| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Institute for Surgical Research and Department of Cardiology, Rikshospitalet, Oslo, N-0027 Norway
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Acute myocardial ischemia
has been associated with abnormal filling patterns in the left
ventricular (LV) apex. We hypothesized that this may in part be due to
postsystolic shortening of ischemic apical segments, which
leads to reversal of early diastolic apical flow. Fourteen open-chest
anesthetized dogs were instrumented with micromanometers in the LV apex
and left atrium and myocardial sonomicrometers in the anterior apical
LV wall. Intraventricular filling by color Doppler and wall motion by
strain Doppler echocardiography (SDE) were assessed from an apical
view. Measurements were taken before and after 5 min of left anterior
descending coronary artery (LAD) occlusion. In four dogs, we measured
the pressure difference between the LV apex and outflow tract. At
baseline, peak early diastolic flow velocities in the distal one-third
of the LV were directed toward apex (9.2 ± 1.6 cm/s). After LAD
occlusion, the velocities reversed (
2.3 ± 0.4 cm/s,
P < 0.01), indicating that blood was ejected from the
apex toward the base during early filling. This interpretation was
confirmed by wall motion analysis, which showed postsystolic shortening
of apical myocardial segments. The postsystolic shortening represented
9.7 ± 1.7% (P < 0.01) and 14.2 ± 2.4%
(P < 0.01) of end-diastolic segment length by SDE and
sonomicrometry, respectively. Consistent with the velocity changes, we
found reversal of the early diastolic pressure gradient from the LV
apex to outflow tract. In the present model, acute LAD occlusion
resulted in reversal of early diastolic apical flow, and this was
attributed to postsystolic shortening of dyskinetic apical segments.
The clinical diagnostic importance of this finding remains to be determined.
strain-Doppler echocardiography; two-dimensional color Doppler; myocardial ischemia; diastolic filling
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
ASSESSMENT OF LEFT VENTRICULAR (LV) intracavitary filling by Doppler echocardiography is one of several noninvasive approaches for studying LV diastolic function. In the normal LV, the initial intraventricular filling wave propagates rapidly toward the apex, and, as demonstrated by color M-mode Doppler, there is near simultaneous onset of filling velocities along the entire LV inflow tract (7). However, in patients with reduced LV ejection fraction or impaired diastolic function, the early diastolic apical filling may be markedly delayed, and this can be measured as slowing of mitral-to-apical flow propagation (1, 13). This has been attributed to a decrease in rate of LV relaxation, which causes a decrease in the driving pressure for mitral-to-apical flow (1, 12, 13), to loss of "apical suction" (12), and enhanced vortex formations due to changes in LV and mitral valve geometry (10).
There is, however, very limited insight into how regional wall motion interacts with intraventricular flow. A common finding in ischemic myocardium is postsystolic (postejection) shortening and consequently delayed onset of diastolic lengthening (8, 16, 17). Therefore, in the ischemic ventricle, there may be substantial regional asynchrony in the onset of myocardial diastolic lengthening, and this in turn may have an impact on intraventricular flow. The paucity of data regarding interactions between regional function and intraventricular filling reflects the limited ability of current imaging modalities to quantify regional myocardial function throughout the different phases of the cardiac cycle. We have recently demonstrated that strain Doppler echocardiography (SDE) represents a noninvasive method to quantify regional function (18). In this regard, SDE appears superior to conventional tissue Doppler imaging, which is strongly influenced by function in neighboring segments and translational effects. Therefore, SDE in combination with color flow imaging may represent a method to study interactions between intraventricular flow and regional wall motion.
The present study was designed to investigate how wall motion abnormalities in the ischemic myocardium interact with intracavitary filling, and the main objective was to determine if postsystolic shortening of ischemic apical segments may lead to a reversal of early diastolic apical flow. The study was done in a dog model, and sonomicrometry was used as a reference method for regional myocardial function.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Fourteen dogs of either sex and an average body weight of 21.2 kg were given thiopentone (25 mg/kg body wt) and morphine (100 mg) intravenously, followed by an infusion of morphine (50-100 mg/h iv) and pentobarbital (50 mg iv) every hour. The animals were artificially ventilated through a cuffed endotracheal tube using room air with 20-50% oxygen. A limb lead was monitored. After a median sternotomy, the pericardium was split from the apex to base, and the edges of the pericardial incision were loosely resutured. Inflatable vascular occluders were placed around the proximal one-third of the left anterior descending coronary artery (LAD). The dog was placed in the right supine position during recordings. The study was approved by the National Animal Experimentation Board.
Pressure Measurements
Via a carotid artery with fluoroscopic guidance, we placed a 5-Fr micromanometer-tipped catheter (model MPC-500, Millar Instruments; Houston, TX) in the LV apical region. Via the appendage, a 5-Fr micromanometer and a fluid-filled catheter were placed in the left atrium (LA). In four dogs, another 5-Fr catheter was positioned in the LV outflow tract just proximal to the aortic valve. All pressure transducers were calibrated with a mercury manometer. The pressures were zero referenced against the fluid-filled LA catheter. Pressure and ECG data were processed via preamplifiers and digitized at 200 Hz for further analysis on a personal computer station.Sonomicrometry
One pair of ultrasonic crystals was implanted in the inner one-half of the myocardium in the anterior LV wall near the apex, aligned parallel with the LV long axis. In four dogs, another pair of crystals was implanted in a nonischemic region in the anterolateral wall near the base, in the perfusion territory of the left circumflex artery. The crystals were connected to a sonomicrometer (Triton Technology; San Diego, CA, or Sonometrics; London, Ontario, Canada).Strain Doppler Echocardiography
The method has previously been described in detail (18). With the use of a combined tissue imaging (3.5 MHz) and Doppler (2.75 MHz) transducer (GE Vingmed Ultrasound; Horten, Norway), we recorded images from an apical view with a frame rate varying from 65 to 106 (mean value 88 frames/s). Strain rate was calculated as the Doppler velocity gradient between two points with a distance of 8 mm, and strain was calculated as the time integral of strain rate (18). An experimental application programmed in Visual C++ (Microsoft; Redmond, WA) was used to extract strain along an M-mode line that was oriented in the direction from apex to base.Two-Dimensional Color Doppler Echocardiography
Both two-dimensional (2-D) color and SDE were recorded from a modified apical two-chamber view by orienting the 2-D image planes through the regions in which we had inserted the segment length crystals, i.e., the anterolateral wall near the apex.The low-velocity filter was set in the range of 1-4 cm/s with a frame rate varying from 38 to 90 (mean value 58 frames/s). The digital color velocity data were transferred to an external computer (Macintosh, Apple Computer) and analyzed with the use of a dedicated analysis program (Echopac, GE Vingmed Ultrasound).
Experimental Protocol
Recordings were first taken at baseline. We then inflated the LAD occluder for a median of 5 min and did recordings during ischemia. Because of interference, sonomicrometry and Doppler echocardiography could not be measured simultaneously. At baseline and during ischemia, we first recorded pressures, ECG and Doppler flow velocities during 10 s and then pressures, and ECG and myocardial segment length during the subsequent 10 s. Because it was not feasible to measure 2-D color flow and strain by Doppler simultaneously, we did the strain Doppler recordings close (within 2 min) to the color flow measurements.At the end of each recording, we induced ventricular extrasystoles and used long diastoles after premature contractions to adjust absolute pressure levels for the micromanometers. Data were recorded with the respirator off and digitized at 200 samples/s. In four dogs, contrast was injected rapidly into the LA before and during LAD occlusion, and 2-D echocardiographic images were recorded immediately after the injection.
Calculations
Pressure-derived variables.
We calculated LV peak systolic pressure, LV end-diastolic pressure, and
the time derivative of LV pressure (dP/dt). The time course
of the fall in LV pressure from peak dP/dt to 5 mmHg above end-diastolic pressure was characterized by the time constant (
) of
an assumed exponential decay to zero pressure (19). For definition of end diastole and end systole, we used the peak R wave of
the ECG and peak LV dP/dt, respectively. We calculated the
time from end diastole to the first diastolic crossover of LV and LA
pressures (onset of transmitral filling). In four dogs, we also
calculated the difference between LV apical and LV outflow tract pressures.
Sonomicrometry-derived variables.
We calculated the following variables: peak systolic shortening [as
the percent change in length (%
L)], as
|
![<IT>÷</IT>(end-diastolic length)]<IT>×</IT>100](/content/vol284/issue6/fulltext/H2343/img002.gif)
|
L), as
|
![ischemic segment)<IT>/</IT>(end-diastolic length)]<IT>×</IT>100](/content/vol284/issue6/fulltext/H2343/img004.gif)
|
L), as
|
![<IT>÷</IT>(end-diastolic length)]<IT>×</IT>100](/content/vol284/issue6/fulltext/H2343/img006.gif)
|
Doppler-derived variables. Doppler measurements of shortening strains were represented by negative values and lengthening strains by positive values. However, to simplify comparison with sonomicrometry, we report strain values in terms of percent shortening: peak systolic shortening and lengthening were calculated as a percentage of end-diastolic dimensions. Postsystolic shortening was calculated as segment shortening after end systole, as a percentage of end-diastolic dimension.
Flow velocities by 2-D color Doppler were recorded along the mitral-to-apical axis. We measured peak intraventricular velocities in the distal one-third of the LV at the time of the first diastolic crossover of LV and LA pressures.Statistical Analysis
Data are presented as means ± SE. Statistical analysis was performed with Student's t-test for paired data. For all statistical comparisons, P < 0.05 was considered significant.| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Hemodynamic variables before and during ischemia
are presented in Table 1 and Fig. 1. Peak
systolic shortening by sonomicrometry and
SDE decreased from 12.5 ± 2.4% to 12.5 ± 2.2%
(P < 0.01) and from 12.6 ± 1.7% to 9.5 ± 1.1% (P < 0.01), respectively, indicating
dyskinesis.
|
|
Figure 2 demonstrates marked changes in
intraventricular filling after LAD occlusion. During baseline, the
early diastolic filling wave by 2-D color Doppler propagated rapidly
towards the apex, as indicated by the uniformly red color throughout
the LV cavity. During LAD occlusion, however, all experiments showed reversal of early diastolic flow in the apex, i.e., the early diastolic
velocities were directed from the apex toward the base. The reversed
apical velocities are represented by the blue-colored area in Fig. 2,
bottom left. To quantify this change in filling, we measured
peak velocities in the distal one-third of the LV at the onset of
transmitral filling, defined as the time of first diastolic crossover
of LV and LA pressures. The peak velocity decreased from 9.2 ± 1.6 cm/s at baseline to 2.3 ± 0.4 cm/s (P < 0.01) during LAD occlusion. The 2-D color pattern suggested that the
transmitral filling wave propagated only a short distance into the LV
and then was redirected toward the LV outflow tract, where it appeared
to rotate in a large vortex. These interpretations were confirmed by
observations with contrast that was injected into the LA (Fig. 2).
Before ischemia, the contrast propagated rapidly toward the
apex and filled the entire LV cavity immediately after the onset of
transmitral filling. During LAD occlusion, the contrast moved toward
the midportion of the LV cavity and then rotated toward the LV outflow
tract, whereas the apex remained free of contrast. Later in diastole,
the contrast moved toward the apex as part of a macrovortex.
|
The reversed apical flow during early LV filling was associated with
postsystolic shortening of the ischemic apical segment (Fig.
1B). Postsystolic shortening by sonomicrometry and SDE
changed from 1.3 ± 0.4% and 0.8 ± 0.4%, respectively, to
14.2 ± 2.4 (P < 0.01) and 9.7 ± 1.7%
(P < 0.01) during LAD occlusion. Figure 1 also
demonstrates the temporal relationships between myocardial segmental
motion and transmitral driving pressure. During LAD occlusion, the
ischemic segment was shortening at the time of LA and LV
pressure crossover, and, as demonstrated in Fig.
3, the postsystolic shortening continued
while the nonischemic segment was lengthening. The
ischemic segment continued to shorten 47 ± 8 and 65 ± 16 ms after the onset of filling by sonomicrometry and SDE,
respectively. The time constant of LV relaxation () increased from
47 ± 4 to 64 ± 7 ms during ischemia
(P < 0.01).
|
Figure 4 displays the intraventricular
pressure gradients as calculated between the apex and LV outflow tract.
During LV ejection, the pressure gradient was directed from the apex
toward the LV outflow tract, and there was a small reversal of the
pressure gradient in late systole. The systolic pressure gradient
decreased after LAD occlusion. During most of the isovolumic relaxation period and during early transmitral filling, the pressure gradient at
baseline was directed toward the apex (peak value 1.1 ± 0.3 mmHg). During LAD occlusion, however, the gradient was reversed during
most of the isovolumic relaxation period (peak value 1.2 ± 0.3 mmHg), consistent with the observed reversal of early diastolic apical
flow velocities. The time from onset of late systolic shortening of the
ischemic segment by sonomicrometry to the peak early diastolic apex-to-outflow tract pressure gradient was 25 ± 3 ms.
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Slowing of mitral-to-apical flow propagation has been observed in patients with acute myocardial ischemia in different clinical settings (11, 13) and has been reproduced in experimental models (1, 12, 13). The etiology of the impaired apical filling is unclear, but several mechanisms have been proposed (10, 12-14). In the present study, we demonstrated that postsystolic shortening of the ischemic myocardium has a profound effect on intraventricular flow. The postsystolic shortening resulted in early diastolic ejection of blood from the apex toward the base, which resulted in markedly disturbed flow at the base of the ventricle, where flow from the apex encountered the transmitral filling wave. The postsystolic shortening was demonstrated by SDE and was confirmed by sonomicrometry. The present study therefore demonstrates the ability of Doppler echocardiography to quantify interactions between intraventricular flow and regional LV wall motion.
Stugaard et al. (13) reported delayed apical filling by color M-mode Doppler during LAD occlusion. In their study, no early diastolic apical flow was reported. This may be due to their velocity filter setting (12 cm/s), which was above the range of reversed apical velocities measured in the present study. The reversed velocities are very low, so the filter setting is critical to capture these velocities. Edvardsen et al. (2) reported reversed flow during the isovolumetric relaxation period in patients with anterior wall infarction. The velocity filter in that study was between 4 and 8 cm/s.
Mechanisms of Delayed Early Diastolic Mitral-to-Apical Flow Propagation
Currently, we have very limited insight into how LV intracavitary flow relates to myocardial properties. This is in part a consequence of the complex geometry of the ventricle and the continuous change in elastic properties of the myocardium throughout the cardiac cycle, which leads to very complex flow patterns. Furthermore, current imaging methods do not provide full visualization of the three-dimensional pattern that composes LV intracavitary flow. Nikolic et al. (6) have shown that regional deformation of the LV, even during the isovolumetric relaxation period, lead to intraventricular pressure gradients and intraventricular flows. As demonstrated by Greenberg et al. (4), intraventricular pressure gradients can even be assessed by color Doppler echocardiography. In 2-D models of nonischemic ventricles, it appears that the intraventricular flow field is represented by a number of vortexes that expand in a circular fashion from the mitral tip region (20). However, during the early phase of filling, while transmitral flow is accelerating, the dominant flow vectors are directed toward the apex (7). This is demonstrated by the 2-D color flow image shown in Fig. 2, which from an apical view shows uniformly red-encoded velocities throughout the ventricle. During this early phase of filling, the propagation velocity of mitral-to-apical flow can be measured by color M-mode Doppler and has been proposed as a measure of diastolic function (1, 3, 4, 13). Experimental data suggest that slowing of flow propagation is in part due to slowing of myocardial relaxation, which leads to a decrease in the mitral-to-apical pressure gradient (12). It also appears that enhanced vortex formation in the diseased ventricle may contribute to slowing of flow propagation as measured by color M-mode Doppler (10). The present study clearly demonstrates that postsystolic shortening of apical myocardial segments may contribute to the impairment of apical filling that is observed during acute ischemia. These different mechanisms are probably related.As demonstrated by sonomicrometry, the ejection of blood from the ischemic apical region started during isovolumic relaxation and persisted for some time after the onset of transmitral filling. Therefore, lengthening of the nonischemic segment (Fig. 3) during early filling may be ascribed not only to transmitral flow but also to redistribution of blood caused by postsystolic shortening. Blood that was ejected from the ischemic segment during early diastole encountered the transmitral jet, which was hindered from propagating toward the apex. As suggested by 2-D color flow and echocontrast, the transmitral flow appeared to propagate only a short distance in the ventricle and then formed macrovortexes that rotated toward the LV outflow tract.
The observed reversal of the intraventricular pressure gradient during ischemia supported the interpretation that postsystolic shortening caused early diastolic ejection of blood from the apical region. At baseline, the pressure gradient during isovolumic relaxation and early filling was directed from the base toward the apex, and intraventricular flow velocities by color flow imaging were directed toward the apex. During LAD occlusion, the pressure gradient during isovolumetric relaxation reversed and was directed toward the base, along with reversal of flow velocities. During ischemia, there was a small time delay of ~25 ms between the onset of late systolic segmental shortening and the peak apex-to-outflow tract pressure gradient, which is consistent with the notion that the gradient is caused by the segmental shortening.
Yellin et al. (20) described intraventricular vortexes that occurred during LV filling due to shear between blood and mitral leaflet surface. The flow reversal described in the present study, however, started during isovolumic relaxation and therefore cannot be attributed to a similar mechanism.
Apical Flow Reversal: Diagnostic Implications
The mechanisms of postsystolic shortening were investigated by Skulstad et al. (9), and it was found that postsystolic shortening was a relatively nonspecific feature of the ischemic myocardium. It could occur in severely ischemic myocardium by an entirely passive process, then representing passive recoil of dyskinetic segments. Postsystolic shortening also occurred in moderately ischemic myocardium and was in part due to delayed active contraction, although passive components did contribute.The present study suggests that color flow imaging may be helpful as an additional diagnostic tool for identifying regions with suspected postsystolic shortening. The finding of early diastolic velocities that are directed from the apex toward the LV base is consistent with postsystolic shortening. Therefore, the two methods are complementary, and their combined use could increase the diagnostic power of echocardiography in the assessment of regional myocardial function. The clinical potential of this approach remains to be investigated.
Limitations
The present animal model differs from a clinical setting in many regards, in particular due to the thoracotomy, the extensive instrumentation, and the use of general anesthesia. However, the regional myocardial responses to coronary occlusion in terms of segmental function should be relatively similar. Therefore, we believe the principal findings of this study may be valid for a clinical situation. This, of course, should be tested in a population with acute myocardial infarction.One significant limitation of SDE is a strong angle dependency (18). In the present study with open-chest animals, we could easily optimize transducer position and therefore minimized this problem. In a clinical setting, however, the problem of angle dependency of the echobeam relative to myocardial fiber orientation may be significant, in particular when studying apical segments.
The present study was limited to short-term ischemia. Potentially, with ischemia of longer duration, resulting in tissue necrosis and stiffening of the myocardium, one might see less passive systolic distension and subsequently less marked postsystolic shortening (5). This in turn may reduce the early diastolic flow reversal.
In conclusion, in the present experimental study, we demonstrated that delayed early diastolic LV apical filling during LAD occlusion may be due to postsystolic shortening of ischemic segments. During isovolumic relaxation and during the early phase of transmitral filling, blood was ejected from the apical region and redistributed toward the basal portions of the cavity. This implies that, in addition to global factors such as the rate of LV relaxation and ventricular geometry, one should consider asynchronous wall motion, and in particular postsystolic shortening, as a mechanism of disturbed intraventricular flow. Potentially, the use of color flow imaging along with SDE may represent a clinical tool for studying interactions between regional function and intraventricular flow. This combined imaging might increase the diagnostic power of echocardiography in the assessment of myocardial function.
| |
ACKNOWLEDGEMENTS |
|---|
S. Urheim, T. Edvardsen, and H. Skulstad were and E. Lyseggen is a recipient of a research fellowship from the Norwegian Council on Cardiovascular Diseases.
| |
FOOTNOTES |
|---|
Address for reprint requests and other correspondence: O. A. Smiseth, Dept. of Cardiology, Rikshospitalet Univ. Hospital, N-0027 Oslo, Norway (E-mail: Otto.Smiseth{at}rikshospitalet.no).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
First published February 6, 2003;10.1152/ajpheart.00320.2002
Received 22 April 2002; accepted in final form 28 January 2003.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Brun, P,
Tribouilloy C,
Duval AM,
Iserin L,
Meguira A,
Pelle G,
and
Dubois-Rande JL.
Left ventricular flow propagation during early filling is related to wall relaxation: a color M-mode Doppler analysis.
J Am Coll Cardiol
20:
420-432,
1992[Abstract].
2.
Edvardsen, T,
Rodevand O,
Aakhus S,
Bjornerheim R,
and
Ihlen H.
Reversal of intraventricular flow propagation during isovolumic relaxation: a marker of anterior wall dysfunction.
J Am Soc Echocardiogr
12:
801-810,
1999[Web of Science][Medline].
3.
Garcia, MJ,
Smedira NG,
Greenberg NL,
Main M,
Firstenberg MS,
Odabashian J,
and
Thomas JD.
Color M-mode Doppler flow propagation velocity is a preload insensitive index of left ventricular relaxation: animal and human validation.
J Am Coll Cardiol
35:
201-208,
2000
4.
Greenberg, NL,
Vandervoort PM,
Firstenberg MS,
Garcia MJ,
and
Thomas JD.
Estimation of diastolic intraventricular pressure gradients by Doppler M-mode echocardiography.
Am J Physiol Heart Circ Physiol
280:
H2507-H2515,
2001
5.
Lyseggen, E,
Skulstad H,
Urheim S,
Rabben SI,
Stugaard M,
and
Smiseth OA.
Myocardial elasticity by strain Doppler echocardiography-a method to identify viable myocardium (Abstract).
Eur Heart J
23, Suppl:
399,
2002
6.
Nikolic, SD,
Feneley MP,
Pajaro OE,
Rankin JS,
and
Yellin EL.
Origin of regional pressure gradients in the left ventricle during early diastole.
Am J Physiol Heart Circ Physiol
268:
H550-H557,
1995
7.
Rodevand, O,
Bjornerheim R,
Edvardsen T,
Smiseth OA,
and
Ihlen H.
Diastolic flow pattern in the normal left ventricle.
J Am Soc Echocardiogr
12:
500-507,
1999[Web of Science][Medline].
8.
Ross, J, Jr,
and
Franklin D.
Analysis of regional myocardial function, dimensions, and wall thickness in the characterization of myocardial ischemia and infarction.
Circulation
53:
I88-I92,
1976.
9.
Skulstad, H,
Edvardsen T,
Urheim S,
Rabben SI,
Stugaard M,
Lyseggen E,
Ihlen H,
and
Smiseth OA.
Postsystolic shortening in ischemic myocardium: active contraction or passive recoil?
Circulation
106:
718-724,
2002
10.
Steen, T,
and
Steen S.
Filling of a model left ventricle studied by colour M mode Doppler.
Cardiovasc Res
28:
1821-1827,
1994
11.
Steine, K,
Flogstad T,
Stugaard M,
and
Smiseth OA.
Early diastolic intraventricular filling pattern in acute myocardial infarction by color M-mode Doppler echocardiography.
J Am Soc Echocardiogr
11:
119-125,
1998[Web of Science][Medline].
12.
Steine, K,
Stugaard M,
and
Smiseth OA.
Mechanisms of retarded apical filling in acute ischemic left ventricular failure.
Circulation
99:
2048-2054,
1999
13.
Stugaard, M,
Smiseth OA,
Risoe C,
and
Ihlen H.
Intraventricular early diastolic filling during acute myocardial ischemia, assessment by multigated color m-mode Doppler echocardiography.
Circulation
88:
2705-2713,
1993
14.
Takatsuji, H,
Mikami T,
Urasawa K,
Teranishi J,
Onozuka H,
Takagi C,
Makita Y,
Matsuo H,
Kusuoka H,
and
Kitabatake A.
A new approach for evaluation of left ventricular diastolic function: spatial and temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography.
J Am Coll Cardiol
27:
365-371,
1996[Abstract].
15.
Takayama, M,
Norris RM,
Brown MA,
Armiger LC,
Rivers JT,
and
White HD.
Postsystolic shortening of acutely ischemic canine myocardium predicts early and late recovery of function after coronary artery reperfusion.
Circulation
78:
994-1007,
1988
16.
Theroux, P,
Ross J, Jr,
Franklin D,
Kemper WS,
and
Sasyama S.
Regional myocardial function in the conscious dog during acute coronary occlusion and responses to morphine, propranolol, nitroglycerin, and lidocaine.
Circulation
53:
302-314,
1976
17.
Tyberg, JV,
Forrester JS,
Wyatt HL,
Goldner SJ,
Parmley WW,
and
Swan HJ.
An analysis of segmental ischemic dysfunction utilizing the pressure-length loop.
Circulation
49:
748-754,
1974
18.
Urheim, S,
Edvardsen T,
Torp H,
Angelsen B,
and
Smiseth OA.
Myocardial strain by Doppler echocardiography. Validation of a new method to quantify regional myocardial function.
Circulation
102:
1158-1164,
2000
19.
Weiss, JL,
Frederiksen JW,
and
Weisfeldt ML.
Hemodynamic determinants of the time-course of fall in canine left ventricular pressure.
J Clin Invest
58:
751-760,
1976[Web of Science][Medline].
20.
Yellin, EL,
Peskin C,
Yoran C,
Koenigsberg M,
Matsumoto M,
Laniado S,
McQueen D,
Shore D,
and
Frater RW.
Mechanisms of mitral valve motion during diastole.
Am J Physiol Heart Circ Physiol
241:
H389-H400,
1981
This article has been cited by other articles:
|
|
 |
|
  E. Lyseggen, T. Vartdal, E. W. Remme, T. Helle-Valle, E. Pettersen, A. Opdahl, T. Edvardsen, and O. A. Smiseth A novel echocardiographic marker of end systole in the ischemic left ventricle: "tug of war" sign Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H645 - H654. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Ganame, R. H. Pignatelli, B. W. Eidem, P. Claus, J. D'hooge, C. J. McMahon, G. Buyse, J. A. Towbin, N. A. Ayres, and L. Mertens Myocardial deformation abnormalities in paediatric hypertrophic cardiomyopathy: are all aetiologies identical? Eur J Echocardiogr, November 1, 2008; 9(6): 784 - 790. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Bijnens, P. Claus, F. Weidemann, J. Strotmann, and G. R. Sutherland Investigating Cardiac Function Using Motion and Deformation Analysis in the Setting of Coronary Artery Disease Circulation, November 20, 2007; 116(21): 2453 - 2464. [Full Text] [PDF]
|
|
|
|
 |
|
 L. Lucats, B. Ghaleh, X. Monnet, P. Colin, A. Bize, and A. Berdeaux Conversion of post-systolic wall thickening into ejectional thickening by selective heart rate reduction during myocardial stunning Eur. Heart J., April 1, 2007; 28(7): 872 - 879. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. P. Sengupta, B. K. Khandheria, J. Korinek, J. Wang, A. Jahangir, J. B. Seward, and M. Belohlavek Apex-to-Base Dispersion in Regional Timing of Left Ventricular Shortening and Lengthening J. Am. Coll. Cardiol., January 3, 2006; 47(1): 163 - 172. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Edvardsen, O. Rodevand, K. Endresen, and H. Ihlen Interaction between left ventricular wall motion and intraventricular flow propagation in acute and chronic ischemia Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H732 - H737. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Carlhall, L. Wigstrom, E. Heiberg, M. Karlsson, A. F. Bolger, and E. Nylander Contribution of mitral annular excursion and shape dynamics to total left ventricular volume change Am J Physiol Heart Circ Physiol, October 1, 2004; 287(4): H1836 - H1841. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. M. Zwanenburg, M. J. W. Gotte, J. P. A. Kuijer, R. M. Heethaar, A. C. van Rossum, and J. T. Marcus Timing of cardiac contraction in humans mapped by high-temporal-resolution MRI tagging: early onset and late peak of shortening in lateral wall Am J Physiol Heart Circ Physiol, May 1, 2004; 286(5): H1872 - H1880. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
