(Circulation. 1999;99:230-236.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Doppler-Derived Mitral Deceleration Time
An Early Strong Predictor of Left Ventricular Remodeling After Reperfused Anterior Acute Myocardial Infarction
From the Division of Cardiology, Careggi Hospital, Florence, Italy.
Correspondence to Giampaolo Cerisano, MD, Division of Cardiology, Careggi Hospital, Viale Morgagni 85, 50134 Firenze. Italy. E-mail carddept{at}tin.it
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—The relation between remodeling and left ventricular (LV) diastolic function has not yet been fully investigated. The aim of this study was to determine whether early assessment of Doppler-derived mitral deceleration time (DT), a measure of LV compliance and filling, may predict progressive LV dilation after acute myocardial infarction (AMI).
Methods and Results—Fifty-one patients (aged 61±11 years; 6
women) with anterior AMI successfully treated with direct
coronary angioplasty underwent 2-dimensional and Doppler
echocardiographic examinations within 24 hours of
admission, at days 3, 7, and 30 and 6 months after the index
infarction. Mitral flow velocities were obtained from the apical
4-chamber view with pulsed Doppler. End-diastolic
volume index (EDVI) and end-systolic volume index (ESVI) were
calculated with the Simpson's rule algorithm. Patients were divided
according to the DT duration assessed at day 3 in 2 groups: group 1
(n=33) with DT >130 ms and group 2 (n=18) with DT 
130 ms. Patency
and restenosis rate at 6 months were similar between the 2
groups (94% group 1 vs 89% group 2; P=0.52; 27% group
1 vs 33% group 2; P=0.64, respectively). LV volume
indexes were similar in both groups at baseline (EDVI: 71±3 group 1 vs
70±3 mL/m2 group 2, P=0.42; ESVI: 43±3
group 1 vs 48±3 mL/m2 group 2, P=0.13,
respectively). From day 3 on, LV volume indexes progressively increased
in group 2 and were significantly larger than those of group 1 at 6
months (LVEDVI 61±3 group 1 vs 104±6 mL/m2 group 2,
P=0.00001; LVESVI 31±3 group 1 vs 73±6
mL/m2 group 2, P=0.00001, respectively). A
significant inverse correlation was found between DT and changes in
EDVI at 6 months (r=-0.68;
P<0.0000001). By stepwise multiple regression
analysis among several clinical, demographic, angiographic, and
echocardiographic variables, DT was the most
powerful predictor of EDVI changes at 6 months (P=0.02).
Conclusions—These data suggest that early estimation (day 3) of Doppler-derived mitral DT provides a simple and accurate mean to predict late LV dilation after reperfused AMI.
Key Words: diastole • remodeling • myocardial infarction • echocardiography
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Ventricular remodeling has emerged as one of the dominant factors that determines the long-term survival of postinfarction patients.1 Several variables have been identified to predict an increase in left ventricular (LV) volume after acute myocardial infarction (AMI). These include infarct size,2 anterior location,3 transmurality of the infarct,4 and patency of the infarct-related artery.5 However, other not-yet well-defined determinants may influence and modify the remodeling process. One of the important functional aspects of remodeling is that it is accompanied by changes in diastolic properties of the left ventricle caused by scar formation, which increases stiffness, and hypertrophy of normal segments, which have delayed relaxation.6 LV dilation may occur early after infarction, probably in part because of elevated filling pressure within the ventricle.5 7 8 Doppler echocardiography has provided a rapid, feasible, and simple noninvasive method of assessing LV filling in various cardiac diseases9 in which diastolic abnormalities have been observed, including AMI.7 10 11 12 Among the various diastolic variables, shortening of the deceleration time (DT) of the early filling wave, indicative of a "restrictive" filling pattern, has been found to correlate with infarct size13 and to predict an adverse outcome of postinfarction patients.11 14 However, no previous study has correlated serial changes in filling patterns with serial changes in LV volumes after AMI. We hypothesized that early assessment of Doppler-derived mitral DT would predict progressive LV dilation after AMI, and serial changes in filling pattern might parallel the evolutionary changes in LV dimensions. To test this hypothesis, we performed a prospective study of patients with first anterior AMI treated with primary coronary angioplasty. To avoid the confounding impact of infarct-related artery patency and residual stenosis on subsequent changes in LV dimensions, only patients in whom anterograde flow was fully restored without significant residual stenosis were included in the study. Serial assessments of Doppler-derived DT were obtained at days 3, 7, and 30 and 6 months after the index infarction.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Patients and Study Protocol
We prospectively studied 72 patients with anterior AMI selected among 142 patients consecutively referred to the catheterization laboratory of Careggi Hospital for emergency coronary angioplasty between April 1996 and January 1997. The study inclusion criteria were (1) confirmed first anterior AMI; (2) successful primary coronary angioplasty (defined as Thrombolysis In Myocardial Infarction Trial [TIMI] flow grade 3 and residual stenosis <30%) within 6 hours of the onset of symptoms or between 6 and 24 hours if there was evidence of continuing ischemia. Exclusion criteria were clinical signs of heart failure or cardiogenic shock in the first week after AMI, postinfarction angina, atrial fibrillation, significant valvular heart disease, and life-limiting noncardiac disease. In particular, no patient with significant (moderate to severe) mitral regurgitation was included in the study. No upper age limit was used. Of the 59 patients selected for the study, 2 (3%) were excluded because of inadequate quality of echocardiographic images and mitral Doppler tracings on the baseline echocardiographic examination. Later, further exclusions were for reinfarction (1) and death (2); an additional 3 patients did not adhere to the follow-up protocol. Thus 51 patients (45 men, 6 women, mean age 61±11 years, range 34 to 89 years) were enrolled in the study. The research protocol was approved by the hospital Ethics Committee, and informed consent was obtained from each patient by one of the investigators. All patients underwent serial assessment of LV filling patterns at days 3 and 7 and LV volumes within 24 hours of admission on days 3 and 7 after the index infarction. A comprehensive echocardiographic examination and repeat coronary angiography were obtained at 1 and 6 months after primary coronary angioplasty in all patients.
Echocardiography
Complete M-mode and 2-dimensional
echocardiography and Doppler ultrasound
examination were performed with commercially available imaging systems
(Aloka model SSD 870 2.5- and 3.5-MHz transducers). LV
diastolic filling patterns were determined by the mitral
inflow pulsed-wave Doppler examination with a 2.5-MHz transducer.
In the apical 4-chamber view, the Doppler sample volume was placed
in the middle of the LV inflow tract 
1 cm below the plane of the
mitral annulus between the mitral leaflet tips, where maximal flow
velocity in early diastole was recorded.15
Special care was taken to align the sample volume as close to
perpendicular as possible to the mitral annular plane. Images were
stored on a videotape by a 0.5-inch VHS cassette recorder (Sony
SVO, 140 PA) for further analysis.
Data Analysis
Two investigators blinded to the clinical and angiographic data
analyzed baseline and follow-up 2-dimensional echocardiograms
and Doppler tracings. Discrepancies were resolved by consensus.
Two-dimensional echocardiographic images were transferred to the hard disk of a Tomtec P90 medical off-line computer analysis system and digitized. LV volumes and ejection fraction (EF) were then measured with the modified Simpson's rule algorithm.16 The mean values of 3 measurements of the technically best cardiac cycles were taken from each examination. The volume indexes were obtained by dividing the volume by the body surface area at each time point. Intraobserver and interobserver variability values in the evaluation of end-systolic and end-diastolic volumes were <5%, indicating the good reproducibility of the measurements.4 On the basis of repeated measurements in individual patients and on the upper 95% confidence limit of the intraobserver variability, an increase in end-diastolic volume index >20% was considered LV dilation.4 The ratio of long-axis length to short-axis length at end diastole and end systole was measured from the apical chamber view and taken as an index of eccentricity, with a value equal to 1 for this index corresponding to a spherical shape and values of >1 representing more ellipsoid shapes.
The dimension of the left atrium was measured at end systole from an M-mode recording at the level of aortic root. LV mass was calculated by the cube formula.17 The left ventricle was divided according to a 16-segment model.16 For each segment, wall motion was scored from 1 (normal) to 4 (dyskinetic). In evaluating regional wall motion abnormalities, attention was also paid to the systolic thickening in the central portion of each segment. Anterior infarct zone was constructed, and in each patient both global and infarct zone wall motion score indexes (WMSI) were derived for baseline and follow-up 2-dimensional echocardiograms.
From Doppler spectra of 3 to 5 consecutive cardiac cycles, average
values were calculated for the following diastolic
variables: peak velocity of early rapid filling wave (E), peak flow
velocity at atrial contraction (A), peak E/A wave velocity ratio, and
DT of early filling. A digitizing pad and microcomputer were used to
analyze the Doppler waveforms (leading edge). To avoid the
influence of heart rate, deceleration time was calculated as the time
between peak E wave and the upper deceleration slope extrapolated to
zero line.15 Cardiac cycles with nonlinear deceleration
slopes and fusion of early and late mitral flow velocity were excluded
from the analysis. A DT >130 ms was classified as
nonrestrictive, and 130 ms was defined as restrictive. This cutoff
point has been shown to be consistent with restrictive
hemodynamics and a powerful independent predictor of
unfavorable outcome after acute myocardial infarction and idiopathic
dilated cardiomyopathy.9 11 12 14 To
avoid the effects of acute ischemia on LV filling
patterns,6 we chose to measure baseline DT on day 3 after
the index infarction.
Statistical Analysis
Continuous data are expressed as mean±SD.
Echocardiographic variables are expressed as
mean±SE. Baseline data were compared by means of the
2 test for categorical variables and
unpaired t test for continuous variables. ANOVA with the
Tukey post hoc test was used to analyze repeated measures of
WMSI, EF, LV volumes, and Doppler-derived diastolic
variables. Simple linear regression analysis was used to
correlate DT, peak creatine kinase, and WMSI with the changes in LV
end-diastolic volume index. Linear regression
analysis was also used to determine intraobserver and
interobserver variability. Linear and multiple regression
analyses were carried out to test the relation between
clinical, echocardiographic, and
hemodynamic variables and DT.
Univariate and multivariate regression
analyses were performed to identify independent correlates of
the changes in LV end-diastolic volume index. A value of
P<0.05 was considered statistically significant.
Statistical analysis was performed with Statistica 4.5 for
Windows (StatSoft, Inc, 1993).
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Baseline Patient Characteristics
Patients were divided into 2 groups according to Doppler echocardiographic mitral pattern assessed at baseline (day 3) Doppler ultrasound examination. Thirty-three patients showed a DT >130 ms (group 1), and 18 had a DT
130 ms (restrictive
LV filling pattern, group 2). All patients were receiving ACE therapy.
There was no significant difference between the 2 groups with respect
to age, sex, frequency of coronary risk factors, time from
onset of symptoms to reperfusion, angiographic collateral grade,
multivessel disease, left atrial size, LV mass index, and Doppler
mitral curves as regard E, A peak velocity, and E/A ratio (Table 1
). However, signs of reduced
infarct size were more common among patients of group 1. These patients
had a markedly (P<0.00001) lower mean peak creatine kinase
and baseline WMSI and a higher EF (Table 1).
|
Since a sizable number of patients with a short DT had an E/A ratio
between 1 and 2, to clarify if this LV inflow pattern was indicative of
pseudonormalization, pulmonary venous flow velocities by
transthoracic pulsed Doppler ultrasound18
and early diastolic velocity of mitral annulus (Ea) by
Doppler tissue imaging19 were measured (Aloka SSD
2002) in 8 consecutive patients with short DT (130 ms; mean 120±7;
range 116 to 126) and an apparently normal (>1<2) E/A ratio (mean
1.2±0.2; range 1.1 to 1.43) 3 days after anterior AMI.
Pulmonary venous flow reversal exceeded the duration of the
mitral A wave in all patients (difference in duration 51±9 ms; range
45 to 75 ms), and the systolic fraction of pulmonary
venous flow (the ratio of systolic to the sum of
systolic and diastolic velocity integral) was
markedly (<0.5) decreased in all patients (mean 0.43±0.03; range 0.40
to 0.49). These data are indicative of elevated LV
end-diastolic pressure and elevated LV pressure before
atrial systole, respectively, despite an apparently normal E/A
ratio.18 In agreement with pulmonary venous flow
velocities recordings, the ratio of transmitral E-wave velocity
to Doppler tissue imaging Ea was elevated (14±3; range 11.7 to
17.5), suggesting an increased LV end-diastolic
pressure.19
Linear and Multiple Regression Analysis Between Clinical
Variables and DT
The correlation coefficients between DT and the clinical,
Doppler echocardiographic, and
hemodynamic variables are shown in Table 2. On multivariate
analysis, DT was independently correlated with peak creatine
kinase (P=0.006) and EF (P=0.018).
|
Angiographic Results
Lesion minimal lumen diameter increased from 0.19±0.30 at
baseline to 3.18±0.42 mm after coronary angioplasty in
group 1 and from 0±0 to 3.23±0.49 mm in group 2.
At 1 month, the angiographic patency rate was 100% in both groups. Lesion minimal diameter was 2.96±0.65 mm in group 1 and 3.35±0.52 mm in group 2 (P=0.016). At 6 months, patency of the infarct-related artery was 94% in group 1 and 89% in group 2 (P=0.52). No significant difference was found in minimal lumen diameter and restenosis rate (>50%) between the 2 groups.
Changes in Regional and Global Ventricular Function and
LV Volumes
At baseline, both global and regional contractile function were
significantly better in group 1 than in group 2 (EF 41±1% vs 30±2%,
P<0.00001; WMSI: 2.43±0.06 vs 2.75±0.03,
P<0.0001). According to ANOVA, a significant progressive
improvement in LVEF was observed in group 1, whereas it remained
unchanged throughout the study period in group 2 (Figure 1A). Comparison between groups by ANOVA
revealed that patients with a DT >130 ms (group 1) had a significantly
higher improvement of global ventricular function at 6
months than did patients with a DT 130 ms. (Figure 1A).
Similarly, the regional contractile function, expressed as WMSI, showed
a higher improvement in patients of group 1 compared with those of
group 2 (Figure 1B). Eleven patients (44%) with LVEF <40% did
not have significant dilation during follow-up. Conversely, 5 (19%)
patients with LVEF 
40% had a significant increase (>20%) in
chamber volume.
|
-
-
End-diastolic and end-systolic volume indexes
were similar in both groups at baseline. From day 3 on, LV volume
indexes progressively increased in group 2 and were significantly
larger than those of patients of group 1 at each study point in time
(Figure 1
, C and D). In patients of group 1,
end-diastolic and end-systolic volume decreased
after 1 month (Figure 1, C and D). Finally, at baseline, eccentricity
index at end diastole and at end systole were similar in
both groups (group 1, 1.58 vs 1.63 group 2, P=0.96; and 1.84
vs 1.85, P=0.99, respectively). The eccentricity index at
end diastole decreased from 1.63 to 1.49 at 6 months in
group 2, indicating a more spherical shape, but increased from 1.58 to
1.63 in group 1 (P=0.0009 for 
group 1 vs group 2).
At end systole, the index decreased from 1.85 to 1.69 in group 2 but
increased from 1.84 to 1.91 in group 1 (P<0.004 for
group 1 vs group 2).
Serial Changes of Filling Pattern
DT increased on day 7 and at 1 and 6 months in both groups (Figure 2). However, the increase in DT was
significantly higher in group 2 on days 3 and 7 than in group 1, so
that the differences between the 2 groups were less pronounced at 1 and
6 months and statistically not significant (Figure 2).
|
Relation of DT to Changes in LV End-Diastolic
Volume Index
In Figure 3, the change in LV
end-diastolic volume index from baseline to 6 months was
plotted against the early filling DT. A significant inverse correlation
was found between the 2 variables (r=-0.68;
P<0.0000001). Similarly, there was a direct relation
between changes in LV end-diastolic volume index and peak
creatine kinase (r=0.66; P<0.0000001) and WMSI
on admission (r=0.48, P<0.0004). A weaker
although statistical significant correlation was found between DT and
the eccentricity index at end diastole at 6 months
(r=.48; P<0.0004) and end systole
(r=.37; P<0.008).
|
The distribution of the DT in patients with and those without LV
dilation at 6 months is shown in Figure 4. All but 2 patients with LV dilation
had shortened DT (130 ms.); in contrast, only 1 patient with a DT
130 ms on day 3 did not develop LV dilation at 6 months.
|
To evaluate the independent contribution of DT to LV dilation, multiple
regression analysis was performed. Variables used for
analysis were as follows: age, Killip class, EF, LV volume
indexes, peak creatine kinase, baseline WMSI, change in WMSI from
baseline to 6 months, onset of reperfusion, collaterals, and
multivessel disease. For multiple regression analysis, factors
showing a P value <0.1 in univariate
analysis were selected. The most important predictor of 6-month
LV dilation was a DT 130 ms (P=0.02), followed by change
in WMSI from baseline to 6 months (P=0.03) and peak creatine
kinase (P=0.09).
Follow-Up
Two patients (1 of group 1 and 1 of group 2) underwent repeat
coronary angioplasty for early (<24 hours) post–myocardial
infarction angina. No patient was lost at 6 months of follow-up. Five
patients had recurrent ischemia at 6 months (3 in group 1 and 2
in group 2). No patient developed congestive heart failure.
Reproducibility
There was an excellent agreement between DT measurements made by a
single observer at 2 time points (intraobserver variability,
r=0.93) and between measurements made by 2 independent
observers (interobserver variability, r=0.91).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The present study suggests that the assessment of LV filling pattern on Doppler echocardiography provides additional and important information in the setting of AMI, allowing identification of patients at high risk for progressive LV dilation within 6 months after AMI. A restrictive filling pattern, as expressed by a short DT, was the most powerful predictor of LV remodeling, and the degree of LV dilation was related to the severity of impairment of LV filling.
LV Diastolic Function and AMI
Although the predominant diastolic abnormality induced
by transient ischemia is an impairment in
relaxation,20 the diastolic filling pattern
may change during AMI, resulting in a restrictive filling
pattern.12 13 Several investigators have in fact observed
an upward shift in the pressure-volume curve during AMI or
ischemia as a result of an increase in resistance to LV filling
or increased chamber stiffness.21 Furthermore, in a few
experimental studies, chamber stiffness increased within 24 hours after
AMI, reverting to normal after several days.6 Increased
chamber stiffness may reflect primary changes in the infarcted
myocardium or simply the ventricular filling on
a steeper portion of its pressure-volume curve.6
Therefore, it is not surprising, in view of the aforementioned effects
of ischemia on LV compliance, that the filling pattern in
patients with large infarcts resembles the filling behavior of those
conditions, such as constrictive pericarditis and restrictive
cardiomyopathies with "restrictive
physiology."
Doppler echocardiography has been used to assess diastolic function in a variety of clinical settings, including AMI.7 10 11 12 Doppler indexes are affected by a number of other physiological factors, including heart rate, LV systolic function, and ventricular preload and afterload.9 However, recent experimental22 data suggest that early filling DT can quantitatively assess LV chamber stiffness independent of heart rate, contractility, and afterload. Conversely, because in many patients diastolic dysfunction may involve both relaxation and chamber stiffness,9 and in view of the dynamic nature of LV filling patterns,15 the ability of the Doppler flow velocity profile as expressed by peak flow velocities (both E and A wave) and their ratio to predict diastolic abnormalities and LV filling pressure is limited.9 15 The results obtained by pulmonary venous flow velocities and Doppler tissue imaging recordings in a small subset of patients in the present study confirm that E/A ratio is less sensitive and specific than DT in assessing filling pressures.23
Restrictive Filling Pattern and LV Remodeling
Previous studies have demonstrated that infarct size is one of the
major factors that promotes LV remodeling.2 On the other
hand, the size of the infarct zone has been shown to influence the
diastolic filling pattern, with the large infarcts
exhibiting a "restrictive" filling pattern.7 13
Therefore, a short DT, indicative of a restrictive filling pattern,
might simply reflect an increasing infarct size and consequently a
higher risk of LV dilation.
In agreement with the aforementioned observations, in the current study the extent of asynergy and peak creatine kinase (as estimates of infarct size) were significantly higher in patients with a short DT. Obviously, this may at least partially account for the difference in LV volumes. However, after controlling for infarct size, DT was the most significant independent predictor of LV dilation. Thus DT appears to be a powerful predictor of LV dilation independent of infarct size. It is conceivable that for comparable infarct size, the transmural extent of necrosis will influences the diastolic properties of left ventricle and the propensity to infarct expansion.4 This speculative hypothesis is supported by the finding on multivariate analysis that the absence of spontaneous recovery of wall motion in the infarct zone was the second most powerful predictor of LV dilation. An alternative hypothesis to explain the relation of DT to ventricular remodeling may not necessarily be related to the extent of myocardial abnormalities that have occurred during the index infarction. DT is inversely related to the LV filling pressure. One may speculate that the LV filling pressure itself can influence subsequent LV dilation due to the changes in wall stress that occur as consequence of the high filling pressures.
Serial Changes of Filling Pattern and LV Remodeling
Experimental and clinical studies have indicated that reperfused
AMI leads to abnormal LV stiffness or relaxation that may improve with
time.24 The results of these studies have suggested that
reperfusion in AMI is associated with "diastolic
stunning," which is an equivalent of the well-known systolic
phenomenon.24 However, experimental studies were hampered
by the fact that periods of occlusion were relatively short, and this
is not usually the case in the clinical setting; in the clinical
studies, follow-up was performed only in a few patients, and LV volumes
were not measured during the short follow-up period. In the present
study, in the group of patients with a baseline short DT, the filling
pattern changed from a restrictive pattern to a "normal" pattern at
6 months after AMI. The biphasic changes in LV filling pattern detected
in the current study are concordant with previous
experimental6 and clinical studies,13
suggesting an early increase in chamber stiffness that subsequently
returns to normal. However, this evolutionary change in filling pattern
may be explained by the healing and remodeling process rather than by a
gradual recovery in diastolic function after reperfusion.
In the early phase of AMI, the infarcted tissue is characterized by
edema and cellular infiltrates, causing the tissue to be less
extensible. Because of the initial LV stiffness, high left atrial
pressures, and rapid increase in LV diastolic pressure
during rapid filling, the diastolic filling pattern becomes
"restrictive," contributing to shortening of the DT. As healing
progresses, the left ventricle becomes more compliant and dilates,
inducing relevant changes in mitral flow velocities, such as
prolongation of DT. Thus serial changes in filling pattern after AMI
parallel the evolutionary changes in LV dimensions. These findings may
provide the critical linkage between restrictive filling pattern and
clinical events after AMI observed in some observational
studies.11 12 14
Study Limitations
One potential limitation of the study is the lack of
simultaneous hemodynamic measurements
obtained with Doppler examinations. However, we did not feel
justified in performing simultaneous cardiac
catheterization to correlate
hemodynamic data with Doppler patterns because
underlying hemodynamic features have been correlated
with diastolic filling variables by
others23 who showed a close inverse correlation
between DT of early filling and pulmonary capillary wedge
pressure irrespective of the filling pattern expressed by the E/A
ratio.
DT of early filling is partially dependent on age and is determined by the interaction of intrinsic diastolic properties and the alterations in hemodynamic conditions and pericardial restraint related to AMI.11 However, it is difficult to control all these factors in a clinical study. Age may be unlikely to have significant impact on our results because age distribution was similar between the restrictive and nonrestrictive groups, and patient age in our series was relatively old (average 60 years) and no correlation was found between age and DT. Although the loading conditions of patients were not characterized, in our study no patient was taking diuretic agents or digitalis, whereas all patients were receiving ACE inhibitor therapy, and no difference in nitrate therapy was found between the restrictive and nonrestrictive group throughout the study period (19% vs 15%, respectively).
Conclusions
This study shows that early noninvasive assessment of transmitral
flow velocity by Doppler echocardiography
allows identification of patients at high risk for progressive LV
dilation within 6 months after anterior reperfused AMI. A restrictive
filling pattern, as expressed by a short (130 ms) DT of early
filling, is the most powerful predictor of LV remodeling, and LV
dilation is related to the severity of impairment of LV filling. Larger
studies are needed to determine the prognostic implications of LV
filling patterns in AMI and the role of Doppler ultrasound in this
setting.
Received May 28, 1998; revision received September 8, 1998; accepted October 1, 1998.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. St. John Sutton M, Pfeffer MA, Plappert T, Rouleau JL, Moye LA, Dagenais GR, Lamas GA, Klein M, Sussex B, Goldman S, Menapace FJ, Parker JO, Lewis S, Sestier F, Gordon DF, McEwan P, Bernstein V, Braunwald E, for the SAVE Investigators. Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction. Circulation. 1994;89:68–75.
2.
Gaudron P, Eilles C, Kugler I, Ertl G. Progressive
left ventricular dysfunction and remodeling after
myocardial infarction: potential mechanisms and early predictors.
Circulation. 1993;87:755–763.
3. Warren SE, Royal H, Markis JE, Grossman W, McKay R. Time course of left ventricular dilation after myocardial infarction: influence of infarct related artery and success of coronary thrombolysis. J Am Coll Cardiol. 1988;11:12–19.[Abstract]
4.
Bolognese L, Cerisano G, Buonamici P, Santini A,
Santoro GM, Antoniucci D, Fazzini PF. Influence of infarct zone
viability on left ventricular remodeling following acute
myocardial infarction. Circulation. 1997;96:3353–3359.
5. Jeremy RW, Hackworthy RA, Bautovich G, Hutton BF, Harris PJ. Infarct artery perfusion and changes in left ventricular volume in the month after acute myocardial infarction, J Am Coll Cardiol 1987; 9:989–995.
6.
Raya TE, Gay RG, Lancaster L, Aguirre M, Moffett C,
Goldman S. Serial changes in left ventricular relaxation
and chamber stiffness after large myocardial infarction in rats.
Circulation. 1988;77:1424–1431.
7. Pipilis A, Meyer TE, Ormerod D, Flather M, Sleight P. Early and late changes in left ventricular filling after acute myocardial infarction and the effect of infarct size. Am J Cardiol. 1992;70:1397–1401.[Medline] [Order article via Infotrieve]
8. Popovic AD, Neskovic AN, Babic R, Obradovic V, Bozinovic LJ, Marinkovic J, Lee J-C, Tan M, Thomas JD. Independent impact of thrombolytic therapy and vessel patency on left ventricular dilation after myocardial infarction: serial echocardiographic follow-up. Circulation. 1994;77:1424–1431.
9. Nishimura RA, Tajik J. Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the clinician's Rosetta Stone. J Am Coll Cardiol. 1997;30:8–18.[Abstract]
10. Chenzbraun A, Keren A, Stern S. Doppler echocardiographic patterns of left ventricular filling in patients early after acute myocardial infarction. Am J Cardiol. 1992;70:711–714.[Medline] [Order article via Infotrieve]
11. Oh JK, Ding ZP, Gersh BJ, Bailey KR, Tajik J. Restrictive left ventricular diastolic filling identifies patients with heart failure after acute myocardial infarction. J Am Soc Echocardiogr. 1992;5:497–503.[Medline] [Order article via Infotrieve]
12. Algom M, Schlesinger Z. Serial changes in left ventricular diastolic indexes derived from Doppler echocardiography after anterior wall acute myocardial infarction. Am J Cardiol. 1995;75:1272–1273.[Medline] [Order article via Infotrieve]
13. Popovic AD, Neskovic AN, Marinkovic J, Lee J-C, Tan M, Thomas JD. Serial assessment of left ventricular chamber stiffness after acute myocardial infarction. Am J Cardiol. 1996;77:361–364.[Medline] [Order article via Infotrieve]
14. Nijland F, Kamp O, Karreman AJP, van Eenige MJ, Visser CE. Prognostic implications of restrictive left ventricular filling in acute myocardial infarction: a serial Doppler echocardiographic study. J Am Coll Cardiol. 1997;30:1618–1624.[Abstract]
15. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insight from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol. 1988;12:426–440.[Abstract]
16. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silverman NH, Tajik AJ. Recommendations for quantification of the left ventricle by two dimensional echocardiography: American Society of Echocardiography Committee on Standards Subcommittee. J Am Soc Echocardiogr. 1989;2:358–367.[Medline] [Order article via Infotrieve]
17.
Devereux RB, Reichek N.
Echocardiographic determination of left
ventricular mass in men: anatomic validation of the method.
Circulation. 1977;55:613–618.
18. Rossvoll O, Hatle LK. Pulmonary venous flow velocities recorded by transthoracic Doppler ultrasound: relation to left ventricular diastolic pressures. J Am Coll Cardiol. 1993;21:1687–1696.[Abstract]
19. Nagueh SF, Middleton KJ, Kopelen HA, Zoghbi WA, Quinones MA. Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol. 1997;30:1527–1533.[Abstract]
20. Labovitz AJ, Lewen MK, Kern M, Vandormael M, Deligonal U, Kennedy HL. Evaluation of left ventricular systolic and diastolic dysfunction during transient myocardial ischemia produced by angioplasty. J Am Coll Cardiol. 1987;10:748–755.[Abstract]
21.
Diamond G, Forrester JS. Effect of coronary
artery disease and acute myocardial infarction on left
ventricular compliance in man. Circulation. 1974;45:11–19.
22.
Little WC, Ohno M, Kitzman DW, Thomas JD, Cheng
C-P. Determination of left ventricular chamber stiffness
from the time for deceleration of early left ventricular
filling. Circulation. 1995;92:1933–1936.
23. Giannuzzi P, Imparato A, Temporelli PL, De Vito F, Silva PL, Scapellato F, Giordano A. Doppler-derived mitral deceleration time of early filling as a strong predictor of pulmonary capillary wedge pressure in postinfarction patients with left ventricular systolic dysfunction. J Am Coll Cardiol. 1994;23:1630–1637.[Abstract]
24.
Williamson BD, Lim MJ, Buda AJ. Transient left
ventricular filling abnormalities (diastolic
stunning) after acute myocardial infarction. Am J
Cardiol. 1990;66:897–903.To assess whether
Doppler-derived mitral deceleration time (DT) may predict left
ventricular (LV) dilation after acute myocardial infarction
(AMI), 51 patients (61±11 years; 6 women) with anterior AMI
successfully treated with direct angioplasty underwent 2-dimensional
and Doppler echocardiographic examinations within
24 hours of admission at days 3, 7, and 30 and 6 months after AMI.
Patients were divided according to the DT duration assessed at day 3 in
2 groups: group 1 (n=33) with DT >130 ms and group 2 (n=18) with DT
130 ms. LV volume indexes were similar in both groups at baseline.
From day 3 on, LV volume indexes progressively increased in group 2 and
were significantly larger than those of patients of group 1 at each
study point in time. By stepwise multiple regression analysis,
DT was the best predictor of end-diastolic volume index
changes at 6 months (P=0.02). Thus DT may predict LV
remodeling after reperfused AMI.[Medline]
[Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  R Mizuno, S Fujimoto, Y Saito, and S Nakamura Depressed recovery of subendocardial perfusion in persistent heart failure after complete revascularisation in diabetic patients with hibernating myocardium Heart, May 1, 2009; 95(10): 830 - 834. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Remmelink, K. D. Sjauw, J. P.S. Henriques, M. M. Vis, R. J. van der Schaaf, K. T. Koch, J. G.P. Tijssen, R. J. de Winter, J. J. Piek, and J. Baan Jr Acute left ventricular dynamic effects of primary percutaneous coronary intervention from occlusion to reperfusion. J. Am. Coll. Cardiol., April 28, 2009; 53(17): 1498 - 1502. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Meta-Analysis Research Group in Echocardiography ( Independent Prognostic Importance of a Restrictive Left Ventricular Filling Pattern After Myocardial Infarction: An Individual Patient Meta-Analysis: Meta-Analysis Research Group in Echocardiography Acute Myocardial Infarction Circulation, May 20, 2008; 117(20): 2591 - 2598. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Strand, S.E. Kjeldsen, H. Gudmundsdottir, I. Os, G. Smith, and R. Bjornerheim Tissue Doppler imaging describes diastolic function in men prone to develop hypertension over twenty years Eur J Echocardiogr, January 1, 2008; 9(1): 34 - 39. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Sestili, C. Coletta, V. Manno, S. Perna, M. Renzi, P. Romano, R. Ricci, and V. Ceci Restrictive mitral inflow pattern is a strong independent predictor of lack of viable myocardium after a first acute myocardial infarction Eur J Echocardiogr, October 1, 2007; 8(5): 332 - 440. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. E. Moller, P. A. Pellikka, G. S. Hillis, and J. K. Oh Prognostic Importance of Diastolic Function and Filling Pressure in Patients With Acute Myocardial Infarction Circulation, August 1, 2006; 114(5): 438 - 444. [Full Text] [PDF]
|
|
|
|
 |
|
 G. Parodi, N. Carrabba, G. M. Santoro, G. Memisha, R. Valenti, P. Buonamici, E. V. Dovellini, and D. Antoniucci Heart Failure and Left Ventricular Remodeling After Reperfused Acute Myocardial Infarction in Patients With Hypertension Hypertension, April 1, 2006; 47(4): 706 - 710. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Carrabba, R. Valenti, G. Parodi, G. M. Santoro, and D. Antoniucci Left Ventricular Remodeling and Heart Failure in Diabetic Patients Treated With Primary Angioplasty for Acute Myocardial Infarction Circulation, October 5, 2004; 110(14): 1974 - 1979. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. F. Azevedo, L. C. Amado, D. L. Kraitchman, B. L. Gerber, N. F. Osman, C. E. Rochitte, T. Edvardsen, and J. A.C. Lima Persistent diastolic dysfunction despite complete systolic functional recovery after reperfused acute myocardial infarction demonstrated by tagged magnetic resonance imaging Eur. Heart J., August 2, 2004; 25(16): 1419 - 1427. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. L. Temporelli, P. Giannuzzi, G. L. Nicolosi, R. Latini, M. G. Franzosi, F. Gentile, L. Tavazzi, A. P. Maggioni, and GISSI-3 Echo Substudy Investigators Doppler-derived mitral deceleration time as a strong prognostic marker of left ventricular remodeling and survival after acute myocardial infarction: Results of the GISSI-3 Echo substudy J. Am. Coll. Cardiol., May 5, 2004; 43(9): 1646 - 1653. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. F.J Mannaerts, J. A van der Heide, O. Kamp, M. G Stoel, J. Twisk, and C. A Visser Early identification of left ventricular remodelling after myocardial infarction, assessed by transthoracic 3D echocardiography Eur. Heart J., April 2, 2004; 25(8): 680 - 687. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Bolognese, N. Carrabba, G. Parodi, G. M. Santoro, P. Buonamici, G. Cerisano, and D. Antoniucci Impact of Microvascular Dysfunction on Left Ventricular Remodeling and Long-Term Clinical Outcome After Primary Coronary Angioplasty for Acute Myocardial Infarction Circulation, March 9, 2004; 109(9): 1121 - 1126. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Hole, C. Hall, and T. Skjaerpe N-terminal proatrial natriuretic peptide predicts two-year remodelling in patients with acute transmural myocardial infarction Eur. Heart J., March 1, 2004; 25(5): 416 - 423. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. S. Hillis, J. E. Moller, P. A. Pellikka, B. J. Gersh, R. S. Wright, S. R. Ommen, G. S. Reeder, and J. K. Oh Noninvasive estimation of left ventricular filling pressure by e/e' is a powerful predictor of survival after acute myocardial infarction J. Am. Coll. Cardiol., February 4, 2004; 43(3): 360 - 367. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C Coletta, A Sestili, F Seccareccia, R Rambaldi, R Ricci, A Galati, R Bigi, N Aspromonte, M Renzi, and V Ceci Influence of contractile reserve and inducible ischaemia on left ventricular remodelling after acute myocardial infarction Heart, October 1, 2003; 89(10): 1138 - 1143. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. E. Moller, G. S. Hillis, J. K. Oh, J. B. Seward, G. S. Reeder, R. S. Wright, S. W. Park, K. R. Bailey, and P. A. Pellikka Left Atrial Volume: A Powerful Predictor of Survival After Acute Myocardial Infarction Circulation, May 6, 2003; 107(17): 2207 - 2212. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Fischer, A. Baessler, H.W. Hense, C. Hengstenberg, M. Muscholl, S. Holmer, A. Doring, U. Broeckel, G. Riegger, and H. Schunkert Prevalence of left ventricular diastolic dysfunction in the community: Results from a Doppler echocardiographic-based survey of a population sample Eur. Heart J., February 2, 2003; 24(4): 320 - 328. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Bolognese, A. N. Neskovic, G. Parodi, G. Cerisano, P. Buonamici, G. M. Santoro, and D. Antoniucci Left Ventricular Remodeling After Primary Coronary Angioplasty: Patterns of Left Ventricular Dilation and Long-Term Prognostic Implications Circulation, October 29, 2002; 106(18): 2351 - 2357. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. C Greaves Role of echocardiography in acute coronary syndromes Heart, October 1, 2002; 88(4): 419 - 425. [Full Text] [PDF]
|
|
|
|
|
|
G. A. Whalley, R. N. Doughty, G. D. Gamble, S. P. Wright, H. J. Walsh, S. A. Muncaster, and N. Sharpe Pseudonormal mitral filling pattern predicts hospital re-admission in patients with congestive heart failure J. Am. Coll. Cardiol., June 5, 2002; 39(11): 1787 - 1795. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S H Poulsen, S E Jensen, J E Moller, and K Egstrup Prognostic value of left ventricular diastolic function and association with heart rate variability after a first acute myocardial infarction Heart, October 1, 2001; 86(4): 376 - 380. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Cerisano, L. Bolognese, P. Buonamici, R. Valenti, N. Carrabba, E. V. Dovellini, P. D. Pucci, G. M. Santoro, and D. Antoniucci Prognostic implications of restrictive left ventricular filling in reperfused anterior acute myocardial infarction J. Am. Coll. Cardiol., March 1, 2001; 37(3): 793 - 799. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. E. Moller, E. Sondergaard, S. H. Poulsen, and K. Egstrup Pseudonormal and restrictive filling patterns predict left ventricular dilation and cardiac death after a first myocardial infarction: a serial color M-mode doppler echocardiographic study J. Am. Coll. Cardiol., November 15, 2000; 36(6): 1841 - 1846. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||