Heparin promotes the formation of extracardiac to coronary anastomoses in a canine model

Unger, Ellis F.; Sheffield, C. D.; Epstein, Stephen E.

doi:10.1152/ajpheart.1991.260.5.h1625

Cited by 38 publications

(17 citation statements)

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“…They observed that selective infusion of heparin into the internal mammary artery promoted the formation of anastomoses between this artery and the myocardial circulation more effectively. 81 Thus, these findings indicated that heparin has the potential to accelerate the rate of collateral development in vivo.…”

Section: Collateral Growthmentioning

confidence: 87%

Recent insights into coronary collateral circulation.

1992

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T he coronary collateral circulation is an alternative source of blood supply to the myocardium jeopardized by failure of the original vessel to provide adequate flow to the major epicardial branches of the coronary artery. There has been considerable debate, however, concerning the functional role of collaterals in humans.1-9 Extensive studies carried out in the past several years in experimental animals, in autopsy materials, or in intact human hearts have confirmed the substantial potential of collaterals in limiting the extent of myocardial ischemia, preventing cell death, and altering the clinical outcome of ischemic heart disease, although these effects depend largely on the rate at which the collateral circulation develops and the magnitude of flow permitted by the newly recruited vessels.Previously More recently, coronary arteriography has permitted correlation of the anatomic appearance of coronary collateral vessels with the underlying coronary artery disease.29 In particular, coronary thrombolysis performed during the first few hours of acute myocardial infarction provided a unique opportunity to evaluate the role of coronary collaterals in minimizing myocardial infarct size.'0-'9 A number of studies suggest that among patients with acute myocardial infarction and unsuccessful intracoronary thrombolytic therapy early after onset of symptoms, subsequent improvement in global function and wall motion in the infarct zone frequently can be expected where residual flow was maintained by extensive collaterals to the region perfused by the infarct-related vessel. 10,12,13,16 We have previously demonstrated that collaterals are a key determinant of the creatine kinase time-activity curve. In patients in whom thrombolysis was unsuccessful but collateral channels are angiographically demonstrable, peak creatine kinase level was attained earlier than in patients without visible collaterals in the absence of recanalization. Thus, collaterals definitely provide significant blood supply to the myocardium at risk'5 (Figure 1)

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Section: Collateral Growthmentioning

confidence: 87%

Recent insights into coronary collateral circulation.

1992

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“…In an experimental study, Unger et al (1991) showed that angiogenic factors can successfully induce neovascularization between extracardiac and coronary arteries, such communications providing significant nutritive flow in more than half of their animals after 8 weeks of treatment. They also noted that myocardial ischemia was the most important factor providing a stimulus for the proliferation of the collateral arteries during the angiogenic treatment.…”

Section: Clinical Applicationsmentioning

confidence: 99%

Extracardiac coronary arterial anastomoses

et al. 2010

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The collateral arterial circulation of the heart has been extensively studied. However, less attention has been paid to extracardiac anastomoses, which may also be of significant clinical importance. In this review, we will describe the most common types of these anastomoses, which include bronchial to coronary arteries and internal thoracic to coronary arteries. In a much lesser degree, anastomoses between coronary arteries and pericardiacophrenic branches of the internal thoracic arteries, anterior mediastinal arteries, intercostal arteries, and esophageal arterial branches have also been described. Knowledge of the likely morphology and function of the anastomoses, therefore, could prove helpful in the clinical evaluation of patients with myocardial ischemia, particularly when selecting candidates for myocardial revascularization.

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“…which could explain its potentiating effect on bFGF [250], Isch aemia is considered a very potent stimulus for the devel opment of collateral circulation in the heart [251] and VEGF may play a crucial role in this. Relative ischaemia also leads to accumulation of adenosine which has a direct angiogenic effect on endothelial cells derived from coro nary microvasculature [252], Another mediator in the development of collateral cir culation may be heparin which, given by infusion, pro moted ingrowth of vessels into the heart from the internal mammary artery [253]. Other experiments suggest that it may be generated locally as protamine inhibited both growth of collaterals in adult dog hearts [254] and growth of capillaries in rat hearts during early postnatal develop ment [255].…”

Section: Vesselsmentioning

confidence: 99%

Postnatal Growth of the Heart and Its Blood Vessels

Hudlická

Brown²

1996

J Vasc Res

100

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Although rapid growth of the heart during early postnatal development ceases with maturation of the organism, the potential for cardiomyocyte growth is not lost and may be observed even in senescent hearts. Rapid developmental heart growth is accompanied by a proportional growth of capillaries but not always of larger vessels, and thus coronary vascular resistance gradually increases. Growth of adult hearts can be enhanced by thyroid hormones, catecholamines and the renin-angiotensin system hormones, but these do not always stimulate growth of coronary vessels. Likewise, chronic exposure to hypoxia leads to growth, mainly of the right ventricle and its vessels but without vascular growth elsewhere in the heart. On the other hand, ischaemia is a potent stimulus for the release of various growth factors involved in the development of collateral circulation. Heart hypertrophy develops in response to training, pressure or volume overload. Training usually leads to growth of larger coronary vessels but little growth of capillaries, except in young animals. However, growth of the capillary bed, but not the resistance vasculature capacity, can be induced by either increased coronary blood flow, bradycardia (electrically or pharmacologically induced) or increased inotropism, all of which are involved in the training stimulus. Thus, what actually promotes growth of larger vessels as opposed to capillaries in training is unclear. Pressure overload hypertrophy is mediated by both the renin-angiotensin system and the response of cardiomyocytes to stretch; both lead to activation of early oncogenes (c-fos, c-jun, c-myc) and angiotensin II activates several protein kinases involved in cell growth. In this condition, growth of larger vessels is inadequate, although some capillary growth may occur. Volume overload leads to cardiomyocyte hypertrophy and hyperplasia and some increase in vascular supply. Deficits in capillary supply in pressure or volume overload hypertrophy can be reversed by chronic administration of ACE inhibitors, dipyridamole, the bradycardic drug alinidine or pacing-induced bradycardia respectively, but in neither case is training effective. Mechanical and humoral factors are involved in growth of cardiomyocytes and vessels. For cardiomyocytes, stretch is most important, activating oncogenes, protein kinases and possibly the inositol phosphate pathway, but not ion channels, with regulation by the balance of angiotensin II, TGF-β1 and IGF-1, but not FGFs. For vessels, growth is stimulated by stretch and shear stress, possibly with involvement of VEGF. Increased shear stress disrupts the glycocalyx on the luminal side of vessels and releases plasminogen activator and metalloproteinases which disrupt the basement membrane and enable endothelial cell migration and proliferation. It also causes rearrangement of the endothelial cytoskeleton and transmission of mechanical signals to the abluminal side disturbing extracellular matrix and causing distortion of capillary basement membrane. Stretch acting from the ablum...

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Heparin promotes the formation of extracardiac to coronary anastomoses in a canine model

Cited by 38 publications

References 0 publications

Recent insights into coronary collateral circulation.

Recent insights into coronary collateral circulation.

Extracardiac coronary arterial anastomoses

Postnatal Growth of the Heart and Its Blood Vessels

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