A multidisciplinary overview of cardiogenic shock.
Cardiogenic shock complicating acute myocardial infarction (AMI) is reviewed from multidisciplinary viewpoints encompassing both basic and clinical aspects. Insights into the absolute obligate aerobic nature of the heart which possesses neither facultative capability nor functional collateral channels, together with O2 diffusion gradients, mitochondrial O2 sensing and anaerobic ATP deficiencies, are described in some detail. Myocardial adaptive responses against energy crisis, termed the Pasteur Effect, and hypoxia inducible factor (HIF)-1 alpha are implicated for cardiomyocyte viability. Oncosis and/or lysosomal autophagy cause such overwhelming numbers (several billions) of cardiomyocyte death, virtually simultaneously following coronary thrombotic occlusion. Apoptosis is briefly described and cardiogenic shock is discussed in terms of the diagnostic criteria by MIRU, unique hemodynamic manifestations, infarct sizes and border zone extension, and potentially jeopardized myocardium in the remote areas. Reperfusion injury, i.e., reactive oxygen species (ROS), is noted as a double-edged sword. The importance of early revascularization by means of PCI, CABG, and IABP support is emphasized according to current guidelines. For innovative promise in the future, de novo development of collateral channels by growth factors and trials of stem cell implantation aimed at myocardial regeneration are introduced.
Okuda
Minoru
M
Department of Medicine, Keio University School of Medicine, Tokyo, Japan. minoru_okuda@mqb.biglobe.ne.jp
D000255:Adenosine Triphosphate / Q000172:deficiency / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D002470:Cell Survival; D003937:Diagnosis, Differential; D004734:Energy Metabolism; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000096:biosynthesis; D008247:Lysosomes / Q000378:metabolism / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D009204:Myocardial Revascularization; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000648:ultrastructure; D010100:Oxygen / Q000378:metabolism*; D012038:Regeneration; D012770:Shock, Cardiogenic; D033581:Stem Cell Transplantation
C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D000255:Adenosine Triphosphate; D010100:Oxygen