Left ventricular hypertrophy in children with blood pressures in the upper quintile of the distribution. The Muscatine Study.

Schieken, Richard M.; Clarke, William R.; Lauer, Ronald M.

doi:10.1161/01.hyp.3.6.669

Cited by 125 publications

(35 citation statements)

References 45 publications

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“…20 Left ventricular mass, although frequently the result of uncontrolled blood pressure in adults, has been found to add significantly to the prediction of future blood pressure in children, with those children with the highest left ventricular mass having the greatest probability of developing higher blood pressures in the future. 21 Similarly, as is the case with adults, weight is a potent predictor of blood pressure, and excessive weight gain during the adolescent years is particularly predictive. 19 Future research in the area of childhood predictors of hypertension will center around refinement of current predictors, development of better laboratory predictors, including investigations of hormonal predictors such as insulin and cationic transporters such as sodium-hydrogen antiporter, and integration of these blood pressure-related predictors with other predictors of diseases having origins that might very well be in childhood, such as hyperlipidemic states and atherosclerosis.…”

Section: Clinical Predictorsmentioning

confidence: 95%

Epidemiology of blood pressure and predictors of hypertension.

Horan

Lenfant

1990

Hypertension

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Hypertension is a clinical disease with a prevalence sufficiently high in acculturated societies to warrant it being designated a serious public health problem. In population studies, blood pressure has been found to be a continuously distributed risk variable with mortality directly related to the level of blood pressure. Thus, hypertension is both a disease and a risk factor. Classic genetic studies suggest that the predisposition for the development of hypertension is an inherited trait that becomes manifest when coupled with one or more environmental insults. Risk factors for hypertension include age, weight, sedentary lifestyle, excessive dietary sodium intake, and excessive alcohol intake. Current and future research is being directed toward the identification of predictors of hypertension that can be conceptualized according to demographic, clinical, genetic, challenge-response, and laboratory predictors. The intent is to identify subjects with a high probability for the development of hypertension in advance of the rise in blood pressure so that appropriate interventions can be implemented as early as possible.

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Section: Clinical Predictorsmentioning

confidence: 95%

Epidemiology of blood pressure and predictors of hypertension.

Horan

Lenfant

1990

Hypertension

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“…This opinion is based on the linear relation between blood pressure and left ventricular hypertrophy in the general population as well as the age-related increase of cardiac hypertrophy in such populations. However, the literature suggests that changes in cardiac function 21 and morphology 22 may be already present in the earliest forms of hypertension. The blood pressure elevations in our experiment, though transient, certainly are not trivial and exceed naturally occurring pressor episodes.…”

Section: Cardiac Hypertrophymentioning

confidence: 99%

Neurogenic pressor episodes fail to cause hypertension, but do induce cardiac hypertrophy.

et al. 1989

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Repeated neurogenic pressor episodes by hindquarter compression were elicited in nine experimental dogs. Conscious dogs underwent 6 hours of compression every day over a period of 9 weeks. The average mean blood pressure increase during the compression periods was 25 mm Hg, but after decompression the blood pressure promptly returned to baseline values. This blood pressure response was constant and did not change over the 9-week period. The blood pressure increase was associated with a significant increase of plasma norepinephrine values. After validity of the model was established, echocardiographic measurements were performed at baseline and after 3, 6, and 9 weeks of compression in six experimental and six time-control dogs. Concentric left ventricular hypertrophy was already detectable at 3 weeks, and at the ninth week, the left ventricular mass was 28% above the baseline value T wo notions are deeply engrained in the traditional thinking about hypertension. The first is that patients with hypertension undergo a phase of "labile" neurogenic hypertension 1 that eventually, through the cumulative effect of pressor episodes, leads to sustained hypertension.2 Second is that labile blood pressure per se is an innocuous condition 3 and that target organ damage is a relatively late complication of sustained hypertension. This attitude largely determines the rather cautious "wait until the blood pressure is permanently elevated" approach to antihypertensive treatment. 4 However, practicing physicians increasingly recognize that some patients with even the mildest forms of hypertension already show signs of left ventricular hypertrophy and that such patients may require early treatment. Received September 21, 1988, accepted December 5, 1988 We developed a model to elicit repeated pressor episodes in dogs. 56 The following lines of evidence obtained in chloralose-anesthetized animals indicate that the blood pressure increase during compression is neurogenic: 1) blood pressure elevation is associated with increase of plasma norepinephrine and plasma renin as well as an acceleration of heart rate; 2) the increase of blood pressure, plasma norepinephrine, and renin are abolished by a low spinal anesthesia; 3) hemodynamically the blood pressure increase is due to an elevation of vascular resistance, and both high resistance and blood pressure are abolished with ganglionic blockade; and 4) the blood pressure response is not altered when the circulation to the hindquarter has been severed through ligation of the vena cava and the lower aorta. This, in turn, suggests that the afferents for the reflex originate in the hindquarters and proves that the response is not dependent on distant effects of the translocated blood or chemical effluents from the compressed area. Our results have been confirmed by Bradley and Hjemdahl 7 who linked the blood pressure response to enhanced neurogenic drive to the kidneys.This model offers unique opportunities to study the effects of transient blood pressure elevation on by guest on May 11, ...

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“…This reported link between cardiac hypertrophy and more elevated rates of NaLi CT in hypertensive groups does not necessarily indicate a direct association, and there are more physiologically plausible explanations. Hypertensive subjects with elevated rates of Na-Li CT could be a subgroup with slight elevations in blood pressure with the normal range before "true" hypertension developed [28,29], or with a greater duration of hypertension [26] or with exaggerated pressor responses to exercise [27], all of which would account for an exaggerated hypertrophic response in this group.…”

Section: Discussionmentioning

confidence: 99%

Association between left ventricular hypertrophy and erythrocyte sodium-lithium exchange in normotensive subjects with and without NIDDM

et al. 1995

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SummaryThe determinants of left ventricular mass in normal control subjects and subjects with non-insulindependent diabetes (NIDDM) are ill-defined. We therefore recorded M-mode and pulsed Doppler echocardiograms and 24-h ambulatory blood pressure in 57 normotensive subjects, 34 with NIDDM and 23 matched non-diabetic control subjects 9 Measurements of erythrocyte sodium-lithium countertransport, plasma angiotensin II, plasma and platelet catecholamines and fasting plasma insulin were also made. Six control subjects (26 %) and 15 diabetic subjects (44 %) had some degree of left ventricular hypertrophy. Subjects with left ventricular hypertrophy (n = 21) had an elevated mean rate of sodium-lithium countertransport (0.40 + 0.13 vs 0.31 + 0.09 mmol. 1-1 9 h-l; p < 0.01), parallel differences being observed in both the diabetic and control groups. Twelve of the subjects with left ventricular hypertrophy (57 %) had elevated rates of sodium-lithium countertransport compared to only seven (19 %) of those without (p < 0.05) 9 There was no consistent difference between those with and without left ventricular hypertrophy in any other clinical or biochemical variable. Multivariate analysis, with the presence or absence of left ventricular hypertrophy as the dependent variable, demonstrated that the maximal rate of sodium-lithium countertransport was the only variable that independently contributed to left ventricular hypertrophy (partial r= 0.35; F~.ss = 7.74; p = 0.007). This study demonstrates for the first time an association between left ventricular hypertrophy and erythrocyte membrane cation transport that is independent of hypertension, is present in both diabetic and non-diabetic groups, and may represent a link between elevated rates of membrane sodium transport and cardiovascular risk. [Diabetologia (1995) non-insulin-dependent diabetes (NIDDM) suffer from cardiovascular disease at a rate in excess of that predicted by known cardiovascular risk factors [5], and there is some limited evidence that NIDDM is independently associated with an increased left ventricular mass [6].Age, body mass index and blood pressure all contribute to population variability in left ventricular mass [7], but the potential contributions of the renin-angiotensin system [8], plasma catecholamines [9], insulin and insulin resistance [10] and membrane cation transport [11] are well recognised, at least in hypertensive populations. NIDDM patients and non-diabetic subjects differ in many of these variables, but whether this contri-

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Left ventricular hypertrophy in children with blood pressures in the upper quintile of the distribution. The Muscatine Study.

Cited by 125 publications

References 45 publications

Epidemiology of blood pressure and predictors of hypertension.

Epidemiology of blood pressure and predictors of hypertension.

Neurogenic pressor episodes fail to cause hypertension, but do induce cardiac hypertrophy.

Association between left ventricular hypertrophy and erythrocyte sodium-lithium exchange in normotensive subjects with and without NIDDM

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