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