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Stem Cell Treatments for Heart Disease is an Option

Stem Cell Treatment for Heart Disease

Cardiovascular diseases remain the biggest cause of deaths worldwide, though over the last two decades, cardiovascular mortality rates have declined in many high-income countries but have increased at an astonishingly fast rate in low- and middle-income countries. The percentage of premature deaths from cardiovascular disease range from 4% in high-income countries to 42% in low-income countries. More than 17 million people died from cardiovascular diseases in 2008. Each year, heart disease kills more Americans than cancer. In recent years, cardiovascular risk in women has been increasing and has killed more women than breast cancer.

Measures to prevent cardiovascular disease may include:

  • Keeping unapposed simple carbohydrates under control, no matter what type: fruit, bread, dairy, etc.
  • decrease emotional stress, or how you react to the environment (traffic, work, deadlines, lifestyle, etc.)
  • a low fat high fiber diet including whole grains and plenty of fresh fruit and vegetables (at least five portions a day)
  • a diet high in complex vegetables and colorful fruit
  • tobacco cessation;
  • limit alcohol consumption;
  • lower blood pressures if elevated through diet and exercise;
  • decrease body fat (BMI);
  • increase daily activity to 30 minutes of any kind of exercise per day at least five times per week

Stem Cell Heart Disease

A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein (CRP) is a common inflammatory marker that has been found to be present in increased levels in patients at risk for cardiovascular disease. Also osteoprotegerin which is involved with regulation of a key inflammatory transcription factor called NF-κB has been found to be a risk factor of cardiovascular disease and mortality. Studies have shown that Stem Cells have shown the ability to reduce inflammation.

Stem Cell Treatments for Heart Disease is an Option at ASCI

Streaming NIH Database:

Related Articles Acute pulmonary edema with new giant V wave immediately after pericardiocentesis. Int J Cardiol. 2016 Jun 01;212:253-4 Authors: Takeuchi T, Fujimoto N, Dohi K, Ino K, Monma F, Katayama N, Ito M PMID: 27054499 [PubMed - indexed for MEDLINE]
Related Articles Hyperglycemia attenuates remifentanil postconditioning-induced cardioprotection against hypoxia/reoxygenation injury in H9c2 cardiomyoblasts. J Surg Res. 2016 Jun 15;203(2):483-90 Authors: Chen L, Chen M, Du J, Wan L, Zhang L, Gu E Abstract BACKGROUND: Hyperglycemia is proposed to be an independent risk factor for cardiovascular morbidity and mortality. Preclinical studies suggest that diabetes mellitus exacerbates myocardial ischemia/reperfusion injury and attenuates the effects of cardioprotective strategies. The cardioprotective effects of postconditioning with the opioid analgesic remifentanil against ischemia/reperfusion injury under the hyperglycemic condition remain contradictory. Therefore, the aim of this study was to investigate the mechanisms by which hyperglycemia affects cardioprotection induced by remifentanil postconditioning. MATERIALS AND METHODS: H9c2 cardiomyoblasts were cultured under the normoglycemic or hyperglycemic condition. Cells were exposed to hypoxia/reoxygenation (H/R) injury followed by hypoxia postconditioning (HPC group) or remifentanil postconditioning (RPC group). Cell viability, injury, and apoptosis were measured after each postconditioning treatment. Activation of endoplasmic reticulum stress (ERS) was analyzed by examining the protein levels of GRP78, CHOP, cleaved caspase-12 and cleaved caspase-3. RESULTS: RPC significantly increased cell viability and reduced apoptosis in normoglycemic cardiomyoblasts, but not in hyperglycemic cardiomyoblasts. HPC and RPC markedly decreased the upregulation of GRP78, CHOP, cleaved caspase 12, and cleaved caspase 3 in response to H/R injury under the normoglycemic condition. Hyperglycemia significantly increased these ERS-associated biomarkers and apoptosis, which could not be reduced by HPC or RPC. CONCLUSIONS: Remifentanil postconditioning protected cardiomyoblasts from H/R injury under normoglycemia, at least in part, through inhibiting ERS-induced apoptosis. Hyperglycemia attenuated the cardioprotection conferred by remifentanil postconditioning, likely as a result of the exacerbated ERS. Inhibiting the ERS response may be an attractive strategy to enhance the cardioprotective effects of postconditioning in diabetic patients. PMID: 27363659 [PubMed - indexed for MEDLINE]