Cardioprotection during ischemia by coronary collateral growth

Abstract

Ischemic heart diseases (IHD) cause millions of deaths around the world annually. While surgical and pharmacological interventions are commonly used to treat patients with IHD, their efficacy varies from patient to patient and is limited by the severity of the disease. One promising, at least theoretically, approach for treating IHD is induction of coronary collateral growth (CCG). Coronary collaterals are arteriole-to-arteriole anastomoses that can undergo expansion and remodeling in the setting of coronary disease when the disease elicits myocardial ischemia and creates a pressure difference across the collateral vessel that creates unidirectional flow. Well-developed collaterals can restore blood flow in the ischemic area of the myocardium and protect the myocardium at risk. Moreover, such collaterals are correlated to reduced mortality and infarct size and better cardiac function during occlusion of coronary arteries. Therefore, understanding the process of CCG is highly important as a potentially viable treatment of IHD. While there are several excellent review articles on this topic, this review will provide a unified overview of the various aspects related to CCG as well as an update of the advancements in the field. We also call for more detailed studies with an interdisciplinary approach to advance our knowledge of CCG. In this review, we will describe growth of coronary collaterals, the various factors that contribute to CCG, animal models used to study CCG, and the cardioprotective effects of coronary collaterals during ischemia. We will also discuss the impairment of CCG in metabolic syndrome and the therapeutic potentials of CCG in IHD.

Correlation Between Ischemia-Modified Albumin Level and Coronary Collateral Circulation

“…When the blood flow of the coronary artery is severely reduced or occluded, anastomotic branches with a diameter of 20-350 μm between the coronary arteries gradually generate functional collateral circulation through a series of mechanisms under the control of end-to-side pressure of the coronary artery [2] . When coronary artery stenosis or occlusion is severe, good CCC can improve myocardial ischemia, protect myocardial contraction function, improve clinical symptoms, reduce the incidence of myocardial infarction, and reduce the size of myocardial infarction, thereby reducing the mortality associated with ischemic events and improving prognosis [3,4,14] . However, the determinants and influencing factors of CCC formation are also complex.…”

Relationship of serum calprotectin, angiopoietin‑1, and angiopoietin‑2 levels with coronary collateral circulation in patients with stable coronary artery disease

“…4 What is more, growth factors released from inflammatory cells (eg, monocytes) that attack the ischemic region in angiogenesis and arteriogenesis are also involved in this process. 1,3,13,14 Some cytokines initiate an inflammatory response by activating transcription factors. This stimulates the endothelium, resulting in a prompt release of presynthesized and stored molecules such as von Willebrand factor, P -selectin, CD63, interleukin 8, endothelin-1, tissue plasminogen activator, and Ang-2.…”

“…This stimulates the endothelium, resulting in a prompt release of presynthesized and stored molecules such as von Willebrand factor, P -selectin, CD63, interleukin 8, endothelin-1, tissue plasminogen activator, and Ang-2. 13 All of them are involved in the control a rapid endothelial response, hemostasis, inflammation, hemodynamic adaptation, and vascular permeability.…”

“…Several studies have shown that inflammatory process and growth factors play an important role in the development of CCC in myocardial ischemia. 13,[22][23][24][25][26] Some biomarkers may be useful for demonstrating the diversity of CCC development. As previously mentioned, calprotectin, Ang-1, and Ang-2 are biomarkers involved in angiogenesis and inflammation.…”

“…18 It was reported that calprotectin catalyzes the formation of reactive oxygen species by activating NADPH oxidase, as well as is involved in the pathogenesis of atherosclerosis by interacting with the receptor for advanced glycation end products and the toll -like receptor and by accelerating the signaling pathway. 13 Katashima et al 19 reported high serum calprotectin levels in patients with acute myocardial infarction. Additionally, the peak calprotectin levels were positively related to peak white blood cell and neutrophil counts along with peak creatine kinase MB isoenzyme and CRP levels.…”