Angiographic correlates of recurrent sustained ventricu+ar tachycardia in chronic ischemic heart disease

We report the angiographic studies of 53 consecutive patients with angiographic coronary artery disease (CAD) and recurrent sustained ventricular tachycardia occurring at least 6 weeks remote from an acute myocardial infarction. Triple-vessel disease was present in 25 patients (47%) double-vessel disease in 19 patients (36%), and single-vessel disease in nine patients (17%). All patients with single-vessel disease had left anterior descending coronary artery obstruction. Patients under 50 years old had significantly fewer diseased vessels than those over 50 years old (1.4 vs 2.4 vessels diseased; p < 0.025). Left ventricular ejection fraction ranged from 0.15 to 0.61 (mean 0.34 f 0.11) and was 0.25 or less in 14 patients (26%). All patients had regional wall motion abnormalities. There was akinesia and/or dyskinesia in 49 patients (92%). Akinesia or dyskinesia was inferior in 17 patients (32%), anteroaplcal in 14 patients (26%) inferoapical in 10 patients (19%) and anteroapicoinferior in 6 patients (11%). Involvement of the septum was noted in 19 patients (36%) and of basal segments in 26 patients (49%). An average of 2.7 (out of seven) segments per patient were dyskinetic or akinetic. Thus multivessel disease, markedly reduced ejection fraction, and severe and extensive regional wall motion abnormalities are generally present. These findings have pathophysiologic as well as clinical and therapeutic implications. The natural history of these patients as well as the results of therapy should be related to the underlying coronary anatomy and left ventricular function. (AM HEART J 105:926, 1963.)

Wilfred Lam, M.D., Raymond Pietras, M.D., Robert Bauernfeind, M.D., Steven Swiryn, M.D., Boris Strasberg, M.D., Edwin Palileo, M.D., and Kenneth M. Rosen, M.D. Chicago, 121.

Coronary artery disease may be complicated by the occurrence of recurrent sustained ventricular tachy- cardia. The natural history as well as the results of therapy should be related to the underlying coro- nary and left ventricular angiographic anatomy and function.1-3 The suitability of surgical approaches and the success of therapy for ventricular tachycar- dia (whether medical or surgical) should be judged in the context of the severity and extent of the underlying coronary disease and left ventricular abnormalities.4

Previous systematic descriptions of the angio- graphic anatomy in patients with recurrent sus-

From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois College of Medicine.

Supported in part by Institutional Training Grant HL 07387, National

Heart, Lung, and Blood Institute, Bethesda, Md., and grants from the Eleanor B. Pillsbury Resident Trust Fund and Bane Estate.

Received for publication Oct. 19, 1981; revision received Feb. 12, 1982; accepted March 3, 1982.

Reprint requests: Wilfred Lam, M.D., University of Illinois Hospital, Cardiology Section, P.O. Box 6998, Chicago, IL 60680.

tained ventricular tachycardia complicating isch- emit heart disease (IHD) have been predominantly in patients selected for surgical therapy of ventricu- lar tachycardia. 5, 6 No previously unselected group of patients has been analyzed in order to assess the spectrum of coronary disease or left ventricular dysfunction associated with this problem. In this report, we describe the coronary and left ventricular angiographic anatomy in 53 consecutive patients referred for recurrent sustained ventricular tachy- cardia complicating chronic coronary artery disease. This study provides insight concerning the biology of ischemic heart disease and the anatomic corre- lates associated with recurrent sustained ventricular tachycardia. In addition, the results of this study are compared to previously reported findings of patients with related clinical problems such as sudden death associated with coronary disease. Our results are also relevant to the selection of surgical modalities of treatment (i.e., coronary bypass grafting, ventric- ular aneurysmectomy, plication, or subendocardial resection) and to the expected life history if ventric- ular tachycardia is palliated.

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METHODS

Patients. The study group consisted of 53 consecutive patients referred to the IJniversity of Illinois Westside Medical Center between 1974 and 1980, who fulfilled the following two criteria for inclusion: (1) Two or more documented episodes of paroxysmal sustained ventricular tachycardia occurring at least 6 weeks remote from an acute myocardial infarction, necessitating either pharma- cologic or electrical conversion for termination, and (2) demonstration of significant coronary artery obstruction at coronary arteriography. Diagnostic cardiac catheteriza- tion has been routinely performed at the University of Illinois Wests:ide Medical Center in patients with recur- rent sustained ventricular tachycardia.

Coronary angiography. The extent and severity of coronary artery disease were assessed angiographically by means of either the Judkins or Sones technique. Coronary artery obstructions were judged from multiple views assessing the reduction in luminal cross-sectional area. A lesion of at least 70% reduction in luminal cross-sectional area was considered significant. The distribution of dis- ease was characterized according to involvement of the left main coronary artery, the left anterior descending coronary artery or the major diagonal branch, the left circumflex coronary artery or the major obtuse marginal branch, and the right coronary artery. An assessment was also made as to whether obstructed vessels received collateral flow and whether coronary artery segments distal to obstructions were diseased and/or less than 1 mm in diameter utilizing the coronary catheter size as a measure of magnification.

LV function. Left ventricular function was assessed by means of resting left vent.ricular end-diastolic pressures and left ventriculography (biplane right and left anterior oblique view in 45 patients and single-plane right anterior oblique view in eight patients). Left ventricular regional wall motion was characterized as normal, hypokinetic, akinetic, or dyskinetic.7 The location of regional wall motion abnormalities was described by five segments in the right anterior oblique view (i.e., anterobasal, anterola- teral, apical, inferior, and inferobasal) and by two seg- ments in the left anterior oblique view (i.e., septal and posterolateral). The left ventricular ejection fraction was calculated as the ratio of the stroke volume to the end-diastolic volume by means of the area-length method of Dodge et al.8 The presence of mitral regurgitation was assessed from the left ventricular angiogram and graded as mild, moderate, or severe.

RESULTS

Clinical findings. The study group consisted of 53 patients (48 men and 5 women) with ages ranging from 34 to 72 years (mean + SD, 59.3 + 7.9). Forty- eight patients had a history of at least one prior clinically documented acute transmural myocardial infarction. One patient had an episode of ventricular fibrillation and the initial ECG showed left bundle branch block. Two patients had no prior clinical

CAD and LV dysfunction in recurrent VT with IHD 929

I1 Normal B Hypokincrio

w Akincsio

100

60

; 60

3

t a 40

20

0 I 2 3 4 5

Jnfero- Antero- Anterior Apicol Inferior basal basal

Fig. 1. Distribution and severity of regional wall motion abnormalities in the patients studied.

infarction but did have pathologic Q waves consis- tent with a previous clinically silent infarction. Two patients did not have clinical or ECG evidence of prior infarction. Two patients had previous aortic valve replacement, one for aortic regurgitation and one for aortic stenosis.

At the time of evaluation at the University of Illinois Westside Medical center, 21 patients (40%) had angina pectoris, 34 patients (64 % ) had exertion- al dyspnea, and 22 patients (42%) had syncope. Six patients (11 W) were New York Heart Association functional class I, 27 patients (57 % ) were functional class II, 17 patients (37%) were functional class III, and 3 patients (6% ) were functional class IV.

The ECG demonstrated infarction patterns in 43 patients (81%) with precordial Q waves in 15 patients (28% ), inferior Q waves in 23 patients (43 % ), and both precordial and inferior Q waves in five patients (9%).

Characteristics of ventricular tachycardia. In 48 patients with previous clinical myocardial infarc- tion, the onset of ventricular tachycardia was an average of 6.53 years after the first clinical infarction with a range of 0 to 24 years and an average of 4.85 years after the last clinical myocardial infarction, The number of sustained episodes of ventricular

930 Lam et al. June. 1983

American Heart Journal

Table I. Frequency of akinetic or dyskinetic segment

No. of segments akinetic or dyskinetic No. of patients

Mean of 2.7 segments per patient.

4 5 9

22 12

0 1 0

Table II. Location of akinetic and dyskinetic areas

Location No. of

patients

Involvement

Septal Posterior Basal

Anterior 2* 1 0 1 Anteroapical 14 11 0 8 Anteroapico- 6 2 1 0

inferior Inferoapical 10 1 3 6 Inferior 17* 3 8 11 Apical 1 0 0 0

Septal 1 1 9 -9 19 12 26

(36’,,) (22T ) (49Crs)

*Includes two patients with both anterior and inferior akinesia and/or dyskinesia.

tachycardia requiring either parenteral drug admin- istration or electrical cardioversion ranged from two to innumerable. Thirty-four patients (64% ) had two or more episodes per month at the time of evalua- tion at the University of Illinois Westside Medical Center. The rates of ventricular tachycardia ranged from 130 to 280 bpm (mean -I SD, 188 of: 35 bpm).

The ventricular tachycardia was characterized by a right bundle branch block pattern in 26 patients (49%) and by a left bundle branch block pattern in 14 patients (26%). In 13 patients (24%) the ventric- ular tachycardia was either polymorphic or the patient had multiple tachycardias with both right and left bundle branch block patterns. Of 42 patients undergoing electrophysiologic study with programmed stimulation, 34 patients had inducible ventricular tachycardia (81% of patients undergoing electrophysiologic study).

Coronary angiographic anatomy. Nine patients (17%) had single-vessel coronary artery disease, 19 patients (36%) had double-vessel disease, and 25 patients (47%) had triple-vessel disease. Two

patients (4%) with triple-vessel disease also had significant left main coronary artery obstruction.

Fifty patients (94 % ) had significant obstruction of the left anterior descending coronary artery, 34 patients (64 % ) had significant left circumflex artery disease, and 38 patients (72%) had significant right coronary artery disease. Total occlusion was present in 17 patients (34%) with left anterior descending disease, in 10 patients (29% ) with left circumflex disease, and in 24 patients (63 % ) with right coro- nary artery disease. In the entire study group, 36 patients (68%) had total occlusion of at least one coronary artery. The distal segment of all totally occluded arteries was at least partially visualized by collateral flow.

All nine patients with single-vessel disease had significant left anterior descending coronary artery disease. Of 122 significantly obstructed arteries, 97 (80 % ) were proximally obstructed without signifi- cant distal disease and with distal lumens greater than 1 mm in diameter. All three patients under 40 years of age had single-vessel left anterior descend- ing disease. For the five patients under 50 years of age, there was an average of 1.4 vessels diseased compared with the 48 patients over 50 years of age who had an average of 2.4 vessels diseased (p < 0.025).

Left ventricular function. Left ventricular end- diastolic pressure ranged from 5 to 43 mm Hg (mean * SD, 16.5 -t 8.5 mm Hg) and was elevated in 33 patients (62%). Left ventricular ejection frac- tion ranged from 0.15 to 0.61 (mean +- SD, 0.339 + 0.113) and was greater than 0.50 in six patients (11% ). Fourteen patients (26%) had an ejection fraction of 0.25 or less. There was no statistically significant difference of the left ventricular ejection fraction based on the number of coronary artery diseased or age.

All patients had wall motion abnormalities. The distribution and severity of wall motion abnormali- ties are shown in Fig. 1. The segments of wall motion abnormalities were supplied by significantly dis- eased coronary arteries in every patient except one who had a previous clinical inferior infarction with an unobstructed right coronary artery. The most severe wall motion abnormalities were dyskinesia in 25 patients (47 %), akinesia in 24 patients (45% ), and hypokinesia in four patients (8 % ). Of the 49 patients with akinesia or dyskinesia, three or more segments were akinetic or dyskinetic in 35 patients (66%) (Table I).

The location of akinesis and/or dyskineeis was most frequently inferior (17 patients, 32% ), then

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Number 6

Location of Wall Motion Abnormality

Inferior

Anterior

Both

L_I Miscclloncous

CAD and LV dysfunction in recurrent VT with IHD 931

Both or RBBB pattern LBBB pattern polymorphic

126) (14) (13)

Septal Wall Motion

Normal

m Hypokinetic

B Akinetic

6

(23) (12) (12) total number in group

Fig. 2. Distribution of regional wall motion abnormalities in patients based upon the ventricular tachycardia morphology. Numbers of patients in each group are given in parentheses.

anteroapical(l4 patients, 26 % ), and then inferoapi- cal (10 patients, 19%) in order of decreasing fre- quency (Table II). Septal involvement with akinesis was present in 19 patients (36%) and was most common in patient with anteroapical akinesis and/ or dyskinesis. Posterolateral involvement with infe- rior akinesis/dyskinesis was present in 12 patients (23%). Akinesis/dyskinesis of the basal segments was present in 26 patients (49%); (9 were anterobas- al and 17 were inferobasal). Mitral regurgitation was present in 10 patients (mild in eight patients, mod- erate in one patient, and severe in one patient). Seven of these 10 patients had akinesis or dyskinesis of the inferior segment. One patient had moderate periprosthetic valvular aortic regurgitation.

The morphology of ventricular tachycardia had no relation to the location of regional wall motion abnormalities or to the presence of septal akinesis or hypokinesis (Fig. 2).

DISCUSSION

The present series of patients with recurrent sustained ventricular tachycardia complicating cor- onary artery disease remote from an acute myocar- dial infarction was characterized by a number of features. Clinically, the patients almost universally had a previous clinical myocardial infarction or ECG evidence of a previous infarction. There was a high frequency of multivessel disease (83%) with only 17% of patients having single-vessel disease. Nota-

bly, all the patients with single-vessel disease had left anterior descending coronary artery obstruction. Patients under 50 years of age had a significantly lower number of vessels diseased compared with patients over 50 years old, and all patients under 40 years of age had single-vessel left anterior descend- ing disease. There was, however, no significant difference in the left ventricular ejection fraction for younger patients.

The left ventricular ejection fraction was general- ly markedly depressed with an average ejection fraction of 0.34. In only 11% of patients was the left ventricular ejection fraction normal. Every patient had regional wall motion abnormalities, which were generally severe and extensive. Ninety-two percent of patients had akinetic and/or dyskinetic segments. The average number of akinetic and/or dyskinetic segments as 2.7 segments per patient (out of seven total segments considered).

The distribution of wall motion abnormalities as widespread with inferior involvement actually more frequent than anterior. Septal and posterior exten- sion were common. Approximately one half of the patients had involvement of either the anterobasal or inferobasal segments. There was no correlation between the morphology of the ventricular tachycar- dia and the distribution of wall motion abnormali- ties. Mitral regurgitation was usually mild and was most frequently seen in patients with inferior wall motion abnormalities.

932 Lam et al. June. 1983

American Heart Journal

Pathophysiologic implications. The patients studied in the present series were selected in order to assess a relatively homogenous group of coronary disease patients with serious ventricular arrhythmias occur- ring outside the setting of an acute myocardial infarction. Although specific mechanisms cannot be delineated in this study, some general occlusions can be made. The mode of electrophysiologic induction (and frequently termination) of chronic recurrent sustained ventricular tachycardia in coronary dis- ease suggests a re-entrant mechanism for this arrhythmia.g lo Our present hypothesis is that exten- sive ischemic scarring is the usual substrate required for the development of these arrhythmias. This hypothesis has been advanced by other investigators and is supported by the data obtained by the present series.4 The universal occurrence of left ventricular regional wall motion abnormalities which are usually both severe and extensive and the almost universal occurrence of previous transmural myocardial infarction in the patients studied sup- port this hypothesis. In addition, patients with single-vessel coronary artery disease had as exten- sive left ventricular disease as patients with multi- vessel disease suggesting that the common thread is the marked severity of left ventricular scarring. That the left anterior descending coronary artery was the uniformly diseased vessel in the patients with single-vessel disease implies that transmural infarctions resulting from this single vessel are the most likely to result in a scar large enough to produce the critical mass of diseased tissue neces- sary to sustain recurrent ventricular tachycardias. It is not clear, however, why a large scar is necessary since the mechanism of the tachycardia may be microre-entrant.g, lo Since most ventricular aneurysms do not manifest sustained ventricular tachycardia, microre-entry may be a generally uncommon phenomenon and a large scar may be necessary to increase the chance of developing microre-entry.

The hypothesis that extensive scarring is required is also consistent with the findings of studies which have correlated higher grades of complex ventricular arrhythmias with more extensive areas of left ven- tricular asynergy in patients with coronary artery disease and postinfarction.lO, 12. l3 Similarly, in studies of coronary artery disease and out-of-hospi- tal ventricular fibrillation, patients with recurrence of ventricular fibrillation had more extensive coro- nary disease and left ventricular wall motion abnor- malities than those with only single episodes.14,15 The present series of patients with generally multi-

vessel disease and severe left ventricular disease closely resembles the patients with recurrent out- of-hospital ventricular fibrillation, suggesting a common anatomic substrate. Indeed, recent reports of patients with out-of-hospital ventricular fibrilla- tion have shown that in some patients the initiating arrhythmia may be ventricular tachycardia which is replicable utilizing programmed stimulation.lfi, I7

Usually ventricular tachycardia originating from the left ventricle would have a right bundle branch block pattern. However, a left bundle branch block morphology is common with recurrent ventricular tachycardias in patients with coronary artery dis- ease in whom the origin of the tachycardia presum- ably is in the left ventricle. Indeed, a left bundle branch block pattern was seen in 26% of the patients in the present series. It has been hypothe- sized that this results from breakthrough of the earliest ventricular activation through the interven- tricular septum. lR In the present series, there was no difference in the distribution of septal wall motion abnormalities between patients with right or left bundle branch block pattern ventricular tachycar- dias.

Clinical and therapeutic implications. The present study has a number of clinical implications regard- ing the life history and management of recurrent sustained ventricular tachycardia complicating chronic coronary artery disease. If medical manage- ment were to achieve total amelioration of chronic recurrent ventricular tachycardia, one could still anticipate significant morbidity and mortality re- lated to the underlying coronary disease and left ventricular dysfunction. 1,a,3 Control of ventricular tachycardia could not be expected to favorably influence the poor prognostic natural history related to the underlying anatomy of the present series of patients.

Since the first report of a successful treatment of ventricular tachycardia by the excision of a left ventricular aneurysm, several surgical approaches to this problem have been advanced.4 Common to the success of all these approaches seems to be the removal or exclusion of a significant amount of diseased tissue. Although initially described with left ventricular aneurysms, excision of akinetic scar without frank aneurysm has also been beneficial. Apparently, coronary artery bypass grafting without removal of scar is unlikely to be successful in the treatment of ventricular tachycardia associated with previous infarctions.5 Thus, although most of the patients in the present series had coronary artery anatomy suitable for bypassing grafting, it seems

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Number 6 CAD and LV dysfunction in recurrent VT with IHD 933

that the critical factor in surgical success would be based on the left ventricular angiographic anatomy. Over one quarter of the patients had very markedly depressed left ventricular function (ejection fraction of 0.25 or less) which would significantly increase the risks of surgery.4F “9 *(’

The majority of patients who have undergone surgery for life-threatening ventricular arrhythmias have had anterior or anteroapical akinesis or dyski- nesis.5*6 The present series actually has plurality of patients with inferior or inferoapical akinesis or dyskinesis. In a recent electrophysiologic study of patients witah recurrent ventricular tachycardia, approximately half the patients studied had a previ- ous inferior wall myocardial infarction.21 Data on inferior aneurysmectomies (for congestive heart fail- ure and particularly for ventricular tachycardia) are very limited.22 Quite possibly, surgical series have been preselected for patients who are more optimal candidates for aneurysmectomy. Inferior aneurysms may be more difficult to excise because of decreased accessibility and a higher risk of resultant mitral regurgitation. Indeed, most of the patients in the present series with mitral regurgitation had primar- ily inferior akinesia or dyskinesia.

Almost one half of the patients studied had akinesis of either the anterobasal or inferobasal segments. Most studies have indicated an increased aneurysmectomy mortality in patients with poor function of the basal segments.*g,20 Also, 36% of patients had septal akinesis suggesting that simple ventricular a.neurysmectomy would probably not be an appropriate approach as the optimal surgery therapy if a ventricular tachycardia arose from the septum in t.hese patients. Endocardial excision or encircling endocardial ventriculotomy with or with- out endocardial intraoperative mapping would appear to be appropriate for these patients.23-25

Conclusions. The present study suggests that chronic recurrent ventricular tachycardia complicat- ing chronic coronary artery disease generally implies multivessel disease and severe and extensive left ventricular regional wall motion abnormalities. Although both medical and/or surgical therapy may be successful in solving the immediate problem of ventricular tachycardia, the long-term prognosis and natural history would be influenced by the underlying coronary artery disease and left ventric- ular dysfunction. Although simple aneurysmectomy may be successful in some patients, a significant proportion at patients may have inoperable disease or may require more sophisticated electrophysiolog- ic and surgical techniques.

Bruschke AVG, Produfit M, Sones FM: Progress study of 590 consecutive nonsurgical cases of coronary disease followed 5-9 years. I. Arterographic correlation. Circulation 47:1147, 1973. Bruschke AVG, Proudfit M, Sones PM Progress study of 590 consecutive nonsurgical cases of coronary disease followed 5-9 years. II. Ventriculographic and other correlations. Circu- lation 47:1154, 1973. Humphries JO, Kuller L, Ross RS, Freesinger GE, Page EE: Natural history of ischemic heart disease in relation to arterographic findings. Circulation 49:489, 1974. Waldo AL, Arciniegas JG, Klein H: Surgical treatment of life-threatening ventricular arrhythmias: The role of intraop- erative mapping and consideration of the presently available surgical techniques. Prog Cardiovasc Dis 23:247, 1981. Buda AJ, Stinson EB, Harrison DC: Surgery for life-threat- ening ventricular tachyarrhythmias. Am J Cardiol 44:1171, 1979.

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Wald RW, Waxman MB, Corey PN, Gunstensen J, Goldman BS: Management of intractable ventricular tachyarrhythmias after myocardial infarction. Am J Cardiol 44:329, 1979. Herman MV, Heinle RA, Klein MD, Gorlin R: Localized disorders in myocardial contraction asynergy and its role in congestive heart failure. N Engl J Med 277:222, 1967. Dodge HT, Sandler H, Ballew DN, Lord JD Jr: The use of biplane angiocardiography for the measurement of left ven- tricular volume in man. AM HEART J 60:762. 1960. Josephson ME, Horowitz LN, Farshidi A, Kastor JA: Recur- rent sustained ventricular tachycardia. 1. Mechanisms. Cir- culation 57:431, 1978. Josephson ME, Horowitz LN, Farshidi A, Spielman SR, Michelson EL, Greenspan AM Sustained ventricular tachy- cardia: Evidence for protected localized reentry. Am J Cardiol 42:416, 1978. Calvert A, Lown B, Gorlin R: Ventricular premature beats and anatomically defined coronary heart disease. Am J Cardiol 39:627, 1977. Califf RM, Burks JM, Behar VS, Margolia JR, Wagner GS: Relationships among ventricular arrhythmias, coronary artery disease, and angiographic and electrocardiographic indication of mvocardial fibrosis. Circulation 57:725. 1978. Schulze RA, Humphries JO, Griffith LSC, Ducci H, &huff S, Baird MG, Mellits ED, Pitt B: Left ventricular and coronary angiographic anatomy: Relationship to ventricular irritability in the late hospital phase of acute myocardial infarction. Circulation 55:839, 1977.

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Weaver WD, Larch GS, Alvarez HA, Cobb LA: Angiographic findings and prognostic indicators in patients resuscitated from sudden cardiac death. Circulation 54:895, 1976. Margolis JR, Hirshfeld JW, McNeer JF, Starrier CF, Rosati RA, Peter RH, Behar VS, Kong Y: Sudden death due to coronary artery disease: A clinical hemodynamic and angio- graphic profile. Circulation 51 and 52(suppl 111):180, 1975. Josephson ME, Horowitz LN, Spielman SR, Greenspan AM Electrophysiologic and hemodynamic studies in patients resuscitated from cardiac arrest. Am J Cardiol 46:948, 1980.

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Ruskin JN, Dimarco JP, Garan H: Out of hospital cardiac arrest. Electrophysiologic observation and selection of longterm antiarrhythmic therapy. N Engl J Med 303:607, 1980. Josephson ME, Horowitz LN, Farshidi A, Spear JF, Kastor JA, Moore EN: Recurrent sustained ventricular tachycardia. 2. Endocardial mapping. Circulation 57:440, 1978. Watson LC, Dickhaus DW, Martin RH: Left ventricular aneurysm. Preoperative hemodynamics, chamber volume and results of aneurysmectomy. Circulation 52:868, 1975. Kapelanski DP, Al-Sadir J, Lambert JJ, Anagnostopoulos CE: Ventriculographic features predictive of surgical out-

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American Heart Journal

come for left ventricular aneurysm. Circulation 58:1167, 1978.

21. Robertson JF, Cain ME, Horowitz LN, Spielman SR, Green- span AM, Waxman HL, Josephson ME: Anatomic and elec- trophysiologic correlates of ventricular tachycardia requiring left ventricular stimulation. Am J Cardiol 48:263, 1981.

22. Loop FD, Effler DB, Webster JS, Graves LK: Posterior ventricular aneurysms. N Engl J Med 288:237, 1973.

23. Josephson ME, Horowitz LN, Spielman SR, Greenspan AM, VandePol C, Harken AH: Comparison of endocardial cathe- ter mapping with intra-operative mapping of ventricular tachycardia. Circulation 61:395, 1980.

24. Josephson ME, Harken AH, Horowitz LN: Endocardial excision: A new surgical technique for the treatment of recurrent ventricular tachycardia. Circulation 60~1430, 1979.

25. Guiraudon G, Fontaine G, Frank R, Escande E, Etievent P, Cabrol C: Encircling endocardial ventriculotomy: A new surgical treatment for life-threatening ventricular tachycar- dias resistant to medical treatment following myocardial infarction. Ann Thorac Surg 26:438, 1978.

Studies of arrhythmias by 241hour pu#y recordings: Reiatiuns~ between atrioventricular block and

The relationship between AV conduction disturbances and sleep states was investigated using continuous polygraphic recordings for one full night. The results were as follows: (1) In the case of first-degree AV block, the phasic shortening of the PQ interval was observed during rapid eye movement (REM) sleep. (2) In the case of second-degree AV block (Wenckebach type), the conduction ratio increased transiently during REM sleep and signifiiant relationships were observed between the number of nonconducted P waves and the mean heart rate in each sleep stage. (3) In the case of advanced AV block, complete AV block was observed less frequently during REM sleep and the period of falling asleep. Since the reproducibility of these results from n,ight to night has not yet been investigated, additional evaluation is required. (AM HEART J 105:934, 1983.)

Kuniaki Otsuka, M.D., Yuhei Ichimaru, M.D., and Takashi Yanaga, M.D. With the collaboration of Yoshinori Sato. Nankoku City, Japan

There have been many reports which show the relationship between sleep states and arrhythmias.‘m3 However, the effect of physiological change in sleep- ing state on atrioventricular (AV) conduction has not yet been studied, except for a case reported by Nevins.4 The present study was designed to estab- lish the relationship between the occurrence of AV block and sleep states.

From the Department of Physiology, Kochi Medical School; and the Department of Bioclimatology and Medicine, Research Institute of Bai- neotherapeutics, Kyushu University.

Received for publication March 20, 1981; revision received Oct. 20, 1981; accepted Feb. 17, 1982.

Reprint requests: Kuniaki Otsuka, M.D., Dept. of Physiology, Kochi Medical School, Oko-Cho Kohasu, Nankoku City, Kochi Prefecture, 781-51, Japan.

METHODS

Patient selection. Four patients with AV conduction disturbances (three men and one woman; average age 28.5 years, ranging from 12 to 65 years) were selected for this study, as shown in Table I. In three of these patients (cases 1,2, and 3) increases in AV conduction disturbances during the nighttime were demonstrated more than twice by 24-hour continuous ECG recordings using the Holter Avionics system5,6 (Model 445 Card&order and Model 660 A Electrocardioscanner), and in another patient (case 4) improvements in the AV conduction disturbances during the nighttime were observed more than twice by 24-hour continuous ECG recordings. The ECG in case 1 showed left anterior fascicular block, that is marked left axis deviation with qR in leads I, aVL, V,, and S in leads II, III, and aV,; there was also sinus bradycardia associated with occasional sinus arrest as well as first-degree AV block. The ECGs in case 2 and 3 showed second-degree AV

934