Inflammation and atherosclerosis
Risk associations in the HUNT surveys
Thesis for the degree of Philosophiae Doctor Trondheim, June 2012
Norwegian University of Science and Technology Faculty of Medicine
Department of Laboratory Medicine, Children’s and Women’s Health
Inga Thorsen Vengen
NTNU
Norwegian University of Science and Technology Thesis for the degree of Philosophiae Doctor Faculty of Medicine
Department of Laboratory Medicine, Children’s and Women’s Health
© Inga Thorsen Vengen
ISBN 978-82-471-3597-6 (printed ver.) ISBN 978-82-471-3598-3 (electronic ver.) ISSN 1503-8181
Doctoral theses at NTNU, 2012:155
Printed by NTNU-trykk
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Cardiovascular diseases
• Ischemic heart disease
• Cerebrovascular disease
• Diseases of the aorta and arteries (including hypertension and peripheral vascular disease)
• Rheumatic heart disease
• Congenital heart disease
• Cardiomyopathies
• Cardiac arrhythmias
Table 1.1 Definition of cardiovascular diseases
Worldwide distribution of major causes of death
Injuries 9%
Communicable diseases* 27%
All-cause CVD 31%
Other non-communicable diseases 33%
Figure 1.1 All-cause CVD is the leading cause of death worldwide. *Communicable, maternal, perinatal and nutritional conditions. Modified from WHO.
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Worldwide distribution of cardiovascular deaths
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Figure 1.2Deaths due to myocardial infarction, stroke and other types of cardiovascular
diseases worldwide. Modified from WHO
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Behavioral risk factors
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Lifestyle related disease
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•Hypertension
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Figure 1.3 Risk factors for atherosclerotic CVD.
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Right coronary artery
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Figure 1.5 Myocardial infarction due to plaque rupture.
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Figure 1.6 Inflammatory cells in the atherosclerotic plaque.
Lipoproteins accumulate in the intima and monocytes are attracted. The monocytes develop into macrophages, which ingest LDL and oxidized LDL and become foam cells. T-helper cells interact with dendritic cells and activate macrophages. Smooth muscle cells proliferate and produce collagen. Neutrophil granulocytes are activated and release substances that can lead to formation of vulnerable plaques. The complement system is involved in the clearing of apoptotic cells. Inefficient removal of dying cells may lead to the formation of a necrotic core.
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