Structure–Function of the Coronary Hierarchy

Tomanek, Robert J.

doi:10.1007/978-1-4614-4887-7_4

Cited by 8 publications

(15 citation statements)

References 157 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We reasoned that the phasic blood flow and pressures unique to the coronary circulation might create—in mouse with its short diastolic intervals—hemodynamic conditions in nascent collaterals favoring their regression. That is, it is known that chronic level of shear stress influences growth of the native coronary collateral circulation: conductance of the coronary network correlates directly with the time in diastole, which is when the majority of coronary perfusion occurs [3,29,30]; after birth the proportion of time in diastole declines since heart rate rapidly increases to 550–600 bpm as mice grow to sexual maturity [24]. Despite this reasoning, collaterals were also absent in in VECAD GFP/+ pups on postnatal day-1 and-2 (data not shown) and in 3 week-old B6 mice (Online Figure 6), when formation of native collaterals in other tissues has achieved the number and diameter present in the adult [17,18].…”

Section: Resultsmentioning

confidence: 99%

“…However, anemia caused biventricular hypertrophy and growth of the overall coronary circulation. Thus, the extent to which the effect of anemia reflects remodeling of pre-existing collaterals, caused by a pressure difference across them [1,6,22] as well as local hypoxia [2,3], and/or neo-collateral formation remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

“…This is similar to brain, where patent neo-collaterals were not seen at day-1.5 after arterial ligation but were present by day-3 [7], and in skeletal muscle where they were not evident at day-2 but present by day-4 [42]. Collateral formation is faster than the onset of growth of arterioles in the surviving (remote) myocardium, which was seen 7 days after a large MI in association with increased wall stress and compensatory hypertrophy [3]. Nevertheless, coronary neo-collateral formation is too slow to prevent development of a necrotic core, which occurs within ~30 minutes after ligation [3,4,43,44].…”

Section: Discussionmentioning

confidence: 99%

“…The left anterior descending coronary artery was ligated 3mm below the left atrial margin (LADX) to produce a small infarction of 10–20% of left ventricle-plus-septum (LVS) wall volume, thus minimizing stimuli for compensatory hypertrophy and vascular growth that otherwise occurs in the normal (remote) myocardium following a large MI [3]. Approximately 99% survival occurred.…”

Section: Methodsmentioning

confidence: 99%

“…It is also not known if occlusive disease can induce new coronary collaterals to form. 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.…”

Section: Introductionmentioning

confidence: 99%

See 4 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

View full text Add to dashboard Cite

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.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

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

View full text Add to dashboard Cite

show abstract

Regulation of Coronary Blood Flow

Goodwill

Dick

Kiel

et al. 2017

Comprehensive Physiology

221

248

View full text Add to dashboard Cite

The heart is uniquely responsible for providing its own blood supply through the coronary circulation. Regulation of coronary blood flow is quite complex and, after over 100 years of dedicated research, is understood to be dictated through multiple mechanisms that include extravascular compressive forces (tissue pressure), coronary perfusion pressure, myogenic, local metabolic, endothelial as well as neural and hormonal influences. While each of these determinants can have profound influence over myocardial perfusion, largely through effects on end-effector ion channels, these mechanisms collectively modulate coronary vascular resistance and act to ensure that the myocardial requirements for oxygen and substrates are adequately provided by the coronary circulation. The purpose of this series of Comprehensive Physiology is to highlight current knowledge regarding the physiologic regulation of coronary blood flow, with emphasis on functional anatomy and the interplay between the physical and biological determinants of myocardial oxygen delivery.

show abstract

Chinese expert consensus on the diagnosis and treatment of coronary microvascular diseases (2023 Edition)

Chen,

Ni,

Huang

et al. 2023

MedComm

View full text Add to dashboard Cite

Since the four working groups of the Chinese Society of Cardiology issued first expert consensus on coronary microvascular diseases (CMVD) in 2017, international consensus documents on CMVD have increased rapidly. Although some of these documents made preliminary recommendations for the diagnosis and treatment of CMVD, they did not provide classification of recommendations and levels of evidence. In order to summarize recent progress in the field of CMVD, standardize the methods and procedures of diagnosis and treatment, and identify the scientific questions for future research, the four working groups of the Chinese Society of Cardiology updated the 2017 version of the Chinese expert consensus on CMVD and adopted a series of measures to ensure the quality of this document. The current consensus has raised a new classification of CMVD, summarized new epidemiological findings for different types of CMVD, analyzed key pathological and molecular mechanisms, evaluated classical and novel diagnostic technologies, recommended diagnostic pathways and criteria, and therapeutic strategies and medications, for patients with CMVD. In view of the current progress and knowledge gaps of CMVD, future directions were proposed. It is hoped that this expert consensus will further expedite the research progress of CMVD in both basic and clinical scenarios.

show abstract

Structure–Function of the Coronary Hierarchy

Cited by 8 publications

References 157 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

Regulation of Coronary Blood Flow

Chinese expert consensus on the diagnosis and treatment of coronary microvascular diseases (2023 Edition)

Contact Info

Product

Resources

About