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Coronary artery disease (CAD) is a well known cause of death and disability in patients worldwide. Although in some countries, mortality rates due to CAD have decreased, CAD is still responsible for one-third of all deaths in patients above the age of 35 years.1 Thus, many studies aim to search for new anti-ischemic therapy to treat CAD.
Collateral arteries provide blood-flow to the myocardium distal to a stenosis in a coronary vessel. Formation of these collateral arteries (arteriogenesis) is related to outcome as well as long-term survival after myocardial infarction.2 Interestingly, there is a significant variation in the arteriogenic response upon coronary stenosis. This variation is seen between different species and also within the same species, especially in mankind.3 In about one-third of patients with CAD, a coronary collateral circulation develops that is capable of restoring myocardial blood flow to a level at which complete blockage of antegrade flow by intracoronary balloon inflation does not lead to angina pectoris (AP) or ischaemia, as assessed by intracoronary derived electrocardiography (ECG). Supposedly, these patients will also not encounter exertional angina, at least not from that specific lesion. In two-thirds of patients, however, the development of the coronary circulation lags behind. Hence, this implies that there is a large potential for proarteriogenic therapy in the treatment of CAD. It also stresses the need to search for factors that …
Contributors Both authors contributed equally in this editorial.
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
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