Pravastatin reduces restenosis two years after percutaneous transluminal coronary angioplasty (REGRESS Trial)

Mulder, Johannes; Bal, Egbert T.; Jukema, J. Wouter; Zwinderman, Aeilko H.; Schalij, Martin J.; Boven, Ad J. van; Bruschke, Albert V.G.

doi:10.1016/s0002-9149(00)01073-0

Cited by 59 publications

(29 citation statements)

References 26 publications

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“…Although the benefits of statins in primary and secondary prevention of atherosclerosis have been widely recognized (17,18), it is less clear whether statins can effectively prevent restenosis in the clinical settings (25,26,29). The approach of liposomal statin treatment is fundamentally different than systemic administration of the free drug in solution, which is not targeted to a specific organ/cell, and from the clinically used drug-eluting stents to inhibit restenosis (60,61).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, accumulating clinical evidence points to the favorable effects of statins on restenosis following stent deployment (22)(23)(24). However, all clinical studies (25)(26)(27)(28), with a single exception (29), have reported a lack of significant effect for statins in preventing restenosis after PCI. Statins, similar to nitrogen-containing bisphosphonates (nBPs), are inhibitors of the mevalonate pathway blocking the prenylation of small GTPases, such as Ras, Rho, and Rac (22).…”

Section: Introductionmentioning

confidence: 99%

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Liposomal Simvastatin Attenuates Neointimal Hyperplasia in Rats

Afergan

David

Epstein

et al. 2010

AAPS J

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Abstract. Monocytes, macrophages, and inflammation play a key role in the process of neointimal proliferation and restenosis. The present study evaluated whether systemic and transient depletion of monocytes could be obtained by a single intravenous (IV) injection of simvastatin liposomes, for the inhibition of neointima formation. Balloon-injured carotid artery rats (n=30) were randomly assigned to treatment groups of free simvastatin, simvastatin in liposomes (3 mg/kg), and saline (control). Stenosis and neointima to media ratio (N/M) were determined 14 days following single IV injection at the time of injury by morphometric analysis. Depletion of circulating monocytes was determined by flow cytometry analyzes of blood specimens. Inhibition of RAW264.7, J774, and THP-1 proliferation by simvastatinloaded liposomes and free simvastatin was determined by the 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide assay. Simvastatin liposomes were successfully formulated and were found to be 1.5-2 times more potent than the free drug in suppressing the proliferation of monocytes/ macrophages in cell cultures of RAW 264.7, J774, and THP-1. IV injection of liposomal simvastatin to carotid-injured rats (3 mg/kg, n=4) resulted in a transient depletion of circulating monocytes, significantly more prolonged than that observed following treatment with free simvastatin. Administration to ballooninjured rats suppressed neointimal growth. N/M at 14 days was 1.56±0.16 and 0.90±0.12, control and simvastatin liposomes, respectively. One single systemic administration of liposomal simvastatin at the time of injury significantly suppresses neointimal formation in the rat model of restenosis, mediated via a partial and transient depletion of circulating monocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Liposomal Simvastatin Attenuates Neointimal Hyperplasia in Rats

Afergan

David

Epstein

et al. 2010

AAPS J

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“…Similar clinical effects were previously reported using pravastatin treatment. 7,26 Early restoration of endothelial function by HMGCoA reductase inhibitors, 17 and associated reduction of transient myocardial ischemia 27 may have resulted in less interventions. Furthermore, a recently published metaanalysis suggests that the clinical benefit of statins vs placebo is proportional to treatment changes in LDL, 28 and it is possible that LDL lowering may be more closely related to long-term than to short-term outcomes.…”

Section: Discussionmentioning

confidence: 99%

Effect of Early Use of Low-Dose Pravastatin on Major Adverse Cardiac Events in Patients With Acute Myocardial Infarction

Sato

Kinjo

Ito

et al. 2008

Circ J

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“…The beneficial effects of statins include a reduction in vascular inflammation, improvement in endothelial function, and a reduction in platelet aggregation and thrombus formation; thus, statins probably influence the vascular wall process after injury (33 ). However, these beneficial effects remain controversial regarding the restenotic process (34,35 ).…”

Section: Statin Therapy and Restenosismentioning

confidence: 99%