Stimulation of coronary collateral growth: Current developments in angiogenesis and future clinical applications

Kass, Richard W.; Kotler, Morris N.; Yazdanfar, Shahriar

doi:10.1016/0002-8703(92)90665-i

Cited by 38 publications

(14 citation statements)

References 75 publications

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“…This research highlights the therapeutic possibilities for controlled vascular development and angiogenesis (Unger et al, 1990). Such treatment, potentially, could both inhibit pathological vascular growth, and enhance the development of collateral arteries subsequent to myocardial ischemia (Kass et al, 1992).…”

Section: Clinical Applicationsmentioning

confidence: 92%

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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Section: Clinical Applicationsmentioning

confidence: 92%

Extracardiac coronary arterial anastomoses

et al. 2010

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“…Its expression -at least in tissue cultures -increases very rapidly during exposure to hypoxia [247] and its half-life is then pro longed from 30 min to 8 h [248], It selectively upregulates expression of proteases involved in the disruption of the basement membrane [249], releasing stored bFGF. 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].…”

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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“…However, as a confounding problem, even when the culprit vessel is occluded, flow may still reach the ischemic territories using a pathway of collateral circulation: pre-existing or newly formed vessels from one coronary vascular bed that connect with an adjacent bed (15)(16)(17). The degree of collateralization varies between species; in the absence of coronary artery disease, it is more extensive in normal dogs than in normal humans (18).…”

mentioning

confidence: 99%

“…The degree of collateralization varies between species; in the absence of coronary artery disease, it is more extensive in normal dogs than in normal humans (18). However, collateral growth and recruitment can be stimulated by gradual narrowing of the coronary arteries, intermittent periods of ischemia or by total occlusion although the former two are more effective (16,19). Because AMI generally occurs in the setting of atherosclerotic narrowed coronary arteries (20), intermittent episodes of ischemia, although often asymptomatic (silent ischemia (5)), may stimulate the growth and proliferation of collateral circulation.…”

mentioning

confidence: 99%