Functional significance of coronary collateral vessels in patients with previous ‘Q’ wave infarction: relation to aneurysm, left ventricular end diastolic pressure and ejection fraction

Banerjee, Amitava; Mohan, Sri Krishna Madan; Ching, G. W. K.; Singh, Shyam

doi:10.1016/0167-5273(93)90244-b

Cited by 15 publications

(11 citation statements)

References 68 publications

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“…[1][2][3][4] In younger individuals, myocardial ischemia induces the development of a collateral supply that partially protects the cardiac tissue from subsequent coronary events. [5][6][7][8] However, angiogenesis is impaired in the cardiac 4,9 -13 and peripheral vascular beds of older individuals, 14,15 and this defect may underlie the increased severity of cardiovascular disease in the geriatric population. Therefore, elucidation of the cellular and molecular pathways that are impaired with aging is critical for developing specific strategies to prevent and reduce the pathogenesis of cardiovascular disease associated with advancing age.…”

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confidence: 99%

Platelet-Derived Growth Factor-AB Limits the Extent of Myocardial Infarction in a Rat Model

et al. 2002

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Platelet-Derived Growth Factor-AB Limits the Extent of Myocardial Infarction in a Rat Model

et al. 2002

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“…Myocardial ischemia provides a potent stimulus to angiogenesis and the subsequent development of collateral vasculature that maintains and/or revitalizes cardiac tissue. [1][2][3][4][5] The mobilization and differentiation of bone marrow-derived endothelial progenitor cells (EPCs) has recently been shown to be important in this process of adult neovascularization. 6 -10 Evidence suggests that EPCs contribute as much as 25% of endothelial cells (ECs) in newly formed blood vessels, 11 and transplantation of EPCs into patients has been demonstrated to induce blood flow recovery in ischemic limbs 12 and increase myocardial viability after infarction.…”

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confidence: 99%

C-Reactive Protein Attenuates Endothelial Progenitor Cell Survival, Differentiation, and Function

et al. 2004

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Background-Myocardial ischemia provides a potent stimulus to angiogenesis, and the mobilization and differentiation of endothelial progenitor cells (EPCs) has been shown to be important in this process. An elevated level of C-reactive protein (CRP) has emerged as one of the most powerful predictors of cardiovascular disease. However, the impact of CRP on EPC biology is unknown. Methods and Results-EPCs were isolated from the peripheral venous blood of healthy male volunteers. Cells were cultured in endothelial cell basal medium-2 in the absence and presence of CRP (5 to 20 g/mL), rosiglitazone (1 mol/L), and/or vascular endothelial growth factor. EPC differentiation, survival, and function were assayed. CRP at concentrations Ն15 g/mL significantly reduced EPC cell number, inhibited the expression of the endothelial cell-specific markers Tie-2, EC-lectin, and VE-cadherin, significantly increased EPC apoptosis, and impaired EPC-induced angiogenesis. EPC-induced angiogenesis was dependent on the presence of nitric oxide, and CRP treatment caused a decrease in endothelial nitric oxide synthase mRNA expression by EPCs. However, all of these detrimental CRP-mediated effects on EPCs were attenuated by pretreatment with rosiglitazone, a peroxisome proliferator-activated receptor-␥ (PPAR␥) agonist. Conclusions-Human recombinant CRP, at concentrations known to predict adverse vascular outcomes, directly inhibits EPC differentiation, survival, and function, key components of angiogenesis and the response to chronic ischemia. This occurs in part via an effect of CRP to reduce EPC eNOS expression. The PPAR␥ agonist rosiglitazone inhibits the negative effects of CRP on EPC biology. The ability of CRP to inhibit EPC differentiation and survival may represent an important mechanism that further links inflammation to cardiovascular disease.

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“…In younger individuals, myocardial ischemia induces the development of a collateral vasculature supply that partially protects the cardiac tissue from subsequent coronary events. [1][2][3][4] However, angiogenesis and endothelial function are impaired with aging and contribute to the increased severity of cardiovascular disease in the geriatric population (for review, see Weinsaft and Edelberg 5 ). Approaches specifically aimed at restoring senescent vascular dysfunction may improve clinical outcomes of older persons with cardiovascular disease in whom present treatments are less effective as compared with younger individuals.…”

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confidence: 99%

Young Adult Bone Marrow–Derived Endothelial Precursor Cells Restore Aging-Impaired Cardiac Angiogenic Function

Edelberg

Tang

Hattori

et al. 2002

Circulation Research

296

199

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Abstract-Delivery of young bone marrow-derived stem cells offers a novel approach for restoring the impaired senescent cardiac angiogenic function that may underlie the increased morbidity and mortality associated with ischemic heart disease in older individuals. Recently, we reported that alterations in endothelial cells of the aging heart lead to a dysregulation in the cardiac myocyte platelet-derived growth factor (PDGF)-B-induced paracrine pathway, which contributes to impaired cardiac angiogenic function. Based on these results, we hypothesized that cellular restoration of the PDGF pathway by bone marrow-derived endothelial precursor cells (EPCs) could reverse the aging-associated decline in angiogenic activity. In vitro studies revealed that young murine (3-month-old) bone marrow-derived EPCs recapitulated the cardiac myocyte-induced expression of PDGF-B, whereas EPCs from the bone marrow of aging mice (18-month-old) did not express PDGF-B when cultured in the presence of cardiac myocytes. Transplantation of young, but not old, genetically marked syngeneic bone marrow cells into intact, unirradiated aging mice that populated the endogenous senescent murine bone marrow incorporated into the neovasculature of subsequently transplanted syngeneic neonatal myocardium. Moreover, the young bone marrow-derived EPCs restored the senescent host angiogenic PDGF-B induction pathway and cardiac angiogenesis, with graft survival and myocardial activity in the aging murine host (cardiac allograft viability: 3-month-old controls,

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Functional significance of coronary collateral vessels in patients with previous ‘Q’ wave infarction: relation to aneurysm, left ventricular end diastolic pressure and ejection fraction

Cited by 15 publications

References 68 publications

Platelet-Derived Growth Factor-AB Limits the Extent of Myocardial Infarction in a Rat Model

Platelet-Derived Growth Factor-AB Limits the Extent of Myocardial Infarction in a Rat Model

C-Reactive Protein Attenuates Endothelial Progenitor Cell Survival, Differentiation, and Function

Young Adult Bone Marrow–Derived Endothelial Precursor Cells Restore Aging-Impaired Cardiac Angiogenic Function

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