The Effect of Short-Term Treatment with Simvastatin on Renal Function in Patients with Peripheral Arterial Disease

Youssef, F. Ben; Gupta, Prakash; Seifalian, Alexander M.; Myint, Fiona; Mikhailidis, Dimitri P.; Hamilton, George

doi:10.1177/000331970405500108

Cited by 74 publications

(50 citation statements)

References 41 publications

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“…[12][13][14] There are now several reports on the effects of statins (mainly atorvastatin and simvastatin) on renal function and SUA levels as well as their contribution to CHD risk reduction. 8,9,[15][16][17][18][19] ACEIs (Group A and C) had a neutral effect on renal function and SUA levels ( Table 2). These differences in renal function may have influenced the RRRs.…”

Section: Discussionmentioning

confidence: 99%

Effect of statins and ACE inhibitors alone and in combination on clinical outcome in patients with coronary heart disease

et al. 2004

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We assessed the 'synergy' of statins and angiotensinconverting enzyme inhibitors (ACEI) in reducing vascular events in patients with coronary heart disease (CHD). The GREek Atorvastatin and CHD Evaluation (GREACE) Study, suggested that aggressive reduction of low density lipoprotein cholesterol to 2.59 mmol/l (o100 mg/dl) significantly reduces morbidity and mortality in CHD patients, in comparison to undertreated patients. In this post hoc analysis of GREACE the patients (n ¼ 1600) were divided into four groups according to long-term treatment: Group A (n ¼ 460 statin þ ACEI), B (n ¼ 420; statin, no ACEI), C (n ¼ 371;no 371;no statin, on ACEI), and D (n ¼ 349; no statin, no ACEI). Analysis of variance was used to assess differences in the relative risk reduction (RRR) in 'all events' (primary end point) between groups. During the 3-year follow-up there were 292 cardiovascular events; 45 (10% of patients) in group A, 61 (14.5%) in group B, 91 in group C (24.5%) and 95 events in group D (27%). The RRR (95% confidence interval (CI) in the primary end point in group A was 31%, (95% CI À48 to À6%, P ¼ 0.01) in comparison to group B, 59% (95% CI À72 to À48%, Po0.0001) to group C and 63% (95% CI À74 to À51%, Po0.0001) to group D. There was no significant difference in RRR between groups C and D (9%, CI À27-10%, P ¼ 0.1). Other factors (eg the blood pressure) that can influence clinical outcome did not differ significantly between the four treatment groups. In conclusion, the statin þ ACEI combination reduces cardiovascular events more than a statin alone and considerably more than an ACEI alone. Aggressive statin use in the absence of an ACEI also substantially reduced cardiovascular events. Treatment with an ACEI in the absence of a statin use reduced clinical events in comparison to patients not treated with an ACEI but not significantly, at least in these small groups of patients.

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Section: Discussionmentioning

confidence: 99%

Effect of statins and ACE inhibitors alone and in combination on clinical outcome in patients with coronary heart disease

et al. 2004

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“…[99][100][101] It is therefore of interest that there is evidence showing that aggressive treatment with statins can improve renal function in high-risk patients and in those with coronary heart disease or peripheral arterial disease. 98,[102][103][104][105] Similarly, there is evidence of an association between statin use and preserved renal function after suprarenal aortic clamping. 106 …”

Section: Smoking and Renal Function In Patients With Aaasmentioning

confidence: 99%

Smoking and Aortic Diseases

Kakafika

Mikhailidis

2007

Circ J

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Cigarette smoking is a major cause of cardiovascular disease (CVD) and is responsible for approximately 11% of the annual total CVD deaths in the United States. 1 Smoking acts synergistically with other vascular risk factors (eg, hypertension, dyslipidaemia and diabetes) to increase vascular morbidity and mortality. 2 However, smoking has a variable magnitude of increased risk for different vascular diseases: the risk is highest for peripheral arterial disease and aortic aneurysm, and is lowest for coronary artery and cerebrovascular diseases. 2 These effects are thought to reverse after smoking cessation. The constituents of cigarette smoke with the major contribution to pathogenesis of vascular disease are nicotine, carbon monoxide, oxidant gases and polycyclic aromatic hydrocarbons. 2 Nonsmokers who are exposed to "secondhand" smoke experience on average a 30% excess risk of ischemic heart disease and nonfatal myocardial infarction. 3 Secondhand smoke exposure has been shown to activate platelets and to produce endothelial dysfunction, in both experimental animals and humans. 3 The mechanisms by which smoking causes acute cardiovascular events include endothelial dysfunction, thrombosis and inflammation.Endothelial dysfunction is an initiating event in atherogenesis, as well as a major factor in causing acute cardiovascular events. Cigarette smoking impairs flow-mediated endothelium-dependent peripheral arterial vasodilatation, an effect that is, at least partly, reversible after smoking Circulation Journal Vol.71, August 2007 cessation. 4 Smokers without atherosclerosis have coronary vasoconstrictor responses to acetylcholine that, in the presence of normal endothelium, produce vasodilatation. 5 Indeed, the oxidant chemicals of smoke degrade nitric oxide (NO) and reduce NO release, with subsequent impairment of vascular dilation and platelet function. 2 Smokers have lower than normal levels of antioxidant vitamins, reflecting their consumption in response to ongoing oxidant stress. 6 In addition, nicotine itself alters the structural and functional characteristics of vascular smooth muscle cells (VSMC) and endothelial cells. 7,8 Experimental data show that human aortic endothelial cells undergo apoptotic changes when they are exposed to cigarette smoke extracts. 9 This process may be prevented by pre-activation of NO synthase by Larginine. 9,10 Furthermore, smoking causes an increase in vascular superoxide production, which results in decreased NO bioactivity and concomitantly increases production of vasoconstrictor eicosanoids. 11 Cigarette smoke extracts, but not nicotine, also inhibit prostacyclin (PGI2: a vasodilator and inhibitor of platelet aggregation) synthesis in human, rabbit and rat vascular tissue. 12 Smoking-mediated endothelial dysfunction also results in reduced secretion of tissue plasminogen activator (tPA) 13 and increased secretion of plasminogen activator inhibitor (PAI)-1, 1 which results in impaired fibrinolysis. This acts in concert with the increased levels of tissue factor and fibrin...

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“…6,36,[38][39][40]53,128 It is also relevant that recent trials have shown that aggressive treatment with statins improves serum creatinine and urate levels. [129][130][131][132][133][134][135][136][137] These findings probably reflect an improved creatinine clearance. In turn, this effect is probably another consequence of improved blood flow following treatment with statins.…”

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confidence: 99%

Statins: another class of antihypertensive agents?

et al. 2006

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The assessment of global cardiovascular risk is an essential step in the management of atherosclerotic disease prevention. Among the risk factors to be addressed are hypertension and hyperlipidaemia; these commonly coexist. A neutral or lipid-friendly antihypertensive agent is probably useful in the presence of lipid abnormalities. Similarly, statins have been shown to decrease cardiovascular risk in hypertensive patients. There is also experimental and clinical evidence that statins have blood pressure (BP)-lowering effects. In this review, we discuss the beneficial effects of statins on BP, and provide an overview of the underlying pathophysiology. We also consider the evidence justifying the use of statins in the management of hypertensive patients.

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The Effect of Short-Term Treatment with Simvastatin on Renal Function in Patients with Peripheral Arterial Disease

Cited by 74 publications

References 41 publications

Effect of statins and ACE inhibitors alone and in combination on clinical outcome in patients with coronary heart disease

Effect of statins and ACE inhibitors alone and in combination on clinical outcome in patients with coronary heart disease

Smoking and Aortic Diseases

Statins: another class of antihypertensive agents?

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