Cardiovascular risk factors cause premature rarefaction of the collateral circulation and greater ischemic tissue injury

Moore, Steven; Zhang, Hua; Maeda, Nobuyo; Doerschuk, Claire M.; Faber, James E.

doi:10.1007/s10456-015-9465-6

Cited by 57 publications

(111 citation statements)

References 85 publications

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“…A surprising finding in this study is that mouse heart lacks native coronary collaterals, given that the strains we examined have collaterals in their brain, skeletal muscle, intestine and skin (ear) [7,11–15,35]. Absence of coronary collaterals, as assessed immediately after ligation, was not due to failure to detect them.…”

Section: Discussionmentioning

confidence: 86%

“…We used an angiographic casting method previously used to quantify native collaterals in other tissues of mouse [7,11–15]. Surprisingly, no coronary collaterals were present in B6 mice (Figure 1) or 7 other inbred strains [C57BLKS (BLKS), A/J, BALB/cBy (BALB/c), C3H-He, CBA, DBA/2, SJL (n≥5 each)], nor in CD1 outbred mice (n=3).…”

Section: Resultsmentioning

confidence: 99%

“…Indirect measures of collateral-dependent blood flow suggest that native collateral extent in heart, brain and lower extremities varies greatly among “healthy” humans, ie, in the absence of CAD [4] or peripheral artery disease [8] or when assessed in the hyper-acute phase of ischemic stroke [9,10], ie, conditions where remodeling—which can also vary among individuals [1–7,11–15]—has not yet taken place. This variation at baseline has been suggested to be a major determinant of the wide variation in the severity of tissue injury when arterial obstruction develops [4,5,7,9–15].…”

Section: Introductionmentioning

confidence: 99%

“…However, recent studies in mice have found that differences in genetic background may be a major factor [5,7,12–15]. Collateral extent in brain varied 46-fold among 21 strains of mice [14], with large variation also present in skeletal muscle and intestine examined in several of the same strains [11–13]. The differences correlated with wide differences in tissue injury in models of acute and chronic arterial obstruction in brain (eg, 30-fold variation in infarct volume [7]) and lower extremities [12,13].…”

Section: Introductionmentioning

confidence: 99%

“…It has generally been assumed [1] (but not without exception [3]) that only remodeling of native collaterals occurs after arterial stenosis or occlusion. However, this assumption remains uncertain because of limitations in resolution of previous angiographic methods: native collaterals can be as small as the smallest arterioles in a tissue (~6–8 microns diameter), are thousands-fold less abundant than nearby arterioles (eg, in skeletal muscle [11]), and can only be anatomically differentiated from the latter by identifying their anastomotic connections. Once collaterals have remodeled after arterial occlusion, their many-fold larger diameter and increased tortuosity makes them somewhat easier to identify.…”

Section: Introductionmentioning

confidence: 99%

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De-novo collateral formation following acute myocardial infarction: Dependence on CCR2+ bone marrow cells

Zhang¹,

Faber²

2015

Journal of Molecular and Cellular Cardiology

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Wide variation exists in the extent (number and diameter) of native pre-existing collaterals in tissues of different strains of mice, with supportive indirect evidence recently appearing for humans. This variation is a major determinant of the wide variation in severity of tissue injury in occlusive vascular disease. Whether such genetic-dependent variation also exists in the heart is unknown because no model exists for study of mouse coronary collaterals. Also owing to methodological limitations, it is not known if ischemia can induce new coronary collaterals to form (“neo-collaterals”) versus remodeling of pre-existing ones. The present study sought to develop a model to study coronary collaterals in mice, determine whether neo-collateral formation occurs, and investigate the responsible mechanisms. Four strains with known rank-ordered differences in collateral extent in brain and skeletal muscle were studied: C57BLKS>C57BL/6>A/J>BALB/c. Unexpectedly, these and 5 additional strains lacked native coronary collaterals. However after ligation, neo-collaterals formed rapidly within 1-to-2 days, reaching their maximum extent in ≤ 7 days. Rank-order for neo-collateral formation differed from the above: C57BL/6>BALB/c>C57BLKS>A/J. Collateral network conductance, infarct volume−1, and contractile function followed this same rank-order. Neo-collateral formation and collateral conductance were reduced and infarct volume increased in MCP1−/− and CCR2−/− mice. Bone-marrow transplant rescued collateral formation in CCR2−/− mice. Involvement of fractalkine→CX3CR1 signaling and endothelial cell proliferation were also identified. This study introduces a model for investigating the coronary collateral circulation in mice, demonstrates that neocollaterals form rapidly after coronary occlusion, and finds that MCP→CCR2-mediated recruitment of myeloid cells is required for this process.

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Section: Discussionmentioning

confidence: 86%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

De-novo collateral formation following acute myocardial infarction: Dependence on CCR2+ bone marrow cells

Zhang¹,

Faber²

2015

Journal of Molecular and Cellular Cardiology

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Leptomeningeal collaterals are associated with modifiable metabolic risk factors

Menon

Smith

Coutts

et al. 2013

Annals of Neurology

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Objective We seek to identify potentially modifiable determinants associated with variability in leptomeningeal collateral status in patients with acute ischemic stroke. Methods Data are from the Keimyung Stroke Registry. Consecutive patients with M1 segment middle cerebral artery (MCA) ± intracranial internal carotid artery (ICA) occlusions on baseline CT-angiography (CTA) from May 2004 to July 2009 were included. Baseline and follow-up imaging was analyzed blinded to all clinical information. Two raters assessed leptomeningeal collaterals on baseline CTA by consensus, using a previously validated regional leptomeningeal score (rLMC). Results Baseline characteristics (n=206) were: mean age 66.9±11.6 years, median baseline NIHSS 14 (IQR 11-20), and median stroke symptom onset to CTA 166 minutes (IQR 96-262), Poor collateral status at baseline (rLMC score 0-10) was seen in 73/206 (35.4%). On univariate analyses, patients with poor collateral status at baseline were older, hypertensive, had higher white blood cell count, blood glucose, D-dimer, serum uric acid levels, and were more likely to have metabolic syndrome. Multivariable modeling identified metabolic syndrome (OR 3.22 95% CI 1.69-6.15, p<0.001), hyperuricemia (per 1 mg/dl OR 1.35 95% CI 1.12-1.62, p<0.01) and older age (per 10 years, OR 1.34 95% CI 1.02-1.77, p=0.03) as independent predictors of poor leptomeningeal collateral status at baseline. Conclusion Metabolic syndrome, hyperuricemia and age are associated with poor leptomeningeal collateral status in patients with acute ischemic stroke.

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The association of interferon‐alpha with development of collateral circulation after artery occlusion

Xing

Wang

Pei

et al. 2021

Clinical Cardiology

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Background: Previous studies have demonstrated that interferon (IFN) signaling is enhanced in patients with poor collateral circulation (CC). However, the role and mechanisms of IFN-alpha in the development of CC remain unknown. Methods:We studied the serum levels of IFN-alpha and coronary CC in a casecontrol study using logistics regression, including 114 coronary chronic total occlusion (CTO) patients with good coronary CC and 94 CTO patients with poor coronary CC. Restricted cubic splines was used to flexibly model the association of the levels of IFN-alpha with the incidence of good CC perfusion restoration after systemic treatment with IFN-alpha was assessed in a mice hind-limb ischemia model. Results:Compared with the first IFN-alpha tertile, the risk of poor CC was higher in the third IFN-alpha tertile (OR: 4.79, 95% CI: 2.22-10.4, p < .001). A cubic spline-smoothing curve showed that the risk of poor CC increased with increasing levels of serum IFNalpha. IFN-alpha inhibited the development of CC in a hindlimb ischemia model. Arterioles of CC in the IFN-alpha group were smaller in diameter than in the control group. Conclusion: Patients with CTO and with poor CC have higher serum levels of IFNalpha than CTO patients with good CC. IFN-alpha might impair the development of CC after artery occlusion. K E Y W O R D S collateral circulation, coronary chronic total occlusion, IFN-alpha 1 | BACKGROUND Development of collateral circulation (CC), also termed as arteriogenesis, is a natural life-preservation mechanism occurring in patients with coronary chronic total occlusion (CTO). Well-developed CC preserves cardiac function, thus reducing cardiac mortality after coronary occlusion. 1,2 Patients with CTO show a great deal of heterogeneity in their arteriogenic responses to artery occlusion. This is affected by multiple factors, including inflammatory factors. 3 The

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Cardiovascular risk factors cause premature rarefaction of the collateral circulation and greater ischemic tissue injury

Cited by 57 publications

References 85 publications

De-novo collateral formation following acute myocardial infarction: Dependence on CCR2+ bone marrow cells

De-novo collateral formation following acute myocardial infarction: Dependence on CCR2+ bone marrow cells

Leptomeningeal collaterals are associated with modifiable metabolic risk factors

The association of interferon‐alpha with development of collateral circulation after artery occlusion

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