Valvular Heart Disease PDF

Valvular Heart Disease (VHD) Dr. Abdul Rehman  Learning Outcomes Enlist the principal mechanisms of heart diseases Describe the causes, pathogenesis, morphology, clinical features and complications of valvular heart diseases Explain the classification, c...

Valvular Heart Disease (VHD) Dr. Abdul Rehman  Learning Outcomes Enlist the principal mechanisms of heart diseases Describe the causes, pathogenesis, morphology, clinical features and complications of valvular heart diseases Explain the classification, causative organisms, pathogenesis, morphology, diagnosis and complications of Infective endocarditis Heart Valve Anatomy and Histology  Valvular Heart Disease Result in stenosis or insufficiency (regurgitation) or both 1. Stenosis: failure of a valve to open completely  impedes forward blood flow - Always a primary cuspal abnormality (calcification, scarring) 2. Insufficiency (Regurgitation): failure of a valve to close completely  allowing reversed blood flow (backflow) - Intrinsic disease of the valve cusps - Disruption of supporting structures - May appear acutely or chronically Abnormal flow through diseased valves  murmurs Valve abnormalities – congenital or acquired (biscupid aortic valve)  Etiology of Acquired Heart Valve Disease caused so II pathom t.is T  Calcific Aortic Stenosis ftg A degenerative valve disease pf11r Joe is Most common cause of aortic stenosis Age related wear and tear Age related arteriosclerosis (role of ATH risk factors) Risk factors: Male, LDL, HTN, smoking Morphology: QQ se Heaped-up calcified masses on the outflow side of the cuspus Cuspal calcification and fibrosis  Clinical features: In anatomically normal valves manifestation begins when the patients reach their 70s and 80s olderAges O O With bicuspid valves onset at earlier age (40–50 Yr) 40 50 a Severe calcific p stenosis  left ventricular outflow aortic obstruction  left ventricular pressure  concentric F left ventricular hypertrophy Fennema hypertrophy Consequences: chronicheartfailure  Mitral Valve Prolapse which hate (Myxomatous Mitral Valve) One or both mitral leaflets are “floppy” and balloon back into the left atrium during systole 0 Women are affected 7 times more frequently than men Can be primary (idiopathic) or secondary Morphology: to Characterized by ballooning or prolapse of mitral leaflets Leaflets- Enlarged, redundant, thick & rubbery Tendinous cords – elongated, L thinned & occasionally ruptured  Histological appearance: Thinning of fibrosa layer of the valve Extension of middle spongiosa layer with increased deposition of myxomatous (mucoid) material Fyxomatous material mucoid Pathogenesis: Largely unknown Underlying intrinsic defect of connective tissue either in its synthesis or remodeling Common features of Marfan syndrome Common feature of Marfan syndrome  Clinical features: No symptoms Majority asymptomatic Symptoms: palpitation, dyspnea or atypical chest pain www Auscultation – midsystolic click with or without an associated regurgitant murmur midsystolic click Complications: with or withoutregurgitant murmur Congestive heart failure  IE Infective Endocarditis (IE) Characterized by microbial infection of heart valves or mural endocardium, often with destruction of the underlying cardiac tissues resulting in bulky, friable vegetations composed of necrotic debris, thrombus and organisms Majorly caused by extracellular bacteria necrotic debal thrombus major cause of infectiveendocarditis Organism B extracellular bacteria Classification of Infective Endocarditis DD viridans Streptococcus previously Ins 0  Pathogenesis of Infective Endocarditis mood 1 HACEK group - (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella)  e Most important condition predisposing to endocarditis is seeding of blood with microbes The portal of entry into the bloodstream infection elsewhere I F Dental or surgical procedure  bacteremia Injection of contaminated material by IV abusers gAbe E TIFamatyin.org ODD to  Erosion into underlying myocardium with abscess formation (ring abscesses) Acute IE of congenitally bicuspid aortic valve Staph. Aureus Ring abscess Systemic emboli Septic infarcts & mycotic aneurysms presence of virulent organisms Microscopic appearance: Subacute IE vegetations often have granulation tissue at their bases Fibrosis Calcification Chronic inflammatory infiltrate may develop Clinical Features: Vegetation pattern in different Diseases Diagnosis of Infective Endocarditis: Complications of Infective Endocarditis:  Non-infected Vegetations Nonbacterial thrombotic endocarditis Libman-Sacks endocarditis 1. Nonbacterial thrombotic endocarditis (NBTE): Characterized by deposition of small sterile thrombi (vegetation) on the leaflets of the cardiac valves Valvular lesions are sterile Usually on previously normal valves  Morphology: Sterile, non-destructive & Bland thrombus without small vegetations inflammation or valve May be single or multiple damage Clinical features: Symptoms are due to embolization to the brain, heart, or other organs Potential nidus for bacterial colonization & the development of IE 2. Libman-Sacks Endocarditis (LSE) Reference (Chapter 9, Page No 327-333)