Prevention of restenosis by lovastatin after successful coronary angioplasty

Sahni, Rakesh; Maniet, Alan R.; Voci, Gerardo; Banka, Vidya S.

doi:10.1016/0002-8703(91)90002-y

Cited by 153 publications

(14 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These trials ranged in length from six months to seven years; there were 17 randomized trials [1][2][3][4]7,9,10,[12][13][14][15]17,18,[26][27][28]30 and 13 open-label studies. 8,11,14,16,[19][20][21][22][23][24][25]29,31 Tables 3 and 4 list the principal findings of the randomized clinical trials and open-label trials, respectively, and show estimates of the frequency of discontinuation of antihyperlipidemic therapy as compared with our findings in the two HMOs.…”

Section: Rates Of Drug Discontinuation In Long-term Clinical Trialsmentioning

confidence: 99%

See 1 more Smart Citation

Discontinuation of Antihyperlipidemic Drugs — Do Rates Reported in Clinical Trials Reflect Rates in Primary Care Settings?

Andrade¹,

Walker²,

Gottlieb³

et al. 1995

N Engl J Med

346

188

View full text Add to dashboard Cite

show abstract

Section: Rates Of Drug Discontinuation In Long-term Clinical Trialsmentioning

confidence: 99%

“…‡Patients in this study were randomly assigned to receive two or more formulations of the same drug. 23 6 mo 37 29.7 (15.0-44.5) Olsson et al 25 6 mo 34 23.5 (9.3-37.8) Varthakavi et al 29 6 mo 36 22.2 (8.6-35.8) HMO 6 mo -26 (21)(22)(23)(24)(25)(26)(27)(28)(29)(30) …”

Section: Lovastatinmentioning

confidence: 99%

Discontinuation of Antihyperlipidemic Drugs — Do Rates Reported in Clinical Trials Reflect Rates in Primary Care Settings?

Andrade¹,

Walker²,

Gottlieb³

et al. 1995

N Engl J Med

346

188

View full text Add to dashboard Cite

show abstract

“…A recent meta-analysis showed that treatment with HMG-CoA reductase inhibitors (statins) decreased the risk of coronary heart disease by 31% and mortality by 21% [2]. Reduction of coronary heart disease with statins involves slowed progression of atherosclerosis, lesion regression [3]and inhibition of the development of new lesions, including the prevention of restenosis following balloon angioplasty [4]and stenting [5]. A major factor to which the success of statins in reducing coronary heart disease is attributed is the reduction of low-density lipoprotein (LDL) cholesterol [2].…”

Section: Introductionmentioning

confidence: 99%

Atorvastatin Treatment Prevents Alterations in Coronary Smooth Muscle Nuclear Ca<sup>2+</sup> Signaling in Diabetic Dyslipidemia

2002

View full text Add to dashboard Cite

Atorvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, alters bulk myoplasmic Ca²⁺ regulation and inhibits phenotypic modulation and proliferation of vascular smooth muscle in culture. Nuclear Ca²⁺ (Ca_n) signaling is tightly coupled to transcriptional events and cell growth. Therefore, we hypothesized that in vivo treatment with atorvastatin would attenuate alterations in mitogen-induced Ca_n signaling associated with coronary atherosclerosis. Three groups of male Yucatan pigs were treated for 20 weeks: controls, alloxan-induced diabetics fed an atherogenic diet and diabetics fed an atherogenic diet plus atorvastatin (80 mg/day). Right coronary artery single-cell cytosolic Ca²⁺ (Ca_c) and Ca_n responses to the mitogen endothelin-1 (5 × 10^–8M) were measured by laser confocal microscopy using the calcium indicator Fluo-4. We observed a 39% increase in Ca_c and a 52% increase in Ca_n responses to endothelin-1 in cells from diabetic dyslipidemic arteries compared to control. These alterations were prevented in animals treated with atorvastatin. We show that during proliferation, the nucleus of a smooth muscle cell becomes rounded and loses the characteristic multilobular shape, clefts and invaginations. Consistent with this, a redistribution of Ca²⁺ stores from a transnuclear morphology in controls to a more perinuclear morphology occurred in cells from diabetic dyslipidemic arteries and was prevented by atorvastatin. In addition, the peak Ca_n responses to endothelin-1 were inversely correlated (r = 0.712) with the extent of the transnuclear distribution of Ca²⁺ stores and directly correlated (r = 0.874) with the extent of atherosclerosis, as assessed in vivo by intravascular ultrasound. These findings indicate that chronic treatment with atorvastatin directly decreases mitogen-induced Ca_n mobilization, which we suggest is related to the spatial localization of Ca_n stores.

show abstract

“…This may be a result of less restenosis among the statin-treated patients. Since a small study in 1991 [26] suggested a potential beneficial effect of statin on restenosis, several additional studies [4,6] have reported similar findings in PCI patients. Moreover, a clinical trial of post-PCI patients [27] reported significantly slower plaque growth in the statin treatment arm compared with usual care.…”

Section: Discussionmentioning

confidence: 91%

Beneficial effects of statins after percutaneous coronary intervention

Zhang

Marroquin

Weissfeld³

et al. 2009

European Journal of Cardiovascular Prevention & Rehabilitat

View full text Add to dashboard Cite

Background Evidence about the efficacy of statin treatment among patients after percutaneous coronary intervention (PCI) is very limited. The rapid advancement in PCI technology and near universal use of adjunctive cardioprotective medications make it necessary to formally assess the effect of statin therapy on cardiac events after PCI. Design This was a multicenter prospective cohort study Methods Patients who received stent implantation and survived to hospital discharge from the National Heart, Lung, and Blood Institute Dynamic Registry from 2004 to 2006 formed the study cohort. Patients with cardiogenic shock, in-hospital adverse events [including myocardial infarction and coronary artery bypass graft surgery (CABG)], liver disease, renal disease, alcoholism, or drug abuse were excluded. The occurrences of death, CABG, and repeat PCI, and repeat revascularization were collected over 1-year follow-up. Results Of the 3227 patients evaluated, 2737 (85%) were prescribed a statin at discharge. By 1-year follow-up, incident events were 98 deaths, 44 CABG, 290 repeat PCI procedures, and 328 repeat revascularizations. After propensity score adjustment, postdischarge statin therapy was associated with lower risks of death [hazard ratio (HR)λ=λ0.58, 95% confidence interval (CI): 0.36–0.93, Pλ=λ0.02], CABG (HRλ=λ0.49, 95% CI: 0.24–1.00, Pλ=λ0.05), and repeat revascularization (HRλ=λ0.74, 95% CI: 0.56–1.00, Pλ=λ0.05). Conclusion These results support the routine use of statin therapy after PCI.

show abstract

Prevention of restenosis by lovastatin after successful coronary angioplasty

Cited by 153 publications

References 29 publications

Discontinuation of Antihyperlipidemic Drugs — Do Rates Reported in Clinical Trials Reflect Rates in Primary Care Settings?

Discontinuation of Antihyperlipidemic Drugs — Do Rates Reported in Clinical Trials Reflect Rates in Primary Care Settings?

Atorvastatin Treatment Prevents Alterations in Coronary Smooth Muscle Nuclear Ca<sup>2+</sup> Signaling in Diabetic Dyslipidemia

Beneficial effects of statins after percutaneous coronary intervention

Contact Info

Product

Resources

About