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Results for “COLLATERAL CIRCULATION”

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[Coronary collateral circulation].

Coronary collaterals are anastomotic connections without an intervening capillary bed between portions of the same coronary artery and between different coronary arteries. The main determinants of coronary collateral circulation are preinfarction angina, severity of coronary artery disease, significant pressure gradient and an increase in shear stress. In presence of pressure gradient the blood flow is redistributed through the preexistent arterioles that connect a high-pressure with a low-pressure area. The consequence is an increased flow velocity and therefore increased shear stress in the collateral arteries, which leads to a marked activation of the endothelium with the subsequent morphological changes, vascular remodeling and activation of growth factors involved in angiogenesis and arteriogenesis. Well-developed coronary collateral circulation can be observed in 25% to 37% of patients with one vessel coronary artery disease and in 74.7% patients with extensive disease. Recruitable collaterals can be evaluated by performing coronary angiography, a qualitative or semiquantitative technique and by measurement of pressure and velocity in distal vascular beds (quantitative technique). Demonstration of well-developed collaterals in patients with angina pectoris or myocardial infarction has been associated with limited infarct size, improved ventricular function, less ventricular aneurysm formation and improved in-hospital and long-term survival.

Collateral Circulation↗
PubMed2003

Collateral circulation.

BACKGROUND: The collateral circulation plays a pivotal role in the pathophysiology of cerebral ischemia. Current knowledge of the collateral circulation remains sparse, largely because of prior limitations in methods for evaluation of these diminutive routes of cerebral blood flow. SUMMARY OF REVIEW: Anatomic descriptions of the collateral circulation often focus on more proximal anastomoses at the circle of Willis, neglecting secondary collateral pathways provided by leptomeningeal vessels. Pathophysiological recruitment of collateral vessels likely depends on the temporal course of numerous compensatory hemodynamic, metabolic, and neural mechanisms. Subsequent endurance of these protective vascular pathways may determine the severity of ischemic injury. Characterization of the collateral circulation with advanced neuroimaging modalities that provide angiographic information and perfusion data may elucidate critical determinants of collateral blood flow. Such information on the status of the collateral circulation may be used to guide therapeutic interventions. Prognostication and risk stratification may also be improved by routine evaluation of collateral blood flow. CONCLUSIONS: Contemporary understanding of the collateral circulation may be greatly enhanced through further refinement of neuroimaging modalities that correlate angiographic findings with perfusion status, providing the basis for future therapeutic and prognostic applications.

Brain↗
PubMed1992

Complete correction of the tetralogy of Fallot in adults using separated extracorporeal circulation to block intrathoracic collateral circulation and improve perfusion of the renal vasculature.

During the last 10 years, complete correction of the tetralogy of Fallot (TOF) has been performed on 28 adult patients using the "separated extracorporeal circulation" (separated ECC) technique developed by us. In addition to the usual ascending aortic and dual right arterial cannulations for ECC, the separated ECC also involved femoral arterial cannulation and the insertion of a catheter with two balloons via the other femoral artery. Flow via the ascending aorta and femoral artery were maintained separately during ECC. The urine output during separated ECC was significantly better than that during ordinary ECC (P < 0.01) and the operative field for intracardiac correction was clearer as a result of blocking the collateral circulation. Thus we believe separated ECC to be a superior method for total correction of TOF in adults, which may enhance the operative outcome.

Adult↗
PubMed2025

Distinct immune-metabolic phenotypes underlie poor coronary collateral circulation.

BACKGROUND: Coronary collateral circulation (CCC) significantly impacts myocardial perfusion and clinical outcomes in coronary artery disease patients, yet the underlying molecular heterogeneity remains inadequately characterized. OBJECTIVE: To identify distinct molecular phenotypes in patients with poor CCC, validate these phenotypes using clinical parameters, and evaluate their prognostic implications. METHODS: This study enrolled 149 patients (80 with good CCC and 69 with poor CCC) for high-throughput proteomic profiling. Unsupervised consensus clustering identified molecular subtypes within poor CCC patients, followed by differential expression analysis and KEGG pathway enrichment. Boruta feature selection was implemented, and multiple machine learning algorithms were tested on clinical data, with XGBoost optimization (accuracy 80.0%, F1-score 80.31%) and SHAP value interpretation. External validation was performed using the MIMIC database. Kaplan-Meier analysis and Cox regression models assessed major adverse cardiovascular events (MACE). RESULTS: Two distinct phenotypes emerged among poor CCC patients: Cluster 1 (n&#x2009;=&#x2009;39, Complement-Driven Vascular Remodeling [CDVR]) and Cluster 2 (n&#x2009;=&#x2009;30, Immuno-Thrombotic Myocardial Dysfunction [ITMD]). An XGBoost model incorporating fasting glucose, eosinophil percentage, and HbA1c achieved excellent discrimination (AUC&#x2009;>&#x2009;0.91). External validation confirmed the phenotype-specific clinical patterns. Notably, Cluster 2 demonstrated significantly higher MACE incidence compared to Cluster 1 (Log-rank p&#x2009;<&#x2009;0.05), with KEGG analysis revealing significant upregulation of platelet activation, diabetic cardiomyopathy, and metabolic pathways in the ITMD phenotype. CONCLUSION: Poor CCC encompasses distinct immune-metabolic phenotypes that can be accurately classified using integrated proteomic-clinical modeling. This classification enables more precise risk stratification and may guide personalized therapeutic strategies for coronary artery disease patients with inadequate collateralization.

Humans↗