January 1996 1 9 8 Levin et al. American Heart Journal
though first described more than 40 years ago, controversy continues to exist over the clinical significance of myocar- dial bridging. A large angiographic study 4 and two necropsy studies 2, 5 have found little or no atherosclerotic plaque formation at the site of the bridge. Therefore it is believed that the myocardial bridge may protect the coronary artery from significant atherosclerosis by limiting its exposure to the forces of the systolic pulse wave and potentially rain- imizing endothelial trauma. However, several reports 69 have disputed this finding, and recent evidence now ques- tions the protective effect afforded by a myocardial bridge.
To our knowledge only three case reports 79 have de- scribed significant coronary artery stenosis at the site of a myocardial bridge documented by angiography. Two cas- es 7, 8 similar to our patient were found after angioplasty of the coronary artery stenosis was performed. One case in- volved the left anterior descending coronary artery 7 and the other the right coronary artery, s The third patient 9 underwent coronary artery bypass graft surgery because of multivessel disease after a myocardial bridge was discov- ered in the left anterior descending coronary artery. In the case described previously the culprit stenosis was at the proximal portion of a myocardial bridge in the left anterior descending coronary artery, and the patient had a similar clinical presentation with chest pain and ST segment ele- vation on the ECG. Myocardial bridging of the coronary segment was not discovered in our case, as in two previous cases, until angioplasty was performed, possibly because of the fixed underlying atherosclerotic stenosis limiting cor- onary inflow and masking systolic compression. Once an- gioplasty was performed, the characteristic "milking ef- fect" consistent with myocardial bridging was noted. Tran- sient coronary occlusion caused by plaque rupture and thrombotic occlusion or vasospasm may have been respon- sible for this patients' event. Fortunately a significant my- ocardial infarction was aborted, and subsequent angina was relieved with conventional angioplasty. Currently the patient has no symptoms.
Myocardial bridging has been associated with angina, myocardial infarction, and sudden death. 3 These clinical events have been attributed to transient coronary occlu- sion (thrombotic or vasospastic) at the site of the myocar- dial bridge when myocardial bridging is the only coronary abnormality present on angiography. Noninvasive clinical studies have shown mixed results ranging from normal exercise treadmill testing to fLxed or reversible defects found on thallium-201 scintigraphy. 3 One invasive report 8 has described coronary vasospasm induced by intracoro- nary acetylcholine at the site of the myocardial bridge, in- dicating endothelial dysfunction. Apparently "kinking" of the entrapped vessel during systole may cause intimal trauma, endothelial damage, or both. Recently Ge et al. 1° reported the presence of atherosclerosis in the coronary segment proximal to the myocardial bridge by intravascu- lar ultrasound and reduced coronary flow reserve by Dop- pler flow wire.
In all reported cases of atherosclerotic narrowing at the site of a myocardial bridge including our own, the initial result was a success; however, optimal therapy of this con-
dition is not known. Until further data are available, treatment should be aimed at relief of symptoms, and clin- ical decisions regarding patients with symptoms and crit- ical stenoses should be made in the standard fashion. Therapeutic decisions in patients with noncritical stenoses may be aided by the use of intravascular ultrasound and intracoronary Doppler flow wire, although this has yet to be proven. In conclusion, we report a rare case of coronary artery stenosis at the site of a myocardial bridge that was apparent only after angioplasty. It is evident from this re- port and others that the presence of myocardial bridging does not necessarily offer protection from significant coro- nary artery disease.
REFERENCES
1. Stolte M, Weis P, Prestele H. Muscle bridges over the left anterior de- scending coronary artery: their influence on arterial disease. Virchows Arch Pathol Anat 1977;375:23-36.
2. Lee SS, Wu TL. The role of mural coronary artery in prevention ofcor- onary atherosclerosis. Arch Pathol 1972;93:32-5.
3. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26:75-88.
4. Channer KS, Bukis E, Hartnell G, Rees JR. Myocardial bridging of the coronary arteries. Clin Radiol 1989;40:355-9.
5. Ishii T, Asuwa N, Masuda S, Ishikawa Y, Kiguchi H, Shimada K. Ath- erosclerosis suppression in the lei~ anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study. Mod Pathol 1991;4:424-31.
6. Edwards JC, Burnsides CN, Swarm RL, Lansing AI. Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 1956;13:235-42.
7. Laifer LI, Weiner BH. Percutaneous transtuminal coronary anglo- plasty of a coronary stenosis at the site of myocardial bridging. Cardi- ology 1991;79:245-8.
8. Munakata K, Sato N, Sasaki Y, Yasutake M, Kusama Y, Takayama M, Kishida H, Hayakawa H. Two cases of variant form angina pectoris as- sociated with myocardial bridge: a possible relationship among coro- nary vasospasm, atherosclerosis and myocardial bridge. Jpn Circ J 1992;56:1248-52.
9. Parashara DK, Ledley GS, Kotler MN,,Yazdanfar S. The combined presence of myocardial bridging and fixed coronary artery stenosis. AM HEART J 1993;125:1170-2.
10. Ge J, Erbel R, Rupprecht H J, Koch L, Kearney P, George G, Haude M, Meyer J. Comparison of intravascular ultrasound and angiography in the assessment of myocardial bridging. Circulation 1994;89:1725-32.
Cardiac tamponade without pericardial effusion after blunt chest trauma
Steven Levin, MD, Ivan Maldonado, MD, Christina Rehm, MD, Steven Ross, MD, and Richard L. Weiss, MD Camden, N.J.
Tension pneumopericardium is an unusual complication in the patient undergoing critical care and may carry a high
From the Department of Surgery and Medicine, Cooper Hospital/Univer- sity Medical Center; the University of Medicine and Dentistry of New Jer- sey; and the Robert Wood Johnson Medical School at Camden.
Reprint requests: Richard L. Weiss, MD, One Cooper Plaza, Camden, NJ 08103. AM HEART J 1996;131:198-200.
Fig. 1. Portable chest x-ray film obtained in t rauma admitt ing area.
Fig. 2. Biplane transesophageal M-mode echocardiogram of right ventricular (RV) outflow tract. S o l i d a r row indi- cates collapse of RV wall in diastole. Note: no pericardial effusion on images. Clear a r row (in RV outflow tract) dem- onstrates normal wall thickening in systole, thereby ex- cluding RV tardokinesia as cause of abnormality.
Fig. 3. Computed tomography scan of chest revealing large retrosternal air compressing the heart.
mortality rate. Typically the patient has hemodynamic in- stability with adequate intravascular volume and stable airway pressure. The chest x-ray film (Fig. 1) shows a small hear t classically surrounded by air. 1 We present a case with normal x-ray film, hemodynamic instability, and a transesophageal echocardiogram suggesting tamponade. However, no pericardial effusion was seen.
The patient was a 57-year-old unrestrained automobile
driver with chronic obstructive pulmonary disease, after undergoing a head-on collision. She had hypotension (sys- tolic blood pressure = 70), bradycardia, tachypneia, and peripheral cyanosis. Her neck veins were not assessable, and she did not have a pulsus paradoxus. She underwent intubation and fluid resuscitation, and her blood pressure was stabilized. An initial chest x-ray film was normal (Fig. 1). Transesophageal echocardiography revealed a normal
January 1996 200 Grigsby et al. American Heart Journal
aorta, no per icardial effusion, but severe diastolic collapse of the r ight ventr icular outflow t rac t consistent wi th tam- ponade (Fig. 2). To assess he r injuries further, a computed tomography scan was obtained and revealed a left pneu- mothorax pneumoper icard ium (Fig. 3). While the com- puted tomography scan was being done, vent i la t ion be- came difficult to perform, and the pa t ien t had hypotension and bradycardia . An emergent needle was passed through the th i rd intercostal space left pa ra s t e rna l decompression. This procedure res tored hemodynamic stabili ty. The pa- t ient was taken to the operat ing room for immedia te explorat ion and definite dra inage of the pericardium. Bi- la te ra l chest tubes were placed, and a subxiphoid pericar- dial window was performed. A significant rush of a i r was re leased from the per icardial sac on opening the pericar- dium. Abdominal explorat ion revealed a rup tured spleen, which was removed, but no hollow viscous injury. Her postoperat ive course was complicated by prolonged respi- ra tory insufficiency and vent i la tor dependence. However, she did not have any cardiac sequelae and eventual ly was discharged to a rehabi l i ta t ion facility.
Cardiac t amponade as a resul t of pneumopericar- d ium has been shown to be a serious problem associated with a high mor ta l i ty ra te (56%). 2 Tension pneumoperi- cardium occurs only ra re ly after b lunt chest t rauma. Most cases occur in association with p rema tu re infants on positive pressure venti lat ion. Other causes include posi- t ive pressure vent i la t ion in pat ients wi th as thma, 3 pene- t r a t ing chest t r auma, and fistulous t racts between infected or cancerous organs contiguous with the per icardial sac.
Macklin 4 provided histelogic evidence of how air from rup tu red alveoli t ravels along peribronchial and perivas- cular sheathes to the lung h i lum and from there gains ac- cess to the per icardial sac. Per icardia l collagenous t issue is not continuous a t the reflection of par ie ta l onto visceral per icard ium near the ostia of the pulmonary veins, which makes dissection of a i r into the per icardia l sac even easi- er. 5 Air in the per icardia l sac has been shown to cause he- modynamic compromise once the pressure within the sac exceeds 145 m m H20 as demons t ra ted by Adcock et al.6 The resul ts of the t ransesophageal echocardiography were ini t ial ly confusing because of the presence of prominent diastolic collapse of the r ight ventricle consistent wi th a tense per icardial effusion, but no effusion was present. Usual ly per icardia l a i r does not allow adequate imaging of the hear t , bu t in this case excellent images were obtained. Subsequent computed tomography resolved the causes of he r instabil i ty, reveal ing pneumoper icard ium and pneu- mothorax (Fig. 2). The ai r was present re t ros te rna l ly and thus did not compromise the image quality, because a i r did not dissect between the esophagus and hear t , which may also account for the normal appearance of the chest x-ray film. In summary, pneumoper icard ium carries a high mor ta l i ty rate, so ear ly diagnosis is important . I t may be present wi th a normal chest x-ray film on presentat ion. This diagnosis should be considered if classic findings of t amponade are seen on echocardiography and no pericar- dial effusion is identified.
REFERENCES 1. Mirvis SE, Indeck M, Shour RM. Posttraumatic tension pneumoperi-
dium resulting in cardiac tamponade. Ann Thorac Surg 1989;37:511-8. 3. Toledo TM, Moore WL, Nash DA, North RL. Spontaneous pneumo-
pericardium in acute asthma. Chest 1972i62:118-20. 4. Macklin CC. Transport of air along sheathes of pulmonary blood yes-
sels from alveoli to mediastinum: clinical applications. Arch Intern Med 1939;64:913-21.
5. Mansfield PB, Graham CB, Beckwith JB, Hall DG, Sauvage LR. Pneu- mopericardium and pneumomediastinum in infants and children. J Pediatr Surg 1973;8:691-8.
6. Adcock JD, Lyons RH, Barnwell JB. The circulatory effects produced in a patient with pneumopericardinm by artificially varying the intra- pericardial pressure. AM HEART J 1940;19:283-91.
Pseudocoarctation of the aorta complicated by saccular aneurysm: Treatment by aortic arch replacement
J. Lee Grigsby, MD, Timothy Galbrai th , MD, Scott Shurmur , MD, and Ubeydul lah Deligonul, MD Omaha, Neb.
Pseudocoarctat ion of the aor ta is a ra re condition described as an elongation of the aortic arch with "kinking" at the level of the l igamentum arter iosum. In this art icle we present a pa t ien t who had a large aneurysm as a compli- cation of pseudocoarctation.
The pa t ien t was a 49-year-old man with recent occur- rence of l ight-headedness after exertion. He denied dysp- nea on exertion, syncope, chest pressure, or fatigue. No his tory of rheumat ic fever or chest t r a u m a was reported. The physical examinat ion was significant for a grade 3/6 ha r sh systolic m u r m u r of the left s ternal border tha t radi- a ted to the carotids and apex of the heart ; $4 was noted. The carotid upst roke was delayed. The pulses were equal throughout without bruits . An echocardiographic exami- nat ion indicated the aortic valve a rea to be 1.1 cm 2 with a mean gradient of 22 m m Hg. The cardiac catheter izat ion was performed percutaneously wi th the r ight femoral ap- proach. Some difficulty was encountered in t ravers ing the aortic arch, which required over-the-wire ca theter ex- changes. An aortic injection demons t ra ted a large saccular aneurysm of the aortic arch (Fig. 1). The arch i tself was noted to be elongated and tor tuous wi th kinking. An 11 m m Hg peak pressure gradient was seen across the a rea of pseudocoarctat ion. Moderate aor t ic stenosis was demon- s t ra ted as shown in Table I. Retrospective review of the medical records noted a rout ine chest x-ray evaluat ion 4 years previously tha t was suspicious for a superior medi-
From the Section of Cardiology, Department of Internal Medicine, Univer- sity of Nebraska Medical Center, Omaha.
Reprint requests: U. Deligonu], MD, Cardiology Section, UNMC, 600 S. 42nd St., Omaha, NE 68198-2265.
