Volume 125, Number 3 American Heart Journal Rechavia et aE. 893 * P c 0.01 vs baseline values A P e 0.005 vs recovery values of nMI r* ; E 40. recovery F maximum ’ 30. MI 5 5 20 nMI I -10 recovery g baseline maximum a ul Rest 0 1 1.5 5 9 minutes Fig. 1. SACE levels in ischemic (IMI) and nonischemic (nMII subjects during exercise test. Table II. SACE activity during the exercise test SACE (nmol/ml/mini Groups -10 0 Maximum Recovery Ischemic (n = 9) "0.78 t 1.99 22.06 f 2.17 ‘25.18 t xv*I I 28.95 t 5.09*i Nonischemic (n = 9) 21.80 c X.70 21.50 k 4.80 2::.30 +- ,'3.10 22.00 k 3.40 *p < 0.01 versus baseline values. tp < 0.005 versus nonischemic at recovery in the event of myocardial ischemia, SACE increases (kininase II) in human endoehelial cells in culture. Adv Exp markedly at maximum effort as well as during recovery. Med Biol 1978;120B:287-90. Our data on SACE activity in nonischemic subjects support 9. Hayes LW, Goguen CA, Ching SF, Slakey LL. Angiotensin- converting enzyme: accumulation in medium from cultured similar results obtained by Milledge and Catley,” who endothelial cells. Biochem Biophys Commun 1978;82:1147-9. found SACE to remain unchanged during extended stress 10. Kasahara Y, Ashihara Y, Harada T. The method for determi- testing (up to 60 minutes) in normal healthy subjects. In nation of angiotensin I converting enzyme (ACE) activity. Clin light of our findings, we propose that SACE elevation could Chem 1981:27:1114-B. 11. Milledge JS, Catley DM. Renin, aldosterone and converting reflect acute endothelial vascular damage (both in general enzyme during exercise and acute hypoxia in humans. J Appl and in particular in the cardiac vasculature) in subjects Physiol 1982;52:3‘20-3. with clinical and ECG signs of myocardial ischemia during stress testing (regardless of the duration of exercise). Protruding left ventricular thrombus REFERENCES formation following blunt chest trauma 1. Erdos EG. The angiotensin I converting enzyme. Fed Proc 1977;36:1760-5. Eldad Rechavia, MD, Shula Imbar, 2. Soffer RL. Angiotensin-converting enzyme and the regulation Yochai Birnbaum, MD, Boris Strasberg, MD, and of vasoactive peptides. Ann Rev Biochem 1976;45:73-94. 3. Skeggs TL, Kahn JR, Shumway NP. The preparation and Samuel Sclarovsky, MD function of the angiotensin-converting enzyme. J Exp Med Petah-Tiqva and Tel-Aviv, Israel 1956;103:295-9. 4. Caldwell PRB, Seegal BG, Hsu RC, Das M, Sofl’er RL. Angiotensin converting enzyme vascular endothelial localiza- tion. Science 1976;191:1050-1. 5I Ryan JW, Ryan US. Correlation of pulmonary structure with From the Cardiovascular Division and Coronary Care Unit. Beilinson Med- pharmacokinetic function. Agents Actions 1976;4:510-4. ical Center, Petah-Tiqva; and the Tel-Aviv University Sackler School of 6. Studdy PR, Lapworth R, Bird R. Angiotensin-converting en- Medicine. zyme and its clinical significance: a review. J Clin Path01 198X36:938-47. Reprint requests: Eldad Rechavia, MD, Cardiovascular Division. Beilinson Medical Center, Petah-Tiqva, 49100 Israel. 7. Wigger HS, Stalcup SA. Distribution and development of an- giotensin-converting enzyme in the fetal and newborn rabbit. AM HEART J 1993;125:893-896. An immunofluorescence study. Lab Invest 1978:38:581-X Copyright 1993 by Moshy-Year Book. Inc. 8. dohnson AR, Erdos EG. Angiotensin I converting enzyme 000’.8703/93/WXl+ .lO 4/4/43467 March 1993 Amencan Heart Journai Fig. 1. ECG showing QS complex in the precordial leads and a right h\lnrl!e branch I)!ock-left anterior hemiblock pattern. Following myocardial contusion, attention has been tradi- 120/80 mm Hg and the pulse rate was 64 beats/min. On ex- tionally directed toward the hemodynamic derangement amination. there was tenderness over t.he left precordium that it produces as well as life-threatening ventricular ar- and a fourth heart sound was audible. As the possibility 01 rhythmias. I,? Little attention has been devoted to the pos- chest trauma was considered, careful anamnesis elicited sible formation of thrambus and the potential thromboem- that the patient had probably sutfered bruising of the left bolic hazards thus evoked. A case is presented of a young anterior chest wali. A chest x-ray film was normal. Contin- patient with normal coronary arteries in whom an unnoted uous monitoring revealed frequent ventricular premature blunt trauma to the chest gave rise to septoapical dyskine- beats and short. runs of ventricular tachycardia. Cardiac sia and protruding left ventricular (LV) thrombus forma- enzyme levels including creatine kinase MB fraction were tion. indicative of infarction. Two-dimensiona echocardiogra- A 35year-old man with no history of heart disease or phy performed the next day showed septoapical dyskine- cardiac risk factors was referred to a surgical department sia and an LV mass protruding into the chamber cavity of our hospital following maxillofacial trauma. He was with marked mobility (Fig. 2). The mass length from apex pushed from a one-story structure, falling on a slanted sur- to the mobile end reached 1.2 cm. Cardiac catheterization face scattered with fairly large poles. An open fracture of demonstrated patent coronary arteries. Ventriculography the left zygomatic bone was accompanied with swelling and was not performed for fear of dislodging the thrombus. The the appearance of hematoma around the lateral aspect of patient was treated by continuous intravenous heparin in- his left eye. Apart from pain at the site of trauma, the pa- fusion (1000 units per hour), followed by warfarin treat- tient complained of blurred vision and troublesome irrita- ment. Follow-up echocardiographic examinat.ion at 1 week, tion in his eye. At the time of admission, no history or ev- 2 weeks, and 1 month later showed gradual regression of the idence of chest trauma was obtained. Three days later, in t.hrombus dimensions, with diminished protrusion and the operating room and just before surgical repair and re- mobility. At a X-month follow-up, echocardiographic find- positioning of the zygomatic fracture, he complained of ings were compatible with mural nonprotruding apical sharp precordial pain on deep inspiration, radiating to his thrombus. No seyuelae of embolization or further ECG left arm. An electrocardiogram (ECG) performed in the changes were noted during the 4-month follow-up period. operating room showed a right bundle branch block-left Ventricular thrombus, logically expected in the setting of anterior hemiblock pattern and QS complex in the precor- myocardial contusion, is surprisingly a relatively rare dial leads (Fig. 1). At this stage, surgery was postponed, and echocardiographic finding. In three prospective echocar- the patient was transferred to the coronary care unit. When diographic studies involving 2’79 individuals, thromhus was seen For the first time in the unit, his blood pressure was documented in none of the patients suff’ering myocardial Volume 125, Number 3 Rechauia et al. 895 American Heart Journal Fig. 2. Two-dimensional two-chamber apical view showing a protruding thrombus in the dyskinetic sep- toapical area of the left ventricle. contusion.“.” However, there is more than anecdotal evi- configuration. Anticoagulation proved to be efficient, de- dence to suggest that in those patients demonstrating wall creasing the size of the thrombus and presumably reducing motion abnormalities related to cardiac contusion, a high the potential risk for embolization. Thrombus formation index of suspicion should be maintained to ensure that no following myocardial contusion may be related either to clinical sequelae of ventricular thrombus may occur. In direct myocardial insult or to compression of a coronary this context, it has been recently concluded by Wisner et artery, resembling myocardial infarction. The first seems al.’ that most of the patients who are prone to life-threat- the more plausible explanation in our patient, who was ening cardiac complications from blunt cardiac injury can thought to have myocardial contusion based on elevation be identified soon after the traumatic event in an emer- of serum cardiac enzymes, electrical instability, mechani- gency room setting. However, one should bear in mind that cal dysfunction, and a normal coronary angiogram. We thrombus could easily be missed if echocardiography is have been able to find in the literature only two reported performed immediately after blunt contusion. As in myo- cases of ventricular protruding thrombus induced by blunt cardial infarction, it is not inconceivable that ventricular chest trauma.*, “’ thrombus, either mural or protruding, will be seen 2 or 3 Cardiac injury is a common and frequently unsuspected days following myocardial contusion, giving rise to a visceral injury. r’ Patients may be free of any cardiac delayed embolic complications As thrombus formation is symptoms or may have transient complaints. In the present promoted by severe wall motion abnormality, echocardio- case, chest trauma was probably masked by the major graphic follow-up is strongly recommended in this subset maxillofacial injury. As we noted, even “innocent” trauma of patients demonstrating early wall motion abnormalities. may result in protruding thrombus formation, and had the Embolic complications in patients with thrombus-re- patient not complained of chest pain, the thrombus could lated myocardial contusion have been sparse.H-12 It remains have gone undetected, with the patient exposed to both debatable whether an echocardiographic finding of a mu- operative and a major delayed embolic risk.” ral thrombus warrants prophylactic anticoagulation.“’ The therapeutic approach might be entirely different when REFERENCES protruding thrombus is apparent, mainly because of its higher propensity (up to 60’, of cases) toward emboliza- 1. Traumatic injury of the heart. Lancet 1990;336:1287-9. 2. Tenser ML. The spectrum of myocardial contusion: a review, tion.‘.l, ” Although anticoagulation has questionable ben- .J Trauma 1985;25:620-7.