Valvular Heart disease
Stenosis is the failure of the valve to open completely leading to obstructing forward flow.
Insufficiency results from failure of a valve to close completely, thereby allowing reversed flow.
Stenosis and regurgitation can occur in pure forms, or may coexist in the same valve.
Valvular disease may affect only a single valve (the mitral valve is the most commonly affected), or more than one valve.
The out come of valvular dis. Depends on the valve involved, the degree of impairment, the tempo of its development and the rate &quality of compensatory mechanism.
Myxomatous mitral valve
Definition: one or both mitral leaflets are floppy and prolapse (Balloon back into the left atrium during systole).
It’s a primary form of myxomatous mitral degeneration.
Affecting women more than men (7:1).
Secondary mitral degeneration can occur in any of a number of settings in which mitral regurgitation is caused by some other entity (IHD).
Rheumatic Valvular Disease RVD
Acute immunologically mediated, multisystem inflammatory disease that occurs a few weeks after an episode of group A?-hemolytic streptococcal pharyngitis.
RHD: It’s the cardiac manifestation of RF.
Its associated with inflammation of the valves, myocardium, or pericardium.
Chronic valvular deformities are the most important consquences of RHD.
The most charecterstic features is diffuse and dense scarring of the valves resulting in permanent dysfunction (mitral stenosis being most common).
Morphological features
Acute RF:
Discrete inflammatory lesions are found in various tissues called Aschoff bodies.
Anitschkow cells (caterpillar cells).
Pancarditis.
Fibrinous or serofibrinous pericarditis.
Fibrinoid necrosis of the valves form verrucae (1-2 mm vegetation).
Pathogenesis of RF
Acute RF is a hypersensitivity reaction.
Host Ab formation against M prot. of certain str. Strains (cross react) with glycoprotein Ag in the Heart, Joint and other T.
Genetic susceptibility.
Morphological features
Chronic RHD:
Charcterized by organization of acute inflammation and subsquent scarring.
Leaflet thickening, commissural fusion and shortening, thickening and fusion of chordae tendineae.
Fishmouth stenosis.
Microscopical features
Neovascularization.
Diffuse fibrosis.
Scarring.
Clinical Features of RF
-ARF us. Age 5-15 y.
-Symp occ. 2-3 w. af str. Pharyngitis.
-Culture negative but increase Ab to streptolysin and anti DNA ase.
-Carditis and arthritis accompanied by fever.
Diagnosis of Rheumatic HD
Serological evidence of previous str. Inf.
Two or more of Jones criteria:
-Carditis.
-Migratory polyarthritis.
-Subcutaneous nodule.
-Erythema marginatum.
-Sydenham chorea.
One of the Jones criteria +nonspecific sig.&symt. Eg. Incr. acute phase prot.
Infective Endocarditis
Definition: serious inf. need prompt Dx.&Rx. Ch. by mic. invasion of the mural endocardium with destruction of the underlying cardiac tissues results in bulky, friable vegetation.
Classification:
-Acute endocarditis.
-Subacute endocarditis.
Morphological Features:
In both types there is friable, bulky and destructive vegetation.
Aorta and mitral valve are the most common.
Vegetation may be single or multiple, involve one or more than one valve.
Abscess formation called ring abscess due to erosion of underlying valve.
Septic infarct.
Microscopical features
Fibrin, infl. cells and microrg. are present.
In sub. there is granulation tissue formation that with the time it will replaced by fibrous tissue with chronic inf. cells inf.
Pathogenesis:
Predisposing factors:
-RHD.
-Mitral valve prolapse.
-Bicuspid aortic valve.
-Calcific aortic stenosis.
-Prosthetic valve replacement.
-Neutropenia & immunodeficiency.
-Sterile fibrin platelets deposits.
Causative micro. depend on underlying risk factor:
Abnormal valve us. infected by viridans streptococci(50-60%).
10-20% caused by staph aureus that can infect the dis. and healthy valve and in IV drug abuse.
Enterococci and gram neg. bacilli rarely the cause.
Culture negative .
Lesions simulating infective endocarditis
Non bacterial thrombotic endocarditis (marantic terminal endocarditisa).
-small thrombi on the heart valves us. in a patchy fashion along the line of cusp closure of mit.&aortic.
-Thought to be cused by hypercoagulable state.
Libman-sacks endocarditis.
-develop in pt. with SLE .
-Can involve the Mitral, Aortic and tricuspid valves.
-The vegitations are sterile, platelet rich and rarely exceed 2 mm in size.
-Fibrinoid necrosis is a charecteristic features.
Disorders of the conduction system:
Damage to the conducting system.
The most vulnerable regions being the AV bundle and the left and right bundles branches.
Acquired causes include:
IHD, Myocarditis, sarcoidosis, connective t.d., infiltrative disorders, and surgical trauma.