Rapid ventricular filling in left ventricular hypertrophy: II. Pathologic hypertrophy

Smith, Vivienne E.; Schulman, Peter; Karimeddini, Mozafareddin K.; White, William Β.; Meeran, Moideen K.; Katz, Arnold M.

doi:10.1016/s0735-1097(85)80425-3

Cited by 207 publications

(59 citation statements)

References 19 publications

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“…7,8 Myocardial structural adaptation of hypertensive cardiovascular disease occurs early in the course of disease, and increased wall thickening can be found even in adolescents whose blood pressure is between the 75th and the 95th percentile for age, which are values considered within the normal range in adults.9,10 Impaired left ventricular filling, because of decreased relaxation in early diastole, is often pre- The sent in hypertensive patients before other arbitrary criteria of LVH are present, such as posterior wall thickness exceeding 1.1 cm, a ventricular mass exceeding an arbitrary value of 134 g/m2, or equally arbitrary voltage and vector criteria on the electrocardiogram. [11][12][13][14][15] In early hypertensive heart disease, impaired filling is predominantly caused by decreased relaxation during early diastole,16-18 whereas in more severe hypertensive heart disease, compliance during late diastole becomes impaired because of an increase in myocardial wall thickness.…”

Section: Point Of Viewmentioning

confidence: 99%

Antihypertensive therapy--going to the heart of the matter.

Messerli

1990

Circulation

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Section: Point Of Viewmentioning

confidence: 99%

Antihypertensive therapy--going to the heart of the matter.

Messerli

1990

Circulation

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“…One of the situations in which diastolic function may hypothetically be altered is chronic pressure overload resulting in pathological hypertrophy (18,30,36,41). RV pressure overload is common in congenital and acquired heart disease and may lead eventually to RV failure or to residual abnormalities in RV function, even after relief of the pressure load (5,7,17).…”

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confidence: 99%

Indexes of diastolic RV function: load dependence and changes after chronic RV pressure overload in lambs

Leeuwenburgh

Steendijk²,

Helbing

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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. Indexes of diastolic RV function: load dependence and changes after chronic RV pressure overload in lambs. Am J Physiol Heart Circ Physiol 282: H1350-H1358, 2002. First published December 13, 2001; 10.1152/ajpheart.00782.2001.-Diastolic function is a major determinant of ventricular performance, especially when loading conditions are altered. We evaluated biventricular diastolic function in lambs and studied possible load dependence of diastolic parameters [minimum first derivative of pressure vs. time (dP/dt min) and time constant of isovolumic relaxation ()] in normal (n ϭ 5) and chronic right ventricular (RV) pressure-overloaded (n ϭ 5) hearts by using an adjustable band on the pulmonary artery (PAB). Pressure-volume relations were measured during preload reduction to obtain the end-diastolic pressure-volume relationship (EDPVR). In normal lambs, absolute dP/dt min and were lower in the RV than in the left ventricle whereas the chamber stiffness constant (b) was roughly the same. After PAB, RV and dP/dt min were significantly higher compared with control. The RV EDPVR indicated impaired diastolic function. During acute pressure reduction, both dP/dt min and showed a relationship with end-systolic pressure. These relationships could explain the increased dP/dt min but not the increased -value after banding. Therefore, the increased after banding reflects intrinsic myocardial changes. We conclude that after chronic RV pressure overload, RV early relaxation is prolonged and diastolic stiffness is increased, both indicative of impaired diastolic function.hemodynamics; hypertrophy; pressure-volume relation; ventricular function, diastole THE IMPORTANCE of diastolic function as a major determinant of ventricular performance has long been recognized. Impaired diastolic function may precede systolic ventricular dysfunction (13,14), and it influences the performance of the contralateral ventricle via ventricular interdependence (23,34,39). The gold standard for determination of right ventricular (RV) [and left ventricular (LV)] diastolic function is still considered to be cardiac catheterization with simultaneous high-fidelity pressure and volume measurements (32).Because RV cineangiography is only sporadically performed during routine diagnostic catheterization and because complex RV geometry hampers adequate RV volume determination, few data are available about RV diastolic function. With the combined pressureconductance catheter it has recently become possible to determine ventricular pressure and volume simultaneously and independently of ventricular geometry in the LV as well as in the RV (3,11).Using this method, we are able to determine parameters of diastolic function such as the end-diastolic pressure-volume relationship (EDPVR) and chamber stiffness constant (b) that are well accepted for LV diastolic analysis. Furthermore, some of the LV relaxation parameters have shown a relationship with load (systolic pressure) that may render them less reliable to characterize intrinsic diastolic properties (26, 33)...

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“…Impaired left ventricular diastolic filling at rest is also a common finding in patients with hypertension, especially in those with ventricular hypertrophy, even in the absence of evidence of decreased systolic performance. [6][7][8][9] The relation between ventricular diastolic filling and the maintenance of adequate systolic function during exercise has not been addressed. As systolic tension development and ejection performance of the left ventricle depends to a large degree on completeness of relaxation and adequate diastolic filling, we hypothesized that impaired left ventricular filling in patients with hypertension might predispose to the reduced systolic functional reserve observed in many patients during exercise.…”

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confidence: 99%

Left ventricular hypertrophy and impaired diastolic filling in essential hypertension. Diastolic mechanisms for systolic dysfunction during exercise.

et al. 1990

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Left ventricular ejection fraction is normal at rest but may respond abnormally to exercise in many patients with essential hypertension. To assess the determinants of the abnormal ejection fraction response to exercise, we performed radionuclide angiography at rest and during exercise in 41 hypertensive patients without coronary artery disease. In 22 patients (group 1), the ejection fraction increased more than 5% during exercise; in the other 19 patients (group 2), the ejection fraction either increased by less than 5% or decreased with exercise. Left ventricular diastolic filling was impaired at rest in patients in group 2 compared with group 1, with reduced peak filling rate (2.5±0.4 vs. 3.1±0.7 end-diastolic volume/sec; p<0.01) and prolonged time to peak filling rate (175±28 vs. 153+±22 msec; p<0.01). Impaired diastolic filling in group 2 was associated with less augmentation in end-diastolic volume during exercise compared with group 1 (p <0.01). These observations were not dependent on the threshold value that was arbitrarily chosen to define an abnormal ejection fraction response, as there were significant correlations for the entire group between the magnitude of change in ejection fraction with exercise and both the resting peak filling rate (r=0.46) and the change in end-diastolic volume with exercise (r=0.62). Echocardiographic left ventricular mass index was greater in group 2 than in group 1 (141±32 vs. 114+±25 g/m2;p<0.01), and for the entire group was significantly related to peak filling rate (r= -0.50) and time to peak filling rate (r= 0.53). Thus, the abnormal ejection fraction response to exercise in patients with hypertension is related to greater left ventricular mass index and impaired diastolic filling, leading to inadequate augmentation of end-diastolic volume during exercise to maintain systolic function. These findings support the concept that exercise-induced systolic dysfunction in hypertensive patients with left ventricular hypertrophy arises predominantly from diastolic mechanisms. (Circulation 1990;81:978-986

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Rapid ventricular filling in left ventricular hypertrophy: II. Pathologic hypertrophy

Cited by 207 publications

References 19 publications

Antihypertensive therapy--going to the heart of the matter.

Antihypertensive therapy--going to the heart of the matter.

Indexes of diastolic RV function: load dependence and changes after chronic RV pressure overload in lambs

Left ventricular hypertrophy and impaired diastolic filling in essential hypertension. Diastolic mechanisms for systolic dysfunction during exercise.

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