Inflammatory markers are associated with left ventricular hypertrophy and diastolic dysfunction in a population-based sample of elderly men and women

Abstract

Markers of inflammation have previously been related to left ventricular (LV) hypertrophy (LVH) in uremic and hypertensive patients. The present study investigated inflammatory markers in relation to LV geometry and diastolic function in a population of elderly persons. In the population-based Prospective Study of the Vasculature in Uppsala Seniors (PIVUS) study (1016 men and women 70 years of age), echocardiograms to determine relative wall thickness (RWT), LV mass index (LVMI) and the E/A-ratio were obtained. Based on RWT and LVMI, four geometric subgroups were defined; normal, concentric remodeling, eccentric and concentric LVH. In all, 10 circulating inflammatory markers were measured. Higher levels of high sensitive C-reactive protein (hsCRP) and E-selectin were seen in the three abnormal geometry groups than in the normal group adjusting for gender, body mass index, systolic and diastolic blood pressure and use of antihypertensive medication. Higher level of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1) and P-selectin were only seen in concentric LVH. Levels of tumor necrosis factor-alpha, interleukin-6, l-selectin, monocyte chemotactic protein-1 and leukocyte count did not differ between the LV groups. l-selectin and hsCRP were related to the E/A-ratio. The adhesion molecules; E-selectin, ICAM-1, VCAM-1, P-selectin and hsCRP were elevated in elderly persons with abnormal LV geometry, especially in concentric LVH, after adjusting for hypertension and obesity. l-selectin and hsCRP were related to LV diastolic function. Further studies are motivated to investigate a pathogenetic role of inflammation for abnormal LV geometry and function.

Angiopoietin-2, Angiopoietin-1 and subclinical cardiovascular disease in Chronic Kidney Disease

“…Masiha et al . reported that inflammatory markers such as high-sensitivity c –reactive protein (hsCRP), ICAM-1, and VCAM-1 were elevated in concentric LVH, and hsCRP was correlated with LV diastolic function, while inflammation might play a pathogenetic role in abnormal LV geometry and function20. On the other hand, Angpt2 is associated with pro-inflammatory responses with P-selectin, E-selectin and VCAM-112.…”

Left ventricular diastolic function and cardiometabolic factors in obese normotensive children

“…In a recent study, inflammatory markers and endothelial activation molecules were found to be associated with LV hypertrophy and diastolic dysfunction in a population-based sample of elderly men and women [11]. We can hypothesize that inflammation that leads to endothelial activation triggers the cardiac fibrosis; therefore, it can play an important role in diastolic dysfunction.…”

“…Recently, both LV hypertrophy and diastolic dysfunction have been found to be associated with systemic inflammation in obese and hypertensive adults [10,11]. This association might be mediated by clinical risk factors that are themselves related to an inflammatory state.…”

Right ventricular hypertrophy in systemic hypertension

“…Ten out of 13 studies [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25]26] included normotensive controls in their series and all but one study [27] showed a significant increase in right ventricular wall thickness in hypertensive patients as compared to their normotensive counterparts. Fig.…”

“…Moreover, elevated left ventricular pressure due to diastolic dysfunction in hypertrophied hearts is an important mechanism leading to venous pulmonary hypertension and to right ventricular pressure overload [12,13]. Finally, left ventricular hypertrophic adaptation to systemic hypertension is multifactorial being sustained by a number of growth factors including aldosterone, catecholamines, angiotensin, insulin, cytokines and inflammatory markers [14,15]. All these circulating or locally produced substances may be responsible of the hypertrophic response of the right ventricular independently of haemodynamic alterations of the pulmonary circulation.…”