The index of myocardial performance and aortic regurgitation: the influence of a volume overload lesion/Miyokard performans indeksi ve aort yetersizligi: hacim yuklenmesi lezyonun etkisi.

ABSTRACT

Objective: The index of myocardial performance (IMP) is a global cardiac function index with prognostic utility in patients with myocardial infarction and dilated cardiomyopathy but is preload dependent. We hypothesized that a volume overload lesion prolonging LV ejection time (LVET) may reduce IMP despite LV dysfunction (LVD).

Methods: The study groups consisted of 35 normals, 26 with LV dysfunction, and 60 with aortic regurgitation (AR): 40 with ejection fraction (EF) >50% (AR+Normal EF) and 20 with ejection fraction [greater than or equal to]50% (AR+Reduced EF). We evaluated consecutive patients in each group with technically adequate 2D and Doppler echocardiography.

Results: When compared to normal subjects (0.357[+ or -]0.122), IMP was increased with LVD (0.604[+ or -]0.278 p<0.001) but was similar in AR+Normal EF patients due to isovolumic relaxation time (IRT) and LVET prolongation. The IMP was lower in AR+Reduced EF group (0.346[+ or -]0.172, p<0.001) as compared to the LVD group due to a prolonged LVET and a reduced IRT and isovolumic contraction time (ICT).

Conclusions: The IMP in AR+Normal EF patients was similar to normals due to IRT and LVET prolongation. The IMP was reduced in AR+Reduced EF patients compared to LVD patients due to IRT and ICT shortening and LVET prolongation. The index of myocardial performance in AR patients should be applied with caution. (Anadolu Kardiyol Derg 2006; 6: 115-20)

Key words: Aortic regurgitation, index of myocardial performance, left ventricular dysfunction 

OZET

Amac: Miyokard performans indeksi (MPI) miyokard infarktuslu ve dilate kardiyomiyopatili hastalarda prognostik degeri olan bir global kardiyak fonksiyon indeksidir, ancak onyuke baglidir. Biz, sol ventrikul ejeksiyon zamanini (SVEZ) uzatan volum yuklenmesine bagli lezyonun sol ventrikul disfonksiyonuna (SVD) ragmen MPI'ni azaltacagini varsaydik.

Yontemler: Calisma gruplanrini 35 normal, SVD'lu 26 hasta ve aort yetersizligi (AY) olan 60 hasta (40'i ejeksiyon fraksiyonu (EF) [superieur ou egal a]50% (AY+Normal EF grubu) ve 20'si ejeksiyon fraksiyonu <50% (AY+dusuk EF grubu) olusturuyordu. Hastalar her grupta ardisik olarak 2 boyutlu ve Doppler ekokardiyografi ile tarafimizdan incelendi.

Bulgular: Normal bireyler (0.357[+ ou -]0.122) ile karsilastirildiginda MPI, SVD'lu (0.604[+ ou -]0.278 p<0.001) hastalarda daha yuksek idi, ancak izovolumik relaksasyon zamaninin (IRZ) ve SVEZ'nin uzamasina bagli olarak AY+Normal EF hasta grubu ve normal grup arasinda fark yok idi. Ayni zamanda SVD'lu gruba gore AY+dusuk EF grubunda MPi (0.346[+ ou -]0.172, p<0.001), SVEZ uzamasi, IRZ ve isovolumik kontraksiyon zamaninin (IKZ) azalmasina bagli olarak kisaldigi tespit edilmistir.

Sonuc: Miyokardiyal performans indeksi, IRZ ve SVEZ uzamasina bagli olarak AY+normal EF'lu hastalarda ve normal bireylerde benzer idi. Sol ventrikul ejeksiyon zamanin uzamasi, IRZ ve IKZ kisalmasina bagli olarak MPi AY+dusuk EF grubunda SVD grubuna gore daha azalmisti. Aort yetersizligi olan hastalarda MPl'nin dikkatle kullamlmasi gerekir. (Anadolu Kardiyol Derg 2006; 6: 115-20)

Anahtar kelimeler: Aort yetersizligi, miyokard performans indeksi, sol ventrikul disfonksiyonu

Introduction

The index of myocardial performance (IMP) is a global left ventricular (LV) performance index that has prognostic significance in patients with cardiomyopathy, congestive heart failure, and following a myocardial infarction (1-3). The IMP is calculated as the Doppler derived sum of the isovolumic contraction time (ICT) and isovolumic relaxation time (IRT) divided by the left ventricular ejection time (LVET) (3). The IMP has been noted to be contractility dependent in clinical studies (4). However, IMP was also preload and afterload dependent in a canine model of normal and reduced LV systolic function (5,6). Specifically, volume loading in a canine model of normal and reduced LV function resulted in a lower IMP by prolonging LVET (5).

Clinically, LV volume overload produced by chronic aortic regurgitation (AR) results in a prolonged LVET (7-11) and may theoretically reduce IMP. As patients with LV dysfunction due to dilated cardiomyopathy or following myocardial infarction have an increased IMP (1-3), the effect of concomitant chronic AR accompanying LV dysfunction has not been well clarified. The purpose of our study was to characterize IMP in patients with chronic AR with both normal LV and reduced LV ejection fractions.

Methods

Patients

This study was approved by the Wayne State University Human Investigation Committee. From 1994 to 1999, we reviewed the echocardiographic database of all the studies that were coded for isolated moderate or greater aortic regurgitation. Patients imaged during an acute illness (pneumonia, gastrointestinal bleeding, endocarditis, sepsis, etc) were excluded in order to avoid any influence on LV function. Consequently, we limited our evaluation to only outpatient imaging. From 1994-1999, approximately 5000 outpatient echocardiograms were performed (25% of all studies). Each study was reviewed for adequacy of echocardiographic images (for evaluation of wall motion and wall thickening and endocardial border detection for assessment of LV volumes). Each study was also evaluated for adequate transmitral and transaortic pulsed, continuous wave, and color flow Doppler. Patient records ware reviewed to exclude patients with coronary artery disease (on the basis of history, electrocardiographic (ECG) evidence of Q waves > 30 msec in 2 consecutive ECG leads, or evidence of ischemic disease by stress test, myocardial perfusion, or cardiac catheterization). Patients with significant valvular regurgitation other than AR (greater than mild valvular regurgitation of another valve), any systolic gradient >10 mm Hg across the aortic or pulmonic valve, evidence of any degree of mitral or tricuspid stenosis, congenital heart disease, or non sinus rhythm were excluded.

We encountered the diagnosis of isolated moderate or greater aortic regurgitation (Doppler echocardiographic criteria: see below) in 98 patients. On further review of the echocardiogram and patient records, we excluded 24 patients for image quality, 5 patients for coexisting aortic stenosis, and akinetic segments in 9 patients. There were 60 patients that fulfilled the criteria. Forty had normal left ventricular ejection fraction (EF) defined as LV ejection fraction [greater than or equal to]50%. Twenty patients had a LV ejection fraction <50%. As comparison groups, from the same time period, we selected all echocardiograms deemed to be normal. We selected an age, sex, and date of study matched group consisting of 35 patients as a comparison for the 40 patients with AR and normal LV ejection fraction (AR+Normal EF) derived from the same 1994-1999 outpatient database. As a comparison group for aortic regurgitation with reduced LV ejection fraction (AR+Reduced EF), we reviewed all the studies with a LV ejection fraction <50% without evidence of valve disease other than mild regurgitation, without a gradient >10 mm Hg across the pulmonic or aortic valve, or any evidence of mitral or tricuspid stenosis, congenital heart disease, or non sinus rhythm. Patients with a remote history of ischemic etiology of LV dysfunction were included as long as their reason for their present evaluation was not ischemic symptoms. We selected an age, sex, and date of study matched group resulting in 26 patients fulfilling the criteria from 1994-1999 outpatient database.

For each patient included, we reviewed patient records and echocardiographic records to determine the presence of hypertension, diabetes, and medication history, which was recorded into a database. Hypertension was defined as a systolic blood pressure [greater than or equal to]140 mm Hg, diastolic blood pressure [greater than or equal to]90 mm Hg, or hypertension treatment. The blood pressure obtained at the time of the echocardiographic study was recorded or if not available, an outpatient blood pressure within 1 month of the study. Diabetes was defined as a fasting blood glucose >125 mg% or diabetes medication or diet treatment.

Echocardiographic Measurements

Echocardiographic images of the left and right ventricles, left and right atria and heart valves ware obtained using a Hewlett-Packard Sonos 2500 (Hewlett Packard, Andover, MA), echocardiograph from multiple parasternal, apical and subcostal views of the heart. Transmitral flow was obtained using an apical four-chamber view with the sample volume at the tips of the mitral leaflets. Transaortic flow was measured from a sample volume in the LV outflow tract just below the aortic valve in the apical three chamber view. Pulsed and continuous wave Doppler and color flow imaging was acquired from all valves to assess regurgitation and presence of a gradient across each of the valves. The degree of aortic regurgitation was determined from the ratio of the color jet height to the LV outflow tract diameter in diastole. A ratio [greater than or equal to] 25% was required for a diagnosis of moderate and [greater than or equal to] 65% for severe aortic regurgitation (12).

Parameters Measured

All of the parameters measured were the average of 3 determinations from consecutive cardiac cycles. The following parameters were obtained using the American Society of Echocardiography standards of measurement for posterior wall dimension, septal wall dimension, end-diastolic dimension, and end-systolic dimension. Left ventricular end-diastolic and end-systolic volumes were obtained from 2 orthogonal apical views using the modified Simpson's rule. Left ventricular ejection fraction was calculated as the difference between end-diastolic and end systolic volume divided by end-diastolic volume (13).

Using transmitral pulsed Doppler, the following indices were obtained: peak rapid filling velocity, peak atrial filling velocity, and their ratio. The rapid deceleration time defined as the time interval from the peak rapid filling velocity to the time the descending segment of the peak rapid filling velocity spectrum crossed the zero baseline (using linear interpolation) was obtained. Transaortic Doppler was used to obtain LVET, which was measured from the onset to the end of the aortic velocity spectrum. The IRT was calculated as the interval from the R wave to the onset of transmitral filling spectrum minus the interval from the R wave to the end of transaortic velocity spectrum (1,2).

The IMP (3)was calculated by the following formula:

IMP=a-b/b

where a= time interval between the end of transmitral velocity spectrum of 1 cardiac cycle to the onset of transmitral mitral velocity spectrum of the next cardiac cycle; and b=LVET.

The ICT was determined by subtracting LVET and IRT from "a". Isovolumic contraction time, IRT, and LVET were divided by the square root of the RR interval to normalize for heart rate and expressed as the respective index (1-3). Index of myocardial performance and IRT calculations involved non-simultaneous measurements of transaortic and transmitral spectral tracings. These spectral tracings are acquired within 1-2 minutes routinely. Heart rate was within 3 beats/minute.

Statistics

Categorical variable were compared using Chi Square or Fisher Exact test depending on cell size. All continuous data were expressed as mean [+ or -] SD. Differences between a variable among stages were assessed using a 1 way analysis of variance. If the F statistic indicated a significant difference existed (P<0.05), then Turkey's test was used to determine where the significant differences existed. A P value <0.05 was considered to be significant. The relationship between variables was determined using least squares linear regression. Forward stepwise multiple linear regression was used to determine the predictors of IMP using all variables with a linear correlation with a P value<0.1.

Results

Table 1 summarizes patient characteristics in the 4 groups. The distribution of New York Heart Association functional class was similar between LV dysfunction and the AR+Reduced EF groups. Both groups had more patients who were functional class II than the normal group. The AR+Normal EF had significantly more patients as functional class II than the normal group. Hypertension (and the use of calcium channel blockers and diuretics) was more common among AR+Normal EF patients than normals. Systolic blood pressures were higher among both AR groups and LVD groups as compared to normals. Both hypertension and diabetes were more common among LV dysfunction patients than AR+Reduced EF patients. Consequently, angiotensin converting enzyme inhibitors, beta blockers, and diuretics were more commonly used with LV dysfunction patients. Two patients in the normal group were using beta blockers for arrhythmias. The etiology and severity of AR was similar in both AR groups.

Parameters of LV size, LV function, and transmitral Doppler are summarized in Table 2. Posterior wall thickness was greater in both groups of AR patients as compared to normals and patients with LVD. As expected, the end diastolic dimension and LV volumes were greater in both AR groups and the LVD group as compared to normals. Patients with AR+Reduced EF had larger LV sizes and volumes as compared to AR+Normal EF patients. Peak rapid filling velocity, E/A, and deceleration time were significantly reduced in the AR+Normal EF group as compared to normals. When compared to the LVD group, E/A was reduced in the AR+Reduced EF group. The cardiac cycle length (RR) was significantly shortened in the LVD and AR+Reduced EF groups as compared to normals and the AR+Normal EF group. The diastolic filling period was shorter in the LVD group as compared to normals and longer in the AR+Normal EF group as compared to AR+Reduced EF possibly reflecting heart rate differences. Patients with AR+Reduced EF demonstrated later ending of aortic flow and an earlier onset of mitral flow as compared to patients in the LVD group. Mitral valve opening was delayed in the AR+Normal EF group as compared to normals and the group with AR+Reduced EF. Similarly mitral valve opening was delayed in the LVD group as compared to normals.

Table 3 summarizes IMP and its components as heart rate adjusted indices. All the components of IMP were expressed as heart rate adjusted indexes. The ICT was prolonged in the LVD group as compared to normals and the AR+Reduced EF group. The IRT was prolonged in the AR+Normal EF group as compared to normals. The IRT was also prolonged in the LVD group as compared to AR+Reduced EF due to aortic flow ending later and mitral flow beginning earlier in the AR+Reduced EF group. Both AR groups demonstrated prolonged LVET's as compared to normals. The LVET in the LVD group was shorter than in normals and in both AR groups (p<0.001). As a consequence, IMP (Fig. 1) was similar to normals in the AR+Normal EF group primarily due to prolongation of both IRT and LVET. However, IMP in the AR+Reduced EF was markedly lower than the LVD group due to a longer LVET and a shorter IRT and ICT despite similar LV ejection fractions. The IMP in the LVD group was increased as compared to normals as expected.

[FIGURE 1 OMITTED]

Using forward stepwise multiple linear regression, in patients with normal LV systolic function, IMP could be predicted (r=0.7612, p<0.0001) from age (r=0.616, p=0.0007) and the diastolic filling period (r=0.471, p=0.0091). The IMP could be predicted (r=0.6415, p<0.001)in patients with LVD from age (r=0.489, p=0.0091) and LV ejection fraction (r=0.386, p=0.0412). In patients with AR+Normal EF, IMP could be predicted (r=0.6655, p<0.001) from deceleration time (r=0.418, p=0.005) and ejection fraction (r=0.397, p=0.019). In patients with AR+Reduced EF, IMP could be predicted (r=0.7728, P<0.0001) from end systolic volume (r=0.450, p=0.0075), E/A (r=0.423, p=0.0086), and LV ejection fraction (r=0.368, p=0.0429).

Discussion

The IMP has been used in the past as a prognostic indicator in patients with cardiomyopathy, congestive heart failure and following a myocardial infarction (1-2). However, IMP has been demonstrated to be preload, afterload, and contractility dependent in human and experimental studies (5,6,14). Chronic AR is both a volume and a pressure overload lesion as end systolic stress tends to be increased (15). We hypothesized that AR as a volume overload lesion would prolong LVET (8-10) and possibly reduce IMP. However, patients with AR also tend to have IRT prolongation (7), which may increase the IMP. The effect of a prolonged LVET and IRT may influence IMP and limit its prognostic value in AR patients. In this study we compared patients with chronic AR and normal LV ejection fraction with age, and sex matched normals. Furthermore, patients with AR+Reduced EF were compared to age and sex matched patients in the LVD group.

We demonstrated that AR+Normal EF patients had a prolonged LVET and IRT resulting in an IMP that did not differ from the normal group. In AR+Reduced EF patients, IMP was significantly lower than in LVD patients primarily due to increased LVET (56 msec longer) and smaller sum of IRT and ICT (58 msec shorter). The increased volume load in AR clearly influenced the IMP by prolonging the LVET. The pressure overload aspect does not appear to be operative, as LVET would be expected to be shorter while ICT and IRT would be longer (6). In patients with AR+Reduced EF, IRT and ICT were similar to normals but shorter than patients with LVD. The IRT was also shorter than in patients with AR+Normal EF. We believe the shortening of IRT in AR+Reduced EF was due to a delay in the end of aortic flow and earlier onset of mitral flow. This might suggest greater elevation of LV filling pressure in the AR+Reduced EF group, but only 4 of 20 patients were functional Class 3 and hemodynamics were not obtained. The ICT can be defined as the time interval from the end of mitral flow to the onset of aortic flow. The ICT shortening in the AR+Reduced EF group was due to an earlier onset of aortic flow as the time to end of aortic flow occurred 17 msec later in the AR+Reduced EF group and LVET was 60 msec longer (nonindexed values). The result would be that the onset of aortic flow occurred 43 msec earlier explaining a large percentage of 29 msec lower ICT index. The finding of an increased IMP in the LVD group may also be in part to the higher incidence of hypertension, coronary disease and diabetes (16,17).

As compared to the AR+Normal EF group, patients with AR+Reduced EF had faster heart rates, shorter diastolic filling periods and started mitral filling earlier resulting in a shorter IRT than patients with AR+Normal EF. Forward stepwise regression revealed that IMP could be predicted from ejection fraction in both AR groups and in the LVD group. Diastolic filling parameters (deceleration time and E/A) in the AR groups suggesting impaired relaxation were also independent predictors of IMP.

Previous Literature

There has been limited work on the influence of AR on IMP. A recent work described IMP in patients prior to and following cardiac surgery for AR (7). Their data differed considerably from the data in our patient group. They demonstrated increases in ICT and IRT and shortening of the LVET. These findings are more consistent with pressure loading with LV dysfunction or cardiomyopathy (1,6) or end stage AR where preload reserve has been exhausted and afterload excess is evident (18, 19). One might suspect that these patients were referred for surgery for congestive heart failure and/or LV dysfunction. Although the estimate of systolic function in their study (fractional shortening) was similar to the estimate of systolic function (ejection fraction) in the AR+Reduced EF group, our values for ICT and IRT were shorter with the LVET being longer. Furthermore, only 4 of 20 patients in our study were functional class III.

Previous data in the literature has noted that the LVET is prolonged in AR, which may have the effect of reducing IMP (8-10). However, previous literature including Haque's study (7) did not stratify patients based on LV systolic function. Our study differs in that we included patients with normal and reduced LV ejection fraction. Other lesions producing LV volume overload may affect IMP and its components differently. With chronic mitral regurgitation, LVET is shorter which may prolong the IMP. This is not surprising, as severe mitral regurgitation has been noted to shorten LVET (7,10,11).

The effect of volume loading on I MP has been demonstrated in canines with and without LV dysfunction and in humans in the operating room. The LVET increased with volume loading (5,20) in both human and experimental studies. However, other studies have not demonstrated preload dependence, but compared patients groups and related IMP to LV size (3).

Limitations

The study has a retrospective design. Consequently, we did not have a consecutive series of patients enrolled since some echocardiograms were not technically adequate. Of importance, the LVD and AR+Reduced EF groups were matched for age, sex, and LV ejection fractions. However, the incidence of coronary disease, hypertension, and diabetes mellitus was significantly higher in the LVD group, which may increase IMP. Consequently, patients in the LVD group had a higher incidence in the use of angiotensin converting enzyme inhibitors and diuretics, which may have an uncertain influence on IMP and its components. Also, patient numbers were small in the AR+Reduced EF group. Second, dichotomization of AR patients based on heart failure symptoms or based on LV ejection fraction is problematic. Symptoms of congestive heart failure may occur with preserved or reduced LV ejection fractions. In fact, the average LV ejection fraction in patients with heart failure and AR were noted to be 45-50% (21,22). We chose an LV ejection fraction of <50% to dichotomize the AR groups purely for comparison with a matched groups of patients with LVD. Although the LV ejection fractions are comparable, the degree of LV systolic dysfunction may not be similar due differing preload and afterload states. Finally, as this was a retrospective study, follow-up was difficult and not evaluated because many patients changed their health care provider.

Clinical Implications

The IMP is most useful as a predictive index when ICT and IRT increase and LVET decrease as in patients post myocardial infarction and with dilated cardiomyopathy (1,2). However, IMP is difficult to interpret in volume overload states as AR with LVET prolongation. In patients with volume overload lesions or patients who experience changes in loading conditions, 1 or more components of IMP may be impacted resulting in an index that may not reflect global cardiac functioning.

Conclusions

Index of myocardial performance had similar values in patients with AR+Normal EF as compared to normal individuals due to an increase in both IRT and LVET. However, in patients with AR+Reduced EF, IMP values were similar to normal patients due primarily to prolongation of LVET. In patients with AR+Reduced EF, IMP values were significantly lower than LVD patients matched for LV ejection fraction due to prolongation of LVET and shortening of the IRT and ICT.

References

(1.) Dujardin KS, Tei C, Yeo TC, Hodge DO, Rossi A, Seward JB. Prognostic value of a Doppler index combining systolic and diastolic performance in idiopathic dilated cardiomyopathy. Am J Cardiol 1998; 82: 1071-6.

(2.) Poulsen SH, Jensen SE, Nielsen JC, Moller JE, Egstrup J. Serial changes and prognostic implications of a Doppler derived index of combined left ventricular systolic and diastolic myocardial performance in acute myocardial infarction. Am J Cardiol 2000; 85: 19-25.

(3.) Tei C, Ling LH, Hodge DO, Bailey KR, Oh JK, Rodeheffer RJ, et al. New index of combined systolic and diastolic myocardial performance: a simple and reproducible measure of cardiac function-a study in normals and dilated cardiomyopathy. J Cardiol 1995; 26: 357-66.

(4.) Cheung MM, Smallhorn JF, Redington AN, Vogel M. The effects of changes in loading conditions and modulation of inotropic state on the myocardial performance index: comparison with conductance catheter measurements. Eur Heart J 2064;25:2238-42.

(5.) Lavine SJ. Effect of heart rate and preload on index of myocardial performance in the normal and abnormal left ventricle. J Am Soc Echocardiogr 2065;18: 133-41.

(6.) Lavine SJ. Index of myocardial performance is afterload dependent in the normal and abnormal left ventricle. J Am Soc Echocardiogr 2005: 18; 342-50.

(7.) Haque A, Otsuji Y, Yoshifuku S, Kumanohoso T, Zhang H, Kisanuki A, et al. Effects of valve dysfunction on Doppler Tei index. J Am Soc Echocardiogr 2002; 15: 877-83.

(8.) Parisi AF, Salzman SH, Schecter E. Systolic time intervals in severe aortic valve disease: changes with surgery and hemodynamic correlations. Circulation 1971; 44:539-47.

(9.) Benchimol A, Matsuo S. Ejection time before and after aortic valve replacement. Am J Cardiol 1971; 27:244-9.

(10.) Moskowitz RL, Wechsler BM. Left ventricular ejection time in aortic and mitral valve disease. Am J Cardiol 1965; 15:869-14.

(11.) Elkins RC, Morrow AG, Vasko JS, Brauwnwald E. The effects of mitral regurgitation on the pattern of instantaneous aortic blood flow: clinical and experimental observations. Circulation 1967; 36:45-53.

(12.) Perry GJ, Helmcke F, Nanda NC, Byard C, Soto B. Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Coll Cardiol 1987; 9: 175-83.

(13.) Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989; 2: 358-67.

(14.) Lind L, Andren B, Arnold J. The Doppler-derived myocardial performance index is determined by both systolic and diastolic function as well as by afterload and left ventricular mass. Echocardiography 2065; 22:211-6.

(15.) Seabra-Gomes R, Parker DJ. Left ventricular function after aortic valve replacement. Br Heart J 1976; 38:45-53.

(16.) Evrengul H, Dursunoglu D, Kaftan A, Kilicaslan F, Tanriverdi H, Kilic M. Relation of insulin resistance and left ventricular function and structure in non-diabetic patients with essential hypertension. Acta Cardiol 2605; 60: 191-8.

(17.) Yakabe K, Ikeda S, Naito T, Yamaguchi K, Iwasaki T, Nishimura E, et al. Left ventricular mass and global function in essential hypertension after antihypertensive therapy. J Int Med Res 2000; 28: 9-19.

(18.) Wisenbaugh T, Spann JF, Carabello BA. Differences in myocardial performance and load between patients with similar amounts of chronic aortic versus chronic mitral regurgitation. J Am Coll Cardiol 1984;3:916-23.

(19.) Sutton M, Plappert T, Spiegel A, Raichlen J, Douglas P, Reichek N, et al. Early postoperative changes in left ventricular chamber size, architecture, and function in aortic stenosis and aortic regurgitation and their relation to intraoperative changes in afterload: A prospective two-dimensional echocardiographic study. Circulation 1987;76:77-89.

(20.) Lutz Jt, Giebler R, Peters J. The Tei-Index is preload dependent and can be measured by transesophageal echocardiography during mechanical ventilation. Eur J Anaesthesiology 2003; 20: 872-7.

(21.) Osbakken MO, Bove AA. Use of left ventricular filling and ejection patterns as assessing severity of chronic mitral and aortic regurgitation. Am J Cardiol 1984; 53:1054-60.

(22.) Lavine SJ, Follansbee WP, Shreiner DP, Krishnaswami K, Reddy PS, Mckee KS. Pattern of left ventricular diastolic filling in chronic aortic regurgitation: A gated blood pool assessment. Am J Cardiol 1985; 55: 127-32.

Aurelio A. Ortiz, Steven J. Lavine

From the Division of Cardiology, Department of Internal Medicine University of Florida/Jacksonville, FL, USA

Table 1. Patient Characteristics

Parameters                 Normals           AR+Normal EF

Age, years            50.6 [+ or -] 5.1   51.6 [+ or -] 7.2
Males/Females, n            20/15               22/18
NYHA Class, n
I                            35                   27
II                            0                   13 **
III                           0                    0
IV                            0                    0
Etiology of AR, n
Bicuspid                     --                    4
Sclerosis                    --                   34
Prolapse                     --                    2
Severity of AR, n
Moderate                     --                   23
Severe                       --                   17
Hypertension, n               0                    8 *
Diabetes, n                   0                    5
Systolic BP, mm Hg     113 [+ or -] 11    136 [+ or -] 19 **
Diastolic BP, mm Hg     68 [+ or -] 12     74 [+ or -] 14
ACEI, n                       0                    5
Beta blockers, n              2                    3
CCB's, n                      0                    6 *
Diuretics, n                  0                    6 *
Digoxin, n                    0                    0

Parameters              AR+Reduced EF             LVD

Age, years                53.2 + 6.5       51.7 [+ or -] 8.6
Males/Females, n             11/9                15/11
NYHA Class, n
I                              7                   13
II                             9                   10
III                            4                    3
IV                             0                    0
Etiology of AR, n
Bicuspid                       4                   --
Sclerosis                     15                   --
Prolapse                       1                   --
Severity of AR, n
Moderate                       9                   --
Severe                        11                   --
Hypertension, n                6 *                 12 *** (^)
Diabetes, n                    4                    9 *** (^)
Systolic BP, mm Hg    141 [+ or -] 20 **   135 [+ or -] 18 **
Diastolic BP, mm Hg    78 [+ or -] 18 *     76 [+ or -] 11 *
ACEI, n                        4               21 *** (^^^)
Beta blockers, n               2                    8 *
CCB's, n                       3                    6 *
Diuretics, n                   5 *                 19 *** (^^)
Digoxin, n                     4                    6 *

* p<0.05, ** p<0.01, *** p<0.001 vs Normal. (^) = p<0.05, (^^) p<0.01,
(^^^) p<0.001 vs AR+ Reduced EF

ACEI--angiotensin converting enzyme inhibitor, AR--aortic
regurgitation, AR+Normal EF--aortic regurgitation with ejection
fraction >50%, AR+Reduced EF--aortic regurgitation with reduced
ejection fraction; systolic dysfunction, BP--blood pressure,
CCB's--calcium channel blockers, LVD--left ventricular dysfunction,
NYHA--New York Heart Association

Table 2. Parameters of LV size, LV function, and transmitral Doppler

Parameters         Normals             AR+Normal EF

PWT, mm        8.3 [+ or -] 1.5   11.2 [+ or -] 3.9 ***
EDD, mm       46.4 [+ or -] 4.1   53.7 [+ or -] 8.4 * (^)
FS, %         39.6 [+ or -] 6.3   39.2 [+ or -] 7.2 (^^)
EDV, ml        112 [+ or -] 21     169 [+ or -] 50 ** (^)
ESV, ml         38 [+ or -] 14      55 [+ or -] 31 * (^^^)
EF, %           66 [+ or -] 7     62.9 [+ or -] 8.4 (^^)
E, cm/s         83 [+ or -] 17      68 [+ or -] 19 *
A, cm/s         61 [+ or -] 10      69 [+ or -] 18
E/A            1.4 [+ or -] 0.3    1.1 [+ or -] 0.4 *
DFP, msec      462 [+ or -] 126    471 [+ or -] 141 (^)
DCT, msec      224 [+ or -] 52     398 [+ or -] 199 ***
R-AVC, msec    375 [+ or -] 35     399 [+ or -] 29
R-MVO, msec    433 [+ or -] 30     468 [+ or -] 39 * (^)
RR, msec       882 [+ or -] 157    870 [+ or -] 163 (^)

Parameters       AR+Reduced EF                LVD

PWT, mm       11.7 [+ or -] 2.6 *     9.2 [+ or -] 1.5 (^^)
EDD, mm       61.7 [+ or -] 9.1 **   63.5 [+ or -] 10.2 **
FS, %         26.1 [+ or -] 3.1 **   25.7 [+ or -] 4.4 ***
EDV, ml        219 [+ or -] 82 ***    229 [+ or -] 81 ***
ESV, ml        111 [+ or -] 29 *      119 [+ or -] 48 ***
EF, %           45 [+ or -] 9 ***      42 [+ or -] 10 ***
E, cm/s         73 [+ or -] 26         81 [+ or -] 29
A, cm/s         73 [+ or -] 26         64 [+ or -] 22
E/A            1.1 [+ or -] 0.6       1.6 [+ or -] 1.2 (^)
DFP, msec      368 [+ or -] 184       382 [+ or -] 118 *
DCT, msec      384 [+ or -] 204 **    235 [+ or -] 82 (^^)
R-AVC, msec    389 [+ or -] 36        372 [+ or -] 31 (^)
R-MVO, msec    435 [+ or -] 44        468 [+ or -] 39 (^)
RR, msec       779 [+ or -] 134 *     759 [+ or -] 109 *

* p<0.05, ** p<0.01, *** p<0.001 vs Normal. (^) = p<0.05, (^^) p<0.01,
(^^^) p<0.001 vs AR+Reduced EF

A--atrial filling velocity, AR--aortic regurgitation, AR+Normal
EF--aortic regurgitation with ejection fraction >50%, AR+Reduced
EF--aortic regurgitation with reduced ejection fraction, systolic
dysfunction, DCT--deceleration time, DFP--diastolic filling period,
E--peak filling velocity, EDD--end-diastolic dimension,
EDV--end-diastolic volume, EF--ejection fraction ESV--end-systolic
volume, FS--fractional shortening, LVD--left ventricular dysfunction,
PWT--posterior wall thickness, R-AVC--R wave to end of aortic flow
interval, R-MVO- R wave to onset of mitral flow interval, RR--cycle
length

Table 3. Components of the Index of Myocardial Performance

Parameters               Normals              AR+Normal EF

ICT index, msec       48 [+ or -] 23         45 [+ or -] 21
IRT index, msec       59 [+ or -] 34         70 [+ or -] 32 (^)
LVET index, msec     301 [+ or -] 29        344 [+ or -] 43 **
IMP                0.357 [+ or -] 0.122   0.342 [+ or -] 0.188

Parameters            AR+Reduced EF                 LVD

ICT index, msec       58 [+ or -] 33         87 [+ or -] 27 *** (^)
IRT index, msec       52 [+ or -] 31         71 [+ or -] 33 (^)
LVET index, msec     325 [+ or -] 45 *      269 [+ or -] 50 ** (^^^)
IMP                0.346 [+ or -] 0.172   0.604 [+ or -]
                                            0.278 *** (^^^)

* p<0.05, ** p<0.01, *** p<0.001 compared to Normals. (^) p<0.05, (^^)
p<0.01, (^^^) p<0.001 compared to AR+Reduced EF

AR--aortic regurgitation, AR+Normal EF--aortic regurgitation with
ejection fraction >50%, AR+Reduced EF--aortic regurgitation with
reduced ejection fraction, systolic dysfunction, LVET--left
ventricular ejection time, ICT--isovolumic contraction time,
IMP--index of myocardial performance, IRT--isovolumic relaxation time