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Project

Do shared “omics” biomarkers reveal a systemic pathogenetic condition explaining association between left ventricular dysfunction and macrovascular disease?

Atherosclerosis is the major disease of the macrovasculature and represents the major cause of morbidity and mortality worldwide due to heart attack and stroke. Heart failure (HF) is another syndrome that represents a major public health problem in developing and developed countries alike. A striking observation is that many of the risk factors predicting HF are also related to macrovascular disease. One mechanism that explains this is ventricular-arterial coupling. Stiffening of the large arteries is an age-dependent process that is accelerated by hypertension or diabetes and causes augmentation of late systolic blood pressure. The left heart ventricle (LV) adapts to the higher systolic load by hypertrophy and stiffening, which may lead to HF. However, an alternative hypothesis is that the change in the LV and macrocirculation are both expressions of systematic alterations driven by processes such as metabolic dysregulation, inflammation and fibrosis. The specific aim of this project is to examine whether structure and function of the macrovasculature are associated with the same proteomic, metabolomic and inflammatory biomarkers, which previous research identified as being mechanistically associated with systolic or diastolic dysfunction and thus lead to new insights in the pathophysiological mechanisms driving disease incidence. This project is based on the population-based FLEMENGHO study whose participants were thoroughly and repeatedly phenotyped.

Date:4 May 2015 →  10 Dec 2018
Keywords:Carotid artery, Intima-media thickness, Inflammatory markers
Disciplines:Cardiac and vascular medicine
Project type:PhD project