scholarly journals Novel echocardiographic method to assess left ventricular chamber stiffness and elevated end-diastolic pressure based on time–velocity integral measurements of pulmonary venous and transmitral flows

2017 ◽  
Vol 19 (11) ◽  
pp. 1260-1267 ◽  
Author(s):  
Kazunori Okada ◽  
Sanae Kaga ◽  
Rika Abiko ◽  
Michito Murayama ◽  
Takuma Hioka ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Chamber ◽  
Time Velocity Integral

Left ventricular diastolic function of remodeled myocardium in dogs with pacing-induced heart failure

1998 ◽  
Vol 274 (3) ◽  
pp. H945-H954 ◽  
Author(s):  
Steven B. Solomon ◽  
Srdjan D. Nikolic ◽  
Stanton A. Glantz ◽  
Edward L. Yellin
Keyword(s):  
Heart Failure ◽  
Elastic Properties ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Elastic Recoil ◽  
Systolic Volume ◽  
Left Ventricular Chamber ◽  
Volume Relation

In patients with heart failure, decreased contractility resulting in high end-diastolic pressures and a restrictive pattern of left ventricular filling produces a decrease in early diastolic filling, suggesting a stiff ventricle. This study investigated the elastic properties of the myocardium and left ventricular chamber and the ability of the heart to utilize elastic recoil to facilitate filling during pacing-induced heart failure in the anesthetized dog. Elastic properties of the myocardium were determined by analyzing the myocardial stress-strain relation. Left ventricular chamber properties were determined by analyzing the pressure-volume relation using a logarithmic approach. Elastic recoil was characterized using a computer-controlled mitral valve occluder to prevent transmitral flow during diastole. We conclude that, during heart failure, the high end-diastolic pressures suggestive of a stiff ventricle are due not to stiffer myocardium but to a ventricle whose chamber compliance characteristics are changed due to geometric remodeling of the myocardium. The restrictive filling pattern is a result of the ventricle being forced to operate on the stiff portion of the diastolic pressure-volume relation to maintain cardiac output. Slowed relaxation and decreased contractility result in an inability of the heart to contract to an end-systolic volume below its diastolic equilibrium volume. Thus the left ventricle cannot utilize elastic recoil to facilitate filling during heart failure.

Estrogen-induced left ventricular chamber enlargement in ewes

1993 ◽  
Vol 264 (4) ◽  
pp. E490-E496 ◽  
Author(s):  
G. D. Giraud ◽  
M. J. Morton ◽  
L. E. Davis ◽  
M. S. Paul ◽  
K. L. Thornburg
Keyword(s):  
Placebo Group ◽  
Stroke Volume ◽  
Inferior Vena ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Chronic Effect ◽  
Inferior Vena Caval ◽  
Intramuscular Dose ◽  
Left Ventricular Chamber ◽  
Chamber Size

We studied the chronic effect of administration of a single large intramuscular dose of 17 beta-estradiol on left ventricular chamber size and output in the ewe. Fourteen oophorectomized ewes were successfully instrumented and studied, with measurements made of left ventricular, aortic, right and left atrial pressures, left ventricular stroke volume, and left ventricular minor axis dimension. Unanesthetized ewes were studied before and 1, 2, and 3 wk after intramuscular administration of 0.6 mg/kg 17 beta-estradiol (7 ewes) or 1.5 ml sesame oil placebo (7 ewes). Left ventricular end-diastolic pressure-end-diastolic dimension (LVEDP-EDD) and left ventricular end-diastolic pressure-stroke volume (LVEDP-SV) relationships were quantified during graded inferior vena caval occlusion and volume infusion. Left ventricular end-diastolic diameter was larger after estrogen but not after placebo administration. The LVEDP-EDD relationship shifted progressively rightward, indicating left ventricular chamber enlargement in the estrogen group but was unchanged in the placebo group. The plateau limb of the LVEDP-SV relationship in the estrogen group shifted up from a mean stroke volume of 77.1-89.5 ml/beat and did not change in the placebo group. We conclude that administration of a single large intramuscular dose of 17 beta-estradiol resulted in left ventricular chamber enlargement and increased stroke volume in the ewe.

Acute Changes in Left Ventricular End Diastolic Pressure following the Transcatheter Closure of an Atrial Septal Defect in Adults

2016 ◽  
Vol 19 (3) ◽  
pp. 145 ◽  
Author(s):  
Young Hwa Kong ◽  
Jinyoung Song ◽  
Kyung Hee Kim ◽  
June Huh ◽  
I-Seok Kang
Keyword(s):  
Elderly Patients ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Transcatheter Closure ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Device Closure ◽  
Acute Changes ◽  
Asd Closure

<strong>Background:</strong> Acute changes in left ventricular diastolic function shortly after ASD closure in elderly patients have not been well known. We aimed to investigate acute changes in left ventricular end diastolic pressure (LVEDP) in elderly patients following transcatheter closure of atrial septal defect (ASD). <br /><strong>Methods:</strong> All 19 adults with ASDs who underwent transcatheter closure between June 2013 and December 2014 were enrolled. LVEDP was measured prior to device closure and compared with that immediately following device closure and 15 minutes after device closure. <br /><strong>Results:</strong> The median age of the patients was 48 years old. The baseline E/e’ and LVEDP values were 8.3 ± 2.8 and 13 ± 3 mmHg. The LVEDP value immediately following closure was 19 ± 4 mmHg, and 15 minutes after closure was 16 ± 4 mmHg. The median increase in the LVEDP value immediately following closure was 6 mmHg, which significantly differed from that prior to closure. The LVEDP 15 minutes after closure decreased but remained significantly higher than the value observed immediately after closure. No significant changes were observed with regard to E/e’ at either 1 day or 3 months following closure. The LVEDP value <br />15 minutes after device closure was significantly correlated with those observed before closure and immediately following closure; however, no significant correlations were observed with regard to patient age, Qp/Qs, E/e’ before closure, or E/e’ 3 months after device closure.<br /><strong>Conclusion:</strong> LVEDP in adults with ASDs significantly increases following device closure. LVEDP before closure predicts LVEDP following device closure.

RELATIVE CONTRIBUTIONS OF FIBROSIS AND CONNEXIN CHANGES TOTHE ATRIAL FIBRILLATION SUBSTRATE DURING THE DEVELOPMENT AND REVERSAL OF CONGESTIVEHEART FAILURE

2008 ◽  
Vol 31 (4) ◽  
pp. 5
Author(s):  
Brett Burstein ◽  
Kunihiro Nishida ◽  
Philippe Comtois ◽  
Louis Villenuve ◽  
Yung-Hsin Yeh ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Potential Model ◽  
Diastolic Pressure ◽  
Recovery Period ◽  
Left Ventricular ◽  
Muscle Bundle ◽  
Protein Ratio ◽  
Conduction Disturbances ◽  
Conduction Abnormalities ◽  
Mrna And Protein Expression

Background: Connexin alterations occur in various atrial fibrillation (AF) paradigms, but their functional significance remains unclear. No data are available regarding the effects of CHF on atrial connexin expression and phosphorylation. We therefore analyzed connexin changes and their contribution to the AF substrate during the development and reversal ofCHF. Methods and Results: Dogs were allocated to three groups: CHF induced by 2-week ventricular tachypacing (CHF, n=15); CHF dogs allowed to recover for 4 weeks after 2-week tachypacing (REC, n=15) and non-paced shams (CTL, n=11). Left ventricular end-diastolic pressure increased with CHF (14.5±1.0*** vs.3.7±0.7, ***P < 0.001 vs. CTL) and normalized upon CHF recovery (5.1±1.0^†††, ^††† P < 0.001 vs. CHF). Real-time PCR and Western-blot analyses revealed connexin43 (Cx43) and connexin40 (Cx40) mRNA and protein expression to be unchanged by CHF and REC. However, CHF caused Cx43 dephosphorylation(by ~73%***) and increased Cx40/Cx43 protein ratio (by ~35%***), with both alterations completely reversing in REC. Immunofluorescent confocal microscopy confirmed connexin protein trends, with a reduction in phosphorylated Cx43 (by ~68%*** in CHF) that returned to control in REC. CHF caused conduction abnormalities (phasedelay-range and heterogeneity index, both P < 0.01) and burst pacing-induced AF prolongation (CTL 22±7s, CHF 1100±171s***, REC 884±220s***) which persisted in the recovery period, along with residual fibrosis (CTL 3.6±0.7%, CHF 14.7±1.5%***, REC13.3±2.3%***). Fibrosis physically interrupted muscle bundle continuity and anionically-based action potential model of canine atrium showed that fibrosiswas able to account for the observed conduction abnormalities. Conclusions: CHF causes connexin-dephosphorylation and Cx40/Cx43ratio increases. With CHF reversal, atrial connexin alterations recover completely, but tissue fibrosis, conduction abnormalities and a substrate forAF remain with fibrosis accounting for conduction abnormalities. Thus, althougha trial connexin changes occur with CHF, they are not essential for conduction disturbances and AF promotion, which appear rather to be related primarily tofibrotic interruption of muscle-bundle continuity.

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