as a factor in heart disorders: crit- angiography. What conclusions are to be ical review and hypothesis. Acta Anat. 1996;157:248- drawn from the 3 positive thallium scans 260. during 1987-1995? With class 3 obstruction of 6. Noble J, Bourassa MG, Petitclerc R. Myocardial bridging and milking effect of the left anterior de- both the left and circumflex arteries angio- scending artery: normal variant or obstruction? Am graphically, the subject could be prone to a J Cardiol. 1976;37:993-999. delay in diastolic filling, thus producing the7. Schwarz ER, Klues HG, von Dahl J, et alo Functional abnormal thallium scan. At the same time, he characteristics of myocardial bridging. Eur Heart J. was able to walk 9 minutes on a treadmill 1997;18:434-442. 8. Geiringer E. The mural coronary. Am Heart J. 1951; with no chest pain, no arrhythmias, and a 41:350-368. normal blood pressure response. He is 68 9. Hansen BE Myocardial covering on epicardial cor- years of age and has not had any life-threat- onary arteries. Scand J Thorac Cardiovasc Surg. 1982; ening cardiac events, has reasonable lipid de- 16:151-155. 10. Bourassa MG, Noble J, Dyrda R, et al. Myocardial terminations, and has not developed any sig- bridges and milking effect of the left anterior de- nificant classic atherosclerotic narrowing of scending artery: normal variant or obstruction? Cir- his coronary arteries. Taken together, all this culation. 1975;51(suppl II):11.