Volume 119

Number 3, Part 1 Brief Communications 6 7 7

REFERENCES

1. Vincent GM, Anderson JL, Marshal HW. Coronary spasm producing coronary thrombosis and myocardial infarction. N Engl J Med 1983;309:220.

2. Shuster EH, Achuff SC, Bell WR, Bulkley BM. Multiple cor- onary thromboses in previously normal coronary arteries: a rare cause of acute myocardial infarction. AM HEART J 1980;99:506.

3. Madjimiltiades S, Covalesky V, Manno BV, Haaz WS, Mintz GS. Coronary arteriegraphic findings in cocaine abuse-in- duced myocardial infarction. Cathet Cardiovasc Diagn 1988;14:33.

4. Abildskov JA, Burgess MG. Neurogenic abnormalities of ven- tricular repolarization. J Electrocardiol 1971;4:87.

5. Parizel G. Life-threatening arrhythmias in subarachnoid hem- orrhage. Angiology 1973;24:17.

6. Stephenson HE Jr. Cardiac arrest and resuscitation. 4th ed. St. Louis: The CV Mosby Company, 1974:160.

7. Myers MG, Norris JW, Hachinski VC, et al. Cardiac sequelae of acute stroke. Stroke 1982;13:838.

Fig. 2. A and B, Left coronary angiograms showing a thrombus in the proximal segment (arrow), and total occlusion near the apex.

profuse surge of catecholamines is almost certain to play a role. Previously recognized cardiac sequelae of central ner- vous system accidents include electrocardiographic abnormali t ies , 4 arrhythmias , 5 cardiac arrest, ~ and myocar- dial necrosis. 7 Most of these complications can be a t t r ib- u ted to autonomic nervous system imbalance. Both coro- nary arterial spasm and pla te le t aggregation may be enhanced by excessive sympathet ic activity. Fur thermore , coronary spasm may occur in the sett ing of hypervent i la- tion, a common occurrence in association with head t r auma and anxiety. We are, however, unaware of any documented cardiac events in head t r auma without demonstrable intracranial hemorrhage. The contr ibution of post- t rau- matic menta l stress to this phenomenon should also be considered.

Coronary artery-to-left ventricle communication with abnormal regional coronary flow demonstrated by ultrafast computed tomography

James Marshall , DO, W. Jay Eldredge, MD, and Peter B. Kurnik, MS, MD. Camden, N.J.

Diffuse fistulas from a coronary ar tery to the left ventric- ular cavity are rare anomalies tha t can resul t in ischemia, but the mechanism is not well understood. We present a pa t ien t with clinical ischemia and demonst ra ted diffuse fistulas in whom abnormali t ies of regional coronary flow were demonst ra ted by ul t rafas t computed tomography.

A 61-year-old man was admi t ted with unstable angina. He had a blood pressure of 110/66 mm Hg, a pulse of 56 beats/min, and an $4 sound but no murmur. An electrocar- diogram showed sinus rhythm, left ventr icular hypertro- phy, and lateral T wave inversion tha t was new. Episodes of chest pain were characterized by deepening symmetric T wave inversion and by relief with nitroglycerin and return to a nonspecific T wave abnormali ty. Catheteriza- tion demonst ra ted normal hemodynamics and oxygen sat- urations. Upon injection of the left coronary artery, the left ventricle was seen to opaci ty via a diffuse communication arising pr imari ly from the distal circumflex coronary ar tery (Fig. 1). There were no significant obstructive coronary le- sions or bridging. Lef t ventr iculography was normal. The pa t ien t was given a regimen of oral propranolol and ni trates and was ambula tory without symptoms. Ultrafast com- puted tomography was performed in the long-axis view us-

From the Cardiology Division, Robert Wood Johnson Medical School/Uni- versity of Medicine and Dentistry of New Jersey. Reprint requests: Peter B. Kurnik, MD, Cardiac Catheterization Labora- tory, Cooper Hospital/University Medical Center, One Cooper Plaza, Cam- den, NJ 08103. 4/4/18121

M a r c h 1 9 9 0

6 7 8 Brief Communications American Heart Journal

F i g . 1. Left ventriculogram achieved during left coronary arteriography, primarily by diffuse communication from the circumflex artery.

ing nonionic contrast medium. Chamber size, wall motion, and cardiac output were normal. Time-density curves were generated for the ascending aorta and for segments of the myocardium (Fig. 2). Estimation of segmental coronary perfusion in the circumflex distribution was 2- to 2.5-fold increased compared with the left anterior descending region. The time-density curve in the anterior descending region demonstrated the typical tissue pattern of low am- plitude and late peaking. In vivid distinction, the time- density curve in the circumflex region demonstrated a pat- tern similar to that of a vascular chamber, parallel to the aortic curve with an early and accentuated peak. These findings document markedly augmented flow through the circumflex distribution in comparison to that of the other coronary beds.

Fistulas draining into the left ventricle make up only 3 % of all coronary artery fistulas, more than 90% of which drain into the right heart of pulmonary arteryJ A subset with diffuse or plexiform communication is probably rare. A large and diffuse network of vessels could permit shunt- ing, with the theoretical potential for myocardial steal of nutrient blood flow at the tissue level. While case reports, including those employing nuclear imaging, substantiate an ischemic syndrome in patients with diffuse coronary- systemic communication, 2, 3 coronary blood flow has not been previously measured in patients with this anomaly.

Attempts at determining shunt flow through discrete, single coronary artery fistulas have been made in a semi- quantitative manner. 4, 5 A shunt that could account for myocardial steal has not been previously demonstrated in patients with plexiform communication. An examination by oxygen saturations in one patient found shunt flow within the range of normal and insufficient to precipitate ischemia. 6 The presence of ventricular hypertrophy in the absence of hypertension (as in our patient) would produce greater sensitivity to subendocadial ischemia in regions susceptible to myocardial steal.

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Fig. 2. Top, Ultrafast computed tomographic section of the left ventricle in the long-axis view demonstrating the ascending aorta (A) and the left anterior descending (L) and circumflex (C) regions. Bottom, Time-density curves in the ascending aorta and two segments of the left ventricular myocardium. The contrast curve in the circum- flex region has more the shape and timing of a vessel or chamber than of a tissue segment and demonstrates perfu- sion 2.5-fold increased over the left anterior descending region.

Ultrafast computed tomography shows promise of being able to measure regional myocardial perfusion, 7 at least qualitatively, a goal that has been difficult to achieve by any noninvasive technique. Indicator dilution theory utilizes the time-contrast density curves of a myocardial segment and a vascular chamber to calculate local perfusion. Our patient demonstrated circumflex region perfusion that was 2.5-fold increased in comparison to left anterior descend- ing region perfusion. The shape of the circumflex region time-density curve had more the appearance of a vessel or chamber than of a tissue segment, correlating with the ar- teriographic appearance of a diffuse coronary artery-left ventricular communication in that location.

We thank Gerald J. Ukrainski, MD, for referring this patient.

R E F E R E N C E S

1. Perloff JK. Congenital coronary arterial fistula. In: The clin- ical recognition of congenital heart disease. 3rd ed. Philadel- phia: W B Saunders Co, 1987:511.

Volume 119 Number 3, Part 1 Brief Communications 6 7 9

2. Duckworth F, Mukharji J, Vetrovec GW. Diffuse coronary ar- tery to left ventricular communications: an unusual cause of demonstrable ischemia. Cathet Cardiovasc Diagn 1987;13: 133-7.

3. Ahmed SS, Hunter B, Regan TJ. Silent left coronary artery- cameral fistula: probable cause of myocardial ischemia. AM HEART J 1982;104:869-70.

4. Cheng TO. Left coronary artery-to-left ventricular fistula: demonstration of coronary steal phenomenon. AM HEART J 1982;104:870-2.

5. Arani DT, Greene DG, Klocke FJ. Coronary artery fistulas emptying into left heart chambers. AM HEART J 1978;96:438- 43.

6. Brewster HP, Goldschlager N, Goldschlager A. Determination of shunt flow in a case of multiple arteriosystemic connections. Cathet Cardiovasc Diagn 1977;4:79-86.

7. Rumberger JA, Feiring AJ, Lipton MJ, Higgins CB, Ell SR, Marcus ML. Use of ultrafast computed tomography to quan- titate regional myocardial perfusion: a preliminary report. J Am Coll Cardiol 1987;9:59-69.

The echocardiographic recognition of an atrial myxoma vegetation

Paul A. Tunick, MD, Ar thur C. Fox, MD, Alfred Culliford, MD, Rober t Levy, MD, and I tzhak Kronzon, MD. New York, N.Y.

From the Departments of Medicine and Surgery, New York University Medical Center.

Reprint requests: Paul A. Tunick, MD, 560 First Ave.-Suite 2E, New York, NY 1O016.

4 /4 /18117

Myxomas are the most common of the pr imary cardiac tumors. 1 They may present with systemic signs and symp- toms such as fever, weight loss, Raynaud 's phenomenon, clubbing, elevated erythrocyte sedimentat ion rate, and anemia. 2 Infected myxomas are very rare, with only 12 cases reported. 314 In none of those cases was the site of in- fection actually documented preoperat ively (or antemor- tem in the unopera ted cases). I f the diagnosis was made at all, i t was inferred tha t the myxoma was infected because of the presence of positive blood cultures: We present the first repor ted visualization of a vegetation on a myxoma as seen by t ransthoracic and t ransesophageal echocardi- ography.

A 58-year-old man was t ransferred from another hospi- tal where the diagnosis of left a tr ial myxoma had been made. He had been admit ted with fever and was found to have an elevated erythrocyte sedimentat ion rate (73 mm/ hr). Three blood cultures grew Streptococcus sanguis. Ap- proximately 6 weeks prior to admission, he had denta l work performed. There was no history of a murmur or hear t dis- ease and no antibiot ic prophylaxis had been given. Over the ensuing weeks the pat ient noted fever as high as 103 ~ F, night sweats, and chills. He also reported a 10-pound weight loss. Physical examinat ion was remarkable for an accentuated first hear t sound and an in termi t tent soft early diastolic sound. Two-dimensional echocardiography re- vealed a large (6.5 cm) mobile mass with several lobulations tha t moved into the mitral orifice in diastole and back into the left a t r ium in systole. On the pole opposite to its point of a t tachment , on the surface tha t entered the mitral ori- fice with each diastole, there was a mobile, thin, shaggy echo tha t was felt to be consistent with a vegetation. For bet ter visualization of this s tructure as well as for bet ter

Fig. 1. Transesophageal echocardiogram showing left a tr ial myxoma and vegetation, aml, Anterior mitral leaflet; LA, left atr ium; LV, left ventricle; pml, posterior mitral leaflet; TU, tumor; black arrow, stalk at- taching tumor to atr ial septum; large curved white arrow, vegetation; four small white arrows, demonstra- t ion of vegetation at taching to tumor. Note tha t the mitral leaflets are normal and are free of vegetation.