aging of the cardiovascular system (continued) chapter 16 p.s. timiras
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Aging of the Cardiovascular System
(continued)Chapter 16
P.S. Timiras
Total or partial occlusion of coronary artery due to plaque rupture and thrombosis can cause angina or frank myocardial infarction.
Plaques likely to rupture termed unstable. Rupture usually occurs in lipid-rich and foam cell-rich peripheral margins and may result in thrombosis and arterial occlusion.
Table 16-5: General Characteristics of Atherosclerotic Lesions
Early onset -- progressiveFocal lesionsEarly lesionsAdvance lesions
Damage, Repair, RegressionProgression of localized lesions influenced by:
Local factors: vessel structure and metabolism, blood turbulenceSystemic factors: diabetes, hypertension, stress, genetic predisposition
Table 16-4: Localized Factors Contributing to Atherosclerosis
Marginal vascularization of arterial wallRelative ischemiaLimited metabolic exchangeBlood turbulence and mechanical stress
• Endothelium-derived relaxing factor (EDRF)/nitric oxide (NO) induce vasal dilation
• Endothelins induce vasal constriction
• Vascular endothelial growth factor (VEGF) induces mitogenesis and promotes angiogenesis and wound healing
• Cytokines participate in repair of vascular wall; promote cell adhesion and stimulate thrombotic activity
Significance of Age Changes in the Vascular Endothelium
*Table 16-2, page 293*
• Endothelial cells line the internal wall (intima) of the blood vessels.
• While the muscle cells and the elastic fibers in the vascular wall regulate blood vessel motility (contraction and relaxation), the endothelial cells, serve as protective lining against trauma, infections, etc,
• Endothelial cells undergo significant changes with aging indicative of abnormal function.
• These alterations by themselves may induce pathology or may predispose with other factors to atherosclerosis
Significance of Age Changes in the Vascular Endothelium*Table 16-2, page 293*Endothelial cells undergo significant changes indicative of abnormal functionThe imbalance of vascular tone is manifested by increased vasoconstriction
Endothelins EDRF, NOVascular integrity (cell proliferation and migration, wall remodeling) and injury repair through local growth factors are impaired
VEGF CytokinesMaintenance of blood fluidity is disrupted with increased cell adherence, blood coagulation, and thrombogenic properties
CytokinesThese alterations by themselves may induce pathology or may predispose with other factors to atherosclerosis
Table 16-6 Probable Role of Ground Substance in EarlyAtherosclerotic Lesions
MAJOR COMPONENTS PROPERTIES
Glucosaminoglycans(proteoglycans)Hyaluronic acid
Viscoelastic (impaired with aging, reduced
mechanical support)CollagenElastin
Water-binding (with aging, reduced hydration,
altered transport)
*Changes in lipids of aorta are listed in Table 16-7 and further discussedby Dr. Forte in relation with the lecture on lipoproteins.
Table 16-8: Theories of Atherosclerosis
• Lipid accumulation• Myoclonal
• Thrombogenic• Inflammation• Free Radicals
**See page 299**
Table 16-10 Symptoms of Angina Pectoris andAcute Myocardial Infarction in the Elderly
Angina Pectoris
Pain, less marked than in adult;may present as headache or epigastric distress
Myocardial Infarction
Variable presentation with chest pain,including breathlessness, confusion, fainting,
GI symptoms, sweating, hypotension, etc.
Regulation of coronary blood
flow:
Vasodilation O2 CO2
Vagal Stimulation
VasoconstrictionAngiotension IISympathetic stimulation
Table 16-11 Major Risk Factors inCoronary Heart Disease
AgeGenetic predispostion
HypertensionDiabetes mellitus
HypercholesterolemiaCigarette smoking
Also:Obesity
Poor physical fitness and lack of exercisePersonality type (?)
High homocysteinemia and Protein C
Table 16-12 Major Types ofCoronary Heart Disease Treatment
Medical treatmentDietExerciseNo smokingPharmacologic agents
Surgical treatmentAortocoronary bypass graft
Percutaneous coronary angioplasty withstreptokinase/ tissue plasminogen activator (TPA)anticoagulant therapy