Effects of simvastatin on blood lipids, vitamin E, coenzyme Q<sub>10</sub> levels and left ventricular function in humans

Colquhoun, David; Jackson, Richard; Walters, Michael J.; Hicks, B.J.; Goldsmith, Jenny F.; Young, Pat; Strakosch, C. R.; Kostner, Karam

doi:10.1111/j.1365-2362.2005.01486.x

Cited by 32 publications

(20 citation statements)

References 42 publications

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“…In another study, the impact of simvastatin on ventricular function was studied in hypercholesterolaemic patients during 6 months of treatment. 40 In contrast to the benefits seen in our study, statin treatment did not result in significant alteration of left ventricular function, as evaluated by echocardiography. As with conflicting data on the impact of statins on insulin resistance, it is possible in this case that the amount of time needed to show a benefit from HMG-CoA reductase inhibitors on ventricular remodelling was greater than that encompassed by the study period.…”

Section: Discussioncontrasting

confidence: 55%

Effects of fluvastatin on insulin resistance and cardiac morphology in hypertensive patients

et al. 2010

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Among hypertensive patients, cardiovascular disease morbidity is common, even in those who are adequately treated. New pharmacological strategies to mitigate the burden of arterial hypertension are needed. This 12-month, randomized, double-blind placebo-controlled study investigated the effect of statin (fluvastatin) treatment on ambulatory blood pressure (ABP), exercise blood pressure (EBP), myocardial structure, endothelial function and insulin resistance in 50 hypertensive patients. At baseline, the groups were comparable in terms of demographic characteristics, ABP, EBP, endothelial function and homeostasis model assessment of insulin resistance (HOMA-IR). At the end of the study, there was no difference between groups in terms of resting systolic blood pressure. However, maximum systolic EBP was lower in the treatment group than in the placebo group (175 ± 18 vs 192 ± 23 mm Hg, Po0.05), as was left ventricular mass index (LVMI; 82±15 vs 100±23, Po0.05), and HOMA-IR index was lower after fluvastatin treatment (2.77 ± 1.46 vs 3.33 ± 1.73, Po0.05). Changes in lipid profile were not correlated with blood pressure, endothelial function, LVMI or HOMA-IR data. In hypertensive patients, fluvastatin can improve maximum systolic EBP, myocardial remodelling and insulin resistance, independently of lipid profile variations and endothelial function.

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Section: Discussioncontrasting

confidence: 55%

Effects of fluvastatin on insulin resistance and cardiac morphology in hypertensive patients

et al. 2010

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“…Interestingly, there is evidence that decreases in CoQ10 and α-tocopherol levels may cause impairment of LV function [14,16] . This is in agreement with our echocardiographic findings of LV dilation and remodeling in this model.…”

Section: Discussionmentioning

confidence: 99%

Chronic cola drinking induces metabolic and cardiac alterations in rats

Milei

Losada²,

Llambí³

et al. 2011

WJC

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AIM:To investigate the effects of chronic drinking of cola beverages on metabolic and echocardiographic parameters in rats. METHODS:Forty-eight male Wistar rats were divided in 3 groups and allowed to drink regular cola (C), diet cola (L), or tap water (W) ad libitum during 6 mo. After this period, 50% of the animals in each group were euthanized. The remaining rats drank tap water ad libitum for an additional 6 mo and were then sacrificed. Rat weight, food, and beverage consumption were measured regularly. Biochemical, echocardiographic and systolic blood pressure data were obtained at baseline, and at 6 mo (treatment) and 12 mo (washout). A complete histopathology study was performed after sacrifice. RESULTS:After 6 mo, C rats had increased body weight (+7%, P < 0.01), increased liquid consumption (+69%, P < 0.001), and decreased food intake (-31%, P < 0.001). C rats showed mild hyperglycemia and hypertriglyceridemia. Normoglycemia (+69%, P < 0.01) and sustained hypertriglyceridemia (+69%, P < 0.01) were observed in C after washout. Both cola beverages induced an increase in left ventricular diastolic diameter (C: +9%, L: +7%, P < 0.05 vs W) and volumes (diastolic C: +26%, L: +22%, P < 0.01 vs W; systolic C: +24%, L: +24%, P < 0.05 vs W) and reduction of relative posterior wall thickness (C: -8%, L: -10%, P < 0.05 vs W). Cardiac output tended to increase (C: +25%, P < 0.05 vs W; L: +17%, not significant vs W). Heart rate was not affected. Pathology findings were scarce, related to aging rather than treatment.CONCLUSION: This experimental model may prove useful to investigate the consequences of high consumption of soft drinks.

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“…As expected, pancreatic insufficient patients demonstrated much lower levels of CoQ (mean=0.31 μg/ml) than pancreatic sufficient patients (mean=0.49 μg/ml, P<0.0001). Because decreased CoQ levels may reflect decreased lipid levels in the serum, CoQ levels should be interpreted in the context of cholesterol levels and, if possible, triglyceride and phospholipid levels as well [149][150][151].…”

Section: Coenzyme Q-10mentioning

confidence: 99%

Antioxidants in cystic fibrosis☆Conclusions from the CF Antioxidant Workshop, Bethesda, Maryland, November 11-12, 2003

Cantin

White

Cross

et al. 2007

Free Radical Biology and Medicine

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Although great strides are being made in the care of individuals with cystic fibrosis (CF), this condition remains the most common fatal hereditary disease in North America. Numerous links exist between progression of CF lung disease and oxidative stress. The defect in CF is the loss of function of the transmembrane conductance regulator (CFTR) protein; recent evidence that CFTR expression and function are modulated by oxidative stress suggests that the loss may result in a poor adaptive response to oxidants. Pancreatic insufficiency in CF also increases susceptibility to deficiencies in lipophilic antioxidants. Finally the airway infection and inflammatory processes in the CF lung are potential sources of oxidants that can affect normal airway physiology and contribute to the mechanisms causing characteristic changes associated with bronchiectasis and loss of lung function. These multiple abnormalities in the oxidant/antioxidant balance raise several possibilities for therapeutic interventions that must be carefully assessed. IntroductionCystic fibrosis (CF) is the most common fatal disease caused by a single gene defect in Europe and North America [1,2]. The defective gene was identified in 1989 [3][4][5] and shown to encode the cystic fibrosis trans-membrane conductance regulator protein (CFTR). CFTR is a cyclic AMP-regulated anion channel with greatest selectivity for chloride, and bicarbonate [6][7][8]. Furthermore, CFTR regulates sodium transport across epithelial membranes through interactions with the epithelial sodium channel ENaC [9], and facilitates the trans-membrane export of the small organic anionic peptide glutathione [10]. The expression of CFTR is located in the apical membrane of epithelial cells that line mucous membranes and submucosal glands ☆ A list of participants may be found in the Acknowledgments.

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Effects of simvastatin on blood lipids, vitamin E, coenzyme Q₁₀ levels and left ventricular function in humans

Cited by 32 publications

References 42 publications

Effects of fluvastatin on insulin resistance and cardiac morphology in hypertensive patients

Effects of fluvastatin on insulin resistance and cardiac morphology in hypertensive patients

Chronic cola drinking induces metabolic and cardiac alterations in rats

Antioxidants in cystic fibrosis☆Conclusions from the CF Antioxidant Workshop, Bethesda, Maryland, November 11-12, 2003

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Effects of simvastatin on blood lipids, vitamin E, coenzyme Q10 levels and left ventricular function in humans

Cited by 32 publications

References 42 publications

Effects of fluvastatin on insulin resistance and cardiac morphology in hypertensive patients

Effects of fluvastatin on insulin resistance and cardiac morphology in hypertensive patients

Chronic cola drinking induces metabolic and cardiac alterations in rats

Antioxidants in cystic fibrosis☆Conclusions from the CF Antioxidant Workshop, Bethesda, Maryland, November 11-12, 2003

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Effects of simvastatin on blood lipids, vitamin E, coenzyme Q₁₀ levels and left ventricular function in humans