Determinants of left ventricular filling and of the diastolic pressure-volume relation.

Gilbert, John; Glantz, Stanton A.

doi:10.1161/01.res.64.5.827

Cited by 382 publications

(166 citation statements)

References 206 publications

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“…None of the myriad of phenomenologic Doppler echo-based parameters proposed to date for diastolic function characterization involves the concept of efficiency (Gilbert et al 1989,Little et al 1990). Accordingly, by deriving an efficiency-based index from a predictive, kinematic (species-independent) model of filling that can be determined using routine echocardiography, we sought to characterize the filling process in a causal, rather than correlative terms.…”

Section: Discussionmentioning

confidence: 99%

The Kinematic Filling Efficiency Index of the Left Ventricle: Contrasting Normal vs. Diabetic Physiology

Zhang

Chung

Riordan

et al. 2007

Ultrasound in Medicine & Biology

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An index of filling efficiency incorporating stiffness and relaxation (S&R) parameters has not been derived or validated although numerous studies have focused on the effects of altered relaxation or stiffness on early rapid filling and diastolic function. Previous studies show that S&R parameters can be obtained from early rapid filling (Doppler E-wave) via kinematic modeling. E-wave contours are governed by harmonic oscillatory motion, modeled via the parameterized diastolic filling (PDF) formalism. The previously validated model determines three (unique) oscillator parameters from each E-wave having established physiologic analogues: x o (load), c (relaxation/viscoelasticity), and k (chamber stiffness). We define the dimensionless, filling-volume based kinematic filling efficiency index (KFEI) as the ratio of the velocity-time integral (VTI) of the actual clinical E-wave contour fit via PDF to the VTI of the PDF model-predicted ideal E-wave contour having the same x o and k, but with no resistance to filling (c=0). To validate the new index, Doppler E-waves from 36 subjects with normal ventricular function, 17 diabetic and 19 well-matched non-diabetic controls, were analyzed. E-wave parameters x o , c, and k and KFEI were computed for each subject and compared. In concordance with prior human and animal studies in which c differentiated between normal and diabetic hearts, KFEI differentiated (p<0.001) between non-diabetics (55.8±3.3%) and diabetics (49.1±3.3%). Thus, the new index introduces and validates the concept of filling efficiency, and using diabetes as a working example, provides quantitative and mechanistic insight into how S&R affects ventricular filling efficiency.

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Section: Discussionmentioning

confidence: 99%

The Kinematic Filling Efficiency Index of the Left Ventricle: Contrasting Normal vs. Diabetic Physiology

Zhang

Chung

Riordan

et al. 2007

Ultrasound in Medicine & Biology

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“…In this study, the time constant of isovolumic LV pressure relaxation (τ) was calculated from the dp/dt versus pressure relation as previously described. 17,18) After the hemodynamic recording, the rabbits were killed with an intravenous overdose of pentobarbital. The heart was immediately excised and placed into ice-cold saline to remove the blood.…”

Section: Methodsmentioning

confidence: 99%

Role of Nitric Oxide in the Progression of Cardiovascular Remodeling Induced by Carotid Arterio-Venous Shunt in Rabbits.

et al. 2003

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SUMMARYDespite a variety of biological roles for nitric oxide (NO) in the cardiovascular system, little is known about whether NO is involved in cardiac hypertrophy. We hypothesized that NO production following a sustained increase in shear stress by volumeoverload modifies the level of cardiac hypertrophy independent of hemodynamic changes. Volume-overload was induced by shunt formation between the left common carotid artery and the external jugular vein in 21 rabbits. These shunt rabbits were randomly assigned to 3 groups: shunt with no treatment (n=8), shunt treated with a low dose of N G -nitro-Larginine methyl ester (L-NAME, 0.5 g/L in drinking water, n=8), and shunt with a high dose of L-NAME (1.5 g/L, n=5). Eight sham operated rabbits were used as controls. Treatments were started immediately after operation and were continued for 6 weeks. Chronic volume-overload by shunt formation caused left ventricular dilatation and arterial enlargement proximal to the fistula. The relative wall thickness of the left ventricle was decreased, indicating eccentric cardiac hypertrophy. L-NAME elevated mean arterial blood pressure (P<0.01) and reduced the increment of cardiac output (P<0.05). L-NAME attenuated ventricular weight (P<0.01), ventricular cavity dilatation (P<0.01), and arterial enlargement (P<0.05). The re-capitulation of atrial natriuretic factor mRNA in the hypertrophied left ventricular myocardium by volume-overload was attenuated with L-NAME. In this model with chronic volume-overload, NO plays a pivotal role in the progression of cardiovascular remodeling by regulating the loading conditions of the heart. (Jpn Heart J 2003; 44: 127-137)

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“…These changes include an increased elastic stiffness due to accumulation of collagen in the myocardial interstitium as well as an increase in myocyte size. 27 These changes are the primary determinants of wall stress at the end of diastole when the heart is fully relaxed. 27 However, an altered rate and extent of ventricular relaxation may be important in the end-diastolic pressure-volume relation, with the extent of relaxation more likely to affect this relation.…”

Section: Discussionmentioning

confidence: 99%

“…27 These changes are the primary determinants of wall stress at the end of diastole when the heart is fully relaxed. 27 However, an altered rate and extent of ventricular relaxation may be important in the end-diastolic pressure-volume relation, with the extent of relaxation more likely to affect this relation. 27 Pressure-overload hypertrophy alters sarcoplasmic reticulum calcium reuptake.…”

Section: Discussionmentioning

confidence: 99%

“…27 However, an altered rate and extent of ventricular relaxation may be important in the end-diastolic pressure-volume relation, with the extent of relaxation more likely to affect this relation. 27 Pressure-overload hypertrophy alters sarcoplasmic reticulum calcium reuptake. 28 This may be related to a reduced coronary reserve, relative myocardial ischemia, and a subsequent slowing of calcium reuptake.…”

Section: Discussionmentioning

confidence: 99%

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Hydrochlorothiazide improves ventricular compliance and thus performance without reducing hypertrophy in renal artery stenosis in rats.

1993

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The effect of hydrochlorothiazide (1 mg/kg per day) on left ventricular (LV) mass and systolic and diastolic function was investigated in two-kidney, one clip (2K1C) renovascular hypertensive rats. Hydrochlorothiazide was administered from 8 weeks, and LV mass and function were measured at 16 weeks after surgery to induce hypertension. Cardiac performance was determined from cardiac output, stroke volume (per 100 g of body weight), and stroke work (per gram of LV weight) versus LV end-diastolic pressure (LVEDP) and versus LV strain relations in anesthetized open-chest, ventilated rats. LV compliance was determined from the LVEDP versus strain relation. Strain was calculated from LV end-diastolic short-axis diameter values. Hydrochlorothiazide reduced systolic blood pressure in 2K1C rats to levels similar to those in sham-operated controls (sham) at 12 weeks after surgery. A reduced afterload failed to influence LV mass, as left LV hypertrophy developed to the same extent in treated 2K1C rats. 2K1C hypertension produced abnormal cardiac performance with altered cardiac output, stroke volume, and stroke work versus LVEDP relations (stroke work versus LVEDP, intercept of 2K1C versus sham,p<0.001). This was attributed to a decreased ventricular compliance (strain versus LVEDP, slope of 2K1C versus sham, p< 0.001). In contrast, hydrochlorothiazide improved ventricular compliance (strain versus LVEDP, slope of 2K1C versus 2K1C hydrochlorothiazide, p<0.01) and thus returned the stroke work versus LVEDP relation to sham values (intercept of 2K1C versus 2K1C hydrochlorothiazide, p< 0.001). We conclude that hydrochlorothiazide reduces blood pressure but not the development of ventricular hypertrophy in 2K1C rats. Although a reduced blood pressure did not produce regression of ventricular hypertrophy, it was associated with an improved ventricular compliance and thus performance. This study underscores the value of equating changes in ventricular hypertrophy with changes in cardiac function when the value of antihypertensive agents is being assessed. Received July 14, 1992; accepted in revised form December 15, 1992. Please note: After the manuscript was accepted, the authors sent a letter and revised manuscript because they discovered they had made a statistical error. The changes were sent to both reviewers. The manuscript with the revised changes was accepted January 27, 1993. ventricular performance. Studies on ventricular function in human hypertension are ethically limited by an inability to assess cardiac function over a range of controlled ventricular filling volumes and pressures. Abnormal ventricular systolic and diastolic functional changes in hypertensive heart disease may be detected only at controlled filling pressures.5 Therefore, improvement of ventricular function with hydrochlorothiazide may be detected only over a range of filling volumes and pressures. The effect of hydrochlorothiazide on cardiac performance at controlled filling volumes and pressures in hypertensive heart disease has not been investiga...

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Determinants of left ventricular filling and of the diastolic pressure-volume relation.

Cited by 382 publications

References 206 publications

The Kinematic Filling Efficiency Index of the Left Ventricle: Contrasting Normal vs. Diabetic Physiology

The Kinematic Filling Efficiency Index of the Left Ventricle: Contrasting Normal vs. Diabetic Physiology

Role of Nitric Oxide in the Progression of Cardiovascular Remodeling Induced by Carotid Arterio-Venous Shunt in Rabbits.

Hydrochlorothiazide improves ventricular compliance and thus performance without reducing hypertrophy in renal artery stenosis in rats.

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