scholarly journals Mechanics of intraventricular filling: study of LV early diastolic pressure gradients and flow velocities

1998 ◽  
Vol 275 (3) ◽  
pp. H1062-H1069 ◽  
Author(s):  
Otto A. Smiseth ◽  
Kjetil Steine ◽  
Gunnar Sandbæk ◽  
Marie Stugaard ◽  
Tor Ø. Gjølberg

This study investigates mechanisms of left ventricular (LV) intracavitary flow during early, rapid filling. In eight coronary artery disease patients with normal LV ejection fraction we recorded simultaneous LV apical and outflow tract pressures and intraventricular flow velocities by color M-mode Doppler echocardiography. In five anesthetized dogs we also recorded left atrial pressure and LV volume by sonomicrometry. In patients, as the early diastolic mitral-to-apical filling wave arrived at the apex, we observed an apex-outflow tract pressure gradient of 3.5 ± 0.3 mmHg (mean ± SE). This pressure gradient correlated with peak early apex-to-outflow tract flow velocity ( r = 0.75, P < 0.05). The gradient was reproduced in the dog model and decreased from 3.1 ± 0.3 to 1.7 ± 0.5 mmHg ( P < 0.05) with caval constriction and increased to 4.2 ± 0.5 mmHg ( P < 0.001) with volume loading. The pressure gradient correlated with peak early transmitral flow (expressed as time derivative of LV volume; r = 0.95) and stroke volume ( r = 0.97). In conclusion, arrival of the early LV filling wave at the apex was associated with a substantial pressure gradient between apex and outflow tract. The pressure gradient was sensitive to changes in preload and correlated strongly with peak early transmitral flow. The significance of this gradient for intraventricular flow propagation in the normal and the diseased heart remains to be determined.

2019 ◽  
Vol 36 (7) ◽  
pp. 1263-1272 ◽  
Author(s):  
Antonio Amador Calvilho Júnior ◽  
Jorge Eduardo Assef ◽  
David Le Bihan ◽  
Rodrigo Bellio de Mattos Barretto ◽  
Antonio Tito Paladino Filho ◽  
...  

1979 ◽  
Vol 236 (2) ◽  
pp. H323-H330 ◽  
Author(s):  
D. Ling ◽  
J. S. Rankin ◽  
C. H. Edwards ◽  
P. A. McHale ◽  
R. W. Anderson

In eight chronically instrumented conscious dogs, apical and middle left ventricular transverse diameters were measured with pulse-transit ultrasonic dimension transducers. Intracavitary apical and midventricular pressures and intrapleural pressure were measured with micromanometers. Both diameters were normalized as a percent extension from the dimension at zero transmural pressure, determined during a transient vena caval occlusion. During the rapid phase of diastolic filling, there was a 2--5 mmHg pressure gradient from the midventricle to the apex. During late rapid filling, the apical transmural pressure and diameter increased more rapidly and reached diastasis 17 +/- 4 ms earlier than the corresponding midventricular measurements (P less than 0.01). The static diastolic pressure-dimension characteristics at the apical and midventricular levels were not significantly different (P greater than 0.30). The dynamic diastolic pressure-dimension relationship was also similar at the two levels and could be represented by a model incorporating parallel viscous properties. Because of regional differences in pressures and dimensions, however, the dynamic relationship could not be modeled when pressure was compared to the dimension at a different level. Thus, diastolic pressures should be measured at the same level as dimensions when assessing left ventricular diastolic mechanics.


1980 ◽  
Vol 238 (2) ◽  
pp. H257-H262
Author(s):  
J. C. Werner ◽  
J. C. Lee ◽  
S. E. Downing

We have shown previously that insulin reduces myocardial injury associated with norepinephrine (NE) infusion in the rabbit (Am. J. Pathol. 93:399--353, 1978). In the present study, left ventricular function (LVF) was assessed from afterload curves obtained by progressive aortic constriction 2--4 days following NE infusion. The initial slope of the function curves (SFC), maximum dP/dt and left ventricular end-diastolic pressure at 120 mmHg ((LVEDP120) were used for comparison. In 4 controls, SFC averaged 23.8 mmHg/cmH2O. In 10 rabbits given NE, the mean slope was 8.4 (P less than 0.01). However, animals pretreated with insulin before being given NE did not differ from controls (SFC, 19.7 mmHg/cmH2O). These performance data were supported by measurements of LVEDP120, which were 2.8, 12.3 and 3.1 cmH2O, respectively (P less than 0.05 and less than 0.02). In spite of the higher LVEDP, max dP/dt120 was significantly lower in the NE group than in the group given insulin. Histological findings and postmortem measurements of LV volume and mass were consistent with the observed differences in LVF. It is concluded that NE damage reduces LVF and this is largely prevented by pretreatment with insulin.


1990 ◽  
Vol 259 (2) ◽  
pp. H457-H463 ◽  
Author(s):  
S. D. Nikolic ◽  
E. L. Yellin ◽  
M. Dahm ◽  
O. Pajaro ◽  
R. W. Frater

This study was designed to investigate the relationship between left ventricular (LV) eccentricity, volume, and passive elastic properties. Eight open-chest fentanyl-anesthetized dogs were instrumented with an LV micromanometer, a remote-controlled mitral valve occluder, and two pairs of ultrasonic crystals to measure anterior-posterior and base-apex dimensions. We identified the presence of elastic recoil forces with negative LV diastolic pressure in nonfilling diastoles (end-systolic volume clamp). Using linear regression analysis we related midwall eccentricity to volume in nonfilling diastoles at the time of LVPmin and at end diastole, and in normal beats at end systole at LVPmin and at end-diastole. Intersection of the end-systolic and end-diastolic lines (transitional volume, Vt = 38.0 + 6.4 ml) divides cycles with and without the presence of elastic recoil forces. Vt is analogous to the equilibrium volume (V0), determined as the volume intercept of the logarithmic passive pressure-volume (P-V) relationship using LV volume estimated from LV weights (V0 nl = 37.6 + 4.4 ml), or the volume intercept of the linearized P-V relationship calculated from a prolate spheroidal model using measured minor and major diameters (V0 l = 44.5 + 3.5 ml). Linear regression analysis was also used to relate the square of peak mitral flow (MF2) with the corresponding atrioventricular pressure gradient (delta P); the slope represents a dissipative constant for the cycles without, P = 0.00058(MF)2 + 0.35 (n = 48, r = 0.73), and with elastic recoil P = 0.00035(MF)2 + 0.21 (n = 24, r = 0.81).(ABSTRACT TRUNCATED AT 250 WORDS)


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Z Zamani ◽  
T J Samuel ◽  
J Wei ◽  
L E J Thomson ◽  
B Tamarappoo ◽  
...  

Abstract Background Women with signs and symptoms of ischemia but no obstructive coronary artery disease (INOCA) are at increased risk of developing heart failure with preserved ejection fraction (HFpEF); however, the exact mechanism for HFpEF progression remains to be elucidated. Prior studies have focused specifically on impaired left ventricular diastolic function in INOCA. We hypothesized that extending our evaluation to include the left atrium (LA)– a key constituent of the transmitral pressure gradient and left ventricular filling– would provide additional, novel, pathophysiological insight. Purpose To evaluate LA function in women with INOCA using cardiac MRI (CMR). Methods We performed retrospective feature tracking analysis of cine images from CMR (Figure 1A), to evaluate LA strain, in 58 INOCA women with normal sinus rhythm (three were excluded due to suboptimal image quality). All strain measurements were performed in duplicate by an experienced investigator blinded to clinical status. We subdivided the cohort by an established threshold of resting left ventricular end diastolic pressure (LVEDP) <12 mmHg vs >12 mmHg, performed invasively within a median of 27 days of the CMR. As illustrated in Figure 1B, LA function was divided into three established phases: (1) reservoir strain, passive expansion of the left atrium from the pulmonary circulation while the mitral valve is closed; (2) conduit strain, passive emptying of the atrium into the ventricle; and (3) booster strain, active emptying of the left atrium following atrial depolarization. Results Reservoir strain was higher in the elevated LVEDP group (n=20, 26.1 + 1.3%) vs. not elevated group (n=35, 22.8 + 0.9%, p=0.03; Figure 1C). In contrast, we observed no group difference in conduit strain (16.5 + 1.0 and 16.5 + 0.7, p=0.78, respectively; Figure 1D), resulting in significantly higher atrial booster strain in the elevated LVEDP group (10.0 + 1.1% and 7.0 + 0.6, p<0.01, respectively; Figure 1E). Conclusions To our knowledge, this is the first report of LA function in women with INOCA. That reservoir strain was higher in subjects with elevated LVEDP provides important pathophysiologic insight regarding diastolic hemodynamics of the LA. The similar conduit function between groups– despite different LVEDP's– strongly suggests a ventricular contribution to the impaired transmitral pressure gradient. Together, these initial proof-of-concept data support the evaluation of LA function in our quest to better understand heart failure progression in INOCA.


2019 ◽  
Vol 44 (5) ◽  
pp. 1050-1062 ◽  
Author(s):  
Shinichiro Niizuma ◽  
Yoshitaka Iwanaga ◽  
Takehiko Washio ◽  
Tadashi Ashida ◽  
Shinsuke Harasawa ◽  
...  

Background: An increased cardiac troponin T (cTnT) level identifies a high-risk group in patients with end-stage renal disease; however, the mechanism of cTnT elevation remains unclear in such patients without acute coronary syndrome (ACS). Therefore, we explored the relationship between cTnT levels and the hemodynamic parameters and the prognostic potential of cTnT in stable patients with chronic hemodialysis (HD). Methods: We included consecutive 174 patients with HD who were referred for coronary angiography due to stable coronary artery disease (CAD), peripheral artery disease (PAD), or heart failure (HF). Hemodynamic measurement was performed, and plasma cTnT, B-type natriuretic peptide (BNP), and A-type natriuretic peptide (ANP) were measured at the same time. The potential of 3 biomarkers to predict all-cause mortality, cardiac death or hospitalized HF, and vascular event was assessed. Results: Increased log cTnT levels were correlated with increased log BNP and log ANP levels (r = 0.531, p < 0.001 and r = 0.411, p < 0.001, respectively). Not increased log cTnT, but increased log BNP and log ANP were associated with the presence of CAD and the extent of CAD. In contrast, they were all associated with the New York Heart Association functional classification and the presence of PAD and significantly correlated with left ventricular end-diastolic pressure (LVEDP) in an independent manner. Increased cTnT and BNP levels were associated with the mortality and hospitalized HF. However, increased cTnT was not associated with vascular events, unlike increased BNP. Conclusions: In patients with chronic HD without ACS, increased cTnT reflected increased LVEDP and the presence of HF or PAD independently, and it did not reflect the presence of CAD in contrast to increased BNP. cTnT and BNP were significant prognostic predictors; however, increased cTnT was associated with HF-related events, not with arteriosclerotic events.


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