Abstract
Coronary artery disease, myocardial infarction, and secondary damages of the myocardium in the form of ischemic heart disease remain major causes of death in Western countries. Beyond traditional risk factors such as smoking, hypertension, dyslipidemia, or diabetes, a positive family history is known to increase risk. The genetic factors underlying this observation remained unknown for decades until genetic studies were able to identify multiple genomic loci contributing to the heritability of the trait. Knowledge of the affected genes and the resulting molecular and cellular mechanisms leads to improved understanding of the pathophysiology leading to coronary atherosclerosis. Major goals are also to improve prevention and therapy of coronary artery disease and its sequelae via improved risk prediction tools and pharmacological targets. In this chapter, we recapitulate recent major findings. We focus on established novel targets and discuss possible further targets which are currently explored in translational studies.
Highlights
Coronary artery disease (CAD) and myocardial infarction (MI) are the main causes of morbidity and mortality
Hyperlipidemia, hypertension, and diabetes mellitus are examples for risk factors which can be treated via pharmacological intervention, whereas smoking and obesity can be addressed by lifestyle interventions
We summarize the developments in the past years which led to the identification of a plethora of genomic loci which are associated with CAD with high statistical certainty
Summary
Coronary artery disease (CAD) and myocardial infarction (MI) are the main causes of morbidity and mortality. The identification of risk factors is a prerequisite to improve prevention and therapy of the disease via gaining knowledge about the underlying pathophysiological processes as well as the identification of therapeutic targets. Age and male gender, which are major risk factors, cannot be addressed therapeutically. A positive family history has been regarded as a non-modifiable risk factor. The underlying risk factors were not known for decades. The methodological spectrum has been vastly expanded to identify novel genetic risk factors of CAD and MI. Details on these methods have been discussed elsewhere (Kessler et al 2016). We aim to briefly mention some important points
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