Chapter I/2: Pathological aspects of myocardial infarction development and its complications

 

Chapter I/2: Pathological aspects of myocardial infarction development and its complications

Tibor Glasz

The chapter structure
feladat

  • I/2.1: Main data of the presented specimen case

  • I/2.2: Description of the specimen

  • I/2.3.: Arteriosclerosis (hardening of arteries, arterial calcification), as the most important disease predisposing to myocardial infarction

    • I/2.3.2: Epidemiological significance

    • I/2.3.3: Lipid metabolism

    • I/2.3.4: Cellular elements of the sclerotic vascular lesions

      • I/2.3.4.1: Endothelial cells

      • I/2.3.4.2: Monocytes/macrophages 

      • I/2.3.4.3: Smooth muscle cells

    • I/2.3.5: Atherogenic theories

      • I/2.3.5.1: ‘Response to injury’ theory 

        • I/2.3.5.1.1: Vascular wall damaging effects, their nature and background

        • I/2.3.5.1.2: Hemodynamical factors of plaque formation

        • I/2.3.5.1.3: The essence of the therory

      • I/2.3.5.2: Lipid theory

      • I/2.3.5.3: Thrombogenic theory

      • I/2.3.5.4: Inflammatory-infectious-autoimmune theory 

    • I/2.3.6: Risk factors

    • I/2.3.7: Morphology of arterial hardening

      • I/2.3.7.1: Anatomical sites of incidence

      • I/2.3.7.2: Appearance types of arterial hardening (AHA classification)

        • I/2.3.7.2.1: Early arteriosclerotic lesion – AHA I

        • I/2.3.7.2.2: Early arteriosclerotic lesion – AHA II

        • I/2.3.7.2.3: Intermediate arteriosclerotic lesion – AHA III

        • I/2.3.7.2.4: Late arteriosclerotic lesion– AHA IV

        • I/2.3.7.2.5: Late arteriosclerotic lesion – AHA V

        • I/2.3.7.2.6: Late arteriosclerotic lesion – AHA VI

        • I/2.3.7.2.7: Plaque stability

        • I/2.3.7.2.8: The organs’ reserves against arteriosclerosis

        • I/2.3.7.2.9: Clinical forms of arteriosclerosis

        • I/2.3.7.2.10: A special and rare form of arterial hardening: Mönckeberg’s medial calcific sclerosis

  • I/2.4: A significant risk factor of cardiovascular diseases: hypertension

    • I/2.4.1: Types of hypertension

      • I/2.4.1.1: Primary (essential) benign hypertension

        • I/2.4.1.1.1: Hypertensive cardiopathy and arterial hardening (arteriosclerosis)

      • I/2.4.1.2: Primary (essential) malignant hypertension

      • I/2.4.1.3: Secondary hypertension

  • I/2.5: Ischemic heart disease syndrome

    • I/2.5.1: Coronary artery hardening (coronary sclerosis) as a cardiac manifestation of arteriosclerosis

      • I/2.5.1.1: Introduction

      • I/2.5.1.2: The causes of coronary artery sclerosis and obstruction

      • I/2.5.1.3: Classification of coronary artery hardening

    • I/2.5.2.:Ischemic heart disease

      • I/2.5.2.1: Concept definition and initiative notes

      • I/2.5.2.2: Causes of ischemic heart disease

      • I/2.5.2.3: Clinicopathological syndromes of ischemic heart disease

        • I/2.5.2.3.1: Angina pectoris

        • I/2.5.2.3.2: Sudden cardiac death

        • I/2.5.2.3.3: Heart attack (acute myocardial infarction)

        • I./2.5.2.3.4: Chronic ischemic heart disease (so-called chronic ischemic cardiopathy) 

    • I/2.5.3: Myocardial infarction (heart attack, myocardial necrosis) 

      • I/2.5.3.1: Introduction

      • I/2.5.3.2: Causes of myocardial infarction

      • I/2.5.3.3: Extension of myocardial infarction

        • I/2.5.3.3.1: Vertical extension of myocardial infarction

        • I/2.5.3.3.2: Horizontal extension of myocardial infarction

      • I/2.5.3.4: Developmental stages of myocardial infarction (post-infarction periods)

      • I/2.5.3.5: Paradoxical myocardial infarction

      • I/2.5.3.6: Progressive myocardial infarction

      • I/2.5.3.7: Complications of myocardial infarction

        • I/2.5.3.7.1: Left heart failure and cardiogenic shock

        • I/2.5.3.7.2.: Left ventricular aneurysm

        • I/2.5.3.7.3: Free ventricular wall rupture, pericardial blood accumulation and tamponade (hemopericardium, pericardial tamponade)

        • I/2.5.3.7.4: Ventricular septal rupture

        • I./2.5.3.7.5: Papillary muscle dysfunction and rupture

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irodalom

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Kádár A, Glasz T: Development of atherosclerosis and plaque biology. Journal of Cardiovascular Surgery 2001; 9: 109-121.

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