the a wave of the apexcardiogram and left ventricular diastolic stiffness

The A Wave of the Apexcardiogram and LeftVentricular Diastolic Stiffness

By THOMAS C. GIBSON, M.B., M.R.C.P., ROBERT MADRY, M.D.,WILLIAM GROSSMAN, M.D., LAMBERT P. MCLAURIN, M.D.,

AND ERNEST CRAIGE, M.D.

SUMMARYThis study was made to determine whether the A wave of the apexcardiogram (ACG), a re-

flection of the late diastolic response of the left ventricle to atrial systole, corresponded in a

quantifiable way to left ventricular late diastolic stiffness (LVDS). Using a combined ultrasonicand hemodynamic technique, the slope of the late diastolic left ventricular pressure/diameter re-

lationship (AP/AD) was calculated in 25 patients and used as a measure of effective LVDS. Mostpatients had valvular heart disease, all were in sinus rhythm and none had regional abnormali-ties of contraction. An ACG was recorded in all and the ratio of the size of the A wave to thetotal amplitude of the ACG wave (A/H) was calculated. When A/H was more than 11%, leftventricular hypertrophy (LVH) and the presence of a fourth heart sound were the rule in thegroup of patients studied.

Using A/H as an independent variable, correlation coefficients were obtained for AP, AD,AP/AD, left ventricular end diastolic pressure (LVEDP), and left ventricular end diastolic vol-ume (LVEDV). Correlation coefficients (r) were: AP = 0.68; AD = -0.05; AP/AD = 0.87;LVEDP =0.73; LVEDV = 0.21. It is concluded that A/H corresponds best to LVDS and is a

useful noninvasive measurement of this property of the left ventricle.

Additional Indexing Words:Echocardiogram Left ventricular pressure-volume relations Left ventricular hypertrophyFourth heart sound Ultrasound Hemodynamics of left ventricle

THE EVALUATION OF LEFT VENTRICU-LAR FUNCTION in man has mainly de-

pended on data obtained by invasive methodswhich are often time consuming, may carrysome risk to the patient, and therefore cannotbe repeated frequently. Accordingly, many investi-gators have sought to correlate information derivedfrom noninvasive procedures with such hemody-namic data. This approach has merit and theapexcardiogram (ACG) has been studied extensive-ly in this context. It has been demonstrated that the

From the Department of Medicine, Division of Cardiolo-gy, and the C. V. Richardson Cardiac CatheterizationLaboratory, University of North Carolina School ofMedicine, Chapel Hill, North Carolina 27514.

Supported by U. S. Public Health Service Grants HL-14833 and GH037.

Dr. Gibson's current address is Medical Center Hospital ofVermont, Burlington, Vermont 05401.

Address for reprints: Ernest Craige, M.D., Department ofMedicine, University of North Carolina School of Medicine,Chapel Hill, North Carolina 27514.

Received August 27, 1973; revision accepted forpublication November 16, 1973.

Circulation, Volume XLIX, March 1974

ACG reflects left ventricular events accurately in aqualitative, and to a lesser extent, quantitativefashion.1-5The recent development in this laboratory of an

index of left ventricular late diastolic stiffness6 hasled us to investigate the correlation of such an indexwith the A wave of the ACG, since bothmeasurements may be regarded as reflecting thelate diastolic response of the left ventricle to atrialsystole. It might be expected that the magnitude ofthe A wave would depend on the degree of leftventricular stiffness. If this were so then the A waveof the ACG would be another useful measurementfor the noninvasive evaluation of this particularfacet of left ventricular function in the individualpatient.

Materials and MethodsTwenty-five patients aged 17 to 62 were studied.

They were selected because they were to undergocardiac catheterization for evaluation of various cardio-vascular diseases. Criteria for inclusion in this groupwere that 1) the patients were in sinus rhythm;2) they were in a comparable basal state for all studiesperformed since no increase in blood pressure, chest

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GIBSON ET AL.

palill, oi- taiclhycardia l)eyond the usual r-estinig rateoccurr.i.ed. This was important since the ACG was aseparate procedure, uisually within 24 hours of thecardiac catheter-ization; 3) technically adequate ACG,left venitricular cavity echocardiograrns anid left ventric-ilar pressuire curves were available.ACG tracings were mnade with the patient in the left

lateral decuibitus positioi, usually at an anigle of 20-30°.A llellige Puilse Microphon-e tranisducer was used, heldby halnid at the poinlt of maximal impulse of the apex.*Quiiet respirationi was usual but occasionally the optimaltraciniig was obtained on expiration. The ACGs wererecorded with a reference phonocardiogram and ECGon a Cambr-idge MC IV Multichannel Data SystemRecorder. The oscilloscope of this recorder was used toverify the proper positioning of the transducer and thepaper speed of the r-ecording was 100 mm per second.Th-e methiod of expressing the ACG data was by theratio of the size of the A wave to the total amplitude ofthe ACG (A/H), and this is illustrated in figure 1. Thisml-ethod was originated by Benlchimol and Dimond7 andhas been used by our laboratory8 and others.9 10 Theheiglht of the A wave was calculated as a fraction of thetotal outwar.d movement in systole (H) and expressedas a percenitage. For all determinations the average ofat least five complexes was used.

Cardiac caitlheterizationi vas carried out in the fastingstate, followinig diazepan (5-10 mgm i.m.) premedica-tioni. Brachial alarteriotomy and retrograde left heartcatheterization vere perforrned with standard #8

*Fritz Hellige & Co., Freiburg, West Germany. Thisapparatus has a flat response at frequencies from 50Hz downto 0.3 Hz, and a timle constant in excess of 3 sec.

.Frelneh catlheters in 15 patients, an-d with high fidelitynic ronmomvneter tipped catleters* in teni patieints.Miicroranometer pressures vere calibrated with amercurx\reference an(l clhecked against the simulta-11eou1s lumi-leni pressture of tlhe,catheter for alignment ofencd-diastolic anid peak-systolic values. No significantbaseline drift was observed in this system. All pressureswere recorded on an Electronics for Medicine DR-12recorder. Left ventricular cineangiography was per-formed in each study, and patients with regionaldisordlers of contractioni were excluded.

Immediately following cardiac output determination,but prior to anigiography, a simultaneous photographicstrip clhai t recording of the electrocardiogram, leftventr-icular pressure and ultrasonically determined leftven-tricular septal and posterior wall motion was made.The ultrasonoscope used was a Smith-Kline InstrumentsCompany Ekolinie 20A coupled to an Electronics forMedicine recorder via an Electronics for MedicineUDA interface channel. Paper speed was 100 mm/seewitlh 0.02 second timelines. The left ventricular cavityrecordin1g was obtainled in a standard manner by theutilizationi of strip cliart scanning as described byFeigenbaum.11 The minor axis used was that in a planeimmediately below thle mitral valve leaflets. Onlyreco-dinigs where it was possible to identify clearly theposterior wall and septal endocardial surfaces wereused. Appropriate damping maneuivers were done inorder to be more certain that true endocardium wasbeing recor-ded. Indocyaniine green or saline wasinijected inito the left ventricular cavity if any doubtexisted.The slope of the late diastolic pressuire-diameter

reclation at the time of left atrial systole (AP/AD) wasmeastired in each patienit, as illtistrated in figure 2. Theonset of left atrial systole was defined with respect to

*Mikrotip, Millar Instruments, Houston, Texas.

LINE AB. D,LUNE COE 2

hP P2-PiA D 0-D

A C

ECGFigre

SECONDS

Figulre 2

ECG ]I fr-

Figure 1

The method of mneasurement for A/H. A = height of Awave, H = total hleight of the apexcardiogram; OM =out-

ward movement; 0 = oint; RFW = rapid filling wave;

SFW slow filling wave. A simultaneous ECG and phono-

cardiogram (PCG) were taken. A!H in this example is 5%k.

Photographic stripchart recordling of simultaneous echocar-diogram, left ventricular pressure (LVP), and EGG from pa-

tient 8. A traced form of the actual record is shown on theright for explanatory purposes. P1 and P2 represent respec-

tively the left ventricular p)ressure.s at onset and peak of leftatrial systole. D1 and D2 are shown by the lines AB andCD representing left ventricular diameters at onset (D1)and peak (D2) of left atrial systole. PW= posterior wall;

LVP = left ventricular pressure.


Si 8Sa2EDM

PCG- LSE

APEX

OM

100-

80-

70-

I 60-ESUr= 50E. 40 -

J 30-20

0

A44



APEXCARDIOGRAM AND DIASTOLIC STIFFNESS

the P wave of the ECG as a reference. The intervalfrom onset of the P wave to onset of left atrial systole inman has been shown to be about 80 msec byBraunwald et al.12 whose method was corrected for the5 msec transmission delay of their pressure measure-

ment system. In this study, no correction was made fortransmission delay through the standard catheters,which averages 10-14 msec in our laboratory,6 since thiswas felt to be less than the error in defining the onset ofthe electrocardiographic P wave.

Having defined P1 and Dl as the left ventriculardiastolic pressures and echocardiographic diameter atthe approximate onset of left atrial systole, we

measured P2 and D2 at the peak of left atrial systole,taken as the peak of the atrial (a) wave in the leftventricular pressure tracing (fig. 2). When there was

no clearly defined "a" wave, P2 and D2 were obtainedat end diastole, defined as occurring 40 msec after theonset of the QRS in the ECG.6 Change in pressure andchange in diameter (AP and AD), defined as P2-P1and D2-D1, thus represent diastolic pressure anddiameter increments occurring in association with leftatrial systole. Their ratio, AP/AD, has been previouslyreported by us as a measure of effective left ventriculardiastolic stiffness (LVDS) .6, 13

Left ventricular end diastolic pressure (LVEDP)was measured in each patient, and left ventricular enddiastolic volume (LVEDV) was calculated from theechocardiographic left ventricular end diastolic diame-ter according to a formula proposed by Teichholz'4(personal communication): V = (7.0/2.4 +D) X D3,where V = volume in cc and D = left ventricular cavitydiameter in cm. The presence or absence of leftventricular hypertrophy (LVH) was derived from thequantified Romhilt and Estes method using a standard12 lead ECG.15 A score of five or more was consideredto indicate left ventricular hypertrophy. The presenceor absence of gallop sounds was established by means ofthe phonocardiogram using Leatham microphones. Thestatistical analyses were performed by standard tech-niques16 using a Wang 600 electronic calculator.

ResultsTable 1 summarizes the over-all data obtained for

the invasive and noninvasive measurements in our

patients. They have been divided into two groups

for the purpose of analysis. Group A consists ofthose patients with A/H of 11% or less, a figure weconsider to be within the limits of normal, andGroup B those with higher A/H. This separation isbased on the level of the mean A/H obtained inour laboratory for normal controls.8

A/H and Left Ventricular Late DiastolicPressure and Volume

Correlation coefficients were calculated for thetotal cohort using A/H as the independent variableand AP, AD, AP/AD, LVEDP, LVEDV as thedependent variables. It can be seen from table 1that AP/AD, LVEDP, and AP correlate best. The


151413

12

10

AP/AD(mm Hg/mm)

9

87

6

5

43

2

.n= 25r = 0.868

* LVHO NO LVH

o(1

0

0

0

00

0

0 * :o 0

0

0

0

2 4 6 8 I0 12 14 16 18 20 22 24 26 28

A/H RATIO (%)

Figure 3

Comparison of ratio of amplitude of A wave to total ampli-tude of ACG (A/H) with left ventricular diastolic stiffness(LVDS). The close relationship between left ventricularhypertrophy (LVH), elevation of A/H above 11% (11 of 12),and LVDS greater than 2.5 mm Hg/mm (12 of 15) is alsoshown.

relationship between A/H and AP/AD is shownin figure 3 (r = 0.868). A lesser correlation(r = 0.730) was also found between A/H andLVEDP (fig. 4). The correlation between A/H andAP was r = 0.684 but AD and LVEDV did not

correlate well.

A/H and Left Ventricular Hypertrophy

A close relationship of the degree of LVDS to thepresence or absence of LVH exists,6 and the level

50

40

30

LVEDP(mm Hg)

20

10

n= 25r = 0.730

* LVH0 NO LVH .

0

0

0 08S0

0

00

2 4 6 8 10 12 14 16 18 20 22 24 26 28

A/H RATIO (%)

Figure 4Comparison of ratio of amplitude of A wave to total ampli-tude of ACG (A/H) with left ventricular end-diastolic pres-

sure (LVEDP). A significant relationship exists. In addition,a close relationship is present between LVEDP greater than12 mm Hg, and the presence of left ventricular hypertrophy(LVH) (14 of 18).

443

n



GIBSON ET AL.

Table 1

Stummary of Patient Data

AP AP/AD LVEDPA/H ap (mm (mm (mm LVEDV

Pt. Age/Sex Diagnosis (%) (mm) Hg) Hg/mm) Jig) (cc) LVH Sa, S4

Group A1. MM 36 F MS, AR 2 1.9 2.7 1.4 6 172 0 02. GP 29 F MS 3 2.0 3.9 2.0 9 148 0 03. BF 40 M MS 4 1.1 2.9 2.7 8 78 0 04. RT 58F MS 5 4.8 2.2 0.5 5 119 0 05. LB 51 F AR, AS, MS 5 1.5 5.2 3.4 13 179 LVII 06. YO 17 F MR 5 2.7 6.O3 2.3 6 166 0 07. PM 30 F VSD 5 2.3 4.5 1.9 12 148 0 08. SH1 25 M AIR 5 1.5 7.2 4.8 26 207 LVII 09. EQ 44 F AR, MR 6 3.4 11.4 3.9 20 210 0 0

10. VW 48 M AR, MS 8 7.1 18.1 2.6 25 172 0 011. WH 62 M AR 10 1.5 9.0 5.9 23 239 LVH 012. RC 53 F MR, MS 11 1.7 5.2 3.2 11 119 0 013. WC 40 F Cardiomyopathy 11 1.9 8.8 4.9 20 135 0 4

Group B14. PG 28 M MS, MR, AR 12 1.9 7.5 4.0 15 172 LVH 415. LS 52 F AR 12 3.4 12.0 3.5 19 200 IIVM 416. WW 49 M CAD 12 2.4 14.3 6.1 18 159 LVH 3.417. JD 33 M AR, MS 13 3.1 12.8 5.0 25 265 LVH ?18. JL 58 M AR 14 3.7 21.0 5.8 39 200 LVIH 419. AT 46 F AS 14 2.1 t3.0 6.3 20 1515 LVH 420. OW 18 F AR 18 7.0 35.5 5.1 5i2 307 LVH 3.421. LD 38 F Cardiomyopathy 18 1.5 9.4 6.6 24 75 0 422. CS 57 M AS 18 1.3 12.0 9.2 23 167 LVH 423. TS 62 M AR 19 2.1 28.0 13.6 40 159 LVHI 424. RB 53 M AS, AR 24 1.1 15.8 14.6 28 119 LVH 425. CS 33 M AR 27 1.8 20.0 11.9 38 315 LVII 3.4Correlations for both groups r -0.051 0.684 0.868 0.730 0.208

Abbreviations: MS = mitral stenosis; MR = mitral regurgitation; AS = aortic stenosis; AR = aorticregurgitation; VSD = ventricular septal defect; CAD = coronary artery disease; LVEDP and LVEDV =

left ventricular end diastolic pressure and volume; LVII = left ventricular hypertrophy; S3, S4 = third andfourth heart sounds. A/H = ratio of height of the A wave to total amplitude of apexcardiogram; AP, AD =change in left ventricular late diastolic pressure and diameter.

of A/H should also reflect this. When Groups A andB were compared this was the case, since three of13 patients in Group A had LVH whereas 11 of 12of Group B had LVH. This difference was highlysignificant (P= 0.0003). The mean value of A/Hfor patients with LVH was 14.5% as compared with7.1% for those without LVH (fig. 5).

A/H and the Fourth Sound

A fourth sound was recorded in only one patientin Group A (1/13), whereas it was the rule inGroup B (11/12). The difference is again highlysignificant as reflected by P < 0.00003. The meanvalue of A/H for patients with a fourth sound was16.6% as compared to 6.3% for those without LVH(fig. 5). In patient 17 it was difficult to identify asound due to an Austin-Flint murmur which

obscured the site where the sound might berecorded on the phonocardiogram.

Discussion

The A wave of the ACG has been used over thepast decade as one indicator of left ventricularfunction. It has been shown to mirror diastolicevents directly recorded from the left ventricle,17, 18reflecting the impact of the late atrial contributionon the filling or already filled left ventricular cavity.It is reasonable to assume that in nonnal man thedistensibility of the left ventricle could accommo-date the changes in pressure and volume broughtabout by this "atrial kick" phenomenon, and thatthe consequent precordial A wave would be of littlemagnitude. Similarly it might be expected that adiseased and poorly functioning left ventricle would


444



APEXCARDIOGRAM AND DIASTOLIC STIFFNESS

n=l14 n=lII n=12 n=l13

Figure 5;Comparison of ratio of amplitude of A wave to total ampli-tude of ACG (A/H) % in patients with and without leftventricular hypertrophy (LVH) and with and without a

fourth heart sound (4). The bars represent mean values andthe horizontal brackets their standard errors.

respond poorly to the added burden of atrial systolein that impaired distensibility leads to dispropor-tionate intraventricular pressure-volume changes,reflected by an increase in the precordial A wave,

often to the extent that it may become palpable.This has been shown in disease states where the "re-

serve of distensibility" of the left ventricle is im-paired, usually in the presence of LVH. In aorticstenosis, aortic regurgitation, idiopathic hyper-trophic subaortic stenosis, cardiomyopathy, andhypertension an abnormal increase in the height ofthe A wave has been described,9' 19, 20 usually asso-

ciated with severe disease. In such studies some pa-

tients did not have large A waves in spite of severe

disease and Tavel has shown that in patients withsevere aortic stenosis the absence of a large A wave

may occur.2' In severe aortic regurgitation a small

or absent A wave may be due to premature closureof the mitral valve leaflets with elevation of leftventricular diastolic pressures above left atrialpressures during most of diastole.22The use of stress with changes in preload and

afterload may alter what was apparently a normalA wave in a patient at rest. Ginn et al. have shownthat subjects with established coronary arterydisease responded to exercise by a near doubling ofthe height of the A wave as measured by A/H.10This is of interest in view of recent studies from our

laboratory which have shown impairment of leftventricular relaxation and consequent increaseddiastolic stiffness during atrial pacing in patientswith coronary artery disease.23 In normal subjects,Circulation, Volume XLIX, March 1974

and those thought to have cardiac ischemia butwith negative coronary cineangiograms, the eleva-tion of A/H was trivial. Ginn et al. also demonstrat-ed that an elevated A/H during an episode ofischemia was appreciably reduced by nitroglycerin.Similar data have been obtained by Benchimol andDimond.7The precise mechanism whereby A wave eleva-

tion occurs is not known. Some have considered that,it is an indicator, not necessarily quantitative, ofchanges in the level of LVEDP, and haveattempted to resolve this by comparing LVEDPwith A/H.24' 25 Voigt, using 58 observations in 18patients, most of whom had coronary artery disease,was able to obtain some correlation (r = 0.57)although this was not striking. He observed that theheight of the precordial A wave depended more onthe height of the A wave seen in the left ventriculartracing, and stated that it therefore depended onthe degree of "atrial kick." Willems, using calibratedprecordial tr.acings in dogs, also showed a relativelyweak correlation (r = 0.48) between the absolutelevel of the precordial A wave and LVEDP.25 Ourown data show a more significant relation of A/Hto LVEDP (r = 0.73), although five of the 13patients with A/H within the limits of normal hadelevated LVEDP. In any discussion of this area,LVEDV must also be considered since it is thepressure-volume relationship that determines com-pliance. Our data indicated that pressure changewas significant whereas end diastolic volume andlate diameter changes were insignificant correlatesof A/H. The index of stiffness AP/AP proved tohave even better correlation with A/H than AP.A most important common denominator in

elevations of A/H and AP/AD was LVH by ECGcriteria, and the only individual with abnormal A/Hbut without LVH was patient 21 who hadrestrictive cardiomyopathy due to cardiac amyloi-dosis and a typical low voltage ECG. It has alsobeen shown that there is a close associationbetween a large A wave and the presence of afourth heart sound; this has been related to elevatedLVEDP.2' In the present study the presence of afourth sound, together with elevation of A/H andECG evidence of LVH, is very well correlated withan abnormal index of late diastolic stiffness of theleft ventricle. This is in keeping with the dataobtained by Shah26 who found that LVH was themajor concomitant of a fourth sound in patientswith cardiomyopathy. Both Shah26 and Craige27have postulated that a process giving rise to LVHwould result in reduced compliance and an elevated

445



GIBSON ET AL.

resistance to filling. The atrial boost would beaugmented and atrial gallop would ensue.The relationship between an index of left

ventricular stiffness and A/H makes the latter auseful noninvasive index of the ability of the leftventricle to accommodate the results of atrialsystole. This relationship is to be expected since themeasurements taken are of identical events. Theapplication of A/H to disease states already existsand it has been shown to be a marker of thecapability of the ventricle to respond to stress. Itshould be an excellent tool for the serial follow-upof patients with generalized left ventricular com-promise.

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human heart from the first derivative of theapexcardiogram. Circulation 36: 933, 1967

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3. VETTER WR, SULLIVAN RW, HYATT KH: Assessment ofquantitative apexcardiography. Am J Cardiol 29:667, 1972

4. MIRSKY I, PASTERNAC A, ELLISON RC: General indexfor the assessment of cardiac function. Am J Cardiol30: 483, 1972

5. TAYLOR DJE, NIXON PGF: Assessment of left ventricularfunction after myocardial infarction. Br Heart J 34:905, 1972

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8. PARKER E, CRAIGE E, HOOD WP: The Austin Flintmurmur and the A wave of the apexcardiogram inaortic regurgitation. Circulation 43: 349, 1971

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18. BENCHIMOL A, DIMOND EG: The normal andabnormal apexcardiogram. Its physiological variationand its relation to intracardiac events. Am J Cardiol12: 368, 1963

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MCLAURIN and ERNEST CRAIGETHOMAS C. GIBSON, ROBERT MADRY, WILLIAM GROSSMAN, LAMBERT P.

The A Wave of the Apexcardiogram and Left Ventricular Diastolic Stiffness

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the a wave of the apexcardiogram and left ventricular diastolic stiffness

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