Serial M-mode Echocardiography in SevereChronic Aortic Regurgitation

IAN G. MCDONALD, M.D., AND V. MICHAEL JELINEK, M.D.

SUMMARY Thirteen patients with severe chronic aortic regurgitation (mean age 52.5 years) were studiedby serial M-mode echocardiography. When first studied, none had breathlessness caused by left ventricularfailure (LVF). Nine of these patients remained asymptomatic over a mean period of 4 years, 3 months (no LVFgroup); the other four patients developed left ventricular failure with dyspnea after a mean interval of 3 years,

11 months (LVF group). For both of these groups, we compared the echocardiographic measurements from thefirst and last of the serial studies. For the LVF group, end-diastolic left ventricular internal dimension in-creased 14%, end-systolic dimension increased 35%, fractional shortening decreased 45% and left atrial dimen-sion increased 62%. All of these changes were significant. For the No LVF group, the change in end-diastolicleft ventricular internal dimension was not significant, but the 6% increase in end-systolic dimension, 10%reduction in fractional shortening and 25% increase in left atrial size were all statistically significant.

Although echocardiography could detect declining left ventricular function in a group of asymptomaticpatients with severe chronic aortic regurgitation, the reproducibility of the technique was limited in individualpatients. Therefore, serial echocardiographic studies should be interpreted in conjunction with clinical assess-

ment and other investigations.

PHYSICIANS often have difficulty deciding when torecommend aortic valve replacement in patients withsevere chronic aortic regurgitation. Depressedmyocardial function may persist after aortic valvereplacement,' and it has been suggested that theoperation might be recommended in some patientswho have a progressive increase in heart size even inthe absence of symptoms.2 However, the asymp-tomatic patient often cannot be convinced of thenecessity for the operation, and our enthusiasm foraortic valve replacement in such patients is stilltempered by the small operative mortality and by theincidence of complications related to the prostheticvalve.8 Should surgery be deferred, myocardial func-tion may progressively deteriorate so that the mor-tality of aortic valve replacement may be increasedand postoperative improvement may be less certain.4Indeed, many reports suggest that delaying aorticvalve replacement might increase operative mortality,especially the late mortality, resulting in less recoveryof left ventricular contraction and less symptomaticimprovement.4-"1 No generally accepted criteria foraortic valve replacement in asymptomatic patientshave emerged; nor is it clear whether it is safe to con-tinue medical treatment in the face of early symptomsuntil there is evidence of progressive deterioration.4Echocardiography is an objective method that can beused to detect impaired left ventricular function.However, it is not clear whether serial M-modeechocardiography is sufficiently sensitive to detectdeclining left ventricular function and hence be ofvalue in the clinical management of severe chronicaortic regurgitation. We analyzed our own experience

From St. Vincent's Hospital and the University of Melbourne,Melbourne, Victoria, Australia.Address for correspondence: Dr. Ian G. McDonald, Director,

Cardiac Investigation Unit, St. Vincent's Hospital, VictoriaParade, Fitzroy, 3065, Victoria, Australia.

Received December 10, 1979; revision accepted May 12, 1980.Circulation 62, No. 6, 1980.

over an 8-year period in an attempt to answer thisquestion.

PatientsFifteen patients with severe chronic aortic

regurgitation were followed medically either becauseaortic valve replacement was not indicated on clinicalgrounds or because the patient refused surgery. Twopatients were subsequently excluded because theechocardiograms were considered unsatisfactory. The13 patients who remained in the study included 11males and two females, with an average age of 52.5years (table 1).

Severe aortic regurgitation was defined as anechocardiographic left ventricular stroke volume of100 ml or more. This criterion was chosen, taking intoaccount the relationship between left ventricularstroke volume and the severity of aortic regur-gitation12 and the results of earlier study of patientswith aortic regurgitation.'3 Thus, Dodge et al. estab-lished that the left ventricular stroke volume in aorticregurgitation increased in direct proportion to themagnitude of regurgitation;'2 in an earlier cross-sectional study of patients with aortic regurgitation,the average value of the echocardiographic left ven-tricular stroke volume was 128.5 ml in severe chronicaortic regurgitation in the absence of left ventricularfailure and 103.1 ml in the presence of failure.'3

Cardiac catheterization was performed in six of the13 patients (patients 1, 4, 6, 10, 11 and 12) and wasrepeated in four to assess progress (patients 1, 10, 11and 12). Coronary angiography and left ventricularangiography were performed in all of these patientsand supine bicycle ergometer exercise was performedin all but patient 4. Left ventricular volumes andregurgitant fractions had been measured only in pa-tient 12. In the remaining patients, the severity ofregurgitation was estimated according to the followingcriteria: the size and amplitude of contraction of theleft ventricular cavity, the appearance of the regurgi-

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VOL 62, No 6, DECEMBER 1980

TABLE 1. Clinical and Echocardiographic Data

Chest IntervalAge Cause of Dyspnea BP radiograph (years, LVIDd LVIDS FS LVSV LA

Pt Sex (years) AR class (mm Hg) CTR PVC ECG months) (cm) (cm) (%) (ml) (cm)

No LVF1 M 16 Rheumatic

182123

2 M 18 Rheumatic2023

3 M 18 Rheumatic20

4 M 25 Rheumatic27

5 M 33 Rheumatic343738

6 M 29 Rheumatic3133

7 M 37 Rheumatic394042

8 M 48 Unknown5053

9 M 21 Unknown2224

IIIIIIIIIIIIIIIIIIIIIIIIII

I

116/56C 0.590.580.630.65

165/40 0.570.560.60

150/20 0.550.54

170/58C 0.630.60

135/50 0.49

0.470.49

108/35 0.490.470.49

145/65 0.52

0.490.51

120/35 0.53

0.54140/50 0.47

0.500.49

+ LVH0 LVH0 LVH (D)0 LVH (D)0 LVH0 LVH0 LVS0 LVH (D)0 LVH (D)0 LVS0 LVS0 LVH- LVH0 LVH0 LVH0 LVH0 LVH0 LVS0 LVH

0 LVH0 LVH0 N- N+ LVH0 LVH0 LVH0 LVH

10 M 36 Rheumatic

11 M 50 Unknown

12 F 56 Rheumatic5861

13 M 51 Unknown52555658

II

IIIIIIIIIIIIIIIIIIIIIIIIIIII

III

III

LVF130/42C 0.65 + LVS

0.65 + LVS0.66 + LVS0.71 + LVS0.69 ++ LVS(D)0.67 + LVS (D)

143/50C 0.61 + LVH (D)

0.60 + LVH (D)0.66 +1+ LVH (D)

147/48C 0.57 + LVH (D)0.57 +0.61 + LVH (D)

135/40 0.55 + LVS0.54 + LVS0.59 ++ LVS (D)

0.66 ++ LVS (D)

Abbreviations: LVF = left ventricular failure; AR = aortic regurgitation; BP = blood pressure; Class = New York HeartAssociation classification; C = intra-arterial blood pressure measured at cardiac catheterization; CTR = cardiothoracic ratio;PVC = pulmonary venous congestion; Interval = time between serial echocardiographs; LVH = left ventricular hypertrophy;LVS = left ventricular strain; (D) = taking digitalis, LVIDd = end-diastolic left ventricular internal dimension; LVID. = end-systolic left ventricular internal dimension; FS = fractional shortening; LVSV = left ventricular stroke volume; LA = left atrialdimension; 0 = no pulmonary venous congestion; + = mild or moderate congestion; + + = severe congestion.

8.32, 7 8.75, 0 8.76, 6 8.6

7.62, 3 7.74, 10 7.5

7.42, 0 7.92, 2 7.2

7.46.0

2, 2 6.34, 2 5.95, 6 6.0

6.02,4 6.84, 4 6.6

7.11, 9 7.13, 4 7.05, 0 7.0

6.42, 0 6.64, 9 6.7

6.31, 8 6.53, 5 6.2

5.85.76.35.85.35.55.74.95.34.85.03.74.24.03.94.25.15.05.55.45.75.54.44.34.94.64.44.5

30342833302924363333323833323530252423241921313627273227

207 4.3255 4.8214 5.6239 6.1172 3.5173 4.1138 5.0176 4.4200 5.2164 4.2171 5.0122 2.1122 2.6103 2.7114 3.0101 2.8115 3.4106 3.7117 5.5114 5.495 5.9108 5.5121 3.6141 4.6118 5.3104 4.6128 4.6101 4.2

1, 1

3, 54, 55, 106, 2

1, 73, 64, 65, 0

2, 64, 0

1, 33, 84, 56, 8

8.58.89.19.08.89.17.06.77.78.18.16.27.27.77.07.67.48.08.0

6.67.47.47.77.98.25.24.65.96.36.44.25.66.24.65.55.76.66.9

22161914101126312322213222183428231814

170 2.2137 3.4179 3.9128 4.0109 5.3103 5.3125 3.4134 3.7147 4.2153 4.7147 4.7115 2.4118 3.0126 4.0158 3.8160 4.1129 4.5121 4.598 4.7

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ECHOCARDIOGRAPHY IN AR/McDonald and Jelinek

tant jet, opacification of the left ventricle and the rateof clearing of contrast from this chamber.'4 161 Cardiaccatheterization was not clinically indicated in theremaining seven patients; in these patients, the se-

verity of aortic regurgitation was confirmed by theclinical signs, in particular by the blood pressure (seetable 1) and the severity of left ventricular dilatationand hypertrophy indicated by the chest radiographand electrocardiograph. None of these patients hadsignificant aortic stenosis, disease of another heartvalve, ischemic heart disease, evidence of unrelatedmyocardial disease or hypertension. Significant aorticstenosis was defined as a peak systolic gradient across

the aortic valve of 10 mm Hg or more and, for thosepatients not subjected to cardiac catheterization, slow-ing of the rate of upstroke of the indirect carotid pulserecording."'

During the period of serial echocardiography, theusual indication for aortic valve replacement in our

Cardiology Unit was clinical left ventricular failure.This was defined as breathlessness that could, clin-ically, be reasonably attributed to pulmonary ve-

nous congestion proved by chest radiography. Fourpatients developed clinical left ventricular failure dur-ing the period of serial study (LVF group) and nine didnot (no LVF group).

Methods

Echocardiography

Our technique has been described previously.'3' 17The description included the method of standardiza-tion, measurement of end-diastolic and end-systolicleft ventricular internal dimensions (LVIDd, LVID.),left atrial dimension, calculation of an index ofmyocardial contraction, fractional shortening (FS)

(FS LVIDd-LVIDg X 10)

and left ventricular stroke volume. Left ventricularvolumes were calculated from the left ventricular in-ternal dimension according to the method ofTeichholz.'8 Errors in the estimation of end-diastolicand end-systolic left ventricular internal dimensionsare additive in the calculation of the index fractionalshortening and cubed in the estimation of left ven-

tricular stroke volume. Hence, we took particular carein reproducing the correctly standardized left ven-

tricular echocardiogram'l in serial recordings and inmeasuring left ventricular dimensions.

Statistical Analysis

For comparison of data from the two groups weused the t test to assess differences in mean values ofeach variable in the light of scatter of results. A secondtype of comparison was also necessary: assessment ofthe significance of differences in echocardiographicvariables between serial studies in one individualpatient. The reproducibility of serial left ventricularechocardiograms differs for each subject, depending

mainly on the quality of the study and ease of stan-dardization. Although the reproducibility for thepatient can be considered informally when makingclinical decisions, insufficient data prevent us fromcalculating statistical reproducibility of measurementsfor each individual. Therefore, we used average valuesfor reproducibility. Reproducibility was establishedseparately for a group of clinically stable patients withsevere left ventricular volume overload due to eitheraortic or mitral regurgitation (table 2).The study included 12 males and three females with

an average age of 38 years. These patients werestudied twice by the same technician, with a mean in-terval between studies of 27 days. The criteria for atechnically acceptable echocardiogram and themethods of routine checking by the supervising physi-cian were identical to our laboratory routine. Signifi-cant changes (measured by paired t test) were con-sidered to be more than 2 standard deviations from themean variation between the paired studies. Thus, asignificant change in end-diastolic left ventricular in-ternal dimension was 4 mm, end-systolic dimension 6mm, fractional shortening 9% and left atrial dimen-sion 8 mm.

Results

Data from serial echocardiography and relevantclinical information are summarized in table 1.Changes in echocardiographic measurements betweenthe first and last of the serial studies are summarizedin table 3.

No LVF GroupThese nine patients were studied over a mean period

of 4 years, 3 months. Comparison of the group meanvalues for echocardiographic measurements recordedat the first and last study disclosed no significantchange in left ventricular end-diastolic internal dimen-sion, but there were statistically significant changesfor the end-systolic internal dimension, fractionalshortening and left atrial dimension (table 3). Thus,end-systolic dimension increased 6% (p < 0.05), frac-tional shortening decreased 10% (p < 0.05) and leftatrial dimension increased 25% (p < 0.01). Theaverage rates of increase of left ventricular end-

TABLE 2. Reproducibility of Echocardiographic Measure-ments in Chronic Severe Left Ventricular Volume Overload(n = 15)

LVIDd LVIDS FS LA(cm) (cm) (%) (cm)

Mean first study 6.53 4.39 33.3 3.57

Mean second study 6.35 4.25 33.3 4.04

Mean difference 0.18 0.14 0.0 0.53

SD 0.20 0.32 4.7 0.40

Abbreviations: LVIDd = end-diastolic left ventricular in-ternal dimension; LVIDe = end-systolic left ventricular in-ternal dimension; FS = fractional shortening; LA = leftatrial dimension.

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VOL 62, No 6, DECEMBER 1980

TABLE 3. Comparison of First and Last Serial Study

LVIDd LVIDM FS LAn (cm) (cm) (%) (cm)

No LVFgroup 9 6.92 4.80 30.88 3.33

-0.75 -0.63 -4.23 -1.497.11 5.12 27.90 4.17

-0.81 -0.65 -4.38 -1.48

LVFgroup 4 7.17 5.15 28.5 2.95

-0.83 0.90 -4.77 -0.678.23 6.92 16.0 4.68

-0.53 -0.78 -3.81 =0.46

Values are mean- SD.Abbreviations: LVIDd end-diastolic left ventricular in-

ternal dimension; LVIDS = end-systolic left ventricular in-ternal dimension; FS = fractional shortening; LA = leftatrial dimension; LVF = left ventricular failure.

diastolic and end-systolic dimension were 0.45 and0.75 mm per year, respectively, and the average rate ofdecline of fractional shortening was 0.7% per year(table 4).Comparison of individual patients, using the

reproducibility criteria of the control study, indicatedthat only patient 6 had a significant increase in bothend-diastolic and end-systolic left ventricular internaldimensions, and patient 3 had a significant increase inend-diastolic dimension only. No patient had a changein fractional shortening that was statistically signifi-cant. In seven patients left atrial dimension increasedsignificantly.

LVF GroupThese patients were studied over a mean period of 5

years, 7 months. During this period, group mean end-diastolic left ventricular internal dimension increased14% between first and last serial study (p < 0.02), end-systolic dimension increased 35% (p < 0.01), the meanvalue of fractional shortening decreased 45%(p < 0.05) and left atrial dimension increased 62%(p < 0.05). The average time from the first echocar-diographic study to left ventricular failure was 3 years,11 months. During this time, the mean rates of in-crease of end-diastolic and end-systolic left ventricularinternal dimensions were 2.05 and 3.21 mm per year,

TABLE 4. Rate of Change Per Year of Left Ventricular In-ternal Dimension and Fractional Shortening

Time LVIDd LVID, FS(yrs, mos) (mm) (mm) (%)

No LVF group 4, 3 0.45 0.75 0.7LVF group

(before LVF) 3, 11 2.05 3.21 2.3

Abbreviations: LVIDd = end-diastolic left ventricular in-ternal dimension; LVID. - end-systolic left ventricular in-ternal dimension; FS = fractional shortening; LVF = leftventricular failure.

respectively, and the rate of decline of fractionalshortening was 2.3% per year (table 4).Each patient had a significant increase in end-

diastolic and end-systolic left ventricular internaldimensions and in the left atrial dimension; fractionalshortening fell significantly in three of the fourpatients.

Patient 7 (fig. 1) was of particular interest becausefractional shortening was subnormal (23%) at the ini-tial study and did not change significantly over thenext 5 years; during this time he remained asymp-tomatic, with no change in physical signs, ECG orchest radiograph.

DiscussionMyocardial Impairment in ChronicSevere Aortic Regurgitation

Chronic severe left ventricular volume overload isknown to cause myocardial damage. The extent ofclinical disability has been related to the age of thepatient and, by inference, to the duration of volumeoverload.20 Left ventricular damage has also beendemonstrated by a variety of techniques in bothanimals and man when the chamber has been sub-jected to prolonged overload,21'28 but clinical detectionof declining left ventricular myocardial function canbe difficult even with the aid of the chest radiographand ECG. Symptoms of left ventricular failure in-dicate a poor prognosis with continued medicaltreatment.29 Unfortunately, important symptoms suchas breathlessness or chest pain are often hard to assesswhen they occur without any objective changes in in-vestigations and may be attributable to anxiety, whichtends to be reinforced by repeated clinical reassess-ments. Nor are radiographic or electrocardiographicchanges always easy to interpret. Although radio-graphic evidence of pulmonary venous congestion30 isimportant, its interpretation is subjective and, in someof our patients, some redistribution of pulmonaryblood flow could be discerned for many years beforesymptoms of left ventricular failure developed. Severecardiac enlargement is an unfavorable sign,313-4 es-pecially if it is progressive, but our studies havedemonstrated that an increase in cardiothoracic ratiomay be caused by progressive left atrial enlargement,with no change in left ventricular size or contraction,as in patients 3, 4, 5, 6 and 8. Furthermore, theprognostic significance of this finding is not yetknown. Severe electrocardiographic left ventricularhypertrophy is also prognostically unfavorable31' 32, 34but may appear only when left ventricular failure isobvious or may be obscured by the effects ofdigitalis.33

Myocardial Impairment Detectedby M-mode Echocardiography

The severity of left ventricular dilatation and ofreduction of fractional shortening demonstrated byechocardiography have been related to the likelihoodof early deterioration of left ventricular function with

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ECHOCARDIOGRAPHY IN AR/McDonald and Jelinek

-LV

FIGURE 1. First (left) and last (right) of the serial echocardiographic studies in patient 7. No significant change was observedover 5 years despite impairment of left ventricular function demonstrated in thefirst echocardiogram. LV = left ventricle; EN= left side of the interventricular septum; PL V = endocardial surface of the posterior left ventricular wall.

progression to failure. Thus, early left ventricularfailure was shown to be more likely when the end-systolic dimension was greater than 5.5 cm35 and aprogressive fall in fractional shortening more likelywhen the left ventricular internal dimensions weremore than 40% above the upper limits of normal(corresponding to LVIDd > 6.5 cm, LVID8 > 4.2cm).38 We studied too few patients to allow us to testthese conclusions. Thus, only two of our patients hadan end-systolic dimension greater than 5 cm at thetime of initial study, and one of them developed leftventricular failure during serial study. The end-diastolic dimension was greater than 6.5 cm and theend-systolic dimension greater than 4.2 cm at initialstudy in three of the four patients who developed leftventricular failure in our study but also in six of thenine patients who did not.Our results suggest that the decline in left ven-

tricular function in asymptomatic patients with severechronic aortic regurgitation is slow but does acceleratein the few years before the onset of left ventricularfailure (table 4). Thus, at the time of initial study ofpatients who developed left ventricular failure, thefractional shortening was 29% and the index was sub-normal in only one of the four patients at that time;however, fractional shortening declined to an averagevalue of 20% during the 4-year period between the ini-tial study and the appearance of dyspnea due to leftventricular failure. Such a rapid decline might reflectacceleration of the degenerative changes in theoverloaded myocardium.21, 22 Alternatively, the onsetof renal sodium retention might cause left ventriculardilatation, resulting in an increase in mural stress andhence left ventricular afterload. In this way, theremight be a terminal vicious circle of progressivelydeclining myocardial function with increasing left ven-tricular dilatation and progressively increasingafterload.

Limitations of M-mode EchocardiographyThe interpretation of serial M-mode echocardio-

graphic measurements in chronic severe aorticregurgitation is hampered by two major problems:limitations of the reproducibility of the technique anda reservation that changes in fractional shorteningmay not always accurately reflect declining myocar-dial function in aortic regurgitation with left ven-tricular failure. The left ventricular echocardiogram isusually easy to record in patients with left ventricularvolume overload but our experience in this study andour routine practice has highlighted some specificproblems limiting reproducibility. For example,echoes from adjacent portions of the interventricularseptum are often recruited serially and superimposedduring systolic contraction, a phenomenon that causesunderestimation of the end-systolic left ventricular in-ternal dimension and overestimation of fractionalshortening and ejection fraction.37 In addition, ourcontrol study demonstrated that, despite careful tech-nique, small variations in standardization of themeasured tracing could result in relative large fluc-tuations in left ventricular dimensions between con-secutive studies.The second problem is that the use of fractional

shortening as an index of myocardial contractionassumes that the cross section of the left ventricle con-tracts symmetrically, and this may not be strictly truein patients with aortic regurgitation and left ven-tricular failure. In fact, there is evidence that shorten-ing of the echocardiographic left ventricular internaldimension, which is expressed as fractional shorten-ing, may overestimate contraction of the left ventricleas a whole.38 The important implication is that impair-ment of left ventricular contraction may actually bemore severe than the echocardiogram suggests andthis would only become apparent if left ventricularangiography were performed.

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1296 CIRCULATION

The results of this study and our clinical experiencehave not encouraged us to rely on M-mode echocar-diographic data alone when assessing individualasymptomatic patients with chronic severe aorticregurgitation. We believe that serial echocardiogramsshould be evaluated in conjunction with the clinicalassessment and other investigations, particularly whendeciding whether to recommend cardiac catheteriza-tion with a view to aortic valve replacement.

References

1. Gault JH, CovellJW, Braunwald E, RossJ Jr: Left ventricularperformance following correction of free aortic regurgitation.Circulation 42: 772, 1970

2. Bonchek LI, Starr A: Ball valve prostheses: current appraisal oflate results. Am J Cardiol 35: 843, 1975

3. Rahimtoola SH: Early valve replacement for preservation ofventricular function? Am J Cardiol 40: 472, 1977

4. Rapaport E: Natural history of aortic and mitral valve disease.Am J Cardiol 35: 221, 1975

5. Kennedy JW, Doces J, Stewart DK: Left ventricular functionbefore and following aortic valve replacement. Circulation 56:944, 1977

6. HirshfeldJW Jr, Epstein SE, Roberts AJ, Glancy DL, MorrowAG: Indices predicting long-term survival after valve replace-ment in patients with aortic regurgitation and patients with aor-tic stenosis. Circulation 50: 1190, 1974

7. Clark CE, Henry WL, Morganroth J, Pearlman AS, Grauer L,Redwood DR, Itscoitz SB, McIntosh CL, Michaelis LL,Morrow AG, Epstein SE: Influence of ejection fraction on theresults of operation in aortic regurgitation. (abstr) Circulation52 (suppl II): II-169, 1975

8. Clark DG, McAnulty JH, Rahimtoola SH: Valve replacementin aortic insufficiency with left ventricular dysfunction. Circula-tion 61: 411, 1980

9. Thompson R, Ahmed M, Seabra-Gomes R, Ilsley C, RichardsA, Yacoub M: The influence of preoperative left ventricularfunction on the results of homograft replacement of the aorticvalve for aortic regurgitation. (abstr) Am J Cardiol 43: 369,1979

10. Samuels DA, Curfman GD, Friedlich AL, Buckley MJ, AustenWG: Valve replacement for aortic regurgitation: Long-termfollow-up with factors influencing the results. Circulation 60:647, 1979

11. Gaasch WH, Andrias CW, Levine HJ: Chronic aorticregurgitation: the effect of aortic valve replacement on left ven-tricular volume, mass and function. Circulation 58: 825, 1978

12. Dodge HT, Kennedy JW, Petersen JL: Quantitativeangiographic methods in the evaluation of valvular heart dis-ease. Prog Cardiovasc Dis 16: 1, 1973

13. McDonald IG: Echocardiographic assessment of left ven-

tricular function in aortic valve disease. Circulation 53: 860,1976

14. Cohn LH, Mason DT, Ross J, Morrow AG, Braunwald E:Preoperative assessment of aortic regurgitation in patients withmitral valve disease. Am J Cardiol 19: 177, 1967

15. Baron MG: Angiographic assessment of aortic insufficiency.Circulation 43: 599, 1971

16. Tavel ME: Clinical Phonocardiography and External PulseRecording. Chicago, Year Book Medical Publishers, 1967

17. McDonald IG, Feigenbaum H, Chang S: Analysis of left ven-

tricular wall motion by reflected ultrasound: application to

assessment of myocardial function. Circulation 46: 14, 197218. Teichholz LE, Kreulen T, Herman MV, Gorlin R: Problems in

echocardiographic volume determinations: echocardiographic-

VOL 62, No 6, DECEMBER 1980

angiographic correlations in the presence or absence ofasynergy. Circulation 37: 7, 1976

19. Sahn DJ, DeMaria A, Kisslo J, Weyman A, The Committee ofM-mode standardization of the American Society of Echocar-diography: Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocar-diographic measurements. Circulation 58: 1072, 1978

20. Goldschlager N, Pfeifer J, Cohn K, Popper R, Selzer A: Thenatural history of aortic regurgitation: a clinical andhaemodynamic study. Am J Med 54: 577, 1973

21. Maron BJ, Ferrans VJ, Roberts WC: Myocardial ultrastruc-ture in patients with chronic aortic valve disease. Am J Cardiol35: 725, 1975

22. Schwarz F, Flameng W, Schaper J, Langebartels F, Sesto M,Hehrlein F, Schlepper M: Myocardial structure and function inpatients with aortic valve disease and their relation to postoperative results. Am J Cardiol 41: 661, 1978

23. Taylor RR, Covell JW, Ross J Jr: Left ventricular function inexperimental aorto-caval fistula with circulatory congestion andfluid retention.-J Clin Invest 47: 1333, 1968

24. Spann JF, Covell JW, Eckberg DL, Sonnenblick EH, Ross JJr, Braunwald E: Contractile performance of the hypertrophiedand chronically failing cat ventricle. Am J Physiol 223: 1150,1972

25. Hildner JJ, Javier RP, Cohen LS, Samet P, Nathan MJ, YahrWZ, Greenberg JJ: Myocardial dysfunction associated withvalvular heart disease. Am J Cardiol 30: 319, 1972

26. Lewis RP, Bristow JD, Griswold HE: Exercise haemodynamicsin aortic regurgitation. Am Heart J 80: 171, 1970

27. Bolen JL, Holloway EL, Zener JC, Harrison DC, AldermanEL: Evaluation of left ventricular function in patients with aor-tic regurgitation using afterload stress. Circulation 53: 132,1976

28. Jelinek VMJ, McDonald IG, Hale GS: Haemodynamic basisfor aortic valve replacement. Br Heart J 36: 69, 1974

29. Dexter L: Evaluation of the results of cardiac surgery. InModern Trends in Cardiology, vol 2, edited by James AM. NewYork, Appleton Century Crofts, 1969, p 311

30. Doyle AE, Goodwin JF, Jarrison CV, Steiner RE: Pulmonaryvascular patterns in pulmonary hypertension. Br Heart J 19:353, 1957

31. Spagnuolo M, Kloth H, Taranta A, Doyle E, Pasternack B:Natural history of rheumatic aortic regurgitation. Criteriapredictive of death, congestive heart failure and angina in youngpatients. Circulation 44: 368, 1971

32. Braun LO, Kincaid OW, McGoon DC: Prognosis of aorticvalve replacement in relation to the preoperative heart size. JThorac Cardiovasc Surg 65: 381, 1973

33. Smith HJ, Neutze JM, Roche AHG, Agnew TM, Barratt-Boyes BG: The natural history of rheumatic aortic regurgita-tion and the indications for surgery. Br Heart J 38: 147, 1976

34. Hirshfeld JW Jr, Epstein SE, Roberts AJ, Glancy DL, MorrowAG: Indices predicting long-term survival after valve replace-ment in patients with aortic regurgitation and patients with aor-tic stenosis. Circulation 50: 1190, 1974

35. Henry WL, Bonow RO, Rosing DR, Epstein SE: Observationson the optimum time for operative intervention for aorticregurgitation. II. Serial echocardiographic evaluation ofasymptomatic patients. Circulation 61: 484, 1980

36. Henry WL, Borer JS, Bonow RO, Rosing DR, Bacharach SL,Green MV, Epstein SE: Functional adaptions of the left ventri-cle to chronic aortic regurgitation. (abstr) Am J Cardiol 43:412, 1979

37. McDonald IG: The problems of M-mode echocardiography. InEchocardiography, edited by Linhart JW, Joyner CR. St Louis,CV Mosby Co. In press

38. Johnson AD, Alpert JS, Francis GS, Vieweg VR, Ochene I,Hagan AD: Assessment of left ventricular function in severeaortic regurgitation. Circulation 54: 975, 1976

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I G McDonald and V M JelinekSerial M-mode echocardiography in severe chronic aortic regurgitation.

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1980 American Heart Association, Inc. All rights reserved.

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