Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction

Silver, Marc A.; Langsjoen, Per H.; Szabo, Szabolcs; Patil, Harish; Zelinger, Allan

doi:10.1016/j.amjcard.2004.07.121

Cited by 82 publications

(53 citation statements)

References 10 publications

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“…Coenzyme Q 10 has previously been shown to inhibit cardiac oxidative stress [12,13]. A protective role for coenzyme Q 10 has been suggested in settings of heart failure outside diabetes [14][15][16]. However, the potential of coenzyme Q 10 to attenuate the structural and functional defects specifically caused by diabetic cardiomyopathy still remains to be elucidated.…”

mentioning

confidence: 99%

Coenzyme Q10 attenuates diastolic dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis in the db/db mouse model of type 2 diabetes

et al. 2012

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confidence: 99%

Coenzyme Q10 attenuates diastolic dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis in the db/db mouse model of type 2 diabetes

et al. 2012

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“…Ubiquinone is a powerful intra-cellular antioxidant and an integral component of the mitochondrial respiratory chain. Very low levels of ubiquinone have been associated with statin-induced rhabdomyolysis (27) and, possibly, cardiac dysfunction (45,46). Statin pharmacokinetics are significantly altered in the critically ill due to changes in protein binding, hepatic metabolism and renal excretion, resulting in significantly higher plasma levels than those found in the general population (28).…”

Section: Discussionmentioning

confidence: 99%

Simvastatin pre-treatment improves survival and mitochondrial function in a 3-day fluid-resuscitated rat model of sepsis

et al. 2017

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Statins may offer protective effects in sepsis through anti-inflammatory, mitochondrial protection and other actions. We thus evaluated the effects of simvastatin on survival, organ and mitochondrial function, tissue and plasma ubiquinone levels and liver transcriptomics in a 3-day rat model of sepsis. Comparisons of rat plasma simvastatin and ubiquinone levels were made against levels sampled in blood from patients with acute lung injury (ALI) enrolled into a trial of statin therapy. Animals received simvastatin by gavage either pre-or postinduction of faecal peritonitis. Control septic animals received vehicle alone. 72-hour survival was significantly greater in statin pre-treated animals (43.7%) compared to both their statin post-treated (12.5%) and control septic (25%) counterparts (p<0.05). Sepsis-induced biochemical derangements in liver and kidney improved with statin therapy, particularly when given pre-insult. Both simvastatin pre-and post-treatment prevented the fall in mitochondrial oxygen consumption in muscle fibers taken from septic animals at 24 hours. This beneficial effect was paralleled by recovery of genes related to fatty acid metabolism. Simvastatin pre-treatment resulted in a significant decrease in myocardial ubiquinone. Patients with ALI had a marked variation in plasma simvastatin acid levels however their ubiquinone/LDL cholesterol ratio did not differ regardless of whether they were receiving statin or placebo. In summary, despite protective effects seen with statin treatment given both pre-and post-insult, survival benefit was only seen with pre-treatment, reflecting experiences in patient studies.Short title: Statin and organ dysfunction in sepsis.

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“…In the study of Silver, et al, 28) patients with hypercholesterolemia but without LV systolic dysfunction had a worsening of LV diastolic function after 3 to 6 months of ATO therapy, but CoQ10 supplementation improved the diastolic dysfunction. On the other hand, the retrospective analyses of large-scale clinical studies 29,30) revealed that statin therapy improved morbidity and mortality in patients with heart failure.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin-Induced Changes in Plasma Coenzyme Q10 and Brain Natriuretic Peptide in Patients With Coronary Artery Disease

et al. 2008

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SUMMARYThe beneficial effects of statins in patients with coronary artery disease (CAD) may be balanced by concerns that statins can depress production of ubiquinone (CoQ10), which serves as a component of mitochondrial energy production and an antioxidant. Accordingly, the effects of atorvastatin (ATO)-induced changes in plasma CoQ10 on BNP and oxidative stress were investigated. In 29 patients with CAD, the plasma levels of CoQ10 and BNP and urinary excretion of 8-iso-prostaglandin F2α (8-iso-PGF) were determined before and after 3-month treatment with ATO. Ten patients had received pravastatin and 10 patients fluvastatin, while 9 patients had not received any statin before ATO. There was a linear correlation between ATO-induced changes in total cholesterol and CoQ10 (r = 0.632, P < 0.01), and an inverse correlation between ATO-induced changes in CoQ10 and BNP (r = -0.497, P < 0.01). There was no significant correlation between ATO-induced changes in CoQ10 and 8-iso-PGF. Multivariate analysis revealed that ATO-induced decreases in plasma CoQ10 were significantly associated with increasing BNP levels. In conclusion, long-term treatment with ATO might increase plasma levels of BNP in patients with CAD when it is accompanied by a greater reduction in plasma CoQ10. However, ATO-induced decreases in CoQ10 might not increase oxidative stress. (Int Heart J 2008; 49: 423-433)

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Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction

Cited by 82 publications

References 10 publications

Coenzyme Q10 attenuates diastolic dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis in the db/db mouse model of type 2 diabetes

Coenzyme Q10 attenuates diastolic dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis in the db/db mouse model of type 2 diabetes

Simvastatin pre-treatment improves survival and mitochondrial function in a 3-day fluid-resuscitated rat model of sepsis

Atorvastatin-Induced Changes in Plasma Coenzyme Q10 and Brain Natriuretic Peptide in Patients With Coronary Artery Disease

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