Endothelial cell function,inflamamtion and infection, acute coronary syndromes, atherosclerosis, coronary flow.
Principal investigator; Pesonen, Erkki, Professor, MD/PhD
Co-workers: Petru Liuba, Postdoc; Ansgar Berg, postdoc,; Hans Öhlin, doc; Kenneth Persson doc; Ilari Paakkari, prof;; Axel Kornerup-Hanssen, prof,; Lennart Truedsson, prof
Vascular endothelial cells have important regulatory functions in preserving the vessel's homestasis and regulating coronary flow. Much of these protective functions are mediated by endothelial NO. Following an endothelial injury there is a decreased bioactivity of endothelial NO. Depending on the intensity and the duration of the injurious stimuli, it may either contribute to acute vascular events, i.e. spasm, thrombosis, or progress toward atherosclerosis.
Children with infection, immunizations and diabetes seem to have decreased endothelial cell function. Myocardial infarction is associated with preceding inflammation. Chlamydia etnerotoxin in circulation is a risk factor for a new infarction and death. A prominent symptom before a coronary attack is tiredness which is associated with elevated microbial antibody titers. Bacteria initiating periodontitis seem to be associated with appearance of stenoses in the coronary arteries. Incresed levels of mannose binding lectin in the serum as well as genes producing plenty of it are associated with increased incidence of acute coronary syndromes. A persistent inflammation exists before the acute event. The increase of serum MMP-8 and TIMP-1 concentrations may reflect plaque instability and tissue damage. TIMP-1 may exert a continuous damaging stimulus on the vascular wall, inducing stimulating smooth muscle cell proliferation and promoting inflammation. If TIMP-1 is “over produced” as a response to acute phase MMP-8 expression or if its production is not suppressed enough during the recovery, the prognosis is poor.
Systemic infections initiate vascular endothelial dysfunction. The mechanisms of atherogenesis and myocardial infarction involve vascular endothelial dysfunction. Infections are risk factors for acute coronary syndromes, intimal thickening of the arteris in children and later atherosclerosis of the coronary arteries. Infections initiate a chronic vascular wall damage and acute infections may precipitate unstable angina pectoris and myocardial infarction.
5 recent original publications
Pirkko Pussinen, SeppoSarna, Mirja Puolakkainen, Hans Öhlin, Timo Sorsa, Erkki Pesonen
The balance of serum matrix metalloproteinase-8 and its tissue inhibitor in acute 2 coronary syndrome and its recurrence
International Journal of Cardiology. 2012; E-pub ahead of print:
Liuba P, Pesonen E, Paakkari I, Batra S, Forslid A, Kovanen P, Pentikainen M, Persson K, Sandstrom S.
Acute Chlamydia pneumoniae infection causes coronary endothelial dysfunction in pigs.
Atherosclerosis. 2003; 167: 215-22.
Elhadi Aburawi, Petru Liuba, Erkki Pesonen, Seppo Ylä-Herttuala, Sture Sjöblad. Acute Respiratory Viral Infections Aggravate Arterial Endothelial Dysfunction in Children with Type 1 Diabetes Mellitus.
Acute Respiratory Viral Infections Aggravate Arterial Endothelial Dysfunction in Children with Type 1 Diabetes Mellitus
Diabetes Care. 2004; 27: 2733-5
Óskarsson G, Pesonen E, Munkhammar P, Sandstrom S, Jogi P.
Normal coronary flow reserve after arterial switch operation for TGA - an intracoronary Doppler guide wire study.
Circulation.. 2002; 10: 1696-702.
Pesonen E, Andsberg E, Ohlin H, Puolakkainen M, Rautelin H, Sarna S, Persson K.
Dual role of infections as risk factors for coronary heart disease
Atherosclerosis. 2007; 192: 370-5
Further publications here (new window)
|Total financing:||MSEK||Gov grant for clinical research ("ALF"):||MSEK|
|Total external financing:||MSEK||Natl and intl prioritized grants:||MSEK|