Sequential Atrioventricular Pacing as a Stress Test

Sequential Atrioventricular Pacing as a Stress Test Evaluation of Left Ventricular Function in Second-Degree AV Heart Block Developing During Atrial Pacing* Demetrios Kimbiris, M.D.,·· and Joseph W. Linhart, M.D.,F.C.C.P.t

pac'"

Advanced or second-degree atrioventricular (A V) heart block pre-eDstiDg or developing duriDg atrial (AP) at low heart rates of < 130 per minute, Umlts the value of AP to stress tbe left ventricle. When Wenkebach type A V block is present, the heart rate can be Increased by administration of atropiDe before atrial pacing or by right ventricular pacing. Atropine, however, occasionaly may cause serious supraventricular or ventricular arrhythmias, and high rate right ventricular padDg is not tolerated by many patients with left ventricular dysfunction because of the absence of the atrial contribution. Twenty-eight out of 101 patients with angina pectoris (27.7 percent) developed second degree AV heart block during atrial pacing studies performed for evaluation of

left ventricular function. In 8 of the 28 patients, sequential AV pacing (SP) w. performed successfuDy, with the heart rate being Increased to 150-167 per minute. In 4 of the 8 patients, left ventricular dysnfunction was demonstra&ed during and immediately after SP. Typical angina pectoris developed in two of the four patien. during SP, one of whom proved to have normal coronary arteriogram. Sequential A V pacing is an altemative metbod to iucrease the heart rate for the purpose of stressing the left ventricle when advanced degree or second-degree A V heart block pre-eDsts or develops during right atrial pacing. In some patients the method of SP might be preferable to adminBtration of atropine or to ventricular pacing.

Right atrial pacing is a well-accepted method for evaluating left ventricular function during cardiac catheterization in patients with coronary artery disease.v" It is a safe and simple procedure to increase the heart rate under controlled conditions, resulting in increased myocardial oxygen consumption and myocardial ischemia. During pacing, important hemodynamic, electrocardiographic and metabolic abnormalities may be observed and left ventricular function assessed. 3.5 The value of this method, however, may be limited: in a significant number of patients, the heart rate cannot be increased because second-degree AV heart block occurs. This limitation of atrial pacing can be overcome by intravenous administration of atropine" or by increasing the heart rate by right ventricular pacing. The intravenous administration of atropine, nevertheless, may cause serious extracardiac and intracardiac side effectsfor example, atrial or ventricular tachycardia." In a number of patients even atropine cannot prevent

the development of block," so that its application is of questionable value. Ventricular pacing at higher rates also may be hazardous, particularly in patients with impaired ventricular function. 8 To avoid the possible undesirable effects of atropine and/ or ventricular pacing, we have successfully used sequential AV pacing in a number of patients in whom AV heart block developed during right atrial pacing at relatively low heart rates.

°From the Division of Cardiology, Hahnemann Medical College and Hospital, Philadelphia, Pennsylvania. . 00 Associate Professor of Medicine. tProfessor and Chairman, Deparbnent of Medicine, Chicago Medical School. Manuscript received July 16; revision accepted September 12. Reprint requests: D1'. Kimbiris, 230 North Broad Street, Philadelphia 19102

540 KIMBIRIS, LINHART

MATERIAL AND METHODS

We performed right atrial pacing in 101 patients with chest pain who had been referred to us for coronary arteriography. The technique of atrial pacing we used was previously reported by Linhart and assoeiates.! We performed rightheart and left-heart catheterization using an antecubital vein and the right brachial artery in the usual manner. A bipolar pacemaker catheter was positioned in the upper right atriwn. The hemodynamics were first recorded at rest; the heart rate then was increased every two to three minutes by increments of 5 to 10 beats per minute, up to a rate of 160 to 167 beats per minute or until the development of angina pectoris, pulsus altemans, or second-degree AV heart block. In 28 (27.7 percent), second-degree AV heart block of the Wenckebach type developed with relatively slow right atrial pacing rates (heart rate 130 beats per minute). In 8 of these 28 patients with AV heart block, sequential AV pacing was performed and the heart rate was increased in this manner. using the external Bifocals pacemaker unit (American Optical

<

CHEST, 67: 5, MAY, 1975

Company) on continuous mode. We used the following method: the pacemaker catheter used for atrial pacing was advanced to the right ventricle; the proximal poles were connected temporarily with the ventricular leads of the Bifocal pacemaker to ensure adequate, constant ventricular pacing. The leads then were disconnected. A second bipolar catheter was inserted through the same vein and positioned in the upper right atrium, whereupon the proximal poles of the atrial pacemaker were connected with the atrial leads of the Bifocal pacemaker. Atrial pacing was then started, with a gradual increase of the rate, until second-degree AV heart block was observed; at that point the rate was gradually decreased until constant 1: 1 conduction was established. We connected the ventricular pacemaker catheter with the ventricular lead of the Bifocal pacemaker, and began sequential pacing with an initially short atrial-ventricular stimulation interval, which we gradually increased to 150-200 msec, When stable sequential pacing was achieved, the rate was increased by 10 beats every 2 to 3 minutes up to 150-167 per minute or until angina pectoris or pulsus altemans developed. Hemodynamic measurements were made at the maximal rate, whereupon

the pacing was abruptly discontinued. After pacing, we made observations of the left ventricular end-diastolic pressure (LVEDP) and the ST segments of the electrocardiogram. REsULTS

The hemodynamics recorded in sinus rhythm and during sequential pacing are shown in Table 1. The resting hemodynamics were normal in all patients. The response to sequential pacing was normal in four, all with normal coronary arteriograms. The left ventriculogram was abnormal in one patient. Figure 1 shows a tracing from a patient with normal response to increased heart rate with sequential AV pacing. One of these four patients experienced atypical chest pain during pacing. The remaining four patients had abnormal responses to sequential pacing, manifested by significant elevation of the left ventricular end-diastolic pres-

Table I-Hemodynamie. in Sin... Rhythm arad SequeratialAY Paeiq

Heart Rate P-R beats/min. m sec.

Pt. Age

46

NSR

M

SP

46

NSR

M

SP

2

CI

Aorta LV Pressure in mmHg (Mean in paren.)

61

160

3.5

124/76

150

90

3.0

120/100 120/4 (110)

64

160

2.94

167

140

3.67

110/90 (120) 105/SO

(104)

Post Pacing LVEDP

124/14 17

110/12 105/4

8

Cor. ArLV teriogram gram

SV

SW

SEP sec.

Angina

104

127

0.36

moderate

N

N

36

52

0.22

91

133

0.33

No

N

N

44

54

0.28

126

176

0.36

moderate

AN

N

33

21

0.18

107

158

0.30

No

AN

CAD

50

69

0.22

Mild

N

N

Mild

AN

CAD

No

AN

N

No

N

N

(95)

3

4

5

6

7

8

51

NSR

M

SP

47

NSR

M

SP

41

NSR

F

SP

35

NSR

M

SP

56

NSR

F

SP

53

NSR

F

SP

54

180

3.41

167

150

2.81

180

4.2

167

96

4.2

79

ISO

2.99

150

140

67

90

2.57

167

170

1.87

53

160

2.28

167/80 (110) 110/90 (100)

167/7 110/37

140/90 140/11 (120) 140/107 140/20 (122)

140/90 (110)

130/80 (95)

140/9

116/68

116/11

150

160

3.1

104/84

104/0

88

220

3.37

155/2

150

ISO

3.14

155/80 (110) 145/90 (110)

CI-Cardiac Index, liters per minute /M2 LV-Left Ventricle SV-Stroke Volume

CHEST, 67: 5, MAY, 1975

18

130/8

100/28

(88)

30

140/12

l00/SO

(90)

20

160/0

18

6

3

84

99

0.28

25

21

0.21

73

76

0.33

35

45

0.20

67

98

0.38

37

55

0.24

SW-Stroke Work in gram-meters N-Normal AN-Abnormal

NSR-Normal Sinus Rhythm SP-8equential Pacing SEP-Systolic Ejection Period

SEQUENTIAL ATRIOVENTRICULAR PACING AS A STRESS TEST 541

~-

,'oJ

~I~. ~~

~

~

~~

"- .~

~

V

II

~~

..- "r

;~ ~~~

~~

~

~ ~

~IJ

-~~~~

I

I,J~

~~"

\ ~~

J

,~

,,~

I

11

I

'--. ~,

I

II

i

~

1\

~

~

-

.

.~.

I'

I'

~

~

~

I

1. Tracing showing normal response o~ the left v ­ tricular end-diastolic pressure (LVEI?P) d~ sequential AV pacing. A, atrial stimulus; V, ventricular stimulus. FIGURE

sure in the period immediately after pacing. During sequential pacing the left ventricular end-diastolic pressure increased significantly in three patients and only slightly decreased in one. Figure 2 shows an abnormal response to cardioacceleration during sequential AV pacing, with significant increase of the LVEDP. The cardiac index did not change in three patients but it did decrease in one patient from 2.57 to 1.87 liters/min M2. Two of these four patients had coronary artery disease (one had three-vessel disease and one single-vessel disease). All of the four patients had abnormal left ventriculograms. Typical angina pectoris developed in one patient with a normal coronary arteriogram and in one with single-vessel disease. DISCUSSION The value of right atrial pacing as a stress test for determining left ventricular function is limited for a Significant number of patients with angina pectoris because of the development of second-degree AV heart block with low atrial pacing rates ~.~

lilliI'",

~~ ~~

I

~, ~

,~~~

i I

~~~.

I I

.~

~

I

~

r

' '~

~

~..~

~~

,~" ,~

IfI'" ~"-~~

l,ilil~~

~,.;

II

~

~

~~

~.~

~

Il~"~

~

JW

I

-

~ ~

~

1\

Ii

~~

~

~

~

PI

FIGURE 2. Tracing showing abnormal response of the L':EDP during sequential AV pacing. There is sigmficant elevation of the LVEDP (Arrow).

542 KIMBIRIS, LINHART

(27.7 percent in our study). Higher pacing rates can be achieved in some of these patients by enhancing the A V conduction with intravenous administration of atropine." However, in some patients significant cardiac acceleration may occur after atropine administration which may persist after cessation of pacing. We personally have observed in several patients, heart rate of 130 to 140 beats per minute after intravenous administration of 1 mg atropine. Under these circumstances, if angina or failure developed .during higher atrial pacing rates, cessation of pacing may not relieve the angina or failure since relative tachycardia will persist. Hence, one of the most important advantages of atrial pacing, that the tachycardia is controlled, is not in eHect. . Serious atrial or ventricular arrhythmias have been reported to occur in patients with acute myocardial infarction after atropine administration," Increased heart rate can be accomplished also by right ventricular pacing. However, previous studies have shown that ventricular pacing impairs left ventricular function, particularly in diseased hearts, not by aberrant ventricular excitation but by the loss of synchronization of atrial and ventricular contractions. ie.n In addition, congestive heart failure has been reported to occur during ventricular pacing. 8 Increasing the heart rate by ventricular ~cing is therefore undesirable. Figure 3 shows a drastic reduction in aortic pressure during ventricular pacing (VP) as compared to the pressure during sequential AV pacing ( SP ) or right atrial pacing ( AP). It has been also shown that sequential atrioventricular pacing with properly timed AV intervals can increase cardiac output in some patients." We performed sequential pacing successfully and without complications in order to stress the left ventricle in all eight patients with angina pectoris, in whom the heart rate could not be increased by right atrial pacing because of the development of AV heart block. Since the method is easy to perform, it is preferable in some patients to intravenous administration of atropine or to ventricular pacing. We conclude, therefore, that SP tachycardia may be of value in assessing left ventricular function in patients in whom the heart rate cannot be increased by atrial pacing because of the development of second-degree AV heart block or in patients in whom advanced degree AV block pre-exists. Although intravenous administration of atropine can improve conduction in the AV node and therefore increase the pacing rate, it should be done with great caution, particularly in patients with coronary artery disease, since sinus tachycardia, atrial

CHEST, 67: 5, MAY, 1975

o FIGURE 3. Simultaneous recording of electrocardiogram and aortic (AO) pressure during ventricular pacing (VP), sequential pacing (SP) and atrial pacing (AP).

tachycardia, or ventricular ·tachycardia can occur," Increasing the heart rate by ventricular pacing also should be avoided since loss of the atrial contribution, particularly with rapid rates, may precipitate left-heart failure in patients with poor left ventricular function. 8

6

7

REFERENCES

1 Sowton GE, Balcon R, Cross D, et al: Measurement of the angina threshold using atrial pacing. A new technique for the study of angina pectoris. Cardiovasc Res 1 :301,. 1967 2 Forrester JS, Helfant RH, Pastemac A, et al: Atrial pacing in coronary heart disease. Effect on hemodynamics, metabolism and coronary circulation. Am J Cardiol 27: 237, 1971 3 Parker JO, Chiong MA, West RO, et al: Sequential alterations in myocardial lactate metabolism, S-T segments, and left ventricular function during angina induced by atrial pacing. Circulation 40:113, 1969 4 Linhart JW, Hildner FJ, Barold SS, et al: Left heart

CHEST, 67: 5, MAY, 1975

5

8 9 10 11

hemodynamics during angina pectoris induced by atrial pacing. Circulation 40:483,1969 Linhart JW: Myocardial function in coronary artery disease determined by atrial pacing. Circulation 44:203, 1971 Kokkinos DV, Katsaros S, Grivas P, et al: Use of atropine for higher right atrial pacing rates. Maximal pacing for diagnosis of coronary artery disease. Br Heart J 35:720, 1973 Massumi RA, Mason DT, Amsterdam EA, et al: Ventricular fibrillation and tachycardia after intravenous atropine for treatment of bradycardias. N Engl J Med 287: 336,1972 Haas, JM, Strait GB: Pacemaker-induced cardiovascular failure. Hemodynamic and angiographic observations. Am J Cardiol 33: 295, 1974 Castillo CA, Berkovits BV, Castellanos A, Jr, et al: Bifocal demand pacing. Chest 59:360, 1971 Samet P, Castillo C, Bernstein WH: Hemodynamic sequelae of atrial, ventricular and sequential abioventricular pacing in cardiac patients. Am Heart J 72: 725, 1966 Samet P, Castillo C, Bernstein WH: Hemodynamic consequences of sequential abiovenbicular pacing. Subjects with normal hearts. Am J CardioI21:207, 1968

SEQUENTIAL ATRIOVENTRICULAR PACING AS A STRESS TEST 543