spectrum of haemodynamic responses to atrial pacing in … · atrial tachy-pacing wasperformed in...

British HeartJournal, 1973, 35, I033-I040.

Spectrum of haemodynamic responses toatrial pacing in coronary artery disease'

P. A. N. Chandraratna, P. M. Shah2, D. H. Kramer, R. J. Davis, and B. F. SchreinerFrom the Cardiology Unit, Department of Medicine, University of Rochester Medical Center,New York I4642, U.S.A.

Atrial tachy-pacing was performed in 34 patients who were divided into 3 groups as follows. Group I: 4patients with obscure chest pain syndromes and normal coronary arteries and haemodynamics; Group 2: 25patients with significant coronary artery disease and angina pectoris; Group 3: 5 patients with coronary arterydisease, left ventricular aneurysm, and left ventricular dysfunction. Pacing produced a reduction in the leftventricular stroke work index and the left ventricular end-diastolic pressure in Group i patients, while thecardiac index and the left ventricular minute work index showed no significant change. Group 2 patientsshowed a variety of responses. Nine patients had a 'normal' response to atrial pacing, namely a fall in leftventricular stroke work index and left ventricular end-diastolic pressure. Of these, .5 had experienced anginaduring pacing and 4 did not; the other I6 had abnormal responses. When considered as a group, there was a

significant decrease in the left ventricular stroke work index and an increase in the left ventricular minutework index, while the left ventricular end-diastolic pressure and cardiac index did not change significantly.Group 3 patients demonstrated a significant fall in the left ventricular end-diastolic pressure and a rise inthe cardiac index and the left ventricular minute work index, while the left ventricular stroke work index wasunchanged. A reduction in the end-diastolic pressure without a fall in stroke work index and with an increasein the minute work index indicate improved myocardial performance in this group ofpatients. It is concludedthat there is a wide spectrum of responses to atrial pacing ranging from no change in left ventricular functionin some patients to gross dysfunction in others. Those with compromised left ventricular function exhibitimproved performance.

Sowton and associates were the first to show thatatrial tachy-pacing produced angina pectoris inpatients with coronary artery disease. Using this asa stress test they showed that chest pain consistentlyoccurred at a particular tension-time index in a givenpatient, and that during angina stroke volume andleft ventricular stroke work decreased while pul-monary artery mean pressure and the pulmonarywedge pressure increased (Sowton et al., I967).Atrial pacing is now widely used in the evaluationof left ventricular function in coronary artery disease(Parker et al., I969; Leighton et al., I969; Dwyer,1970; Linhart, I97I). It has been a useful methodReceived 29 March I973.1 This work was supported in part by a MIRU contract andgrants from the National Heart and Lung Institute, Bethesda,Maryland, U.S.A.2 This work was done during Dr. Shah's tenure ofan AmericanHeart Association Teaching Scholar Award.

of studying the effects of drugs in angina pectoris(Frick et al., I968) and more recently has beenemployed to assess the results of coronary arterysurgery (Ross et al., 1972).

Parker and associates using left ventricular cathe-terization found that when heart rate was increasedby atrial pacing the normal response was a fall instroke work index and left ventricular end-diastolicpressure (Parker et al., I969). In contrast whenangina occurred, left ventricular dysfunction wassuggested because of a rise in end-diastolic pressureand a decrease in stroke work index. The rise inend-diastolic pressure, moreover, was most con-spicuous in the first few beats after brief interrup-tion of pacing. More recently, Linhart observed thatsimilar changes suggesting left ventricular dysfunc-tion might occur in patients with ischaemic heartdisease who do not develop angina during atrial

copyright. on N

ovember 10, 2020 by guest. P

rotected byhttp://heart.bm

j.com/

Br H

eart J: first published as 10.1136/hrt.35.10.1033 on 1 October 1973. D

ownloaded from

http://heart.bmj.com/

1034 Chandraratna, Shah, Kramer, Davis, and Schreiner

pacing and that in some patients abnormal functionappeared before the onset of angina (Linhart, I97I).Both groups of authors chose to construct ventricu-lar function curves relating left ventricular end-diastolic pressure to stroke work index with pacingintervention. These relations do not represent theclassic Frank-Starling function curves nor do theyduplicate the concepts of Sarnoff and Berglund whoderived a given function curve only in the presenceof a constant inotropic state (Sarnoff and Berglund,I954). The Bowditch effect whereby an increasedheart rate results in an augmented inotropic statehas been largely discounted in these pacing studies.The purposes of the present study are (i) to show

that there is a wide spectrum of responses to atrialpacing in patients with symptomatic coronary arterydisease; (2) to indicate that patients with anginamay have a normal response or a conspicuously ab-normal response, whereas those with ventricularaneurysm and left ventricular failure may show animprovement in cardiac performance during atrialpacing. It is further emphasized that pacing fimctioncurves in fact represent points on different functioncurves as classically expressed.

MethodsThirty-four symptomatic patients with suspected coron-ary artery disease were studied. The patients weredivided into three groups. Group I consisted of 4 men(age range I9 to 6o years) with atypical chest painsyndromes who had normal coronary arteries and nodetectable cardiac abnormality. Group 2 comprised 25patients, 20 men and 5 women (age range 33 to 68 years)who had disabling angina pectoris (Class III New YorkHeart Association Classification) and coronary arterydisease documented by selective coronary angiographywith the exception of Case 17 who had chest pain withelectrocardiographic abnormalities of ischaemia duringpacing, but had insignificant lesions in her coronaryangiogram. Group 3 was composed of 5 men (age 30 to63 years) who had left ventricular aneurysm and evidenceof cardiac decompensation.

Right and left heart catheterizations were performedin the postabsorptive state under pentobarbitone seda-tion. A flow-directed Swan Ganz catheter was passedinto the pulmonary artery via the right antecubitalvein. A bipolar pacing catheter was placed in the coron-ary sinus, or in the right atrium. A cannula was placedin a brachial artery. Left heart catheterization was per-formed using either the Brockenbrough transseptal tech-nique or the Seldinger retrograde technique from afemoral artery. Lead II and lead Vs of the electrocardio-gram were monitored. The pulmonary artery, pulmonaryartery wedge or left atrial pressure, left ventricular, andbrachial artery pressures were recorded on a Brush re-corder through Statham P23dB strain gauge transducers.The zero reference point used was 5 cm below the sternalangle. Mean pressures were determined by electronicintegration. The left ventricular end-diastolic pressure

measurementwas facilitated byusing ahighgain and paperspeed of 50 or Ioo mm/sec. The end-diastolic pressurewas measured at the point where the downslope of the'a$ wave was interrupted by the upstroke of left ventri-cular pressure rise. With rapid heart rates when thistransition could not be precisely discerned, the pressurewas read at o0o4 sec after onset of QRS at both controland paced rates. All pressures were measured over tworespiratory cycles and averaged. The 'pace-off LV end-diastolic pressure' was obtained after transient interrup-tion of pacing. The left ventricular end-diastolic pressurefrom ten consecutive beats after cessation of pacing wasaveraged. Cardiac output determinations were made bythe dye dilution technique using indocyanine greeninjected into the pulmonary artery and sampled from thebrachial artery through a Gilford densitometer.1 Theleft ventricular stroke work index in g m/beat and minutework were calculated using standard formulae.

Control pressures were measured and cardiac outputwas determined in duplicate. Atrial pacing was thenbegun with increments in heart rate of Io to 20 beats/minute at a time with continuous pressure recordings.Measurements of cardiac output were made in duplicateafter pacing for 5 minutes at each heart rate. Whenchest pain or discomfort similar to that experienced bythe patient during exertion occurred with pacing, nofurther increase in heart rate was attempted. In otherpatients the heart rate was progressively increased,usually to a maximum of I5o/minute. In some patientsthis heart rate could not be achieved because of impairedAV conduction (Cases 25, 31, 32, 33).

After haemodynamic studies, left ventricular angio-cardiography was performed in each patient. Selectivecoronary arteriography was carried out on a subsequentday by the Judkins technique.

ResultsHaemodynamic dataThe haemodynamic data of individual patients arepresented in Table i. The mean values for eachgroup are shown in Table 2. Eighteen patients inGroup 2 and i patient in Group 3 developed anginaduring pacing. The control heart rates beforepacing were similar in Groups i and 2, but weresomewhat higher in Group 3 patients. The cardiacindex during the control period and pacing was notsignificantly different in Groups i and 2, but wassignificantly higher during pacing in Group 3patients. The left ventricular end-diastolic pressuredecreased significantly during atrial pacing inGroups i and 3, but there was no significant changein Group 2. A significant fall in the left ventricularstroke work index was observed during pacing inGroups I and 2, but no change occurred in Group3. The left ventricular minute work index increasedsignificantly during atrial pacing in Groups 2 and3, but remained unchanged in Group i.

1 Model I03 IR.

copyright. on N



j.com/

Br H


ownloaded from


Spectrum of haemodynamic responses to atrial pacing in coronary artery disease 1035

The relation of end-diastolic pressure to strokework index for patients in Groups I, 2, and 3, wasexamined. The mean value and the standard errorof the mean during the control period and duringpacing are shown in Fig. x. All 4 patients in Groupi showed normal responses to atrial pacing, i.e.a fall in end-diastolic pressure and a concomitantdecrease in stroke work index.

Seven patients in Group 2 did not experience an-gina during pacing. Of these, 4 showed a fall instroke work index as well as end-diastolic pressure,in 2 there was a fall in stroke work index with a risein end-diastolic pressure, and the remaining patientshowed a fall in stroke work index with no changein end-diastolic pressure. Five of the i8 patients inGroup 2 who developed angina during pacing hada fall in both stroke work index and end-diastolicpressure; the other I3 had increased end-diastolicpressure associated with a fall in stroke work index.When considered as a group; they demonstrated asignificant fall in stroke work index during pacingwith no change in end-diastolic pressure (Fig. i).Four of the 5 patients in Group 3 showed a fall inend-diastolic pressure and a rise in stroke workindex during pacing. Fig. i shows that these patientswhen considered as a group demonstrate a fall in

701 Groupi

60

E

30-

20 .1 , L

4 8 12 8LVEDP (mm Hg)

Group2

12 I16 24 28 32

FIG . i The relation between left ventricular strokework index (LVSWI g m/beat) and left ventricularend-diastolic pressure (LVEDP mmHg) is illustrated.The mean value and the standard error of the meanfor each group, during the control period and duringpacing, are given. The control and pacing values are

joined and the arrows point toward the pacing values.Group I patients show a significant reduction in thestroke work index and end-diastolic pressure duringpacing (P < o-os). There is a reduction in stroke workindex in Group 2 patients with pacing (P<o-oox),while the end-diastolic pressure shows no significantchange. The end-diastolic pressure in Group 3 patientsdecreased with pacing (P < o.ox), while the strokework index did not change significantly.

_ 5-

EE 4.

- 3.

-J 2

GrouPi

4 8 12 8 12 16 20 24 28 32LVEDP (mm Hq)

FIG. 2 This shows the relation between left ventricu-lar minute work index (LVMWI kg m/min) and theleft ventricular end-diastolic pressure (LVEDP mm-Hg). The mean value and the standard error of themean for each group, during the control period andduring pacing, are given. The control and pacingvalues are joined and the arrows point toward thepacing values. Group I patients show a reduction inthe end-diastolic pressure (P < o os), but no significantchange in the LV minute work index, during pacing.There is an increase in the latter in Group 2 patientswith pacing (P< o-or) while the end-diastolic pressureis unchanged. The end-diastolic pressure in Group 3patients decreased with pacing (P < o.oI) and thiswas associated with an increase in the minute workindex (P<o-oi).

end-diastolic pressure during pacing with no signifi-cant change in stroke work index. The relationbetween minute work index and end-diastolic pres-sure was also examined (Fig. 2). Again, a spectrumof responses was seen. When considered together,Group I patients demonstrated a significant fall inend-diastolic pressure, but no significant change inthe minute work index. There was a rise in theminute work index during atrial pacing in Group 2,but no change was observed in the end-diastolicpressure. The increase in minute work index waslargely due to increase in systemic arterial pressure,especially in those experiencing angina. Group 3patients, however, had a significant rise in minutework index and a fall in end-diastolic pressure whenthe heart rate was increased. Pacing was interruptedand end-diastolic pressure during the subsequentI0 beats measured in 20 patients. In 4 patients (Case5, II, I6, and 22) the end-diastolic pressure rosefrom a normal value during pacing to a distinctlyabnormal one with pace interruption, thus unmask-ing an abnormality in left ventricular fimction.

Direct left atrial pressures during the controlperiod and during atrial pacing were measured inI7 patients. In 9 patients the end-diastolic pressure

copyright. on N



j.com/

Br H


ownloaded from


-1036 Chandraratna, Shah, Kramer, Davis, and Schreiner

TABLE i Haemodynamic data of patients studied

Case State Heart LV end- Pace off Left atrial Brachial Cardiac LV stroke LV minuteNo. rate/min diastolic LV end- mean artery index work index work index

pressure diastolic (mmHg) mean (I./min per (g m/beat) (kg m/min)(mmHg) pressure (mmHg) m2)

(mmHg)

Group II Control 65

Pace I502 Control 60

Pace Ioo3 Control 75

Pace I454 Control 80

Pace I50Group 2

5 Control 75Pace I50

6 Control t00Pace I50



9 Control 78Pace 125

Io Control 75Pace I20

II Control 78Pace* I50

12 Control 8oPace* I55

I3 Control 60Pace* I35

14 Control 85Pace* Ioo

I5 Control 70Pace* 105

I6 Control 65Pace* I30

17 Control 82Pace* 143

I8 Control 60Pace* 90



21 Control 65Pace* I07




25 Control 58Pace 97





I08 I3 9

I5I0 I28 - 6

57 4I 3

6 78 20 II

I2 - I0I0 147 4

5 6

I3 8

I3 '4I3 9i8 - 10

I3 10

7 I0I3 86 20 8

8 720 30 I36 - 38

I327 2510 768 _

II I88 6

5 3Io - 525 3012 77 I3 II

9 - 6

23 28

9 7II 8

Io - 6

II I5 76 35 I0 76- 8

i6 25 I7i6 - II

I3 2325 - -

34 -

I5 12

6 IoI5 - Io25 I7 I52I - I932 32 40

97 2-80

95 2-74I05 3-I0I05 4-2090 3-04Ioo 3-30ioo 3-10I05 2-98

ioo 3-I0I05 2-90II0 4-o8I20 4-05I05 3.I6I00 3-04ioo 3 83II0 3-9685 I.6588 i-8iI25 2-60I25 2.4I82 3-2690 3-46I30 3.35I40 3.5675 2-4680 2-5490 2-58II5 2-66I20 2-91I20 2'97II0 2-92I05 2-84II0 3-30I15 2-8680 2-4385 2-0097 2-40I02 2-88II0 2-86I30 3.4792 2.73II7 3°09I42 2-60I95 2-8895 2-70Ioo 2-50I25 2.76I50 3o00145 2-50I6o 3-4099 3-38112 3'07I32 2-89147 3.8295 2-7II25 3-05I25 3.I8I70 3.I7

66-226-569.755473'5230

5527

57425328

565321

I752.237.342-727.87540°559.7I9-834.2

34.364-544.866-930.I56324I.6I9.556.i26-656-637.750'545-579.769.547.526.55842'774.773.I52-526.5836548-345.473.565

4-303.974-205*503'504'504-i64'50

3.904'055'7063o04'504-204.80560i-642I23.924.523.32

4 I56-oo6-303-482.702-903-424.5I4'704-503.904'704.562-50I.753-003-604-205.453'304.905.oo7-603-483'404.355.754.396*903*603.444-807-803-384-854-806-30

copyright. on N



j.com/

Br H


ownloaded from



TABLE I continued

Case State Heart LVend- Pace off Left atrial Brachial Cardiac LV stroke LV minuteNo. rate/min diastolic LV end- mean artery index work index work index

pressure diastolic (mmHg) mean (I./mnn per (g m/beat) (kg mlmin)(mmHg) pressure (mmHg) mi2)

(mmHg)

Group 330 Control I20 37 37 I05 21II I8-2 2-i8

Pace I50 28 38 28 I05 2.23 2I.5 3-2031 Control 75 - - 82 I-88 I7 i-28

Pace 110 i8 - 80 2-24 20 212032 Control 95 33 0-9 3-00 25-9 2.46

Pace I25 30 - 30 IOO 3-65 30 3'7533 Control 85 28 23 80 iv8o I7.I IP45

Pace I20 25 - 90 21-0 2I 2-5034 Control 68 26 13 I35 2-6I 66-3 4-50

Pace* 145 i8 22 I5 150 2-70 35.6 5.I5

* The asterisks indicate patients who developed angina during pacing, and the values given are those observed during pace-induced angina.

TABLE 2 Summary of haemodynamic data. The mean values ± standard error are given

Heart LV end-dias- Left atrial Brachial Cardiac index LV stroke LV minuteratw/min tolic pressure mean (mmHg) artery mean (I. min per work index work index

(mmHg) (mmHg) mi2) (gm/beat) (kg m/min)

Group IControl 70SEPace I36SE

Group 2Control 72SEPace 124SE

I2+ II4+2NS

8

14

I07 2-9±4 +0-II20 3-0±5 +0*I

P<o-ooI NS

56-6 4-0±3 +0±239 4.7±3 ±0+3P<o-ooi P<o-oI

Group 3Control 89SEPace 130SE

Note: Statistical method was standard paired 't' test.

I0+26

+2P<oo5

5.0

6

98±3IOI±3NS

3-0+0-1

3.3±0+3NS

587+635-6±7P<oo5

4-0+0-24.6

±0+3NS

30+224+2P <o-oi

27

24

98+1084

±24NS

2-3+0-22-6

±03P<oo5

28-9±925 9±3NS

2-4_o*63.4

±o*6P<oor

copyright. on N



j.com/

Br H


ownloaded from


1038 Chandraratna, Shah, Kraner, Davis, and Schreiner

decreased during atrial pacing and it was unchangedin one patient. In 8 of these the left atrial meanpressure either increased (6) or remained the same(2) and in the 2 other patients there was a con-comitant decrease in left atrial mean. This decrep-ancy in the trends of the end-diastolic and meanpressures during atrial pacing is due to spuriousrise in the left atrial mean resulting from fusion ofthe 'a' and 'v' waves (Leighton et al., I969; Khajaand Parker, I97I). In the 7 patients in whom theend-diastolic pressure increased during pacing therewas a corresponding rise in the left atrial mean ineach case.Unusual responses were observed in 2 patients in

Group 2 (Fig. 3). One patient (Case 14) developedangina when the heart rate was increased from 6oto go beats/minute. The mean LA pressure rosefrom 5 mmHg to 30 mmHg with a 'V' wave of 40mmHg. Another patient (Case 29) experienced an-

Case 14 v40 v /

c 20 E 20 -

Ea10 3 E lo

Control Pace

Case 29

o ~~~~oo

a,40 Vv

80-

E 20 E 40I

E101- E 20]

Control Pace off

FIG. 3 The pressure tracings of two patients whoshowed unusual responses to pacing are illustrated.The upper panel shows the direct left atrial pressuretrace of Case 14 during the control period (on the left)and during pace-induced angina (on the right). Notethe tall ' V' wave in the tracing on the right, with a

sharp Y descent suggestive of mitral incompetence.Case 29 (lower panel) had mitral incompetence at restas shown by a tall ' V' wave in the pulmonary arterywedge pressure tracing (trace on the left). Duringpace-induced angina the 'V' wave became more pro-nounced. The tall 'V' wave persisted for severalminutes when pacing was stopped (trace on the right),suggesting a sharp accentuation ofmitral incompetence.

gina on increasing the heart rate from 65 to 97 aminute, with a rise in the 'V' wave of the pulmonarywedge pressure from 40 mmHg to I00 mmHg whichpersisted for several minutes when pacing was dis-continued (Fig. 3).

DiscussionSeveral investigations have supported the originalobservations of Bowditch (I871) that an increase infrequency of cardiac stimulation augments ventricu-lar performance (Woodworth, I902). Mitchell andassociates studied the effects of heart rate on ventri-cular performance in the areflexic dog heart, inwhich the stroke volume and the mean aortic pres-sures were maintained constant (Mitchell, Wallace,and Skinner, I963). Their results suggested thatthere was an increased velocity and force of con-traction when the heart rate was increased. Sonnen-blick and associates investigated the influence ofheart rate on the dynamics ofthe intact human ven-tricle (Sonnenblick, Morrow, and Williams, I966).The maximum rate of force development increasedwhen the rate was raised, but there was little effecton the peak contractile force, suggesting that in manthere is a 'velocity staircase' rather than a 'forcestaircase'. A more recent report indicates that themaximal intrinsic velocity of contractile elements(Vmax) is increased significantly during atrial pacingsuggesting an augmented contractile state (Bowyeret al., I97I).The use of atrial pacing as a stress test for evalua-

tion of patients with coronary artery disease hasbeen shown to be of practical value. Some investi-gators have attempted to construct Sarnoff functioncurves relating left ventricular end-diastolic pressureto stroke work based on data obtained at differentheart rates. Though pacing 'function curves' areshown to be different in the normal and in thediseased ventricle, one has reservations about con-structing curves following interventions that areconstantly changing myocardial contractility. Apacing 'functioncurve'isprobablyderived from join-ing points on different ventricular function curves.The results of the present study show that though

'normal' patients respond uniformly to pacing witha fall in left ventricular end-diastolic pressure andstroke work index (normal response), those withcoronary artery disease exhibit a wide spectrum ofresponses. In patients with stable angina pectoriswithout evidence of left ventricular dysfunction at

rest, end-diastolic pressure fails to decrease as strokework index falls at heart rates sufficient to developangina. Indeed, transient interruption of pacing mayunmask conspicuously raised left ventricular end-diastolic pressure (abnormal response). However, 26

copyright. on N



j.com/

Br H


ownloaded from



per cent of patients in Group 2 in the present studyhad decreased end-diastolic pressure and strokework index after pacing despite the development ofangina. On the other hand, of the 7 patients inGroup 2 in whom pacing stress was insufficient toprovoke angina, the haemodynamic response was'normal' in 4 and abnormal in 3.This wide variationin haemodynamic response to pacing could not becorrelated with the location or number of occlusivelesions in the coronary arterial tree. These resultsare not significantly different from individual patientdata previously published (Linhart, I97I). Becauseof the significant increase of false positive and falsenegative results, pacing stress may not be reliablyused as a diagnostic intervention in this group ofpatients.

Furthermore, patients having clinical evidence ofcongestive failure associated with coronary arterydisease manifested a significant improvement in leftventricular function after pacing at more rapid heartrates. Four of 5 patients in this group showed asignificant fall in end-diastolic pressure associatedwith an increase in stroke work index. This haemo-dynamic improvement may be due to the positiveinotropic effect of tachycardia (Bowditch effect)on nonischaemic areas of the ventricle.The haemodynamic responses to pacing may be

further influenced by the development of mitralregurgitation as was seen in two patients in Group 2.Case I4 probably developed papillary muscle dys-function and mitral regurgitation when stressed toangina as indicated by a sharp rise in the left atrialmean pressure from 5 to 30 mmHg. Similarly inCase 29 the pronounced increase of the 'V' wave inthe left atrial pressure from 40 to I00 mmHg reflectssharp accentuation of mitral regurgitation with theonset of pace-induced angina. Lesser degrees ofmitral regurgitation in other patients may havegone undetected and could alter the relation be-tween left ventricular stroke work index and leftventricular end-diastolic pressure.Abnormal rise in end-diastolic pressure in the

majority of patients paced to angina may reflecteither decreased compliance from ischaemia or leftventricular dysfunction. The latter hypothesis issupported by angiographic observations on leftventricular wall motion made in our laboratory(Davis et al., 1972). Areas of akinetic and dyskineticmotion were observed after pace-induced angina inseveral patients. These findings support similarobservations made by Dwyer (1970).

In conclusion, though a pacing stress is a usefulintervention to study patients with stable anginapectoris, it may be unreliable in at least one-fourthof patients. A normal response to pacing stress can-not be equated with an absence of myocardial

ischaemia from coronary artery disease since exer-cise treadmill test may be strongly positive even atlow work loads. Patients with ischaemic heartdisease show a wide spectrum of responses to atrialpacing. Left ventricular fimction may either be'normal' with a drop in left ventricular end-diastolicpressure along with stroke work index, or may begrossly 'abnormal' with a rise in end-diastolic pres-sure despite a fall in stroke work index. Evaluationof left ventricular function may be further complica-ted by the development of mitral regurgitation fromischaemic dysfunction of papillary muscle. Finally,patients with ischaemic heart disease having clinicalleft ventricular failure associated with ventricularaneurysm may show significant improvement inventricular performance as evidenced by decreasedend-diastolic pressure with increase in stroke workindex.

ReferencesBowditch, H. P. (I87I). Uber die Eigenthumlichkeiten der

Reizbarkeit, welche die Muskelfasern des Herzens zeigen.Berichte iiber die Verhandlungen der Koniglich SachsischenGesellschaft der Wissenschaften zur Leipzig, 23, 652.

Bowyer, A. F., Allen, R. L., Schmidt, P. E., and Johns, V. J.,Jr. (197I). Contractile element velocity during pacemakertachycardia in man (abstract). Circulation, 44, Suppl. 2, 44.

Davis, R. J., Shah, P. M., Schreiner, B. F., Lipchik, E. 0.,and Kramer, D. H. (I972). Effects of pace induced anginaon left ventricular wall motion (abstract). Circulation, 46,Suppl. 2, I44.

Dwyer, E. M. (I970). Left ventricular pressure-volume altera-tions and regional disorders of contraction during myo-cardial ischemia induced by atrial pacing. Circulation, 42,IIII.

Frick, M. H., Balcon, R., Cross, D., and Sowton, E. (I968).Hemodynamic effects of nitroglycerin in patients withangina pectoris studied by an atrial pacing method.Circulation, 37, I60.

Khaja, F., and Parker, J. 0. (I97I). Dissociation of left atrialpressure and left ventricular end-diastolic pressure duringpacing induced tachycardia (abstract). Circulation, 44,Suppl. 2, I86.

Leighton, R. F., Zaron, S. J., Robinson, J. L., and Weissler,A. M. (I969). Effects of atrial pacing on left ventricularperformance in patients with heart disease. Circulation, 40,6i5.

Linhart, J. W. (197I). Myocardial function in coronary arterydisease determined by atrial pacing. Circulation, 44, 203.

Mitchell, J. H., Wallace, A. G., and Skinner, N. S., Jr. (I963).Intrinsic effects of heart rate on left ventricular perform-ance. American Journal of Physiology, 205, 41.

Parker, J. 0., Ledwich, J. R., West, R. 0., and Case, R. B.(I969). Reversible cardiac failure during angina pectoris.Circulation, 39, 745.

Ross, D., Sutton, R., Dow, J., Gonzalez-Lavin, L., Hendrix,G., Jefferson, K., McDonald, L., Petch, M., Smithen, C.,and Sowton, E. (I972). Venous graft surgery in treatmentof coronary heart disease. British Medical Jourxal, 2, 644.

Sarnoff, S. J., and Berglund, E. (I954). Starling's law of theheart studied by means of simultaneous right and leftventricular function curves in the dog. Circulation, 9, 706.

copyright. on N



j.com/

Br H


ownloaded from


1040 Chandraratna, Shah, Kramer, Davis, and Schreiner

Sonnenblick, E. H., Morrow, A. G., and WiLliams, J. F., Jr.(I966). Effects of heart rate on the dynamics of forcedevelopment in the intact human ventricle. Circulation,33, 945.

Sowton, G. E., Balcon, R., Cross, D., and Frick, M. H. (I967).Measurement of the angina threshold using atrial pacing.Cardiovascular Research, I, 30I.

Woodworth, R. S. (1902). Maximal contraction, staircase-contraction, refractory period, and compensatory pause, ofthe heart. American Journal of Physiology, 8, 2I3.

Requests for reprints to Dr. P. M. Shah, CardiologyUnit, Strong Memorial Hospital, 260 Crittenden Blvd.,Rochester, New York I4642, U.S.A.

copyright. on N



j.com/

Br H


ownloaded from


spectrum of haemodynamic responses to atrial pacing in … · atrial tachy-pacing wasperformed in...

Documents