Physical Activity in the Prevention and Treatment of Coronary Artery Disease

Ephraim Bernhard Winzer, Felix Woitek, Axel Linke, Ephraim Bernhard Winzer, Felix Woitek, Axel Linke

No abstract available

Keywords: coronary artery disease; endothelium; exercise training; physical exercise; prevention.

Figures

Figure 1
Figure 1
Impact of regular physical activity on mortality in primary prevention. Low cardiorespiratory fitness, obesity, arterial hypertension, diabetes mellitus, and dyslipidemia contribute to increased mortality (+). Regular physical activity improves fitness (+) and counteracts the development of risk factors (−).
Figure 2
Figure 2
Endothelial function and repair. Endothelial NO synthase (eNOS) produces NO via conversion of l‐arginine (l‐Arg.) to l‐citrulline in the presence of tetrahydrobiopterin (BH4) and calcium‐calmodulin. Shear stress activates eNOS activity by phosphorylation at serine 1177 (S1177). This process is mediated by phosphatidylinositol 3‐kinase (PI3K), phosphoinositide‐dependent kinase (PDK), and protein kinase B (AKT). NO easily diffuses through plasma membranes. In smooth muscle cells, NO activates guanylate cyclase, which, in turn, converts GTP to cGMP. A reduction of the intracellular calcium concentration (Ca2+) leads to hyperpolarization of the cell membrane and, consequently, smooth muscle relaxation. NO is broken down in the presence of reactive oxygen species (ROS), mainly superoxide, generating peroxynitrite. Peroxynitrite, in turn, oxidates BH4 and promotes eNOS uncoupling, resulting in eNOS‐derived superoxide production. Additional sources of superoxide are heme oxygenase (HO1/2), myeloperoxidase, cytochrome P450, the mitochondrial electron transport chain, and nicotinamide‐adenine dinucleotide [phosphate], reduced form (NAD[P]H) oxidase, which is activated by tumor necrosis factor α and angiotensin II via the angiotensin II receptor type 1 (AT1‐R). Extracellular superoxide dismutase (ecSOD) scavenges superoxide. Vessel growth and arteriolarization of capillaries are mediated by vascular endothelial growth factor (VEGF), transforming growth factor ß (TGF), platelet‐derived growth factor (PDGF), fibroblast growth factors 1 and 2 (FGFs 1/2), and insulin‐like growth factor (IGF). Circulating progenitor cells (CPCs), mobilized from the bone marrow, contribute to repair of the damaged endothelium and the formation of new vascular structures. Homing of CPCs is mediated by the binding of CXC‐chemokine receptor type 4 (CXCR4) to stromal cell–derived factor‐1 (SDF‐1), which is secreted at the site of injury. The adhesion molecule P‐selectin mediates the rolling of blood cells on the surface of the endothelium and initiates the activation of platelets and adhesion of leukocytes at the site of injury, allowing them to transmigrate the endothelial layer and perpetuate an inflammatory atherosclerotic process via the secretion of interleukins and chemokines. Question marks indicate that there are several other endothelial‐derived relaxing and constricting factors that affect different ion channels, transporters, and second messengers. Further alterations within the vascular smooth muscle cell and perivascular adipose tissue are involved in the regulation of the vascular tone, but they are not in the focus herein.
Figure 3
Figure 3
Mechanisms of improved collateral blood flow. Improvement of collateral blood flow in occlusive coronary artery disease in response to exercise training might be a consequence of the following: (1) angiogenesis, which is the sprouting of endothelial cells from preexisting capillaries and the formation of a capillary network; (2) the arteriolarization of capillaries and microvessels; or (3) improved vasomotor function of conduit arteries and resistance vessels of the collateral supply arteries.

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