Left Ventricular Hypertrophy, Subclinical Atherosclerosis, and Inflammation

Abstract

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...

Normative Temporal Values of CRP and ESR in Unilateral and Staged Bilateral TKA

“…However, we believe we covered typical times for routine practice. Fourth, the levels of CRP and ESR are influenced by the presence of systemic conditions [6,9,18,24]. In our study, we found no differences in the prevalence of the systemic conditions between the unilateral and staged bilateral groups.…”

“…The data on the fortysecond and ninetieth postoperative days only were compared between the unilateral and the second knee bilateral groups. Because the levels of CRP and ESR are influenced by the presence of other systemic conditions (diabetes mellitus, cardiac diseases, chronic lung and kidney disease, and cancers) [6,9,18,24], proportions of patients with the systemic conditions were compared between the unilateral and the staged bilateral groups. There were no differences in the prevalence of systemic conditions between the unilateral and staged bilateral groups (20.3% versus 27.9%; p [ 0.05, chi square test).…”

Incremental role of resting myocardial computed tomography perfusion for predicting physiologically significant coronary artery disease: A machine learning approach

“…The myocardial thickness and Describe cut-off points: CT stenosis, C70% coronary stenosis by CCTA; Resting CTP, C30 of likelihood (%) of having a perfusion defect; significant ischemia, B0.8 by invasive fractional flow reserve PPV, positive predictive value; NPV, negative predictive value; CT, computed tomography; CTP, computed tomography perfusion ratio of subendocardium perfusion to subepicardial perfusion are easily obtainable parameters when performed using CTP analysis and are closely related to ischemia. Indeed, previous data suggest that a high myocardial thickness is associated with atherosclerotic burden and elevated inflammatory activity, 29 and was found to be an independent predictor of adverse events in addition to coronary atherosclerosis and myocardial ischemia. 30 It is also well known that there are significant relationships between the subendocardium-tosubepicardial perfusion ratio and ischemia.…”

Left Ventricular Hypertrophy Development, Associated With Genetic Polymorphism of Inflammatory Mediators

“…накопилось значительное число наблюдений, которые свидетельствуют в пользу участия факторов, традиционно относимых к сис-теме воспаления, в развитии гипертрофии левого желудочка. В популяционных исследованиях выяв-лена ассоциация уровня С-реактивного белка (СРБ) и толщины стенки левого желудочка [1], механизм которой неясен -обнаружено, что ГМЛЖ может предсказывать при длительном наблюдении последу-ющее повышение СРБ [2]. Найдены эксперименталь-ные подтверждения участия интерлейкина-6 (ИЛ-6) и фактора некроза опухоли альфа в развитии ГМЛЖ [3].…”

“…Есть данные об ассоциации уровня СРБ c уровнем АД и развитием ГМЛЖ [1]. Биохимической основой для взаимосвязи между развитием ГМЛЖ и уровнем СРБ является то, что, стимулируя синтез адгезивных молекул и матрикс-ных металлопротеиназ, СРБ активирует тучные клетки, которые могут синтезировать факторы роста и потенцировать развитие фиброза миокарда.…”