Relation of Left Ventricular Concentric Remodeling to Levels of C-Reactive Protein and Serum Amyloid A in Patients With Essential Hypertension

Tsioufis, Costas; Stougiannos, Pavlos; Kakkavas, Apostolis; Toutouza, Marina; Mariolis, Argiris; Vlasseros, I.; Stefanadis, Christodoulos; Kallikazaros, Ioannis

doi:10.1016/j.amjcard.2005.03.054

Cited by 38 publications

(40 citation statements)

References 21 publications

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“…35 Subsequently, 2 studies of hypertensive patients determined that increased LV wall thickness (concentric remodeling) or echocardiographic LVH were associated with elevations of CRP. 34,54 Herein, we found that increasing quartiles of LV wall thickness and concentricity were associated with elevated CRP in stepwise fashion in both men and women. However, the association of LVH with CRP did not persist in multivariable analysis after adjusting for body composition, lipid levels, age, and other confounders, suggesting that CRP was elevated in patients with LVH because of risk factors common to the development of LVH and CRP elevation.…”

Section: Discussionmentioning

confidence: 93%

“…30 -32 Yet another emerging hypothesis is that LVH itself is a low-level inflammatory state, as has been suggested recently from animal 33 and human studies. 34,35 If this is the case, one could postulate that the proinflammatory state associated with LVH may increase the risk of ASHD and incident myocardial infarction.The Dallas Heart Study is a large, ethnically diverse, population-based sample of Dallas County, Tex, in which subjects underwent cardiac MRI and coronary electron beam CT (EBCT) and had serum C-reactive protein (CRP) measured, affording an ideal opportunity to determine the mechanisms by which LVH increases the risk of ASHD. In this study we tested the following 2 hypotheses: LVH is independently associated with extent of subclinical atherosclerosis as measured by CAC, and LVH is independently associated with an elevation in CRP.…”

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Left Ventricular Hypertrophy, Subclinical Atherosclerosis, and Inflammation

et al. 2007

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Abstract-To elucidate mechanisms by which left ventricular (LV) hypertrophy (LVH) increases the risk of atherosclerotic heart disease, we sought to determine whether LVH is independently associated with coronary artery calcium (CAC) and serum C-reactive protein (CRP) levels in the general population. The Dallas Heart Study is a population-based sample in which 2633 individuals underwent cardiac MRI to measure LV structure, electron beam CT to measure CAC, and measurement of plasma CRP. We used univariate and multivariable analyses to determine whether LV mass and markers of concentric LV hypertrophy or dilation were associated with CAC and CRP. Increasing quartiles of LV mass indexed to fat-free mass, LV wall thickness, and concentricity, but not LV volume, were associated with CAC in both men and women (PϽ0.001). After adjustment for traditional cardiovascular risk factors and statin use, LV wall thickness and concentricity remained associated with CAC in linear regression (PϽ0.001 for each). These associations were particularly robust in blacks. LV wall thickness and concentricity were also associated with elevated CRP levels (Pϭ0.001 for both) in gender-stratified univariate analyses, although these associations did not persist in multivariable analysis. In conclusion, concentric LVH is an independent risk factor for subclinical atherosclerosis. LVH is also associated with an inflammatory state as reflected in elevated CRP levels, although this relationship appears to be mediated by comorbid conditions. These data likely explain in part why individuals with LVH are at increased risk for myocardial infarction. , whether determined by the ECG 1-9 or echocardiogram, 6 -8,10 -18 has been associated with various adverse cardiovascular outcomes, including mortality, myocardial infarction, and heart failure. Although there has been considerable speculation as to why LVH is such an important marker of risk, 19,20 the basic mechanisms that predispose patients with LVH to develop atherosclerotic heart disease (ASHD) are not known. Previous hypotheses have included abnormalities in the coronary vasculature 21-25 or platelets, 26 increased blood viscosity, 27 and a prothrombotic state. 28 In addition to these factors, which may contribute to reduced myocardial oxygen supply, myocardial oxygen demand is also increased in patients with LVH. 20 Another simple explanation for the association of LVH and ASHD is that LVH reflects target organ damage from concomitant risk factors, such as hypertension, thus providing a noninvasive barometer of the extent of ASHD. The association of LVH with atherosclerosis in other vascular territories, for example, the carotid artery, 29 supports this hypothesis. There are scant data as to whether LVH is associated with the burden of coronary atherosclerosis as estimated by coronary artery calcium (CAC). 30 -32 Yet another emerging hypothesis is that LVH itself is a low-level inflammatory state, as has been suggested recently from animal 33 and human studies. 34,35 If this is the case, one co...

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Section: Discussionmentioning

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Left Ventricular Hypertrophy, Subclinical Atherosclerosis, and Inflammation

et al. 2007

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“…11,12 As described earlier, the data were initially saved on the machine's archive (digital archive, raw data), and measurements were subsequently carried out by two independent operators, blinded to the patients' demographics and BP status. 13 The standard 2D and M-mode measurements, such as interventricular septum thickness, LV posterior wall thickness and LV end-systolic and end-diastolic diameter were averaged from five consecutive cardiac cycles. The LV mass was calculated using the regression equation recommended by the American Society of Echocardiography 14 and was indexed for body surface area to estimate the LV mass index.…”

Section: Study Populationmentioning

confidence: 99%

Left ventricular mass but not geometry determines left atrial size in the early stages of hypertension

et al. 2009

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We investigated whether the type of left ventricular (LV) geometry is associated with left atrial (LA) size as determined either by LA diameter or by volume, indexed for body surface area, in essential hypertensives. A total of 339 consecutive, untreated, hypertensives (aged 51.8 years, 234 males) underwent 24-h ambulatory blood pressure (BP) monitoring and estimation of LA diameter and volume, as well as LV structure and function by echocardiography. LV hypertrophy was present in 130 (38.3%) patients whereas normal geometry (LV-NG), concentric remodeling (LV-CR), concentric hypertrophy (LV-CH) and eccentric hypertrophy (LV-EH) represented 34.5, 27.1, 25.7 and 12.7%, respectively. Patients with either LV-CH or LV-EH had increased LA diameter index compared with those with either LV-NG (by 1.1 mm m -2 , Po0.01 and 1.4 mm m -2 , P ¼ 0.003, respectively) or LV-CR (by 1.3 mm m -2 , P ¼ 0.003 and 1.6 mm m -2 , P ¼ 0.001, respectively). Similarly, patients with either LV-CH or LV-EH had significantly increased LA volume index compared with those with either LV-NG (by 3.2 ml m -2 , Po0.001 and 3.4 ml m -2 , Po0.005, respectively) or LV-CR (by 4.5 and 4.7 ml m -2 , respectively, Po0.001 for both). Multiple linear regression analysis showed that the independent predictors of both LA volume and diameter index were LV mass index, 24-h pulse pressure and E/Em.LA size assessed either by its diameter or by volume is closely related only to LV mass index and not to any specific LV geometric pattern in the early stages of essential hypertension.

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“…5 Furthermore, the association of microalbuminuria and left ventricular concentric remodelling with increased hs-CRP supports the participation of inflammatory mechanisms in the manifestation of target organ damage in essential hypertensives. 6,7 Subjects with blunted nocturnal fall in blood pressure (BP), defined as non-dippers, exhibit a higher prevalence of target organ damage such as left ventricular hypertrophy, microalbuminuria, silent cerebrovascular disease and peripheral arterial changes, 8 thus being at higher risk for cardiovascular events. A critical point is whether this unfavourable outcome should be attributed to an accompanying increased haemodynamic load or to the actual failure to decrease BP levels during night time.…”

Section: Introductionmentioning

confidence: 99%

Disturbed circadian blood pressure rhythm and C-reactive protein in essential hypertension

et al. 2008

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We investigated the effect of the diverse definition criteria of the dipping and non-dipping status on the assessed differences in inflammatory activation between dippers and non-dippers with essential hypertension. 269 consecutive subjects (188 males, aged 50 ± 7 years) with untreated stage I-II essential hypertension underwent ambulatory blood pressure (BP) monitoring and high-sensitivity C-reactive protein (hs-CRP) level determination. The population was classified into dippers and non-dippers based on the three following different definitions: true non-dippers (TND): non-dippers (nocturnal fall of systolic and diastolic BP of o10% of the daytime values, n ¼ 95) and dippers (the remaining subjects, n ¼ 174); true dippers and true non-dippers (TD-TND): non-dippers (nocturnal fall of systolic and diastolic BPo10%, n ¼ 95) and dippers (nocturnal fall of systolic and diastolic BPX10%, n ¼ 75); systolic nondippers (SND): non-dippers (nocturnal systolic BP fall of o10% of the daytime values, n ¼ 145) and dippers (the remaining subjects, n ¼ 124). Non-dippers compared to dippers in the TND, TD-TND and SND classification exhibited higher levels of log hs-CRP (by 0.11 mg l À1 , P ¼ 0.02; 0.13 mg l À1, P ¼ 0.03 and 0.14 mg l À1, P ¼ 0.02, respectively) and 24 h pulse pressure (PP) (by 4 mm Hg, P ¼ 0.006; by 5 mm Hg, P ¼ 0.003 and by 5 mm Hg, Po0.0001, respectively). Twenty-four hour PP and nocturnal systolic BP fall were independent predictors of log hs-CRP (Po0.05 for both) in multiple regression analysis. In conclusion, essential hypertensive nondippers compared to dippers exhibit higher hs-CRP values, irrespective of the dipping status definition. Furthermore, ambulatory PP and nocturnal systolic BP fall interrelate and participate in the inflammatory processes that accompany non-dipping state.

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Relation of Left Ventricular Concentric Remodeling to Levels of C-Reactive Protein and Serum Amyloid A in Patients With Essential Hypertension

Cited by 38 publications

References 21 publications

Left Ventricular Hypertrophy, Subclinical Atherosclerosis, and Inflammation

Left Ventricular Hypertrophy, Subclinical Atherosclerosis, and Inflammation

Left ventricular mass but not geometry determines left atrial size in the early stages of hypertension

Disturbed circadian blood pressure rhythm and C-reactive protein in essential hypertension

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