patients suggests that support devices may be associated with an increased morbidity and mortality.7

This study demonstrates that angioplasty of LMCA stenosis can be performed with a high success rate and suggests that angioplasty of unprotected LMCA is a viable option for patients with prohibitive surgical risk. However, the data should be interpreted cautiously, since selection bias and a relatively small number of patients may have contributed to these favorable results. Further- more, close follow-up is essential because a high resteno- sis rate may occur in these patients,’ and a significant proportion of these patients require additional revascu- larization procedures during the ensuing years.

1. O’Keefe JH, Hartzler GO, Rutherford BD, McConahay DR, Johnson WL, Giorgi LV, Ligon RW. Left main coronary angioplasty: early and late results of 127 acute and elective procedures. Am J Cardiol 1989;64:144-147.

2. Ryan TJ, Faxon DP, Gunnar RM, Kennedy JW, King SB III, Loop FD, Peterson KL, Reeves TJ, Williams DO, Winters WL, Jr, Fisch C, D&an&is RW, Dodge HT, Reeves TJ, Weinberg SL. Guidelines for percutaneous transluminal coronary angioplasty. A report of the American College of Cardiology/American Heart Association task force on assessment of diagnostic and therapeutic cardio- vascular procedures (subcommittee on percutaneous transluminal coronary angi- oplasty). Circulation 1988;78:486-502. 3. Stertzer SH, Wallsh E, Bruno MS. Evaluation of transluminal coronary angioplasty in left main coronary artery stenosis (abstr). Am J Cardiol 1981;47:396. 4. Shani J, Gelbfish J, Rivera M, Hollander G, Greengart A, Lichstein E. Percutaneous transluminal coronary angioplasty: relationship between restenosis and inflation times (abstr). J Ant Coil Cardiol 1987;964A. 5. Kaltenbach M, Beyer J, Walter S, Klepzig H, Shmidt SL. Prolonged applica- tion of pressure in transluminal coronary angioplasty. C&et Curdiouasc Diagn 1984;10:213-219. 6. DiSciascio G, V&row GW, Lewis SA, Nath A, Cole SK, Edwards VL. Clinica! and angiographic recurrence following PTCA for nonacute total oc- clusions: comparison of one- versus five-minute inflations. Am Hearr J 1990;120:529-532. 7. Herz I, Fried G, Feld H, Lichstein E, Greengart A, Hollander G, Shani J. High risk PTCA without cardiopulmonary support (abstr). Circuhztion 1990;82(suppl III):III-654.

Symmetry, Broken Symmetry, and Restored Symmetry of Apparent Pure Ventricular Parasystole Agustin Castellanos, MD, Pedro Fernandez, MD, Federicd Moleiro, MD, Albert0 Interian, Jr., MD, and Robert J. Myerburg, MD

P revious reports dealing with the dynamics of “pure” parasystole using mathematic and elec- tronic (pacing-induced) models, respectively,

showed that a number of predictions emerged naturally from mathematic analysis. 1,2 Therefore, it appeared of interest to determine whether they would also apply to a series of patients with clinical (apparently) “pure” ven- tricular parasystole who were monitored for relatively long periods of time. In contrast to previous studies, Glass et al’ had the ingenious idea of analyzing the number of sinus beats interposed between 2 consecutive manifest parasytolic beats. They observed that, with the rates being practically constant, a detailed mathematic de- scription could be made using 2 parameters: the ratio of ectopic cycle length to sinus cycle length and the ratio of ventricular refractory period to sinus cycle length. From a correlation of these parameters 3 basic rules emerged: ( 1) There are at most 3 different values for the number of sinus beats in between parasystolic beats. (2) Only 1 of these values is odd. (3) The sum of the 2 lesser values is 1 less than the larger value.

From the Division of Cardiology, Department of Medicine, University of Miami School of Medicine, P.O. Box 016960, Miami, Florida 33101. This study was supported in part by research grant HL-28 130 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. Man- uscript received January 28, 1991; revised manuscript received March 15,1991, and accepted March 18.

We attempted to determine whether symmetry (a term extrapolated from Kaku and Trainer,l’ here meaning that sinus andparasystolic rhythms could be linked by the aforementioned mathematic rules) was present in 10 cases in whom continuous ventricular parasystole had been reprospectively identified. In 9 patients, the diagnosis was made by 24-hour Holter recordings and in I the diagnosis was made by long ( 1 to 3 minutes) rhythm strips obtained at frequent inter- vals from a coronary care unit monitoring device.

Table I lists the pertinent information. In the man- ner of Glass et a1,1a234 we defined the refractory period as the shortest interval between a sinus-induced QRS complex and a parasystolic beat. We attempted to identify symmetry once the diagnosis of parasystole had been made, when sinus cycle length and ectopic cycle length were first found to be “‘constant” (i.e., with variations of <f-5%). We found symmetry in all patients.3 At the time at which this initial symmetry occurred, the refractory period ranged between 380 and 540 ms and the ectopic cycle length between 1,040 and 2,330 ms. The ectopic cycle length/sinus cycle length ratio varied between 1.58 and 2.74 and the refractory period/sinus cycle length ratios between 0.43 and 0.64. When these values were plotted in the refractory period/sinus cycle length, ectopic cycle length/sinus cycle length plane used by Glass et al,’

256 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68 JULY 15, 1991

TABLE I Values, Ratios and Symmetries of Apparent Pure Parasystole

TEKS RP/TS Pt. Ratio Ratio

1 1.63 0.59 2 1.68 0.50 3 1.65 0.50 4 1.73 0.60 5 1.58 0.43 6 1.59 0.47 7 2.74 0.64 8 2.39 0.56 9 2.24 0.54

10 2.23 0.49

RP = refractory period; TE = ectopic cycle length; TS = sinus cycle length.

Symmetry: Numbers

1,2, 4 1,294 1, 2, 4 1,2, 4 1,2,4 1,294 2,7, 10 2,7, 10 1, 6, 8 1, 6, 8

TE

1,040 1,280 1,320 1,210 1,520 1,480 2,330 2,220 1,500 1,920

TS

640 760 800 700 960 930 850 930 670 860

RP

380 380 400 420 410 440 540 520 360 420

they yielded the expected number of sinus beats be- tween consecutive manifest parasystolic beats (hereby considered as the numbers of symmetry). These val- ues were the same as those directly counted on electro- cardiographic paper running at a speed of 25 mm/s (Table I). Although the latter was that at which all measurements were performed, some illustrations will be presented at slower paper speeds since they were those at which I or more minutes of recording time could be best presented as a single figure. The numbers of initial symmetry were 1, 2 and 4 in 6 patients: 2, 7 and IO in 2 patients: and I, 6 and 8 in 2 patients. However, in all patients this initial symme- try was broken and subsequently restored.L6

An example is shown in Figure I. It shows the well- known characteristics that for many years have been attributed to “pure” parasystole.s In this example, where the corresponding ratios were 0.59 and 1.63, respectively, the X in the corresponding region indi- cated the predicted 3 values (1, 2 and 4) which were

precisely the number (in parentheses, below the rhythm strip) of hand-counted sinus beats between manifest parasystolic beats. In Figure 2, ectopic cycle length was 2,330 ms; sinus cycle length, 850 ms; and refractory period, 540 ms. Thus, the corresponding ectopic cycle length/sinus cycle length and refractory period/sinus cycle length ratios had values of 2.74 and 0.54, respectively. Consequently, the numbers of ini- tial symmetry were 2, 7 and 10.’ Figure 3 (top), ob- tained 40 seconds later, at a slower paper speed (with each horizontal line representing 20 seconds of re- cording time), reveals that when sinus cycle length varied erratically (increasing and decreasing), the symmetry was broken, since number I3 appeared sev- eral times (instead of number 1O).3Js However, when the initial conditions (previous values) recurred 2 minutes later, the preexisting symmetry was restored, as can be seen in the lower panel where the number of sinus beats between parasystoiic beats was again 2, 7 and 1O.3

FIGURE 1. Apparent “pure” ventricular parasystoie. Tracing obtained at a paper speed of 25 mm/s. The diagram, from Glass et al,l depicts the mathematically predicted number of sinus beats in be- tween ectopic beats in the refractory peri- od (RP)/sinus cycle length (TS), ectoptc cy- cle length (TE)TrS plane for pure parasys- tole. For each region, the allowed values are indicated by 3 integers. The location X in parameter space correspondr; to the predicted numbers in this case (1,Z and 4) that coincide with the numbers of di- rectly counted interposed sinus beats. The latter (numbers of symmetry) are shown in parentheses below the rhythm strip, where the corresponding time intervals are expressed in milliseconds. F = fusion beat (also considered a manifest dis- charge)‘; X = morphology of totally mani- fest parasystolic discharges. (Reproduced with permission from the American Physi- ological Society.)

1 SYMM;TRY: 1,2,4 F

99

(4)

i 3120 =

i

(2) x 1’) 20803 A

1040x3

X (2) ;

1040x2 T 1040 2100 =

1050x2

(FROM GLASS ET ALI

TE / Ts = 163 Pm W) .

RP / TS (360) (640) = Ov5’

BRIEF REPORTS 257

Figure 4 (top) depicts how the initial symmetry was lost for other reasons.2 It occurred when sinus cycle length changed, but not erratically.2 Note that sinus cycle length decreased persistently (to 900 ms) whereas ectopic cycle length and refractory peri- od remained constant. Therefore, the ectopic cycle length/sinus cycle length ratio and the refractory pe- riod/sinus cycle length ratio became 2.59 and 0.53, respectiuely.’ Consequently, in the refractory period/ sinus cycle length, ectopic cycle length/sinus cycle length plane of Glass et al, there was a shift to the 2,4,

and 7 zone. The initial symmetry recurred when the cycle length again increased to the original values so that the initial conditions resumed (bottom).

Our report corroborates that predictions regarding the number of sinus beats between parasystolic beats could be made for a group of patients with apparent “pure” ventricular parasystole. This had been reported by Gordon et al2 in a patient having parasystole with “weak” modulation. Moreover, in a study of modulated parasystole, Courtemanche et al4 noted that rhythms associated with quasiperiod~city obeyed the rules derived

SYMMETRY : 2,7, 10 TE/TS: 2.74 RPITS: 54

2330

FIGURE 2. Apparent ‘pure” ventricutar parasystete. Recerdings were obtained at a paper speed of 25 mm/s. The 2 strips are continuous. The numbers circted (2,7 and 10) m the numbers of symmetry, i.e., of sinus beats interpesed between con- secutive manifest parasystotii beats. 7hb arrowheadat the beginning of the fop indiites that there yere 5 additional sinus beats between the immediately preceding mantfest parasystogi discharge (not shown) and the first discharge QC) seen in this fig- ure. Ahhreviatiem as in Figure 1.

BROKEN SYMMETRY: SEE NUMBER 13

RESTORED SYMMETRY : 2,7,10 39

FIGURE 3. Same patient as in Figure 2; recordings were obtained at a sbwer paper speed. Eacu horizontal he reprem& 20 seconds of recording time. 7ep pane/ shows that the symmetry was test because number 13 (instead of 10) appeared 3 times during 1 minute. This eccurred when the sinus cyde tength changed erratically. In the boffom 2 strips, the preexisting symme- try was restored when the initjal conditions resumed (the sinus cyde tength again attained a constant vatue stmilar to the preex- is&g value).

SHIFT TO 2,4,7, ZONE WHEN TE (2330)/TS(900j~2.59;RPklSO)/TS(9OOk0.53 +‘.‘:23 ::-

x+@+=x @ xt@+x

ORIGINAL SYMMETRY RESTORED WHEN TE/TSz2.70; RP/TS-0.56 - X

FIGURE 4. Same patient as in Figures 2 and 3. Loss of the preexisting symmetry occprhg when the siw cyck length (TS) in- creased consistentty (top). *is caused in the RP/t’S, TE/t3 plane, of Gtass et ai,’ a shii to the 2,4 and 7 zone. Note Utat these were precisety the nmnbsr of sinus beats interposed between manifest parasystogi peats. Bottom, ths preexisting symmetry was restored when the initial conditions resumed (7S became persistentiy shorter). Abbreviations as in Figure 1.

258 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68 JULY 15, 1991

for “pure” parasystole. They also observed that these rules were also fulfilled in some sporadic cases reported by other investigators.

The mathematic relation under consideration - symmetry - was found in all our patients.3 Precisely, its identification, not the exact moment at which parasytole was diagnosed, was considered as the starting point of the current study. However, initial symmetry did not last for long periods of time (only minutes), considering that the tracings were obtained for 24 hours. A review of the tapes showed that the lost symmetry resulted from the fact that the physiologic parameters tended to change as time went by. Of the 3 pertinent parameters, we have ob- served that in absence of exit block, refractory periods tended to be constant. Yet, sinus cycle length and ectopic cycle length (the former more than the latter) were seen to be changing variables. In fact, it is well known that sinus cycle lengths show frequent fluctuations. More- over, parasystolic cycle lengths are also not constant, but less so than the former.5 Although not analyzed as such in this study, it is possible to consider that during a 24- hour period parasystole shows not 1 but several symme- tries, with the corresponding numbers depending on the

different values that the changing parameters attain throughout the monitoring time (Figures 2 and 4).

Finally, in our patients, the possibility that the ar- rhythmia diagnosed as “pure” parasystole may have been parasystole with “weak” modulation cannot be completely excluded. Because there were some variations in parasystolic cycle lengths during the overall (long- term) recording time, fluctuations attributed to changes in the timing of automatic discharges could have reflect- cd lesser degrees of modulation than degrees of variations of automaticity. However, this in no way would invali- date our study since, as previously mentioned, “weak” modulation may obey the rules of pure parasytole.2,4

1. Glass L, Goldberger AL, Belair J. Dynamics of pure parasystole. Am J Physiol 1986;251:H841-H847. 2. Gordon D, Scagliotti D, Courtemanche MT Glass L. A clinical study of the dynamics of parasystole. PACE 1989;12:1412-1418. 3. Kaku M, Trainer J. Beyond Einstein. The cosmic quest for the theory of the universe. New York: Bantam Books, 1987;109:121-123. 4. Courtemanche M, Glass L, Rosengarten MD, Goldberger AL. Beyond pure parasystole: promises and problems in modeling complex arrhythmias. Am J Physiol 1989;257:H693-H706. 5. Scherf D, Schott A. Extrasystoles and Allied Arrhythmias. 2nd ed. Chicago: Year Book Medical Publishers, 1973:271-272. 6. Hawking SW. A Brief History of Time. New York: Bantam Books, 1988;71.

Effects of Amiodarone on Serum Lipoprotein Levels Stewart G. Albert, MD, Larry E. Alves, MD, and Edward P. Rose, MD

A miodarone is an antiarrhythmic agent approved for the treatment of recalcitrant ventricular ar- rhythmias. It is an amphiphilic-iodinated organ-

ic compound with a prolonged elimination rate, and has been associated with a high incidence of thyroid dysfunc- tion.’ In a previous evaluation of the effects of amioda- rone, serum cholesterol was monitored as a systemic marker for thyroid dysfunction.2 Unexpectedly, there were uniform increases in serum cholesterol independent of thyroid hormone status. Controversy exists as to whether there are changes in serum cholesterol levels in patients receiving amiodarone,2-6 and it is important to define the action of this drug on high-risk patients who already have heart disease.

Twenty-seven patients (I 5 men and I2 women: 18 with paroxysmal ventricular tachycardia, 6 with mul- tiform ventricular arrhythmias associated with arte-

From the Divisions of Endocrinology and Cardiology, Department of Internal Medicine, St. Louis University School of Medicine, 1402 South Grand Boulevard, St. Louis, Missouri 63104, and the Depart- ment of Internal Medicine, Memorial Hospital, Belleville, Illinois. Manuscript received December 17, 1990; revised manuscript received March 11, 1991, and accepted March 18.

riosclerotic cardiovascular disease and 3 with symp- tomatic atrialflbrillation; mean age f standard error of the mean 70 f 2 years) who required amiodarone for the control of severe symptomatic arrhythmias were followed prospectively. The clinical procedures for monitoringfor efficacy and adverse reactions were described previously.2 Amiodarone was given at a loading dose of 400 to 600 mg/day initially followed by a maintenance dose of 200 mg/day. If the arrhyth- mia was refractory as assessed by electrocardiogra- phy and ambulatory monitoring or by exercise testing, the initial dose was repeated. When necessary the maintenance dose was titrated upward. The mainte- nance dose was also adjusted downward according to adverse side effects, predominantly symptomatic bradycardias. Many patients with arteriosclerotic cardiovascular disease had underlying hypercholes- terolemia, and 3 had been receiving stable doses of gemfibrozil; 3 had started receiving lovastatin either previously (n = I) or at baseline (n = 2) concomitant- ly with the amiodarone. Fifteen subjects were receiv- ing thiazides and 2 were receiving estrogens; these medications were started before the amiodarone and

BRIEF REPORTS 259