25 Feb Blood Amyloid Level Linked to Mortality from Heart Disease
MedicalResearch.com Interview with:
Prof. Konstantinos Stellos, MD, DM, MRCP, DSc, FAHA, FESC
Professor of Medicine, Chair of Cardiovascular Medicine, Chair of Epitranscriptomics
Lead, Vascular Biology & Medicine Theme
Hon. Consultant Cardiologist, Newcastle Hospitals NHS Foundation Trust
Biosciences Institute Faculty of Medical Sciences
MedicalResearch.com: What is the background for this seminar? Can you tell us a little about how amyloid is made and stored?
Response: Patients are afraid that they may die due to a heart attack – a major cause of death worldwide- or if they live long they may get dementia compromising severely their quality of life in their last years of life. Many years ago we asked the question whether there is a link between these two ageing-associated diseases. For this reason we studied the clinical value of amyloid-beta peptides in patients with coronary heart disease.
We chose to study the amyloid-beta peptides, which are the cleavage product of the beta- and gamma-secretases of the mother protein amyloid precursor protein, because amyloid-beta plaques in brain is the hallmark of Alzheimer’s disease. Following amyloid precursor protein (APP) gene transcription, APP is cleaved in the nonamyloidogenic pathway (plasma membrane) by α- and γ- secretases or in the amyloidogenic pathway (endosomes) by β- and γ- secretases. The later pathway generates amyloid beta (Αβ) peptides that are released extracellularly. Αβ accumulation in blood or tissues may result from enhanced production/cleavage or by impaired degradation and/or clearance. The related mechanisms are depicted in Figure 2 of our publication in JACC: http://www.onlinejacc.org/content/75/8/952
MedicalResearch.com: What are the main findings?
1) Excess in blood Αβ1-40 levels exerts detrimental effects in vascular and blood cells promoting endothelial activation, atherosclerosis, and atherothrombosis. See also Figure 3 of the same publication.
2) A single measurement of circulating Aβ1-40 at presentation was independently associated with mortality in coronary heart disease. Importantly, Αβ1-40 substantially improved risk stratification into correct risk categories over established risk models in both chronic and acute coronary syndromes.
3) Lifestyle modifications and several cardiovascular medications may affect Aβ1-40 blood levels.
MedicalResearch.com: What should readers take away from your report?
Response: Aβ, an aging-induced peptide and the hallmark of the amyloid hypothesis of Alzheimer’s disease, constitutes an independent cardiovascular risk factor.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Response: Clinical application of this peptide as a biomarker needs further research to set reference values and thus allow its investigation as part of novel prognostic algorithms in coronary heart disease.
There are no disclosures related to this work.
The Alzheimer’s Disease Amyloid-Beta Hypothesis in Cardiovascular Aging and Disease
Dimitrios A. Stakos, Kimon Stamatelopoulos, Dimitrios Bampatsias, Marco Sachse, Eleftherios Zormpas, Nikolaos I. Vlachogiannis, Simon Tual-Chalot, Konstantinos Stellos
J Am Coll Cardiol. 2020 Mar, 75 (8) 952-967.
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Last Updated on February 25, 2020 by Marie Benz MD FAAD