A brief etymology of the collateral circulation (original) (raw)
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Quo vadis collateral blood flow? A commentary on a highly cited paper
Cardiovascular Research, 2000
front' hypothesis by Reimer and Jennings [3] had anticipated this finding, showing that infarcts start in the The highly cited landmark paper by the Hearse-Yellon subendocardium and move wave-front like toward the group from the year 1987 [1] still stands out for its epicardium along the edges of the perfusion territory. thoroughness and stringency of approach. Above all, the As always, the paper in question had its predecessors. information contained in it is still valid and is not Our group had presented similar results in rats, rabbits, superceded by new results obtained by more modern pigs and dogs at a meeting organized by Hearse and Yellon methods. On the contrary, 'modern' methods in hemo-and our results were published in the proceeding book of dynamics often lack the precision of the gold standards that conference . We were elated by the fact that the that we were used to. Blood flow studies in animals are Hearse-Yellon group eventually confirmed our previous now often performed with the less rigorous clinical tech-results. This is the way that science should work but often niques. Part of the problem is that the more precise and doesn't. more sensitive, older methods have become so expensive Our studies were done to find out the major deter-(radioactive waste and cadaver disposal) that their use has minants of infarct size and apart from the size of the become prohibitive. vascular territory perfused by the occluded artery (1) and The strength of the Maxwell-Hearse-Yellon paper is the duration of occlusion , infarcts were significantly that collateral blood flow was measured over a wide range determined by collateral blood flow (3). With the excepof the mammalian kingdom using the same method thereby tion, of course, of those species that had no collaterals, making the results comparable. The objective was to time seemed to be the most important determinant. obtain a more rational basis for experiments dealing with About the same time that the Hearse-Yellon paper ischemia and its modulation and to come to a more appeared, a fourth determinant of infarct size was discovmeaningful selection of the right animal model for the ered. Ischemia tolerance can be manipulated by ischemic question to be tested: rats, rabbits and pigs that have preconditioning . We had shown earlier that in animals practically no collateral flow are well suited for ischemia with significant collateral flow myocardial oxygen contolerance studies. Dogs, cats and guinea pigs with their sumption at the moment of occlusion constituted the 5th variable and often sizeable collateral flow are well suited determinant of infarct size . for studies of vascular adaptation to ischemia.
Coronary Collateral Circulation
Clinical Cardiology, 1991
The occurrence and influence of coronary collateral circulation and obstruction of the supplying coronary arteries on left ventricular contractility, prevalence of myocardial infarction, and bicycle exercise ergometer test were studied in a random sample of 286 patients with angioprdphically documented coronary artery disease. Collaterals appeared increasingly in all three main coronary arteries with grade of obstruction. The highest prevalence of collatcrals occurred in stenosis of the right coronary artery (60%), followed by the left descending artery (45%); they occurred least in the left circumflex artery (21 74) (p<O.OOl). The frequency of intra-arterial collateral circulation was 4 2 % , 11 %, and 12%, respectively (p<O.OOI). With total occlusion of the left anterior descending coronary artery, 22 % of the patients had normokinetic anterior and apical left ventricular wall when collaterals were present. More often, the inferior wall showed normid contraction with total occlusion of the right coronary artely and collaterals [52 %, p < 0.001 compared with left anterior descending artery (LAD)]. The prevalence of inferior myocardial infarction was 39%, with collateral circulation to the totally occluded right coronary artery. The respective prevalence of anterior infarction and total occlusion in the left coronary artery was 58% (p <0.02). The presence or absence of collaterals had no obvious influence on ST-segment response during bicycle ergometer test. In triple-vessel disease, peak work capacity was better when collaterals to LAD were not jeopardized (427 kpm) than when jeopardized (32 1 kpm) (p<0.02).
The collateral circulation of the heart
BMC Medicine, 2013
The coronary arteries have been regarded as end arteries for decades. However, there are functionally relevant anastomotic vessels, known as collateral arteries, which interconnect epicardial coronary arteries. These vessels provide an alternative source of blood supply to the myocardium in cases of occlusive coronary artery disease. The relevance of these collateral arteries is a matter of ongoing debate, but increasing evidence indicates a relevant protective role in patients with coronary artery disease. The collateral circulation can be assessed by different methods; the gold standard involves intracoronary pressure measurements. While the first clinical trials to therapeutically induce growth of collateral arteries have been unavailing, recent pilot studies using external counterpulsation or growth factors such as granulocyte colony stimulating factor (G-CSF) have shown promising results.
Acute development of collateral circulation and therapeutic prospects in ischemic stroke
Neural Regeneration Research, 2016
Acute development of collateral circulation and therapeutic prospects in ischemic stroke The treatment of acute ischemic stroke has entered a new era recently because of the consistent success in endovascular therapy with or without the administration of intravenous recombinant tissue plasminogen activator (IV rtPA). In acute ischemic stroke, tissues that remain alive despite low cerebral blood flow but that are at risk for progressing into infarction are considered to be 'ischemic penumbra.' Both IV rtPA and endovascular therapies can rescue penumbral tissue by recanalizing occluded cerebral arteries. However, even after successful recanalization, some patients show little neurologic improvement, possibly because the penumbral area had already progressed into the irreversibly damaged ischemic core or because hemorrhagic transformation occurred after the recanalization therapy. Collateral circulation has the potential to protect against these ischemic injuries by maintaining cerebral blood flow, and we have focused on collateral circulation in this context. A deterioration in the quality of the collateral circulation
The Pathophysiology of Collateral Circulation in Acute Ischemic Stroke
Diagnostics
Cerebral collateral circulation is a network of blood vessels which stabilizes blood flow and maintains cerebral perfusion whenever the main arteries fail to provide an adequate blood supply, as happens in ischemic stroke. These arterial networks are able to divert blood flow to hypoperfused cerebral areas. The extent of the collateral circulation determines the volume of the salvageable tissue, the so-called “penumbra”. Clinically, this is associated with greater efficacy of reperfusion therapies (thrombolysis and thrombectomy) in terms of better short- and long-term functional outcomes, lower incidence of hemorrhagic transformation and of malignant oedema, and smaller cerebral infarctions. Recent advancements in brain imaging techniques (CT and MRI) allow us to study these anastomotic networks in detail and increase the likelihood of making effective therapeutic choices. In this narrative review we will investigate the pathophysiology, the clinical aspects, and the possible diagno...
Basic Research in Cardiology, 2009
Following an arterial occlusion outward remodeling of pre-existent inter-connecting arterioles occurs by proliferation of vascular smooth muscle and endothelial cells. This is initiated by deformation of the endothelial cells through increased pulsatile fluid shear stress (FSS) caused by the steep pressure gradient between the high pre-occlusive and the very low post-occlusive pressure regions that are interconnected by collateral vessels. Shear stress leads to the activation and expression of all NOS isoforms and NO production, followed by endothelial VEGF secretion, which induces MCP-1 synthesis in endothelium and in the smooth muscle of the media. This leads to attraction and activation of monocytes and T-cells into the adventitial space (peripheral collateral vessels) or attachment of these cells to the endothelium (coronary collaterals). Mononuclear cells produce proteases and growth factors to digest the extra-cellular scaffold and allow motility and provide space for the new cells. They also produce NO from iNOS, which is essential for arteriogenesis. The bulk of new tissue production is carried by the smooth muscles of the media, which transform their phenotype from a contractile into a synthetic and proliferative one. Important roles are played by actin binding proteins like ABRA, cofilin, and thymosin beta 4 which determine actin polymerization and maturation. Integrins and connexins are markedly up-regulated. A key role in this concerted action which leads to a 2-to-20 fold increase in vascular diameter, depending on species size (mouse versus human) are the transcription factors AP-1, egr-1, carp, ets, by the Rho pathway and by the Mitogen Activated Kinases ERK-1 and -2. In spite of the enormous increase in tissue mass (up to 50-fold) the degree of functional restoration of blood flow capacity is incomplete and ends at 30% of maximal conductance (coronary) and 40% in the vascular periphery. The process of arteriogenesis can be drastically stimulated by increases in FSS (arterio-venous fistulas) and can be completely blocked by inhibition of NO production, by pharmacological blockade of VEGF-A and by the inhibition of the Rho-pathway. Pharmacological stimulation of arteriogenesis, important for the treatment of arterial occlusive diseases, seems feasible with NO donors.
Medical Hypotheses, 2010
The internal thoracic arteries (ITAs) are a source of &amp;amp;amp;amp;amp;quot;noncoronary collateral circulation&amp;amp;amp;amp;amp;quot; (NCCC), or &amp;amp;amp;amp;amp;quot;noncoronary collateral blood flow&amp;amp;amp;amp;amp;quot; (NCCBF). The hypothesis herein is that enhancement of NCCC may represent an alternative means of myocardial blood supply: (1) Ligature of the ITAs creates a local hypertensive status and increases the perfusion pressure within the channels leading to the heart; (2) Myocardial ischemic stimulus diverts most ITA-related collateral flow to the heart rather than to the chest wall; (3) The ITAs may develop neo-collaterals owing to their ischemia-related plastic potential; (4) Angiogenic growth factor administration within the ITAs enhances neo-collateral development. These elements may pave the way for a new field of cardiovascular research aimed at enhancing NCCC as a new therapeutic option for ischemic heart disease.
Cerebral collateral circulation in experimental ischemic stroke
Experimental & translational stroke medicine, 2016
Cerebral collateral circulation is a subsidiary vascular network, which is dynamically recruited after arterial occlusion, and represents a powerful determinant of ischemic stroke outcome. Although several methods may be used for assessing cerebral collaterals in the acute phase of ischemic stroke in humans and rodents, they are generally underutilized. Experimental stroke models may play a unique role in understanding the adaptive response of cerebral collaterals during ischemia and their potential for therapeutic modulation. The systematic assessment of collateral perfusion in experimental stroke models may be used as a "stratification factor" in multiple regression analysis of neuroprotection studies, in order to control the within-group variability. Exploring the modulatory mechanisms of cerebral collaterals in stroke models may promote the translational development of therapeutic strategies for increasing collateral flow and directly compare them in term of efficacy, ...