Cardiovascular Safety of VEGF-Targeting Therapies: Current Evidence and Handling Strategies

Girardi, Fabio; Franceschi, Enrico; Brandes, Alba A.

doi:10.1634/theoncologist.2009-0235

Cited by 40 publications

(25 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…150 In a metaanalysis including 3784 patients, the RR for HF was 4.74 compared with placebo, and the reported incidence was 1.7% to 4%. [151][152][153] These effects did not appear to be dose-dependent or clearly related to different concomitant chemotherapy regimens. Singlecenter reports of small numbers of patients also suggest that a decline in LVEF occurs early during therapy and is potentially reversible.…”

mentioning

confidence: 85%

Drugs That May Cause or Exacerbate Heart Failure

Page¹,

O’Bryant²,

Cheng³

et al. 2016

Circulation

348

185

View full text Add to dashboard Cite

Heart failure is a common, costly, and debilitating syndrome that is associated with a highly complex drug regimen, a large number of comorbidities, and a large and often disparate number of healthcare providers. All of these factors conspire to increase the risk of heart failure exacerbation by direct myocardial toxicity, drug-drug interactions, or both. This scientific statement is designed to serve as a comprehensive and accessible source of drugs that may cause or exacerbate heart failure to assist healthcare providers in improving the quality of care for these patients.

show abstract

mentioning

confidence: 85%

Drugs That May Cause or Exacerbate Heart Failure

Page¹,

O’Bryant²,

Cheng³

et al. 2016

Circulation

348

185

View full text Add to dashboard Cite

show abstract

“…However, its potential involvement in injury and premature atherosclerotic disease in patients with MS remains to be clarified. Moreover, inflammatory imbalances, viewed by increased pro-inflammatory cytokines, such as TNF-α and/or reduced anti-inflammatory and anti-atherogenic molecules, including adiponectin, have been considered key factors for the CVR in other pathologies [13,14] and deserve attention in MS. A similar effect has been given to the phenomenon of angiogenesis, being the vascular endothelial growth factor (VEGF) a new biomarker with increased importance [15,16].…”

Section: Introductionmentioning

confidence: 92%

New Markers of Early Cardiovascular Risk in Multiple Sclerosis Patients: Oxidized-LDL Correlates with Clinical Staging

et al. 2013

View full text Add to dashboard Cite

Abstract. OBJECTIVES:This study aimed to characterize a population of multiple sclerosis (MS) patients in terms of traditional and new cardiovascular risk factors and assess their putative correlation with clinical disease activity (evaluated by the Expanded Disability Status Scale [EDSS] 00 (28.25-40.25) years and scoring a median of 2.00 (1.50-3.13) in EDSS. Comparing with controls, the most relevant differences encountered were: increased serum triglycerides (P < 0.001), Ox-LDL (P < 0.001) as well as Ox-LDL/LDL ratio and reduced small HDL (P = 0.040), accompanied by a trend to increased VEGF concentration. LDL content, especially Ox-LDL, showed positive and significant correlation with EDSS (r = 0.458; P = 0.011) and VEGF (r = 0.453; P = 0.014). CONCLUSIONS: MS patients presented a profile of early CV risk, being Ox-LDL contents a putative good marker and having correlation with the clinical activity of the disease.

show abstract

“…FGF-1 can impact on the early stages of angiogenesis by upregulating MMP-1 expression, FGF-2 can induce synthesis of MMP-2, 3, 7, 9, 10, 11, and 13, PDGF promotes MMP-13 transcription, and VEGF can stimulate the production of MMP-2 [184,185,186,187], all major contributors to EC migration and atherosclerotic plaque vulnerability, therefore modulation of growth factor binding may decrease MMP secretion and prevent EC migration to combine two potent mechanisms of plaque stabilization. Unfortunately, clinical trials of monoclonal antibodies for some proangiogenic growth factors/receptors, especially those targeting VEGF, have demonstrated a prohibitively high rate of cardiovascular complications [188]. Exploration of this paradox with the ApoE knockout mouse has yielded conflicting results.…”

Section: Targets To Promote Plaque Stabilizationmentioning

confidence: 99%

Multidimensional Contribution of Matrix Metalloproteinases to Atherosclerotic Plaque Vulnerability: Multiple Mechanisms of Inhibition to Promote Stability

Ruddy¹,

Ikonomidis²,

Jones³

2016

J Vasc Res

View full text Add to dashboard Cite

The prevalence of atherosclerotic disease continues to increase, and despite significant reductions in major cardiovascular events with current medical interventions, an additional therapeutic window exists. Atherosclerotic plaque growth is a complex integration of cholesterol penetration, inflammatory cell infiltration, vascular smooth muscle cell (VSMC) migration, and neovascular invasion. A family of matrix-degrading proteases, the matrix metalloproteinases (MMPs), contributes to all phases of vascular remodeling. The contribution of specific MMPs to endothelial cell integrity and VSMC migration in atherosclerotic lesion initiation and progression has been confirmed by the increased expression of these proteases in plasma and plaque specimens. Endogenous blockade of MMPs by the tissue inhibitors of metalloproteinases (TIMPs) may attenuate proteolysis in some regions, but the progression of matrix degeneration suggests that MMPs predominate in atherosclerotic plaque, precipitating vulnerability. Plaque neovascularization also contributes to instability and, coupling the known role of MMPs in angiogenesis to that of atherosclerotic plaque growth, interest in targeting MMPs to facilitate plaque stabilization continues to accumulate. This article aims to review the contributions of MMPs and TIMPs to atherosclerotic plaque expansion, neovascularization, and rupture vulnerability with an interest in promoting targeted therapies to improve plaque stabilization and decrease the risk of major cardiovascular events.

show abstract

Cardiovascular Safety of VEGF-Targeting Therapies: Current Evidence and Handling Strategies

Cited by 40 publications

References 61 publications

Drugs That May Cause or Exacerbate Heart Failure

Drugs That May Cause or Exacerbate Heart Failure

New Markers of Early Cardiovascular Risk in Multiple Sclerosis Patients: Oxidized-LDL Correlates with Clinical Staging

Multidimensional Contribution of Matrix Metalloproteinases to Atherosclerotic Plaque Vulnerability: Multiple Mechanisms of Inhibition to Promote Stability

Contact Info

Product

Resources

About