Cardiovascular Pathology

Valvular Heart Disease

• Valve function: to maintain unidirectional blood flow through the heart. Hence any loss of one-way flow will result in pathology.
• Valve histology: a layer of endothelium overlying dense collagen fibrosa layer. Beneath that is a core of loose connective tissue to allow movement and facing the ventricle is a layer of elastin.
• Valve disease: can be either pure or a mix of the following:
- Stenosis: impaired forward flow due to narrowing of the valve entrance
- Regurgitation: incompetence of the valve to close fully allowing reverse flow
• Detection methods: cardiac auscultation and echocardiography (ultrasound of the heart)
- Diastolic murmurs: mitral or tricuspid stenosis – after ventricular ejection and relaxation, valves open and blood rushes into the ventricle against resistance producing murmur. The murmur diminishes until atrial contraction which augments the sound before ventricular systole and 1st heart sound. Aortic or pulmonary incompetence – after systole, recoil of blood through the valves produces a murmur but diminishes as greater vessel pressure drops.
- Systolic murmus: mitral and tricuspid incompetence – after 1st heart sound, ventricular contraction cause blood to squirt through the valves into the atrium producing murmur that diminishes. Aortic and pulmonary stenosis – during ventricular ejection, blood squirting through the narrowed valve produce murmur which increases with progression of ejection but diminishes toward the end.
• Development defect in connective tissue:
- Stenosis of aortic and pulmonary valve
- Leaflet abnormalities: e.g. bicuspid aortic valve. As it is normally 3 cusps, the valve will be vulnerable to pathology. Under long term stress, calcification may occur.
- Myxomatous degeneration of mitral valve: mitral valve prolapsed. Usually as a result in Marfan syndrome or other inherited connective tissue disorder. The disease is often asymptomatic but may increase risk of infective endocarditis and mitral insufficiency.
• Dystrophic calcification: occurs in local areas after extensive/chronic cell injury as a result of dead or dying cells accumulating calcium, e.g. mitochondria and membrane bound vesicle accumulate Ca2+in response to injury.
- Heart valves under long term stress such as bicuspid valves can suffer cumulative damage and lead to cell injury and calcification.
- Annular mitral calcification: calcium formed around the base of the valve on the ring which may or may not affect function
- Aortic stenosis calcification: calcified valves blocks blood flow
• Infection: colonization by pathogen causing valve damage
- Infective endocarditis: colonization and invasion of the heart valve specifically by a microbe often after “polluting” the blood through IV drug abuse or surgery. Lesions or vegetations are formed and these inflammatory nodules can break and cause embolization (obstruction of blood vessels).
- Histology of endocarditis: extensive acute inflammatory cells with many nuclei and dense numbers of fibroblasts and fibrin.
- Acute infection: high virulence organism that attack a normal valve and cause destruction and mortality, e.g. Straph. Aureus
- Sub-acute infection: low virulence organism that attack previously abnormal valve (congenital reasons) and cause insidious damage, e.g. Straph. Viridans
• Post-infection: common disease is rheumatic fever which is an acute multi-system inflammatory disease that occurs only after infection of the nasopharynx with group A streptococcus. It causes valve vegetations, Aschoff bodies and pericarditis which progress to chronic valve deformities, e.g. mitral stenosis
- Pathology: antibodies against streptococcal M proteins cross-react with antigens in the heart creating an autoimmune response. It predisposes infective endocarditis
- Aschoff bodies: focal points of edematous inflammatory connective tissue surrounded by lymphocytes, plasma cells and prominently enlarged macrophages.
• Non-bacterial thrombotic endocarditis (marantic endocarditisis): deposition of fibrin and platelets on heart valves that may occur when a patient is in a hypercoagulable state due to cancer or sepsis etc.
- Thrombosis: inappropriate activation of coagulation on the heart valve leads to thrombosis, e.g. occurs on prosthetic valves hence patient required to be on anti-coagulant drug. Thrombo-emboli can break off and block vessels.
• Carcinoid tumours: neoplasms arising form the neuroendocrine cells or their precursors. Growth of local tumours secretes a variety of bioactive products such as serotonin, that appear to cause plaque-like thickenings in the right side of the heart.
- Plaque thickenings: composed largely of smooth muscles and affect the tricuspid and pulmonary valves.

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