Relation of metformin treatment to clinical events in diabetic patients undergoing percutaneous intervention

Kao, John; Tobis, Jonathan M.; McClelland, Robyn L.; Heaton, Melissa R; Davis, Barry R.; Holmes, David R.; Currier, Jesse W.

doi:10.1016/j.amjcard.2004.02.028

Cited by 85 publications

(53 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Metformin has beneficial effects on heart in human and experimental animals, decreasing cardiovascular mortality and the risk of myocardial infarct in humans and improving left ventricular functions in experimental animals [15][16][17]19]. Although metformin reduces protein synthesis in cardiac myocyte [22], it is unknown whether metformin inhibits cardiac hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

“…Patients who received metformin therapy demonstrate significant improvement all-cause and cardiovascular mortality when compared with patients who received sulphonylurea therapy [15,16]. Metformin treatment also reduces the risk of myocardial infarct in diabetic patients [17]. Recently, metformin was revealed to be an AMP activated protein kinase (AMPK) activator [18] and low doses metformin significantly improves left ventricular function and survival via activation of AMPK [19].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

Cha

Choi

Kim

et al. 2010

Korean J Physiol Pharmacol

View full text Add to dashboard Cite

ABBREVIATIONS: AMPK, AMP-activated protein kinase; ANP, atrial natriuretic peptide; GPx1, glutathione peroxidase 1; IL-6, interleukin-6; MMP-2, matrix metallopeptidase 2; MMP-9, matrix metallopeptidase 9; TGF-β, transforming growth factor-β. The present study examined whether metformin treatment prevents isoporterenol-induced cardiac hypertrophy in mice. Chronic subcutaneous infusion of isoproterenol (15 mg/kg/24 h) for 1 week using an osmotic minipump induced cardiac hypertrophy measured by the heart-to-body weight ratio and left ventricular posterior wall thickness. Cardiac hypertrophy was accompanied with increased interleukin-6 (IL-6), transforming growth factor (TGF)-β, atrial natriuretic peptide (ANP), collagen I and III, and matrix metallopeptidase 2 (MMP-2). Coinfusion of metformin (150 mg/kg/24 h) with isoproterenol partially inhibited cardiac hypertrophy that was followed by reduced IL-6, TGF-β, ANP, collagen I and III, and MMP-2. Chronic subcutaneous infusion of metformin did not increase AMP-activated protein kinase (AMPK) activity in heart, although acute intraperitoneal injection of metformin (10 mg/kg) increased AMPK activity. Isoproterenol increased nitrotyrosine levels and mRNA expression of antioxidant enzyme glutathione peroxidase and metformin treatment normalized these changes. These results suggest that metformin inhibits cardiac hypertrophy through attenuating oxidative stress.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

Cha

Choi

Kim

et al. 2010

Korean J Physiol Pharmacol

View full text Add to dashboard Cite

show abstract

“…In humans, metformin supplementation has been shown to reduce adiposity (40) and mortality rates in diabetic individuals, most effectively in obese and insulin-resistant individuals (41)(42)(43). Although the data so far are promising, further study is needed to show whether metformin is able to extend life span in healthy rodents, primates, and humans.…”

Section: Glucose and Insulin Homeostasismentioning

confidence: 99%

Dietary Interventions to Extend Life Span and Health Span Based on Calorie Restriction

Minor

Allard

Younts

et al. 2010

The Journals of Gerontology Series A: Biological Sciences and M

View full text Add to dashboard Cite

The societal impact of obesity, diabetes, and other metabolic disorders continues to rise despite increasing evidence of their negative long-term consequences on health span, longevity, and aging. Unfortunately, dietary management and exercise frequently fail as remedies, underscoring the need for the development of alternative interventions to successfully treat metabolic disorders and enhance life span and health span. Using calorie restriction (CR)-which is well known to improve both health and longevity in controlled studies-as their benchmark, gerontologists are coming closer to identifying dietary and pharmacological therapies that may be applicable to aging humans. This review covers some of the more promising interventions targeted to affect pathways implicated in the aging process as well as variations on classical CR that may be better suited to human adaptation.

show abstract

“…Although this study has shown similar effects of different glucose-lowering drugs in monotherapy prior to MI on the prognosis after the MI, concerns about differences in the risk of developing cardiovascular disease, including MI, among users of different glucose-lowering drugs remain [7,[26][27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Type of preadmission glucose-lowering treatment and prognosis among patients hospitalised with myocardial infarction: a nationwide follow-up study

2008

View full text Add to dashboard Cite

Aims/hypothesis We examined whether the type of preadmission glucose-lowering treatments explained differences in mortality rate and risk of readmission with myocardial infarction (MI) and heart failure following first-time hospitalisation for MI in patients with type 2 diabetes mellitus. Methods We conducted a nationwide population-based followup study among all Danish patients hospitalised with firsttime MI from 1996 to 2004. Data on use of glucose-lowering drugs and other medications, comorbidities, socioeconomic status, laboratory findings, readmission with MI and heart failure, and death were obtained from medical databases. We computed mortality rates and rates of MI and heart failure readmission, according to type of glucose-lowering treatment and used Cox's proportional hazards regression analysis to compute hazard ratios (HRs) as estimates of relative risks. Results We identified 8,494 MI patients with type 2 diabetes mellitus. The overall cumulative 30 day and 1 year mortality rates were 22.2 and 36.6%, respectively. Patients not receiving any glucose-lowering drugs (adjusted 30 day HR: 0.79, 95% CI: 0.57-1.10) and users of any combination (adjusted 30 day HR: 1.43, 95% CI: 0.98-2.09) had the lowest and highest mortality rates, respectively, when compared with users of sulfonylureas. We found that glycaemic control had no impact on the risk estimates in a subanalysis including biochemical laboratory data. We found no differences in the risk of new MI and heart failure between the different glucose-lowering agents. Conclusions/interpretation Type of preadmission glucoselowering treatment in monotherapy is not associated with substantial differences in prognosis following hospitalisation with MI. However, patients treated with any combination had increased mortality rates.

show abstract

Relation of metformin treatment to clinical events in diabetic patients undergoing percutaneous intervention

Cited by 85 publications

References 18 publications

Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

Dietary Interventions to Extend Life Span and Health Span Based on Calorie Restriction

Type of preadmission glucose-lowering treatment and prognosis among patients hospitalised with myocardial infarction: a nationwide follow-up study

Contact Info

Product

Resources

About