(Circulation. 1999;99:2048-2054.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Mechanisms of Retarded Apical Filling in Acute Ischemic Left Ventricular Failure
From the Institute for Surgical Research, Rikshospitalet, Oslo, and Medical Department, Aker University Hospital, University of Oslo, Norway.
Correspondence to Prof Otto A. Smiseth, Institute for Surgical Research, Rikshospitalet, N-0027 Oslo, Norway. E-mail o.a.smiseth{at}rh.uio.no
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Abstract |
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Background—We examined the hypothesis that retardation of apical filling as measured by color M-mode Doppler echocardiography in the diseased left ventricle (LV) reflects a decrease in the intraventricular mitral-to-apical pressure gradient.
Methods and Results—In 9 open-chest anesthetized dogs,
micromanometers were placed near the mitral tip and
in the apical region. From the color M-mode Doppler images, the
time delay (TD) between peak velocity at the mitral tip and the apical
region was determined as an index of LV flow propagation. Acute
ischemic LV failure was induced by coronary
microembolization. Induction of ischemia caused a marked
increase in LV end-diastolic pressure and a decrease in LV
ejection fraction. The time constant of LV isovolumic apical pressure
decay (
) increased from 31±8 to 49±16 ms
(P<0.001). The peak early diastolic
mitral-to-apical pressure gradient (
PLVmitral-apex)
decreased from 1.9±0.9 to 0.7±0.5 mm Hg
(P<0.01), and TD increased from 5±3 to 57±26 ms
(P<0.001). The slowing of flow propagation was limited
to the apical portion of the LV cavity. The TD correlated with
PLVmitral-apex (r=-0.94,
P<0.01) and with (r=0.92,
P<0.01). Before ischemia, the mitral-to-apical
flow propagation velocity far exceeded the velocity of the individual
blood cells, whereas during ischemia, flow propagation velocity
approximated the blood velocity.
Conclusions—Retardation of apical filling in acute ischemic failure was attributed to a decrease in the mitral-to-apical driving pressure, reflecting slowing of LV relaxation. The slowing of flow propagation appeared to represent a shift in apical filling from a pattern of column motion to a pattern dominated by convection.
Key Words: diastole • echocardiography • ischemia • heart failure • pressure
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Several clinical studies that used color M-mode Doppler echocardiography (CMD) have demonstrated marked disturbances of left ventricular (LV) intracavitary flow in acute myocardial ischemia and in ischemic and nonischemic cardiomyopathy.1 2 3 4 5 6 A consistent finding in the diseased ventricle has been retardation of early diastolic apical filling as measured by CMD.1 2 3 4 5 6 Furthermore, the impairment of apical filling in the ischemic and failing ventricle is associated with prolongation of the time constant of isovolumic pressure decay (
).1 2 3 4 Accordingly,
intraventricular flow propagation has been proposed
as a noninvasive method to assess LV relaxation.1 2 3 4 One
potential mechanism could be that slowing of relaxation leads to a
decrease in driving pressures for intraventricular
flow, and this in turn causes slowing of flow propagation. Nearly 2 decades ago, Ling et al7 described an early diastolic intraventricular pressure gradient between LV base and apex, probably representing the driving force for base-to-apical flow during early filling. More recently, Courtois et al8 demonstrated reduction of the base-to-apical pressure gradient after induction of acute ischemia in dogs. The present study was designed to test the hypothesis that retardation of early diastolic apical filling in acute myocardial ischemia reflects reduction of the intraventricular base-to-apical pressure gradient subsequent to impairment of LV relaxation.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Animal Preparation
Nine dogs of either sex weighing 18 to 30 kg (21.8±3.9 kg) were anesthetized by thiopental sodium 25 mg · kg-1 · body wt-1 and 100 mg of morphine IV, followed by infusion of morphine 50 to 100 mg/h IV and pentobarbital 50 mg IV every 1.5 hours. The animals were artificially ventilated through a cuffed endotracheal tube.
The chest was opened by a median sternotomy. After instrumentation, the edges of the pericardial incision were loosely resutured. A pacing lead was placed in the right ventricle and connected to an external pacemaker (Medtronic 5325). After the data collections were finished, the dogs were killed by an overdose of pentobarbital.
The protocol was approved by the ethical committee of the institution.
Instrumentation and Measurements
Pressure
A 7F fluid-filled catheter was placed in the aortic arch for
monitoring of aortic pressure. A micromanometer
(Konigsberg Instruments) was placed in the apex via a stab wound in the
apical dimple. A 5F micromanometer-tipped catheter
(model MPC-500, Millar Instruments) was introduced into the LV via a
pulmonary vein and placed near the mitral tip (Figure 1
). Another micromanometric catheter (7F)
with a fluid lumen (model SPC-471A, Millar) was inserted into the left
atrium (Figure 1).
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At the end of each recording, we induced extrasystoles by the right ventricular pacing catheter in the right ventricle. Long diastoles after premature contractions were used to adjust absolute pressure levels. By comparing the LV peak pressures during nonejecting premature contractions (ie, LV pressure rise with no rise in aortic pressure), we confirmed that the gain setting was similar for the 2 LV manometers.
Sonomicrometry
Three pairs of ultrasonic crystals were implanted in the
endocardium of the LV to measure the anterior-posterior (Dap),
septal-lateral (Dsl), and the base-apex (Dla) dimensions. The crystals
were connected to a sonomicrometer (Triton Technology
Inc).
Color M-Mode Doppler
Ultrasonic measurements were performed with a Vingmed CFM 700
cardiac scanner (Vingmed Sound). The cursor line was placed centrally
in the LV inflow tract, including both mitral and apical flow, and
velocities were measured along this line. The velocity filter was set
to 8 to 12 cm/s. The recorded velocity, time, and depth values were
digitized and transferred to an external computer (MacIntosh 11ci,
Apple Computer, Inc).
Experimental Protocol
Pressures, dimensions, and ECG were recorded by a Gould ES
2000, and the data were simultaneously digitized for later
analysis (CVSOFT, Odessa Computers). Recordings were
done with the dogs in the supine position at end expiration and with
the ventilator off. Pressures, ECG, and Doppler flow velocities
were recorded for 10 seconds, followed by pressures, ECG, and
dimensions during the subsequent 10 seconds. The recordings
were obtained first at baseline and then during acute ischemic
LV failure by repeated injections of plastic microspheres
(50 µm) according to the method of Smiseth and
Mjøs.9
Data Analysis
Pressures
From the LV apical pressure tracing
(PLVapex), the following pressures were
calculated: peak-systolic, end-diastolic, and the
maximum time derivative (dP/dtmax). We calculated
for both PLVapex and
PLVmitral using the derivative
method.10 R values for ln dP/dt versus pressure
for PLVmitral and PLVapex
were >0.97 in all the dogs at baseline and at LV failure. Left atrial
pressure (PLA) was measured at first diastolic crossover
with the 2 LV pressures. Transmitral and
intraventricular pressure differences were
calculated as PLA minus PLVmitral and
PLVmitral minus PLVapex,
respectively. For both LV pressures, we measured early
diastolic pressure nadirs and the time from LA/LV crossover
to pressure nadir.
Sonomicrometry
End-systolic and end-diastolic volumes were
calculated as a general ellipsoid by use of the equation,
volume=
/6xDapxDslxDla.11
Color M-Mode Doppler
Analyses were performed as described by Stugaard
et2 3 with the software program EchoDisp (Vingmed
Sound).
The CMD images were decoded into numerical values. Each pixel represented a velocity, averaged over a distance of 2.3 mm in the mitral-to-apical (depth) axis and 5 ms in the time (horizontal) axis. An algorithm was used to identify the peak velocity at the mitral tip level and in every second pixel (0.46 cm) toward the apical region. The time delay (TD) in milliseconds between occurrence of peak velocity at the mitral tip (first level) and the apical region (fifth level) was used as an index of early diastolic mitral-to-apical flow propagation.
As an estimate of the time for 1 blood cell to travel from the mitral tip to apex, we used the average of the peak velocities at all 5 levels along this distance.
Statistics
Data are presented as mean±SD. For comparisons of the
data, paired t test and ANOVA were performed. Regression
analyses were done according to Glantz and
Slinker12 with a multiple regression model, including
dummy variables to account for between-subject differences. The
level of significance was a value of P<0.05.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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LV Function Before and After Coronary Microembolization
Coronary microembolization caused a marked increase in LV end-diastolic apical pressure (EDP), from 7±3 to 17±4 mm Hg (P<0.001), and a decrease in LV ejection fraction from 0.35±0.06 to 0.23±0.05 (P<0.001). Stroke volume was maintained because of a compensatory increase in end-diastolic volume from 20±6 to 32±7 mL (P<0.001). There was a decrease in LV dP/dtmax from 2107±726 to 1182±486 mm Hg/s (P<0.01) and a downward and rightward shift of the end-systolic pressure-volume relationship (Figure 2
), consistent with substantial
depression of LV systolic function.
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The of PLVapex increased from 31±8 to 49±16
ms (P<0.01), whereas of PLVmitral
increased from 34±4 to 46±15 ms (P<0.05) after induction
of LV failure. Although tended to be shorter for
PLVapex than for PLVmitral,
the difference did not reach statistical significance during baseline
(P=0.08) or during LV failure (P=0.9) (Table 1).
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Timing of LV Filling by CMD
Before induction of LV failure, the CMD recordings showed
rapid and nearly simultaneous onset of
diastolic flow along the entire LV inflow tract, with peak
velocity almost at the same time in the apical and in the mitral
region. Accordingly, the TD between peak velocity at the mitral tip and
that in the apical region was small (Figure 3A and Table 2).
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After induction of LV failure, the onset of diastolic
apical flow became retarded, and the TD index increased from 5±3 to
57±26 ms (P<0.001) (Figure 4A and Table 2
). This flow
disturbance was predominantly an apical phenomenon, and the
retardation of filling was not seen at the measurement level 0.46 cm
distal to the mitral tip (Table 2). From the next measurement
level (0.92 cm), the TD increased progressively toward the apex (Table 2).
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During LV failure, peak early diastolic filling velocities in the apical region were reduced from 0.30±0.07 to 0.19±0.05 m/s (P<0.01), and at the mitral tip from 0.53±0.06 to 0.37±0.12 m/s (P<0.01). Averaged peak velocities at the 5 velocity levels from the mitral tip to apex decreased from 0.44±0.04 m/s at baseline to 0.29±0.9 m/s (P<0.01) during LV failure.
Intraventricular Pressure Gradients
Figure 3 shows simultaneous flow velocities and
intraventricular pressures before coronary
embolization in a representative experiment. During
onset of early diastolic mitral-to-apical flow,
PLVapex was falling at a faster rate than
PLVmitral, thereby establishing a pressure
gradient toward the apex. Note also that early diastolic
pressure nadir in the apex was lower (P<0.05) (Table 2 and Figure 3B) and occurred earlier
(P<0.001) than at the mitral tip (Table 2 and Figure 3B).
After coronary microembolization, the 2 pressure nadirs were
elevated to approximately the same level and nearly coincided (Table 2, Figure 4B). Thus, the
intraventricular mitral-to-apical peak pressure
gradient (PLVmitral-apex) was markedly
reduced, from 1.9±0.9 to 0.7±0.5 mm Hg (P<0.01)
(Table 2). There was a less marked decrease of the peak
transmitral pressure gradient
(PLA-PLVmitral), from 2.4±0.7 to
1.7±0.7 mm Hg (P<0.01) (Table 2).
Relationship Between Timing of Apical Filling,
Intraventricular Pressure Gradients, and LV
Function
As demonstrated in the upper panel of Figure 5, the TD index showed a negative
correlation with PLVmitral-apex
(r=0.94, P<0.01). This relationship tended to be
stronger after logarithmic transformation of the data
(r=-0.98, P<0.001) (Figure 5, lower
panel). There was a positive correlation between TD and
(r=0.92, P<0.01). TD also correlated strongly
with LV ejection fraction (r=-0.91, P<0.01) and
end-systolic volume (r=0.91, P<0.01).
There was no significant correlation between TD and PLA, heart rate, or
LV systolic pressure. PLVmitral-apex
correlated strongly with end-systolic volume
(r=-0.95, P<0.01) and (r=-0.84,
P<0.05).
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, n=9) and
during (
, n=7) ischemic LV failure (in 2 dogs, during
failure, pressure and velocity data were not recorded
simultaneously). Bottom, Same data after logarithmic
transformation. In 2 dogs, at baseline, TD=0 and therefore is not
included in log-transformed plot.
Figure 6 shows a
representative dog with simultaneous apical
velocities and pressures. Before ischemia, apical flow was
accelerating while apical pressure was falling. During ischemic
LV failure, however, apical flow was accelerating while apical pressure
was rising.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In the present study, retardation of apical filling during acute ischemic LV failure was associated with marked reduction of the intraventricular mitral-to-apical pressure gradient. There was a strong negative correlation between the intraventricular pressure gradient and
,
suggesting that the decrease in pressure gradient is due to slowing of
LV relaxation. The present data therefore suggest that retardation
of apical filling during ischemia may be causally related to
slowing of relaxation.
Mechanisms of Apical Flow Velocities
Although the present study demonstrates a significant
correlation between the mitral-to-apical pressure gradient and flow
propagation, the gradient in the nonischemic ventricle varied
widely, ie, between 1 and 3 mm Hg, with very little variation in
the TD index of flow propagation (Figure 5, upper panel). The
prolongation of TD was not evident until the pressure difference
dropped to <1 mm Hg, which occurred after induction of
ischemic LV failure. Therefore, there may not be a simple
linear relationship between the inflow tract pressure gradient and
Doppler indices of mitral-to-apical flow propagation. Logarithmic
transformation of the intraventricular pressure
gradients was consistent with this assumption (Figure 5, lower panel).
Analysis of the color Doppler images of LV filling suggests that the rapid onset of apical flow in the nonischemic ventricle and the retarded apical filling during ischemia reflect entirely different flow phenomena. In the nonischemic ventricle, onset of flow and peak velocities occurred nearly simultaneously along the entire LV inflow tract, with a short TD of 5±3 ms. Given a distance from the mitral tip to the apical level of 1.84 cm and a TD of 5 ms, the apparent flow propagation velocity would be 3.7 m/s. Peak velocity at the mitral tip, however, was 0.53±0.06 m/s, and even if this velocity had been maintained toward the apex, 1 blood cell would use 35 ms to propagate from the mitral tip to the apical level. Therefore, the short TD between peak velocities at the mitral tip and the apical region in the nonischemic ventricle cannot be attributed to convection or motion of the individual volume elements but could reflect the propagation velocity of the blood wave front. This nearly simultaneous onset of flow along the LV inflow tract resembles motion of an entire column of blood in the inflow tract. The latter interpretation is consistent with the conclusions of Steen and Steen13 from an in vitro model study that simulated LV filling.
During ischemic failure, there was rapid propagation of flow into the basal portion of the LV cavity, but in the apex, the early flow component was lost. Instead, apical filling occurred later in diastole, and peak apical velocities were seen when transmitral velocities approached zero. These observations are not consistent with column motion of blood in the apical region but rather most likely represent convection. This notion is supported by an additional analysis, which incorporated the flow velocities measured at 5 levels between the mitral tip and the apical region. This gives an estimate of the time for 1 blood cell to move from the mitral tip to apex. By this analysis, we calculated a mitral-to-apical propagation time of 63 ms, which compares well with the measured TD of 57±26 ms during failure. Therefore, in the present heart failure model, it appears that blood enters the LV as a column, but propagation of flow into the apical portion is slow and compatible with convection. In 2 additional dogs, we did supplementary measurements with high-frame-rate 2-dimensional color Doppler (Vingmed system 5). Before ischemia, the flow wave propagated rapidly toward the apex, whereas during ischemia, the early rapid filling wave was aborted in the basal portion of the LV, similar to the findings with CMD. Accordingly, the TD, as measured by CMD, appears to represent different flow phenomena during baseline and during ischemia. This may limit the ability of TD index of flow propagation to serve as a quantitative index of LV relaxation.
Mitral-to-Apical Flow Propagation, "Diastolic
Suction," and Inertial Forces
Courtois et al8 hypothesized that loss of the
early-diastolic base-to-apex pressure gradient during
myocardial ischemia and the subsequent flow disturbance
is due to loss of elastic recoil. Nicolic et al14
demonstrated that the base-to-apical pressure gradient was a function
of the diastolic restoring forces. Consistent with
this, we observed a strong negative correlation between
mitral-to-apical pressure gradient and LV end-systolic volume.
The present study was not designed to quantify the contribution
from elastic recoil to mitral-to-apical flow propagation. However, by
applying principles of wave propagation
analysis15 16 and relating apical pressure and
velocities, it may be possible to tell which mechanism is dominating,
that is, whether blood is "sucked" or "pushed" toward the apex.
If blood is sucked into the apical region, one would predict a decrease
in apical pressure while flow accelerates toward the apex. Conversely,
if blood is pushed toward the apex, one would predict a rise in apical
pressure while flow accelerates toward the apex. Figure 6
displays velocity and pressure in early diastole before
ischemia and demonstrates that flow is accelerating and apical
pressure is falling. This is compatible with suction of blood toward
the apex. During ischemia, however, apical pressure is rising
when flow accelerates toward the apex. The latter observation cannot be
ascribed to a net suction effect. Therefore, the marked slowing of
mitral-to-apical flow propagation during ischemic failure might
be attributed to loss of diastolic suction.
The strong correlation between TD and end-systolic volume could in part reflect inertial effects during LV failure, when a larger intraventricular mass needs to be accelerated. This interpretation is consistent with the study by Greenberg et al,17 which recently demonstrated the importance of inertia for LV filling.
Limitations
The functional differences between the present animal model
and patients with coronary artery disease or congestive
cardiomyopathy are obvious. In our model, heart
rate was high and LV ejection fraction was less than normal, probably
because of the combined effect of anesthesia and the
extensive instrumentation. A high heart rate will shorten
diastole, which might represent a problem in the
study of diastolic intraventricular
flow. In the present study, however, we investigated
early-diastolic filling, and heart rate is less of a
problem than for studies of mid or late diastolic filling.
Moreover, we have previously demonstrated that pacing
tachycardia from 120 bpm to heart rates of 150 bpm caused
no significant change in the mitral-to-apical flow propagation
velocity.2 Before induction of ischemia,
intraventricular flow propagation in the
present model was rapid and resembled flow propagation in the
normal human heart.1 2
The microembolization model has proved to be a highly reproducible model for induction of ischemic LV failure, and its hemodynamic characteristics are in many ways similar to the hemodynamic features of patients with acute ischemic LV failure. This includes a decrease in LV systolic pressure, an increase in LV EDP, dilatation of the LV, and elevated systemic vascular resistance.9 Furthermore, we have previously shown that this model, in a reproducible manner, gives retardation of apical filling similar to that seen in patients with ischemic LV failure.3 Therefore, although the preparation has significant limitations, we believe the model is valid for investigating mechanisms of impairment of apical filling in the ischemic ventricle, which was the main objective of this study.
The observed mitral-to-apical pressure differences were small, and one might question whether they were beyond the resolution of our system. Throughout each experiment, however, pressures were repeatedly adjusted to zero during pacing-induced long diastoles, and similar gain setting for the 2 pressure sensors was confirmed by comparing peak systolic pressures during nonejecting beats.
Conclusions
Retardation of apical filling in acute myocardial ischemia
was associated with slowing of LV relaxation and a marked reduction of
the intraventricular mitral-to-apical pressure
gradient. In the nonischemic ventricle, the dominant
early-diastolic flow propagated rapidly toward the apex
with a speed far exceeding that of the blood cells, thus resembling
column motion. During ischemia, however, the penetration of
this column flow into the LV was markedly reduced. In the apical
region, flow propagation was slower and approximated the velocity of
the individual blood cells, which is compatible with a change in apical
filling to a pattern dominated by convection.
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Acknowledgments |
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Kjetil Steine is a recipient of a clinical research fellowship from the University of Oslo, Norway. The study was also financed by the Norwegian Council on Cardiovascular Diseases and the Norwegian Research Council. We thank engineer Roger Ødegaard for important technical assistance, university secretary Maureen Raw for helpful advice and assistance in computer management, and Dr Thor Edvardsen and Dr Stig Urheim for their beneficial collaboration in the laboratory.
Received July 30, 1998; revision received December 1, 1998; accepted December 17, 1998.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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1. Brun P, Tribouilloy C, Duval AM, Iserin L, Meguira A, Pelle G, 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. 1992;20:420–432.[Abstract]
2.
Stugaard M, Smiseth OA, Risøe C, Ihlen H.
Intraventricular early diastolic
filling during acute myocardial ischemia: assessment by
multigated color M-mode Doppler
echocardiography. Circulation. 1993;88:2705–2713.
3. Stugaard M, Risøe C, Ihlen H, Smiseth OA. Intracavitary filling pattern in the failing left ventricle assessed by color M-mode Doppler. J Am Coll Cardiol. 1994;20:663–670.
4. Takatsuji H, Mikami T, Urasawa K, Teranishi J-I, Onozuka H, Takagi C, Makita Y, Matsuo H, Kusuoka H, 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. 1996;27:365–371.[Abstract]
5. Steine K, Fløgstad T, Stugaard M, Smiseth OA. Early diastolic intraventricular filling pattern in acute myocardial infarction by color M-mode Doppler echocardiography. J Am Soc Echocardiogr. 1998;11:119–125.[Medline] [Order article via Infotrieve]
6. Garcia MJ, Ares MA, Asher C, Rodriguez L, Vandervoort P, Thomas JD. An index of early left ventricular filling that combined with pulsed Doppler peak E velocity may estimate capillary wedge pressure. J Am Coll Cardiol. 1997;29:448–454.[Abstract]
7. Ling D, Rankin JS, Edwards CH II, McHale PA, Anderson RW. Regional diastolic mechanics of the left ventricle in the conscious dog. Am J Physiol. 1979;236:H323–H330.
8.
Courtois MA, Sandor J, Kovacs J, Ludbrook PA.
Physiological early diastolic
intraventricular gradient is lost during acute
myocardial ischemia. Circulation. 1990;81:1688–1696.
9. Smiseth OA, Mjøs OD. A reproducible and stable model of acute ischemic left ventricular failure in dogs. Clin Physiol. 1982;2:225–239.[Medline] [Order article via Infotrieve]
10. Craig WE, Murgo JP, Pasipoularides A. Evaluation of time course of left ventricular isovolumic relaxation in humans. In: Grossman W, Lorell BH, eds. Diastolic Relaxation of the Heart. Boston, Mass: Martinus Nijhoff; 1988:125–132.
11.
Little WC, Freeman GL, O'Rourke RA.
Simultaneous determination of left ventricular
end-systolic pressure-volume and pressure-dimension
relationships in closed-chest dogs. Circulation. 1985;71:1301–1308.
12. Glantz SA, Slinker BK. Primer of Applied Regression and Analysis of Variance. New York, NY: McGraw-Hill; 1990.
13.
Steen T, Steen S. Filling of a model left ventricle
studied by colour M mode Doppler. Cardiovasc Res. 1994;28:1821–1827.
14.
Nikolic SD, Feneley MP, Pajaro OE, Rankin JS, Yellin
EL. Origin of regional pressure gradients in the left ventricle during
early diastole. Am J Physiol. 1995;268:H550–H557.
15. Parker KH, Jones CHJ. Forward and backward running waves in the arteries: analysis using the method of characteristics. J Biomech Eng. 1990;112:322–326.[Medline] [Order article via Infotrieve]
16. MacRae JM, Sun YH, Isaac DL, Dobson GM, Cheng CP, Little WC, Parker KH, Tyberg JV. Wave-intensity analysis: a new approach to left ventricular filling dynamics. Heart Vessels. 1997;12:53–59.[Medline] [Order article via Infotrieve]
17.
Greenberg NL, Vandervoort PM, Thomas JD.
Instantaneous diastolic transmitral pressure differences
from color Doppler M mode echocardiography.
Am J Physiol. 1996;271:H1267–H1276.
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N. L. Greenberg, P. M. Vandervoort, M. S. Firstenberg, M. J. Garcia, and J. D. Thomas Estimation of diastolic intraventricular pressure gradients by Doppler M-mode echocardiography Am J Physiol Heart Circ Physiol, June 1, 2001; 280(6): H2507 - H2515. [Abstract] [Full Text] [PDF]
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