Myocardial redox stress and remodeling in metabolic syndrome, type 2 diabetes mellitus, and congestive heart failure.
Over the past three decades, we have witnessed an improvement of survival in those patients with the trio of metabolic syndrome, prediabetes, and overt type 2 diabetes mellitus. Revolutionary changes in technology and an improved understanding of the mechanisms involved in acute coronary syndromes have resulted in this observation. Due to advances in coronary care, we are currently at a crossroads, wherein, the mortality from acute cardiovascular events have been declining and the mortality associated with this trio has been increasing due to congestive heart failure (CHF). This intersect between the two causes of death represent a challenge for the future, as the numbers of patients with this deadly trio are undergoing exponential growth not only in the U.S. but also abroad as more countries undergo urbanization and adopt a western-type lifestyle of over nutrition and under exercise. Thus, we live to die another day. There are multiple metabolic toxicities in this toxic trio, which predispose to an increase in reactive oxygen species and resultant redox stress within the vascular intima and myocardium. By aggressively reducing the elevated substrates producing reactive oxygen species we may be able to restore our individual, endogenous, potent, antioxidant (antiredoxidant) network. Appropriately, we need to examine the mechanisms that result in the development and transition from diastolic and systolic dysfunction to the clinical syndrome of overt CHF with its inherent increase in morbidity and mortality.
Hayden
Melvin R
MR
Department of Family and Community Medicine University of Missouri Columbia, Missouri 65020, USA. mrh29@usmo.com
Tyagi
Suresh C
SC
D003327:Coronary Disease / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism*; D005109:Extracellular Matrix / Q000378:metabolism; D006333:Heart Failure / Q000378:metabolism* / Q000401:mortality; D006801:Humans; D007333:Insulin Resistance; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D061965:Matrix Metalloproteinase Inhibitors; D024821:Metabolic Syndrome / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D009765:Obesity / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
D061965:Matrix Metalloproteinase Inhibitors; D017382:Reactive Oxygen Species; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D020780:Matrix Metalloproteinase 9