Prediction for Coronary Collateral Development.

Cardiovascular disease (CVD) is the second leading cause of death in Taiwan and coronary artery disease (CAD) is the most important CVD causing morbidity and mortality in the world. The coronary collateral development and formation of collateral anastomosis were initiated by vasculogenesis during embryogenesis. Those collaterals do not vanish in neonate but decrease in caliber that numerous anastomosis are found in the normal heart. The recruitment and augmentation of these receded collateral arteries have been recognized as a response in severe stenotic coronary artery when myocardial ischemia is presented. A well-functioning collateral circulation play an important role in preserving myocardial contractility, reduced angina symptom and saves lives in patient with chronic CAD during the time of coronary occlusion. Although the inter-individual variability and mechanism to develop coronary collateral circulation are complex, hypoxia or hypoperfusion may directly stimulate angiogenesis and arteriogenesis that both play important roles in collateral vessel formation. Several cytokines and factors involving in these processes include vascular endothelial growth factor, nitric oxide, angiopoietin, matrix metalloproteinases, and shear forces. Although angiogenic growth factors have revealed some promising results in small clinical trials and animal models, none of these approaches were successfully applied into clinical practice. Because this biochemical arteriogenesis may share potential inflammatory process related to atherosclerosis that might have harmful effect in coronary artery disease. One of the natural ways to augment coronary collateral formation is physical exercise by increasing vascular shear stress in performed coronary anastomosis. In a randomized clinical trial, coronary collateral flow index showed significant improvement in the exercise group. Other clinical trials had showed external counterpulsation therapy (ECP) had positive effect on increasing coronary collateral circulation by triggering arteriogenesis revealing that ECP is a tool in relieving symptom in CAD patients. As mentioned above, the development of collateral circulation is affected not only by cytokines but also by many clinical factors like diabetes mellitus, severity of CAD vessels and coronary ectasia. These clinical scenarios might influence the plasma level of inflammatory markers, cytokines, and oxidative stress that are also affected by nutritional status. The prognostic nutrition index (PNI) was the first nutritional assessment tool that provided quantitative estimation of operative risk from 1979. By calculating albumin and lymphocyte counts reflecting both nutritional status and inflammation of patient, PNI is a useful tool to predict the prognosis of cancer, cardiovascular surgery and CAD. In general, malnutrition had been identified as an independent predictor of worsening prognosis among patient with chronic disease including CAD. Although CAD has better outcomes after coronary revascularization, malnutrition is still associated with higher risk of cardiac events in CAD patients. The development of atherosclerosis had also been associated with inflammation and malnutrition in patients with chronic kidney disease. The other study supporting association of inflammation and malnutrition is abnormal coronary microvascular function in patient with cardiomyopathy. Although nutritional status might be associated with coronary collateral development as reported by Akbu a K et al., nonnutritional factors included inflammation, renal function and fluid status were affect clinical nutrition assessment. It indicated that its difficulty in explanation how