L2- Pathology of Ischemic Heart Disease

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Aug 23, 2009
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CLINICAL MANFESTATIOS OF ISCHEMIC HEART DISEASE SIZE OF HE PROBLEM ATHEROTHROMBOTIC CORONARY HEART DISEASE RISK FACTORS FOR IHD CLINICAL PRESENTATION DIAGNOSIS AND INVESTIGATIONS THERAPY PREVENTION SIZE OF THE PROBLEM IHD is now the leading cause of death worldwide, and it is expected that the rate of IHD will accelerate in the next decades, contributed to by; 1.aging of population 2.Alarming increase in the prevalence of obesity, type 2 DM, and metabolic syndrome 3.Rise in CV risk factors (smoking, stress) among young generations The WHO estimates that by 2020 the global number of deaths from IHD will have risen from 7.1 in 2002 to 11.1 millions FIGURE 35-2B The structure of normal arteries. A, Elastic artery. Note the concentric laminae of elastic tissue that form “sandwiches” with successive layers of smooth muscle cells. Each level of the elastic arterial tree has a characteristic number of elastic laminae. B, Muscular artery. The smooth muscle cells are surrounded by a collagenous matrix but lack the concentric rings of well organized elastic tissue characteristic of the larger arteries. FIGURE 35-3 The endothelial thrombotic balance. This diagram depicts the anticoagulant profibrinolytic functions of the endothelial cell  (left) and certain procoagulant and antifibrinolytic functions (right). PAi = plasminogen activator inhibitor; PGI2 = prostacyclin; t-PA = tissue type plasminogen activator; vWf = von Willebrand factor. FIGURE 35-4 Schematic of the evolution of the atherosclerotic plaque. 1: Accumulation of lipoprotein particles in the intima. The modification of these lipoproteins is depicted by the darker color. Modifications include oxidation and glycation. 2: Oxidative stress, including products found in modified lipoproteins, can induce local cytokine elaboration. 3: The cytokines thus induced increase expression of adhesion molecules for leukocytes that cause their attachment and chemoattractant molecules th
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