1074 Brief Communications June, 1982

funerican Heart Journal

90 set

Fig. 1. ECG lead II immediately postcardioversion show- ing transient ST elevation with rapid sequential return to baseline within 90 seconds.

logic evidence of myocardial injury in animals.” However, in patients with transient ST elevation following cardio- version, cardiac CPK isoenzymes and myocardial scintig- raphy with technetium-99m-pyrophosphate and thallium- 201 have failed to reveal evidence of myocardial damage, suggesting that a mechanism other than myocardial necro- sis is operative.” Following abrupt coronary artery ligation, ST elevation does not begin until 45 seconds have elapsed.6 In our case, maximal ST elevation occurred immediately following cardioversion. In dogs, DC cardio- version elicits a vagotonic reflex which decreases coronary vascular resistance.’ These findings imply that transient ST elevation following cardioversion is unlikely to be caused by electrical-induced coronary spasm.

Embryonic heart cells in tissue culture maintain elec- trophysiologic properties similar to intact myocardium.R If current nine times depolarization threshold is passed through a heart cell culture, depolarization occurs which may persist for many seconds to minutes, as the ability to spontaneously depolarize is restored and resting mem- brane potential approaches baseline intracellular negativ- ity?” When a critical mass of myocardial cells in the intact heart undergoes sustained depolarization, a difference in electrical potential exists between the depolarized and normal tissue. This could be reflected as ST elevation in the negative recording leads of the surface ECG. Since ST elevation occurs most frequently in the myocardium clos- est to the origin of countershock current, it is postulated that the higher current density to which such tissue is exposed results in localized ST elevation.” While the possibility of inducing coronary artery spasm suggests caution when electively cardioverting patients with vari- ant or rest angina, the available evidence appears to indicate that DC cardioversion is unlikely to cause vaso- spasm. Thus transient ST elevation postcardioversion is apparently unassociated with myocardial necrosis and, in

contrast, could be explained by sustained depolarization of the regional myocardium most exposed to highest current density.

REFERENCES

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4.

5.

6.

7.

8.

9.

Sussman RM, Wallenberg DH, Cohen M: Myocardial changes after direct current electroshock. JAMA 189:739. 1964. Gertz SD, Merin G, Pasternak RC, Gotsman MS, Blaumanis DR, Nelson E: Endotheiial cell damage and thrombosis following partial coronary constriction: Relevance to the pathogenesis of myocardial infarction. Isr .I Med Sci 14384, 1978. Lepeschkin E. dories .JL, Rush S, ,Jones RE: Analysis of cardiac damage following elective cardiac defibrillation. Car- diac Defibrillation Conference, Purdue llniversity. Lafayette, tnd.. Oct., 1975. pp 85-90. Dahl CF. F:wy GA. Warner ED, Thomas ED: Myocardial necrosis from direct current countershock: Effect of paddle electrode size and time int.erval between discharges. Circula- tion 50:956, 1974. Chun PK, Davia JE, Donohue DJ: ST segment elevation with elective cardioversion. Circulation 63:2X), 1980. Weiner .JM, Apstein CS, Arthur ,JH. Pirzada FA, Hood WH .Ir: Per&tam-e of myocardial injury following brief periods of coronary occlusion. Cardiovasc Res 10:678. 1976. Cobb FR. Wallace AC,, Wagner GS: Cardiac inotropic and coronary vascular responses ttr rountershock. Circ Res 23X31. 1968. Sperelakis N: Electrical properties of embryonic heart cells. In DeMello WC. editor: Electrical phenomena in the heart. New York, 1972, Academic Press, Inc, p 1. .Innes ,JL. Rush S. *Jones RE, Lepeshkin E: (‘ultured chick heart cells as a model for cardioversion trauma. Fed Proc 323431. 197:I.

Diastolic prolapse in the flail mitral valve syndrome: A new observation providing differentiation from the mitral valve prolapse syndrome

George Cherian, D.M. (Card), Chuwa Tei, M.D., Pravin M. Shah, M.D., and Maylene Wong, M.D. Los Angeles, Calif.

The spectrum of echocardiographic manifestations in the mitral valve prolapse (MVP) syndrome] and the features of the flail mitral valve (FMV) syndrome have been described.‘” In the FMV syndrome, there is loss of coaptation at the tip of the valve leaflets and the tip of the abnormal leaflet points towards the left atrium (LA).” Since the mitral valve starts to float back into a “closed”

From the Ijepartment 01 Medicine, University U[ f’alifornia School r>t Medicine, and U’adsw<ltth Veterans Administratim Medical Center.

Received tar publication Feh. 11. 1982: accepted Feb. 22. 1982.

Reprint requests: George Cherian. D.M.. C’ardiology Section (691/l 11E). Wadsworth VA Medical Center. Wilshire and Sawtelle Rlvdn., Los Angeles. (‘A 900X

0002-8703/82/061074 + 02$00.20/O c 198“ The C. V. Mosby Co.

Volume 103 Number 6

Fig. 1. Three stop frames in diastole from a FMV patient in atria1 fibrillation. The flail anterior mitral leaflet (AML) in early diastole (frame A) is pointing towards the left ventricle (LV). In a later frame (B), before the QRS it has already moved posteriorly into the left atrium (LA). Frame C at the beginning of the QRS complex shows a similar finding. PW = posterior LV wall; PML = posterior mitral leaflet; IVS = interventricular septum.

position even before the onset of ventricular systole, the unsupported flail leaflet can be expected in some instances to float in and out of the LA, independent of ventricular systole. We examined the timing of mitral leaflet displacement posterosuperiorly past the mitral anular plane into the LA in I2 patients with FMV and in 23 with MVP. The timing of leaflet displacement was related to the ECG using a single-frame analysis tech- nique. Apical four-chamber and parasternal long-axis two-dimensional echocardiograms (2DE) were studied independently by three observers, by initially covering the ECG signal and later exposing it, after the timing of prolapse was identified. Nine patients with FMV were in sinus rhythm and three were in atria1 fibrillation (AF). Eight had flail posterior and four had flail anterior leaflets.

All of the 12 FMV patients showed an initial abnormal leaflet displacement past the mitral anular plane into the LA in diastole prior to the onset of the QRS complex (Fig. 1). On the other hand, in all 23 patients with MVP, the prolapse of the leaflet was noted only after the QRS complex. In the FMV patients in AF, the interval between the abnormal leaflet, displacement and the QRS varied

Brief Communicafions 1075

Fig. 2. Four stop frames from a FMV patient showing the biphasic movement in diastole during sinus rhythm of the flail posterior mitral leaflet (PML) indicated by the arrow. In mid-diastole (A), the leaflet points towards the left ventricle (LV); just before the P wave (B) the PML has moved posteriorly into the left atrium (LA). After atria1 systole (C) the PML is now pointing towards the LV, and again back towards the LA in frame D before the QRS. AML = anterior mitral leaflet.

from 67 to 363 msec, being greater with a longer R-R interval. In five of nine patients with FMV in sinus rhythm, the diastolic prolapse of the abnormal leaflet was biphasic, once before the P wave, and after floating back into the left ventricle, again before the QRS complex (Fig. 2). In the remaining four, this occurred only before the QRS complex. Diastolic prolapse in the FMV syndrome, hitherto undescribed, is an interesting observation which could be a useful additional sign in its differentiation from MVP.

REFERENCES

1. DeMaria AD, King JF, Bogren HG, Lies JE, Mason DT: The variable spectrum of echocardiographic manifestations of the mitral valve prolapse syndrome. Circulation 50:33, 1974.

2. Sweatman T, Seizer A, Kamagaki M, Cohn K: Echocardio- graphic diagnosis of mitral regurgitation due to ruptured chordae tendineae. Circulation 46:580, 1972.

3. Duchak JM Jr, Chang S, Feigenbaum H: Echocardiographic features of torn chordae tendineae. Am J Cardiol 29:260, 1972.

4. Burgess J, Clark R, Kamigaki M, Cohn K: Echocardiographic findings in different types of mitral regurgitation. Circulation 48:97, 1973.

5. Feigenbaum H: Echocardiography. Philadelphia, 1981, Lea & Febiger, p 267.