Molecular imaging targets of cardiac remodeling

Abstract

Left ventricular (LV) remodeling is a major determinant of the clinical course and outcome of systolic heart failure (HF). Activation of neurohormonal and inflammatory cytokine pathways and their effects on intracellular signal transduction cascades through stimulation of membrane-bound receptors mediate LV remodeling. Although major advances have been made in clinical management of HF through large randomized trials, its prognosis remains poor. Interindividual differences, often genetically based, are increasingly recognized as important determinants of LV remodeling. Identification of the influence of these individual factors on the clinical course of HF has stimulated a search for specific pathophysiologic mechanisms that operate at the individual level and can be targeted directly. This article summarizes the current application of molecular imaging techniques to the understanding of the cellular and molecular mechanisms involved in LV remodeling in an attempt to provide the tools necessary for personalized, truly "evidence-based" assessment, serial evaluation, and monitoring of HF.

Association of Long Noncoding RNA Expression Signatures with Stress-Induced Myocardial Perfusion Defects

“…However, other microvascular heart conditions, such as dysregulated stress adaptation and cardiac remodeling, can also lead to a positive thallium stress test and affect the patient's quality of life. Advanced nuclear molecular imaging techniques have been developed to detect molecules along the pathophysiological pathways of cardiac remodeling [27][28][29]. However, these techniques require advanced radiopharmaceuticals or modalities.…”

Astragaloside IV inhibits ventricular remodeling and improves fatty acid utilization in rats with chronic heart failure

“…A 5- and 10-year survival rate of CHF patients is estimated to be 50 and 10%, respectively, and is even lower in developing countries [ 6 , 7 ]. Ventricular remodeling, including ventricular wall thickening, ventricle dilation, and collagen fiber proliferation, is an important pathological feature of CHF and contributes to ventricular dysfunction, and increase in oxygen consumption, and even cardiac death [ 8 , 9 ]. Inhibiting ventricular remodeling is thus a primary treatment target for CHF patients and a large number of studies have been carried out to achieve this objective [ 10 ].…”