Ischemic heart disease is the most important cause of death worldwide. It is etiologically multifactorial and genetically heterogeneous, inflammatory disease. Clinical and epidemiological studies have documented that strong risk factors such as increased serum cholesterol, diabetes mellitus, hypertension, age, male sex, and family history predict the risk for coronary artery disease. However, it is influenced by environmental factors, such as smoking and diet, but also by of other pathophysiological mechanisms such as coagulation disorders, and lipopolysaccharide release from mouth and intestine. These traits are also genetically influenced. Twin studies estimates heritability of death from CAD to be 38-57%.

An atherosclerotic plaque development is characterized by accumulation of modified LDL and infiltration of inflammatory cells. Both of these are necessary for the generation of an inflammatory response of the arterial wall. Without inflammation, LDL-cholesterol accumulation does not induce the formation of a vulnerable plaque. Once activated, inflammatory cells secrete a myriad of cytokines that promote inflammation. T-cell repertoire depends on these cytokines, and they can either promote or suppress inflammation. The system that regulates inflammation, immunity and cellular defensive mechanisms lies in big part in the Major Histocompatibility Complex region on chromosome 6p21.31. This area contains Human leucocyte antigen (HLA) genes. HLA-driven antigen presentation to T cells is essential for adaptive immune responses. For example ApoB-derived peptides may stimulate proliferation of the antigen-specific T cell clone and aggravation of atherogenesis.

We have shown that a novel haplotype in chromosome 6p21, combining HLA-DRB1*01 and BTNL2 was more than three times more common in acute coronary syndrome patients than in control subjects. This haplotype could be found in 14.5% of genetically selected ACS patients and in 4.4% of controls. This haplotype cannot be found with GWAS due to the fact that there is no universal SNP for detecting HLA-DRB1*01, which has to be first detected by PCR or sequencing. In another study we have shown that a genetic variants on chromosome 1p13.3 are associated with non-ST elevation myocardial infarction and to the expression of DRAM2 gene.

Our epidemiological studies have revealed that blood transfusions for acute coronary syndrome patients are connected to higher long term mortality, which may be explained by increased incidence of cancers among transfusion receivers’. Also we have shown that adherence to statin use is connected to decreased mortality after myocardial infarction.

Our Takotsubo-cardiomyopathy studies have discovered that ECG is not reliable method to distinguish Takotsubo-cardiomyopathy from acute coronary syndrome, but high TIMP-1 may help in distinction.


We carry on basic and translational research from pathogenesis and immunogenetics to epidemiology and clinical drug trials. Our aim is to discover basic mechanisms behind coronary artery disease, and to influence them in order so that patients in our cardiological clinic would benefit of our research.

Ongoing studies are based on large collected materials such as Corogene-study, ASO-material and the hearts' explanted during transplantation. Epidemiological studies are based mainly on over ten years follow up data of Corogene-study. Clinical drug trials are located in Meilahti Hospital, Heart and Lung Center. Pathogenesis, inflammation, immunogenetics studies are done in Haartman-institute.



  • Extraction
  • Sequencing (Sanger, NGS)
  • qPCR
  • Specialised methods: HLA typing and MLPA



  • Tissue and WBC extraction
  • Reverse transcription and qPCR



  • Histological and fluorescent stainings
  • Deep learning network AI image analyses
  • µCT scans and 3D image analyses