Prevention of Restenosis by Lovastatin After Successful Coronary Angioplasty

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

doi:10.1097/00008483-199201000-00013

Cited by 28 publications

(41 citation statements)

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“…[27][28][29][30][31] Myocardial perfusion studies [32][33][34] and endothelial function studies 35,36) have shown clinical and functional improvements before the detection of lesional atherosclerotic regression. They also showed an improvement in vasodilatory function of vascular endothelium at the level of the coronary 30,37,38) and peripheral circulation 39) through the use of HMG-coA reductase inhibitors alone or in combination with antioxidant therapy. 29,40) Hemostatic and inflammatory processes are possibly affected by pravastatin.…”

Section: Discussionmentioning

confidence: 97%

Pravastatin Protection from Cold Stress in Myocardium of Rats.

et al. 2003

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SUMMARYThe aim of this research was to evaluate the possible protective effect of pravastatin on ultrastructural alterations induced by cold stress in the myocardium of rats.Sixteen EPM-Wistar rats (Rattus norvegicus albinus) were used and distributed into four groups: 1) control; 2) pravastatin; 3) cold stress, and 4) pravastatin + cold stress. A daily oral dose of 10 mg/kg of weight of pravastatin was administered to each rat in groups 2 and 4 for 15 days. The stress induced by cold was obtained by keeping the group 3 and 4 rats in a freezer at -8°C for 4 hours. The animals were killed and the heart and fragments of the left ventricles (LV) were removed and processed prior to conducting electron microscopic analysis.The ultrastructural alterations in cardiomyocytes were quantified through the number of mitochondrial cristae pattern (cristalysis). The group subjected only to cold stress showed a significant increase in cristalysis (391.9) when compared with control group (42.0). In the cold stress and pravastatin pretreatment group, a statistically significant (96.9)*, P<0.05 cristalysis reduction was observed when compared with cold stress group. The mitochondrial cristalysis profiles of the control and pravastatin groups were 42.0 and 65.7, respectively.Cold stress induced a significant increase in the rate of mitochondrial cristalysis. In the group that received pravastatin and was exposed to cold stress, the drug protected the LV cardiomyocytes. This fact was confirmed by a reduction mitochondrial cristalysis pattern. (Jpn Heart J 2003; 44: 243-255)

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Section: Discussionmentioning

confidence: 97%

Pravastatin Protection from Cold Stress in Myocardium of Rats.

et al. 2003

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“…39 Lovastatin prevents restenosis in hypercholesterolemic rabbits undergoing femoral balloon angioplasty 19 and reduces restenosis rates after percutaneous transluminal coronary angioplasty in humans. 20 However, it is difficult to extrapolate from these studies any direct effect of vastatins on arterial myocyte proliferation. The former study was pursued in hypercholesterolemic animals; in the clinical study, a significant reduction of serum cholesterol was observed in the lovastatin-treated patients, even though no clear correlations between plasma cholesterol levels and restenosis rates were observed.…”

Section: Discussionmentioning

confidence: 99%

“…16 - 18 Aggressive lipid-lowering treatment with lovastatin prevented restenosis after balloon angioplasty in hypercholesterolemic rabbits 19 and humans. 20 However, no correlations between serum cholesterol and restenosis were found in percutaneous transluminal coronary angioplasty patients.…”

mentioning

confidence: 99%

HMG CoA reductase inhibitors. In vivo effects on carotid intimal thickening in normocholesterolemic rabbits.

Soma

Donetti

Parolini

et al. 1993

Arterioscler Thromb

210

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The in vivo activity of different 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (vastatins) on neointimal formation induced by insertion of a flexible collar around one carotid artery of normocholesterolemic rabbits was investigated. The contralateral carotid artery served as a sham control. Pravastatin, lovastatin, simvastatin, and fluvastatin were given mixed with food at daily doses of 20 ing/kg body wt for 2 weeks starting on the day of collar placement. The treatment with vastatins did not modify rabbit plasma cholesterol concentrations. The neointimal formation was assessed by measuring the cross-sectional thickness of intimal and medial tissues of fixed arteries with light microscopy. Fourteen days after collar placement, intimal hyperplasia (mostly cellular) was pronounced in treated carotid arteries. The intimal/medial (I/M) tissue ratio was 12-fold higher in treated arteries than in arteries without the collar (0.36±0.04 versus 0.03±0.02). Animals treated with lovastatin (R=12), simvastatin (n=12), and fluvastatin (R=12) showed significantly less neointimal formation; I/M tissue ratios were 0.24±0.03, 0.20±0.03, and 0.17±0.03, respectively. The inhibition elicited by pravastatin (n=12, 032 ±0.03) did not reach statistical significance. or-Actin antibody immunofluorescence analysis of serial sections revealed that cells present in the hyperplastic intima were mostly myocytes. Rates of intimal myocyte proliferation were also measured by incorporation of 5-bromo-2'-deoxyuridine, a thymidine analogue, into replicating DNA. Immunofluorescence analysis showed that 5-bromo-2'-deoxyuridine was actively incorporated into intimal myocytes after insertion of the collar, with a labeling index (percent of labeled myocytes) of 2.15 after 14 days. Labeling indexes for pravastatin-, lovastatin-, simvastatin-, and fluvastatin-treated carotid arteries were 2.01, 1.32,1.23, and 1.20, respectively, suggesting a direct effect of vastatins on arterial myocyte proliferation. The different responsiveness shown by the vastatins tested may be attributed to the differences in their capacity to penetrate cell membranes and their potency in inhibiting the HMG CoA reductase enzyme. We conclude that the inhibition of carotid intimal myocyte proliferation by these vastatins is independent of their effect on plasma cholesterol concentrations. -11 suggesting that the hypolipidemic effect is

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“…Numerous pharmacological approaches and devices have been evaluated in an attempt to prevent restenosis. Fish oil, and trapidil (growth inhibitor) have shown promise in some trials [48,49]. Some trials that failed to demonstrate the benefit of a particular pharmacologic agent may have too few patients and uses adequate doses.…”

Section: Management Of Restenosismentioning

confidence: 99%

Short Term and Long Term Complications after Percutaneous Transluminal Coronary Angioplasty (PTCA)

Sharma¹

2017

IJCH

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Background: The nonsurgical treatment of arteries narrowed by atherosclerosis was introduced in 1964, when Dotter and Judkin performed transluminal angioplasty of femoral artery stenoses [1]. In 1970, Gruntzig modified the dilation catheter to allow its use in coronary arteries dilation [2]. Subsequently, In 1977 he performed the first Percutaneous Transluminal Coronary Angioplasty (PTCA) in a patient. Since onward, PTCA has been used in many patients with stable angina, unstable angina or acute myocardial infarction. Its use was initially limited to the treatment of discrete stenoses in proximal segment of a coronary artery, but improvements in equipments and techniques have lead its use in patients with stenoses, that are more complex or located in distal arterial segments and in patients relatively at high risk for complications [3]. Despite the wider application of PTCA, the success rate remained high. Over the past decade, the number of procedure performed has steadily increased, with over 300,000 performed in united state in 1990 [4].

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Prevention of Restenosis by Lovastatin After Successful Coronary Angioplasty

Cited by 28 publications

References 0 publications

Pravastatin Protection from Cold Stress in Myocardium of Rats.

Pravastatin Protection from Cold Stress in Myocardium of Rats.

HMG CoA reductase inhibitors. In vivo effects on carotid intimal thickening in normocholesterolemic rabbits.

Short Term and Long Term Complications after Percutaneous Transluminal Coronary Angioplasty (PTCA)

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