Literature DB >> 16513517

Metabolic syndrome in patients with acute myocardial infarction is associated with increased infarct size and in-hospital complications.

Leonardo C Clavijo1, Tina L Pinto, Pramod K Kuchulakanti, Rebecca Torguson, William W Chu, Lowell F Satler, Kenneth M Kent, William O Suddath, Augusto D Pichard, Ron Waksman.   

Abstract

BACKGROUND: Metabolic syndrome (MS), the combination of hypertension, obesity, dyslipidemia, and insulin resistance, is a precursor of diabetes mellitus (DM) and highly prevalent among patients with acute myocardial infarction (AMI). Diabetes mellitus is associated with larger infarct size and worse outcomes after AMI. This study examined infarct size and short-term outcomes among nondiabetic patients with MS following contemporary treatment of AMI.
METHODS: Four hundred five consecutive patients with AMI treated with primary percutaneous coronary intervention were evaluated. Patients with diabetes (n=105) were excluded. Those with MS (n=167) included patients with three or more of the following criteria: hypertension, elevated fasting blood glucose, hypertriglyceridemia, low high-density lipoprotein, and obesity [body mass index (BMI)> or =30]. The control group (n=133) included patients without MS or DM.
RESULTS: Baseline characteristics were similar except for hypertension, BMI, and dyslipidemia, which by study design were higher in the MS group. The MS group had larger infarct size as determined by peak creatine kinase-MB (79.8+/-133.8 vs. 30.84+/-51.5, P<.001). Overall in-hospital complications were higher in patients with MS (21.1% vs. 9.2%, P=.003). Metabolic syndrome is associated with a 10-fold increased risk of acute renal failure after myocardial infarction (7.9% vs. 0.8%, P=.007).
CONCLUSION: Metabolic syndrome in nondiabetic patients with AMI is associated with larger infarct size, more in-hospital complications, and a marked increase of acute renal failure. Awareness of MS and preventative measures is crucial in this population to minimize infarct size and decrease morbidity after AMI.

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Year:  2006        PMID: 16513517     DOI: 10.1016/j.carrev.2005.10.007

Source DB:  PubMed          Journal:  Cardiovasc Revasc Med        ISSN: 1878-0938


  17 in total

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Review 3.  Obesity and vulnerability of the CNS.

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4.  Discordant signaling and autophagy response to fasting in hearts of obese mice: Implications for ischemia tolerance.

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7.  Impaired contractile recovery after low-flow myocardial ischemia in a porcine model of metabolic syndrome.

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Review 8.  The assessment of endothelial function: from research into clinical practice.

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Journal:  Circulation       Date:  2012-08-07       Impact factor: 29.690

9.  Boosting autophagy in the diabetic heart: a translational perspective.

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Journal:  Cardiovasc Diagn Ther       Date:  2015-10

10.  The novel adipocytokine visfatin exerts direct cardioprotective effects.

Authors:  Shiang Y Lim; Sean M Davidson; Ajeev J Paramanathan; Christopher C T Smith; Derek M Yellon; Derek J Hausenloy
Journal:  J Cell Mol Med       Date:  2008-04-08       Impact factor: 5.310

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