Top Banner
Coronary Heart Disease
14
Welcome message from author
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Transcript
Page 1: Coronary Heart Disease

Coronary Heart Disease

Page 2: Coronary Heart Disease
Page 3: Coronary Heart Disease
Page 4: Coronary Heart Disease

Risk factors

Abnormal lipidsSmoking

HypertensionDiabetes mellitus

Abdominal obesityPsychosocial factors

Consumption of too few fruits and vegetables.Too much alcohol

Lack of regular physical activity.

Page 5: Coronary Heart Disease
Page 6: Coronary Heart Disease

• Lipid metabolism in relation to formation of atherosclerotic lesions. Fatty acids from dietary lipids are reesterified in intestinal cells and exported as protein-containing chylomicrons. Lipoprotein lipase from endothelial cells catalyzes the release of triglycerides from the chylomicrons, and the chylomicron remnants are taken up by the liver. In the liver, they take up cholesterol and are released into the bloodstream as very low density lipoprotein (VLDL) particles. These engage in exchange reactions with intermediate-density lipoproteins (IDL) and high-density lipoproteins (HDL). Low-density lipoprotein (LDL) particles are formed, and these constitute the major source of cholesterol for the tissues. Oxidized LDL enter the macrophages and smooth muscle cells, forming foam cells. In addition, HDL carry cholesterol from tissues to the liver for excretion in the bile, and LDL receptors in the liver (not shown) take up VLDL, IDL, and LDL, lowering circulating cholesterol. 6

Page 7: Coronary Heart Disease
Page 8: Coronary Heart Disease

• Formation of a fatty streak in an artery. Following vascular injury, monocytes bind to the endothelium, then cross it to the subendothelial space and become activated tissue microphages. The macrophages take up oxidized LDL, becoming foam cells. T cells release cytokines, which also activate macrophages. In addition, the cytokines cause smooth muscle cells to proliferate. Under the influence of growth factors, the smooth muscle cells then move to the subendothelial space, where they produce collagen and take up LDL, adding to the population of foam cells.

Page 9: Coronary Heart Disease
Page 10: Coronary Heart Disease

• Mechanisms of production of atheroma. A: Structure of normal muscular artery. The adventitia, or outermost layer of the artery, consists principally of recognizable fibroblasts intermixed with smooth muscle cells loosely arranged between bundles of collagen and surrounded by proteoglycans. It is usually separated from the media by a discontinuous sheet of elastic tissue, the external elastic lamina. B: Platelet aggregates, or microthrombi, which may form as a result of adherence of the platelets to the exposed subendothelial connective tissue. Platelets that adhere to the connective tissue release granules whose constituents may gain entry into the arterial wall. Platelet factors thus interact with plasma constituents in the artery wall and may stimulate events shown in the next illustration. C: Smooth muscle cells migrating from the media into the intima through fenestrae in the internal elastic lamina and actively multiplying within the intima. Endothelial cells regenerate in an attempt to recover the exposed intima, which thickens rapidly, owing to smooth muscle proliferation and formation of new connective tissue.

Page 11: Coronary Heart Disease

Plaque rupture

• Many atherosclerotic plaques remain stable or progress only gradually.

• Rupture, often related to the inflammatory process.

• The rupture causes…– Turbulent flow– Extrusion of lipids and fatty gruel– Exposure of tissue factor

Page 12: Coronary Heart Disease

• All result in a cascade of events culminating in intravascular thrombosis.

• The outcome of these events is…– Complete vessel occlusion.– Partial vessel occlusion (causing the symptoms

of unstable angina or myocardial infarction)– Restabilization often with more severe stenosis.

• Transient occlusion and/or embolization of platelet and thrombin debris, which may result in elevation in serum troponin, predispose to clinical events and portend a worse prognosis.

Page 13: Coronary Heart Disease

• Goal: Complete cessation. No exposure to environmental tobacco smoke.

• Goal: For patients with blood pressure 140/90 mm Hg (or 130/80 mm Hg for individuals with chronic kidney disease or diabetes.

• Assess fasting lipid profile in all patients, and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event.

Page 14: Coronary Heart Disease

• Assess body mass index and/or waist circumference on each visit and consistently.

• Encourage weight maintenance/reduction through an appropriate balance of physical activity, caloric intake.