Role of Intraventricular Dispersion of Early Diastolic Filling in Indicating Left Ventricular Diastolic Dysfunction: Assessment by Color M-Mode Inflow Propagation Velocity

Cardiology ◽  
2001 ◽  
Vol 95 (3) ◽  
pp. 151-155 ◽  
Author(s):  
Wen-Chol Voon ◽  
Chih-Hsin Huang ◽  
Sheng-Hsiung Sheu
Keyword(s):  
Diastolic Dysfunction ◽  
Propagation Velocity ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Ventricular Diastolic Dysfunction

A Hydrodynamic Efficiency Parameter as a Novel Left Ventricular Diastolic Dysfunction Diagnostic Metric

2008 ◽  
Author(s):  
Kelley C. Stewart ◽  
Rahul Kumar ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
William C. Little
Keyword(s):  
Diastolic Dysfunction ◽  
Critical Role ◽  
Propagation Speed ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Ventricular Diastolic Dysfunction ◽  
Efficiency Parameter ◽  
Wave Propagation Speed ◽  
The Relationship

Numerous studies have shown that cardiac diastolic dysfunction and diastolic filling play a critical role in dictating overall cardiac health and demonstrated that the filling wave propagation speed is a significant index of the severity of diastolic dysfunction [1, 2]. However, the governing flow physics underlying the relationship between propagation speed and diastolic dysfunction are poorly understood. More importantly, currently there is no reliable metric to allow clinicians the ability to diagnose cardiac dysfunction on the basis of the wave filling speed.

Left Ventricular Vortex Ring Dynamics and Their Association to Early Diastolic Filling

2011 ◽  
Author(s):  
Kelley C. Stewart ◽  
John J. Charonko ◽  
Takahiro Ohara ◽  
William C. Little ◽  
Pavlos P. Vlachos
Keyword(s):  
Diastolic Dysfunction ◽  
Left Atrial ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Compensatory Mechanisms ◽  
Ring Dynamics ◽  
Ventricular Diastolic Dysfunction ◽  
Ventricular Filling ◽  
Early Filling

Diastolic dysfunction is the impairment of the filling in the left ventricle. Patients with left ventricular diastolic dysfunction (LVDD) lose the ability to adjust left ventricular filling properties without increasing left atrial pressure [1]. Although LVDD is very prevalent, it currently remains difficult to diagnose due to inherent atrioventricular compensatory mechanisms including increased heart rate, increased left ventricular (LV) contractility, and increased left atrial (LA) pressure. Although variations within the early diastolic filling velocity have been previously observed [2], the physical mechanism for the deceleration of the early filling wave is not understood.

scholarly journals P897 The role of oxidative stress and inflammation for stress induced left ventricular diastolic dysfunction in non-severe chronic obstructive pulmonary disease patients

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
Z Cherneva ◽  
V L Lozanov ◽  
P S Sugareva ◽  
R C H Cherneva
Keyword(s):  
Oxidative Stress ◽  
Diastolic Dysfunction ◽  
Left Ventricular Diastolic Dysfunction ◽  
Urine Concentration ◽  
Left Ventricular ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Ventricular Diastolic Dysfunction ◽  
Severe Copd

Abstract Background Oxidative stress and inflammation have been implicated in the pathogenesis of diastolic dysfunction (DD) and are both present in chronic obstructive pulmonary disease (COPD). Purpose To evaluate the role of oxidative stress markers (8-isoprostane) and inflammation (prostaglandin E2, resistin) in the pathogenesis of stress induced left ventricular diastolic dysfunction (LVDD) in non-severe COPD. Materials and methods 104 patients with non-severe COPD (FEV1 > 50%) and preserved left ventricular ejection fraction >50% underwent incremental cardio-pulmonary exercise testing (CPET). Echocardiography was performed before CPET and 1-2 minutes after peak exercise. Peak E/e’ ratio >15 was a marker for stress LVDD. Urine concentration of 8-isoprostanes was assumed as surrogate marker for oxidative stress; urine concentration of prostaglandine-E2 and plasma resistin levels as inflammatory markers. Mass spectrometry was applied for 8-isoprostane and prostglandine E2 (Cayman. Chemical) measurement. Values were normalised to urine creatinine (µmol/l/cre). ELISA was applied for resistin measurement (Raybio_Human) (ng/ml). Results Patients were divided into two groups: subjects with stress LVDD (67) and subjects without stress LVDD (37). 8-isoprostane levels were higher in subjects with LVDD vs those without LVDD (32.9 vs 29.67µmol/l/cre; p< 0.05). The same is observed regarding resistin plasma levels (22.51 vs 15.68ng/ml). Urine concentrations of prostaglandin E2 did not differ between the two groups (50.76 vs 51.07 µmol/l/cre) Conclusions In non-severe COPD patients the levels of oxidative stress (8-isoprostanes) and inflammation (resistin) seem to be associated with stress induced left ventricular diastolic dysfunction.

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