Immediate Effect of Aortic ValveReplacement for Aortic Stenosis on LeftVentricular Diastolic Chamber Stiffness

Patrice A. McKenney, MD, Carl S. Apstein, MD, Lisa A. Mendes, MD,Gilbert P. Connelly, MD, Gabriel S. Aldea, MD, Richard J. Shemin, MD, and

Ravin Davidoff, MB, BCh

Diastolic dysfunction is common after coronary arterybypass surgery, and we hypothesized that left ventricu-lar (LV) hypertrophy associated with aortic stenosis maylead to worsening LV diastolic function after aortic valvereplacement for aortic stenosis. Transesophageal echo-cardiographic LV images and simultaneous pulmonaryarterial wedge pressures were used to define the LVdiastolic pressure cross-sectional area relation beforeand immediately after aortic valve replacement for aor-tic stenosis in 14 patients. In all patients, LV diastolic

chamber stiffness increased, as evidenced by a leftwardshift in the LV diastolic pressure cross-sectional arearelation. At comparable LV filling (pulmonary arterialwedge) pressures the mean LV end-diastolic cross-sec-tional area preoperatively was 17.9 6 1.7 cm2, butdecreased by 32% after aortic valve replacement to12.1 6 1.2 cm2 (p 5 0.0001). In conclusion, after aorticvalve replacement, diastolic chamber stiffness increasedin all patients. Q1999 by Excerpta Medica, Inc.

(Am J Cardiol 1999;84:914–918)

In patients who have undergone aortic valve replace-ment for aortic stenosis, postoperative morbidity

and mortality is related to the degree of left ventricular(LV) hypertrophy, especially when the preoperativerelative wall thickness is high.1 The responsible mech-anisms are unknown, but may be related to diastolicrather than systolic dysfunction. Diastolic dysfunctionis frequent after coronary artery bypass surgery in theabsence of LV hypertrophy.2 Because experimentalstudies have shown that LV hypertrophy is associatedwith exaggerated diastolic dysfunction after ischemiaand reperfusion,3–7 we hypothesized that postopera-tive diastolic dysfunction might be increased aftervalve replacement for aortic stenosis.

METHODSPatient selection and surgical procedures: All pa-

tients undergoing elective aortic valve replacement foraortic stenosis with or without coronary artery bypasssurgery were eligible for the study. Patients wereexcluded from the study if the rhythm was other thannormal sinus rhythm or if they had more than mildaortic regurgitation. The study protocol was approvedby the Institutional Review Board, and informed con-sent was obtained from all patients. To ensure com-parable pre- and postoperative hemodynamic condi-tions at the time of study, patients were excluded fromanalysis if comparable pulmonary arterial wedge pres-sures were not obtained before and immediately after

surgery, if.21 mitral insufficiency was present ei-ther pre- or postoperatively, if the degree of mitralinsufficiency changed between the pre- and postoper-ative study, or if the patient experienced tachycardiaafter surgery (defined as a heart rate.100 beats/min).

Of 20 enrolled patients with aortic stenosis, 14patients (5 men and 9 women) were analyzed. Exclu-sions included lack of a comparable pre- and postop-erative pulmonary arterial wedge pressure (n5 3),and postoperative heart rate.100 beats/min (n5 3).Mean age was 72 years (range 68 to 86). There were2 patients with 3-vessel, 4 with 2-vessel, 2 patientswith single-vessel coronary artery disease, and 6 withno significant coronary artery disease. Four were oncalcium channel blockers (29%), 2 were onb blockers(14%), and 5 were on nitrates (36%) before surgery.Preoperative cardiac medications (except aspirin)were continued on the day of surgery. Preoperativeejection fraction was 63%, mean aortic gradient was486 5 mm Hg, and mean aortic valve area was 0.760.1 cm2. Demographic and relevant clinical and he-modynamic data are shown in Table I.

All patients received sufentanyl anesthesia. Sixpatients underwent aortic valve replacement only, and8 had concomitant coronary artery bypass surgery.The time on cardiopulmonary bypass averaged 11167 minutes. Aortic cross-clamp time averaged 686 4minutes. Crystalloid cardioplegia was given to 10patients, and 4 patients received blood cardioplegia.More specifically, 9 patients received anterograde andretrograde crystalloid cardioplegia, 1 patient receivedanterograde crystalloid and no retrograde cardiople-gia, and the remaining 4 received anterograde bloodand retrograde blood cardioplegia. At the time ofechocardiographic and hemodynamic measurements,the bladder temperature averaged 37.1°C6 0.3°C.One patient received epinephrine transiently due to

From the Cardiology Section, Department of Medicine, Evans Memo-rial Department of Clinical Research; Department of Anesthesiologyand the Department of Cardiothoracic Surgery, Boston Medical Cen-ter and Boston University School of Medicine, Boston, Massachusetts.Manuscript received June 29, 1998; revised manuscript received andaccepted December 24, 1998.

Address for reprints: Ravin Davidoff, MB, BCh, Section of Cardi-ology, Boston Medical Center, 88 East Newton Street, Boston, Mas-sachusetts 02118. E-mail: ravin.davidoff@bmc.org.

914 ©1999 by Excerpta Medica, Inc. All rights reserved. 0002-9149/99/$–see front matterThe American Journal of Cardiology Vol. 84 October 15, 1999 PII S0002-9149(99)00465-8

vasodilation while rewarming, but all were hemodynam-ically stable at the time of echocardiographic measure-ments. Six patients received low-dose dopamine (2 to 5mg/kg/min) after the procedure.

Clinical anaylsis: Clinical variables that could influ-ence diastolic function were assessed. Preoperative vari-ables included age, gender, coronary artery disease, hy-pertension, diabetes mellitus, medications, preoperativeejection fraction by ventriculogram, preoperative wallthickness by echocardiogram, and preoperative aorticvalve area and aortic valvular mean pressure gradientdetermined by cardiac catheterization. Operative vari-ables included the number of vessels bypassed, type ofanesthesia, time on cardiopulmonary bypass, type andmethod of delivery of cardioplegia, temperature afterbypass, hematocrit after bypass, and use of postoperativeinotropic agents or vasopressors.

Assessment of diastolic chamber stiffness: Diastolicchamber stiffness was defined as LV diastolic pressurerelative to volume as previously described.2 The pul-monary arterial wedge pressure at end-expiration wasmeasured as an index of mean LV diastolic pressure(filling pressure). LV end-diastolic area was used asan index of end-diastolic volume. Diastolic chamberstiffness was then evaluated by LV volume loading tocreate a LV diastolic pressure cross-sectional arearelation. Comparisons between pre- and postoperativediastolic chamber stiffness were made by measuringLV end-diastolic areas at similar pulmonary arterialwedge pressures (within 2 mm Hg).

Echocardiographic assessment: The 2-dimensionalcross-sectional LV end-diastolic area, determinedfrom transesophageal echocardiographic images at thesame mid-papillary level before and immediately aftersurgery, was measured as an index of diastolic vol-

ume. End-diastolic areas were determined as the averageof 3 consecutive hand-traced images at each loadingcondition, utilizing off-line analysis on the Freeland GTICine View Plus system (TomTec Company, Denver,Colorado). LV wall thickness was measured, accordingto American Society of Echocardiography guidelines, onthe preoperative transthoracic echocardiogram in theparasternal long-axis view.8 To obtain comparable mea-surements of wall thickness before and after surgery,end-diastolic wall thickness was also measured beforeand immediately after surgery on the transesophagealechocardiogram in the transgastric view at the mid-pap-illary level. Systolic function was assessed by measuringthe fractional area change on the transesophageal echo-cardiogram before and after surgery. This was calculatedas: fractional area change (%)5 100 3 [end-diastolicarea2 end-systolic area]/end-diastolic area. Wall motionwas assessed in multiple views before and after bypasssurgery.

Diastolic LV filling was also assessed by Doppleranalysis of mitral inflow in the 4-chamber view beforeand after aortic valve replacement at similar pre- andpostoperative pulmonary arterial wedge pressures.The deceleration time was measured as the time frompeak filling during early diastole (peak of the E wave)to baseline. All echocardiograms were analyzed by 2cardiologists in a blinded fashion.

Data collection: Preoperative hemodynamic andechocardiographic measurements were obtained 15minutes after anesthetic induction once the patient wasstable, and postoperative measurements were madeimmediately after aortic valve replacement, within 30minutes after coming off cardiopulmonary bypass,once hemodynamic stabilization had occurred. If fill-ing pressures were low, the patient was volume loaded

TABLE I Demographic, Clinical, Hemodynamic, and Echocardiographic Features

PatientAge (yrs)

& Sex

LV–AAPeak

SystolicGradient(mm Hg)

LV–AAMean

Gradient(mm Hg)

AVA(cm2)

AR(0–41)

MR(0–41)

EF(%)

Pre-opMAP

(mm Hg)

Post-opMAP

(mm Hg)

# CAs2 .50%(in diam)

DArea(%)

1 82 M 81* 28 0.6 0 0 89 62 48 3 47.62 68 F 50† 37 0.6 0 0 68 94 82 1 14.03 77 M 80* 28 0.8 0 2 62 67 66 3 17.34 65 M — 76 0.6 2 1 55 71 73 2 58.25 47 F 52* 31 1.1 0 0 47 71 68 2 14.16 74 M 74* 42 0.7 1 0 75 76 71 2 31.07 79 F — 39 0.9 T 2 60 73 52 1 36.18 76 F 54† 45 0.7 1 0 80 78 84 2 31.19 65 F 90† 85 0.4 1 1 65 79 68 0 18.6

10 62 F 83* 38 1.0 2 0 55 93 82 0 44.411 77 F 49† 47 0.7 T 0 85 86 58 0 16.912 86 M 80* 40 0.6 1 1 40 104 82 0 29.913 73 F 100* 70 0.7 1 2 77 60 68 0 44.314 77 F 46† 43 0.7 0 0 25 60 68 0 40.1

Average 72 69.91 44.14 0.72 63.07 78 69.385 31.696 SD 6 9.92 6 18.59 6 21.43 0.18 6 17.94 6 12.56 6 11.59 14.12

*By echo-Doppler; †at cardiac catheterization.Patients 1 to 8 had coronary artery bypass graft surgery in addition to AVR.AA 5 ascending aorta; AR 5 aortic regurgitation; AVA 5 aortic valve area; CAs 5 coronary arteries; D AREA 5 % decrease in end-diastolic area pre- and

postoperatively at comparable pulmonary arterial wedge pressure; EF 5 ejection fraction; MAP 5 mean arterial pressure; MR 5 mitral regurgitation; PAWP 5

pulmonary arterial wedge pressure.

VALVULAR HEART DISEASE/DIASTOLIC FUNCTION AFTER VALVE REPLACEMENT 915

intravenously with 1 to 2 liters of normal saline, andmeasurements were obtained before and after volumeloading.

Statistical analysis: Pre- and postoperative datawere compared by the Student’s pairedt test, witheach patient serving as his own control. A p value of,0.05 was considered significant. All data are pre-sented as the mean6 SEM.

RESULTSSystolic function: Systolic function did not decrease

in any patient postoperatively. The mean preoperativefractional area change of 626 4% was unchangedafter surgery, again averaging 626 4%. No new orworsened wall motion abnormalities developed post-operatively.

Diastolic chamber stiffness: LV end-diastolic cross-sectional area (measured at comparable pulmonaryarterial wedge pressures) was 17.96 1.7 cm2 preop-eratively, and decreased by 32% postoperatively to12.1 6 1.2 cm2 (p 5 0.0001) (Figure 1). In eachpatient there was a decrease in end-diastolic areabetween the pre- and postoperative measurements at

comparable pulmonary arterialwedge pressures (Figure 2). Therewas no detectable increase in post-operative wall thickness relative tothe preoperative measurement.Comparison of patients who hadonly aortic valve replacement withthose who had concomitant coro-nary artery bypass grafting demon-strated no difference in the magni-tude of LV area change (Table I).There was no relation between thedegree of mitral regurgitation beforeaortic valve replacement and the in-crease in diastolic stiffness.

The pulmonary arterial wedgepressure was maintained constantlyat a mean of 146 1 mm Hg preop-eratively and 146 1 mm Hg post-operatively at the time of the echo-

cardiographic assessment of LV diastolic cross-sec-tional area. The mean heart rate increased slightlyafter surgery in all patients from 636 4 beats/minbefore surgery to 826 3 beats/min after surgery. Bydesign, no patient had a heart rate of.100 beats/minafter surgery. The mean arterial pressure decreasedonly slightly, averaging 786 4 mm Hg preoperativelyand 706 3 mm Hg postoperatively (p5 0.02). Theaverage hematocrit decreased by 15 points, from 3961% to 246 1% immediately after surgery.

Mitral inflow velocities: Mitral inflow decelerationtime (measured at comparable pulmonary arterialwedge pressures) decreased from 2606 30 ms pre-operatively to 1086 4 ms after surgery (p5 0.0001)(Figure 3). The peak E-wave velocity, peak A-wavevelocity, and E/A ratio were not significantly differentafter surgery (Table II).

DISCUSSIONOur principal findings were that marked LV dia-

stolic dysfunction occurred immediately after aorticvalve replacement for aortic stenosis. Recently, thepresence of high relative wall thickness has also beenidentified as a risk factor for mortality after aorticvalve replacement for aortic stenosis.1 The mechanismfor this is unknown, but the increased morbidity andmortality after aortic valve replacement in patientswith excessive hypertrophy relative to the cavity di-mension may be due to increased postoperative dia-stolic dysfunction, because the presence of pressureoverload hypertrophy has been shown to amplify thediastolic dysfunction that occurs with ischemia andreperfusion.3–7

The effects of aortic valve replacement on postop-erative diastolic function appear controversial. In 1study of patients with aortic stenosis that compareddiastolic function preoperatively and 6 months post-operatively, the LV end-diastolic pressure, mean leftatrial pressure, elastic stiffness, and stiffness constantwere all elevated before aortic valve surgery, and 6months after aortic valve replacement, LV end-dia-stolic wall thickness and stiffness constant remained

FIGURE 1. Comparison of LV end-diastolic areas at a similar pulmonary arterialwedge pressure (PCWP) before (Pre) and immediately after (Post) aortic valve replace-ment for aortic stenosis (AVR).

FIGURE 2. Comparison of LV end-diastolic (LVED) area in individ-ual patients before (Pre) and after (Post) aortic valve replace-ment.

916 THE AMERICAN JOURNAL OF CARDIOLOGYT VOL. 84 OCTOBER 15, 1999

moderately elevated.9 In contrast, no change in dia-stolic function could be detected in the first 6 hoursafter aortic valve replacement for aortic stenosis whendP/dt and rate of dimensional change were assessed.10

Our results indicate that a simple index of LV diastolicchamber stiffness (end-diastolic cross-sectional arearelative to LV filling pressure) reveals a very frequentincrease in LV diastolic stiffness in the immediatepostoperative period.

There are several mechanisms by which diastolicchamber stiffness may be increased after aortic valvereplacement in aortic stenosis. Previously, we haveshown that new diastolic dysfunction is frequentlypresent after cardiac surgery among patients with normalLV wall thickness.2 Furthermore, the hypertrophied ven-tricle has been shown to be especially susceptible todiastolic dysfunction after ischemia and reperfusion.3,4,11

Possible contributing mechanisms include abnormal cor-onary flow regulation and diminished coronary vasodi-lator reserve in the hypertrophied heart.12 Postischemicreperfusion has been associated with increased diastolicchamber stiffness due to increased coronary turgor, cy-tosolic calcium overload, and rapid pH changes13 as wellas a reduced glycolytic capacity, reduced levels of aden-osine triphosphate and creatine phosphate, and an alteredcellular sodium and calcium homeostasis.3–7 Moreover,hypertrophied myocardium has a greater dependency onthe glycolytic pathway to preserve diastolic functionduring tissue hypoxia than nonhypertrophied myocardi-um.5,14 Temperature changes and pharmacologic influ-ences can affect LV diastolic compliance.15,16

The type and method of delivery of cardioplegiamay also be important, because retrograde cardiople-gia may lead to extracellular edema and potentiallyincrease diastolic chamber stiffness.2,17,18However, inthe present study, when patients were stratified ac-cording to the type and method of cardioplegia, therewas no correlation with extent of worsening of dia-stolic dysfunction postoperatively. The groups weresmall and thus small differences may not have beendetected. Although we expected to find an increase inwall thickness postoperatively due to a combination ofthe decrease in LV area and possible myocardial

edema after bypass, we were unableto detect a significant change. Thismay be because small changes inwall thickness could not be detectedadequately by echocardiography.Thus, although we cannot define themechanism, patients with significantLV hypertrophy secondary to aorticstenosis preoperatively appear torepresent a group that is more sus-ceptible to factors that have the po-tential to worsen diastolic dysfunc-tion immediately after cardiac sur-gery.

The mitral inflow profiles, ob-tained at comparable pulmonary ar-terial wedge pressures, revealed nosignificant differences in the peak Ewave, peak A wave, and E/A ratio

between pre- and postoperative measurements. How-ever, the deceleration times decreased significantlyfrom the pre- to postoperative measurements. Little etal19 have shown that, in response to phenylephrineinfusion, the early LV diastolic filling decelerationtime decreases as LV stiffness increases acutely. Asstiffness increases, LV diastolic pressure increasesmore rapidly for a given amount of LV filling, therebytruncating early LV inflow and the measured deceler-ation time. Thus, our observed shortening of the de-celeration time is consistent with the postoperativeincrease in LV chamber stiffness as measured by thedecrease in LV end-diastolic areas at comparable pre-and postoperative pulmonary arterial wedge pressures.

Study limitations: We used LV diastolic pressure-areameasurements as a clinically useful surrogate for pres-sure-volume measurements. In a canine model, LV pres-sure-area loops during volume manipulation were quan-titatively similar to pressure-volume relations.20

Heart rates were slightly elevated postoperatively,averaging 63 beats/min before surgery and 82 beats/min after surgery. In normal subjects, there was nochange in the LV end-diastolic dimension when theheart rate was increased within the physiologicrange.21 Thus, this relatively minor increase in post-operative heart rate is unlikely to have significantlyaffected ventricular filling or our assessment of dia-stolic chamber stiffness.

Clinical implications: Marked LV hypertrophy, man-ifested as a marked increase in LV wall thickness, hasbeen found to be associated with a significantly in-creased risk of postoperative mortality after aorticvalve replacement for aortic stenosis.1 Postoperativediastolic dysfunction may contribute to this increasedmortality. Excessive LV hypertrophy and/or a rela-tively small chamber size, coupled with postoperativediastolic dysfunction, could result in significant im-pairment of LV filling. The underfilled left ventriclecould then be susceptible to dynamic obstruction dur-ing systole with intracavitary acceleration of flow.22

Recognizing the presence of postoperative dia-stolic dysfunction could significantly alter treatmentstrategies. In the presence of increased LV diastolic

FIGURE 3. Comparison of mitral deceleration time before (Pre) and immediately after(Post) aortic valve replacement (AVR) at a similar pulmonary arterial wedge pressure.

VALVULAR HEART DISEASE/DIASTOLIC FUNCTION AFTER VALVE REPLACEMENT 917

stiffness a normal or increased LV filling pressuredoes not rule out an underfilled left ventricle. Anunderfilled left ventricle with a small stroke volumeresponds poorly to inotropic medications and is par-ticularly susceptible to atrial arrhythmias and the lossof the atrial contribution to LV filling. Orsinelli et al1

noted that after aortic valve replacement several pa-tients improved hemodynamically when treated withvolume replacement and the addition of calcium chan-nel blockers orb blockers. Similarly, Lee et al23

described a patient with severe aortic stenosis andhypertrophic cardiomyopathy who could not beweaned from bypass despite maximal measures tosupport systolic function, but had a marked improve-ment after administration of a calcium blocking agent.They suggested that the effect of this agent was toimprove cardiac output by correcting diastolic abnor-malities. Our study confirms the importance of LVdiastolic chamber stiffness early after aortic valvereplacement in patients with aortic stenosis.

1. Orsinelli DA, Aurigemma GP, Battista S, Krendel S, Gaasch WH. Leftventricular hypertrophy and mortality after aortic valve replacement for aorticstenosis. A high risk subgroup identified by preoperative relative wall thickness.J Am Coll Cardiol1993;22:1679–1683.2. McKenney PA, Apstein CS, Mendes LA, Connelly GP, Aldea GS, Shemin RJ,Davidoff RD. Increased left ventricular diastolic chamber stiffness immediatelyafter coronary artery bypass surgery.J Am Coll Cardiol1994;24:1189–1194.3. Gaasch WH, Zile MR, Hoshino PK, Weinberg EO, Rhodes DR, Apstein CS.Tolerance of the hypertrophic heart to ischemia: studies in compensated andfailing dog hearts with pressure overload hypertrophy.Circulation 1990;81:1644–1653.4. Mochizuki T, Eberli FR, Ngoy S, Apstein CS, Lorell BH. Effects of briefrepetitive ischemia on contractility, relaxation, and coronary flow: exaggeratedpostischemic diastolic dysfunction in pressure-overload hypertrophy.CirculationRes1993;73:550–558.5. Cunningham MJ, Apstein CS, Weinberg EO, Vogel WM, Lorell BH. Influenceof glucose and insulin on the exaggerated diastolic and systolic dysfunction ofhypertrophied rat hearts during hypoxia.Circulation Res1990;66:406–415.6. Eberli FR, Apstein CS, Ngoy S, Lorell BH. Exacerbation of left ventricularischemic diastolic dysfunction by pressure-overload hypertrophy: modificationby specific inhibition of cardiac angiotensin converting enzyme.Circulation Res1992;70:931-943.7. Wexler LF, Lorell BH, Monomura S, Weinberg EO, Ingwall JS, Apstein CS.

Enhanced sensitivity to hypoxia-induced diastolic dysfunction in pressure-over-load left ventricular hypertrophy in the rat: role of high energy phosphatedepletion.Circulation Res1988;62:766–775.8. Sahn DJ, DeMaria AN, Kisslo J, Weyman AE. The Committee on M-modeStandardization of the American Society of Echocardiography. Recommenda-tions regarding quantitation in M-mode echocardiography: result of a survey ofechocardiographic measurements.Circulation 1978;58:1072–1083.9. Schwarz F, Flameng W, Schaper J, Hehrlein F. Correlation between myocar-dial structure and diastolic properties of the heart in chronic aortic valve disease:effects of corrective surgery.Am J Cardiol1978;42:895–903.10. Jin XY, Pepper JR, Brecker SJ, Carey JA, Gibson DG. Early changes in leftventricular function after aortic valve replacement for isolated aortic stenosis.Am J Cardiol1994;74:1142–1146.11. Menasche P, Grousset C, Apstein CS, Marotte F, Mousa C, Piwnica A.Increased injury of hypertrophied myocardium with ischemic arrest: preservationwith hypothermia and cardioplegia.Am Heart J1985;110:1204–209.12. Polese A, DeCesare N, Montorsi P, Fabbiochi F, Guazzi M, Loaldi A, GuazziMD. Upward shift of the lower range of coronary flow autoregulation in hypertensivepatients with hypertrophy of the left ventricle.Circulation 1991;83:845–853.13. Apstein CS, Lorell BH. The physiologic basis of left ventricular diastolicdysfunction.J Card Surg1988;3:475–485.14. Kagaya Y, Weinberg EO, Ito N, Mochizuki T, Barry WH, Lorell BH. Glycolyticinhibition: effects on diastolic relaxation and intracellular calcium handing in hyper-trophied rat ventricular myocytes.J Clin Invest1995;95:2766–2776.15. Ivanov J, Wiesel RD, Mickleborough LL, Hilton JD, McLaughlin PR.Rewarming hypovolemia after aortocoronary bypass surgery.Crit Care Med1984;12:1049–1054.16. Moores WY, Weiskopf RB, Baysinger M, Utley JR. Effects of halothane andmorphine sulfate on myocardial compliance following total cardiopulmonarybypass.J Thorac Cardiovasc Surg1981;81:163–170.17. Schaper J, Walter P, Scheld H, Hehrlein F. The effects of retrograde perfusionof cardioplegic solution in cardiac operations.J Thorac Cardiovasc Surg1985;90:882–887.18. McKenney PA, Davidoff R, Mendes LA, Connelly GP, Aldea GS, SheminRJ, Apstein CS. Retrograde cardioplegia increases diastolic chamber stiffnessafter coronary artery bypass surgery (abstr).J Am Coll Cardiol1995;396A.19. Little WC, Ohno M, Kitzman DW, Thomas JD, Cheng C-P. Determination ofleft ventricular chamber stiffness from the time for deceleration of early leftventricular filling.Circulation 1995;92:1933–1939.20. Gorcsan J, Romand JA, Mandarino WA, Deneault LG, Pinsky MR. Assessmentof left ventricular performance by on-line pressure-area relations using echocardio-graphic automated border detection.J Am Coll Cardiol1994;23:242–252.21. Harrison MR, Clifton GD, Pennell AT, DeMaria AN. Effect of heart rate onleft ventricular diastolic transmitral flow velocity patterns assessed by Dopplerechocardiography in normal subjects.Am J Cardiol1991;67:622–627.22. Aurigemma G, Battista S, Orsinelli D, Sweeney A, Pape L, Cuenoud H.Abnormal left ventricular intracavitary flow acceleration in patients undergoingaortic valve replacement for aortic stenosis. A marker for high postoperativemorbidity and mortality.Circulation 1992;86:926–936.23. Lee TH, DiSesa VJ, Cohn LH, Lilly LS, Antman EM. Correction ofintraoperative diastolic myocardial dysfunction with nifedipine.Clin Cardiol1983;6:549–552.

TABLE II Mitral Flow Doppler Profiles

Patient

Peak E (m/s) Peak A (m/s) E/A DT (sec)

Pre Post Pre Post Pre Post Pre Post

1 0.41 0.59 0.46 0.40 0.89 1.45 0.416 0.1282 – – – – – – – –3 0.65 0.62 0.72 1.06 0.90 0.58 0.290 0.0624 0.80 0.79 0.54 0.72 1.48 1.10 0.182 0.0855 0.71 0.57 0.52 0.60 1.36 0.95 0.367 0.1906 0.34 0.44 0.36 0.31 0.97 1.43 0.198 0.1347 0.79 0.63 0.72 0.73 1.10 0.86 0.348 0.1548 0.52 0.51 0.43 0.66 1.22 0.77 0.278 0.0469 0.83 1.06 0.77 0.95 1.08 1.12 0.169 0.090

10 – 1.00 – – – – 0.202 0.06811 0.42 0.76 0.87 1.20 0.48 0.64 0.125 0.16012 – – – – – – – –13 0.77 0.61 0.76 0.90 1.01 0.68 0.318 0.05114 0.67 0.57 0.92 0.65 0.73 0.88 0.179 0.133

Average 0.628 0.679 0.643 0.74 1.02 0.951 0.256 0.108*6 SD 6 0.18 6 0.188 6 0.190 6 0.18 6 0.11 6 0.400 6 0.170 6 0.004

*p 5 0.0001 before versus after DT.A 5 peak late mitral inflow velocity; DT 5 deceleration time; E 5 peak early mitral inflow velocity.

918 THE AMERICAN JOURNAL OF CARDIOLOGYT VOL. 84 OCTOBER 15, 1999