Statin use is associated with enhanced collateralization of severely diseased coronary arteries

Pourati, Isaac; Kimmelstiel, Carey; Rand, William; Karas, Richard H.

doi:10.1016/s0002-8703(03)00413-7

Cited by 52 publications

(34 citation statements)

References 25 publications

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“…Secondly, vasoactive drugs, such as ACE inhibitors, angiotensin receptor blockers, and statins, could have positive effects on endothelial function (44 -46). Moreover, statin use has been shown to be associated with enhanced collateralization in patients with documented coronary artery disease (47). Although the use of lipidlowering agents was equally distributed in our study population, patients with the metabolic syndrome use ACE inhibitors or angiotensin receptor blockers significantly more often than patients without the metabolic syndrome (28 vs. 11%, P ϭ 0.001).…”

Section: Olijhoek and Associatesmentioning

confidence: 78%

Presence of the Metabolic Syndrome Does Not Impair Coronary Collateral Vessel Formation in Patients With Documented Coronary Artery Disease

Olijhoek

Koerselman²,

Jaegere³

et al. 2005

Diabetes Care

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OBJECTIVE -The metabolic syndrome confers an increased risk for cardiovascular morbidity and mortality. The presence of coronary collaterals may have beneficial effects during myocardial ischemia and may improve cardiovascular outcome in patients with coronary artery disease. Impaired collateral formation could be one of the reasons for the increased cardiovascular risk in patients with the metabolic syndrome. The aim of the present study was to determine the influence of the metabolic syndrome and insulin resistance on the presence of coronary collaterals. RESEARCH DESIGNS AND METHODS-We conducted a cross-sectional study in 227 patients referred for elective percutaneous transluminal coronary angioplasty to the University Medical Centre Utrecht. The metabolic syndrome was diagnosed according to Adult Treatment Panel III, and homeostasis model assessment of insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI) were used to quantify insulin resistance. Coronary collaterals were graded with Rentrop's classification. Rentrop grade Ն1 indicated the presence of collaterals. Results were adjusted for age, sex, and severity of coronary artery disease.RESULTS -A total of 103 patients (45%) were diagnosed with the metabolic syndrome. There was no association between the metabolic syndrome and the presence of coronary collateral formation (odds ratio [OR] 1.2 [95% CI 0.7-2.0]). Also, the degree of insulin resistance was not related to the presence of coronary collaterals. The OR for HOMA-IR (highest versus lowest tertile) was 0.7 (0.3-1.5) and for QUICKI (lowest versus highest tertile) 0.8 (0.4 -1.6).CONCLUSIONS -The metabolic syndrome and insulin resistance are not related to the presence of coronary collaterals in patients with documented coronary artery disease. Diabetes Care 28:683-689, 2005T he metabolic syndrome is a cluster of generally accepted cardiovascular risk factors such as impaired glucose metabolism, elevated blood pressure, dyslipidemia, and central obesity (1). Also, other often not routinely measured cardiovascular risk factors (e.g., inflammation, increased oxidative stress, increased small dense LDL cholesterol, impaired fibrinolysis, hypercoagulability, and hyperinsulinemia) cluster in this syndrome (2). The underlying pathophysiology is still not fully clarified, but insulin resistance is a major characteristic. Increased adipose tissue mass is involved in the development of insulin resistance by metabolic alterations such as changes in the production of cytokines (3,4).The prevalence of the metabolic syndrome is high, amounting to 24% in an apparently healthy westernized population (5). In patients with manifest vascular disease, the prevalence is 46% (6). The number of subjects with the metabolic syndrome is likely to increase in the coming years due to the increased prevalence of obesity. Patients with the metabolic syndrome are at an increased risk for cardiovascular morbidity and mortality (7)(8)(9)(10)(11)(12). Several studies report a two-to threefold increase...

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Section: Olijhoek and Associatesmentioning

confidence: 78%

Presence of the Metabolic Syndrome Does Not Impair Coronary Collateral Vessel Formation in Patients With Documented Coronary Artery Disease

Olijhoek

Koerselman²,

Jaegere³

et al. 2005

Diabetes Care

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“…Secondly, higher atherosclerotic burden at the time of presentation may explain the observed shift in the presentation patterns toward more benign clinical forms for at least 2 reasons: first, coronary occlusions at the site of a critical stenosis functionally might be less important than coronary occlusion of mild-to-moderate stenoses because the amount of coronary flow that is interrupted might be already small and, second, critical stenoses might have promoted collateral development which further attenuates the clinical presentation of acute coronary occlusion. There are reports that statins may enhance coronary collateral formation in patients with severe CAD [33]. Thirdly, within the group of patients presenting with ACS, these effects may explain the increased proportions of unstable angina and NSTEMI, known to have a higher atherosclerotic burden than patients with STEMI [34].…”

Section: Discussionmentioning

confidence: 98%

Statin pretreatment and presentation patterns in patients with coronary artery disease

Ndrepepa¹,

Fusaro²,

King³

et al. 2013

Cardiol J.

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“…PϭNS, *PϽ0.01 compared with control. Prior reports about the effect of statins on angiogenesis have been conflicting between a stance of promotion 14,15,32 and inhibition. 33,34 These discrepant data may result from the different cell types used or may be attributed to the different statin concentrations.…”

Section: Discussionmentioning

confidence: 99%

Neuronal Nitric Oxide Synthase Mediates Statin-Induced Restoration of Vasa Nervorum and Reversal of Diabetic Neuropathy

et al. 2005

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Background-Peripheral neuropathy is a frequent and major complication of diabetes. Methods and Results-Severe peripheral neuropathy developed in type II diabetic mice, characterized by significant slowing of motor and sensory nerve conduction velocities. Rosuvastatin restored nerve vascularity, including vessel size, and nerve function also recovered to the levels of nondiabetic mice. Neuronal nitric oxide synthase expression in sciatic nerves was reduced in diabetic mice but was preserved by rosuvastatin. Coadministration of a nitric oxide synthase inhibitor with rosuvastatin attenuated the beneficial effects of rosuvastatin on nerve function and limited the recovery of vasa nervorum and nerve function. In vitro, rosuvastatin inhibited downregulation of neuronal nitric oxide synthase expression induced by high-glucose conditions in cultured Schwann cells. Furthermore, Akt phosphorylation in Schwann cells, downregulated by high-glucose conditions, was also restored by rosuvastatin, consistent with the change of neuronal nitric oxide synthase expression. Akt inhibition independently reduced neuronal nitric oxide synthase expression in Schwann cells in low-glucose cultures. Conclusions-These data indicate that the HMG-CoA reductase inhibitor rosuvastatin has a favorable effect on diabetic neuropathy independent of its cholesterol-lowering effect. Our data provide evidence that this effect may be mediated in part via neuronal nitric oxide synthase/nitric oxide and phosphatidylinositol 3-kinase/Akt-signaling pathways and also suggest that restoration or preservation of the microcirculation of the sciatic nerve may be involved.

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Statin use is associated with enhanced collateralization of severely diseased coronary arteries

Cited by 52 publications

References 25 publications

Presence of the Metabolic Syndrome Does Not Impair Coronary Collateral Vessel Formation in Patients With Documented Coronary Artery Disease

Presence of the Metabolic Syndrome Does Not Impair Coronary Collateral Vessel Formation in Patients With Documented Coronary Artery Disease

Statin pretreatment and presentation patterns in patients with coronary artery disease

Neuronal Nitric Oxide Synthase Mediates Statin-Induced Restoration of Vasa Nervorum and Reversal of Diabetic Neuropathy

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