Endocarditis and pericarditis CVS5 Hisham Alkhalidi

Inefective endocarditis (IE) a serious infection, characterized by: – Microbial invasion of heart valves or mural endocardium – Often with destruction of the underlying cardiac tissues – Results in bulky, friable vegetations composed of necrotic debris, thrombus, and organisms

IE, Types Acute endocarditis, usually: – Suggests a destructive infection – Involvement of a highly virulent organism (staph. Aureus) – Attacking a previously normal valve – Death within days to weeks in more than 50% of patients despite antibiotics and surgery Subacute endocarditis: – Low virulence organisms (strept. Viridans) – Colonizing a previously abnormal heart, especially when there are deformed valves – The disease typically appears insidiously – Follows a protracted course of weeks to months – Most patients recover after appropriate antibiotic therapy

Clinical presentation and complications Acute: – Fever, rigor, malaise – Large vegetation -> emboli: Infarction Metastatic infection Distant organs like spleen, brain or heart Kidney: Ag-Ab complex -> GN-> nephrotic syndrome or Renal failure – Congestive heart failure due to valve disease – Can lead to ring abscess and perforation of the aorta and myocardium – Death up to 60%

Subacute: – Insidious – Splenomegaly – Non specific fever, weight loss – Small vegetations, so less embolic – Low mortality

Murmurs are present in 90% of patients with left-sided lesions, but these may merely relate to the pre-existing cardiac abnormality predisposing to IE Diagnosis is largely made on the basis of positive blood cultures, echocardiographic findings, and other clinical and laboratory findings

Pathogenesis Bacteremia is a pre-requisite – Other organs infection – IV drug abuse: Usually Staph aureus, right heart side (Tricuspid) – Dental or surgical procedure – Trivial injury, skin, gut, urinary bladder Contributory condition is immunosupression and neutropenia

Favorable conditions of infections Congenital defects Chronic RHD MV Prolapse Deg. Calcific stenosis Bicusped aorta Prosthetic valve (5% in 5 years) Indwelling catheters

Diagnsosis Blood C/S is a major step Duke’s criteria

Nonbacterial Thrombotic Endocarditis NBTE (Marantic endocarditis) – Attributed to: Disseminated intravascular coagulation Hypercoagulability – Association with malignancy (specially adenocarinoma)

Gross: loose adherent groups of small nodules on the lines of valve closure (similar to those of acute rheumatic fever), valve leaflets are normal Micro: SMALL, sterile, fibrin and platelets aggregates, no inflammation or fibrosis. Clinically asymptomatic, if large -> may embolize, may become infected. Typically mitral valve

Endocarditis associated with SLE Unknown etiology Both sides of the valve Deformity to the valve by healing of fibrinoid necrosis and mucoid degeneration Sterile

Pericarditis Primary vs secondery Acute vs chronic Uremia is the most common systemic disorder associated with pericarditis

Pericarditis Serous Fibrinous, serofibrinous Purulent Hemorrhagic Caseous

Pericarditis Serous: – Exudate – Non bacterial causes: Rheumatic fever SLE Tumor Uremia Primary viral

Pericarditis Fibrinous, serofibrinous Same causes of serous Most commonly due to MI Purulent – Bacteria (staph, strept, pneuomcocus) – Fungi – Parasite – Can lead to mediastionpericaridtis or congestive pericarditis

Pericarditis Hemorrhagic: – Blood + fibrin or pus – Surgery – TB – Tumor Caseous: – TB – Fungi – Fibrocalcific constrictive pericarditis

Healing Resolution Fibrosis: – Epicardial plaque – Thin – Thick massive adhesion

Adhesive mediastinopericarditis: – heart contracts against the surrounding structures Constrictive pericarditis: – 1 cm thick dense fibrous obliteration with Ca ++ – Limit diastolic expansion and cardiac output

Chronic Pericarditis: Morphology Ranges from delicates adhesions to dense fibrotic scars that obliterate the pericardial space. In extreme cases the heart can’t expand during diastole : constrictive pericarditis

Clinical picture Atypical chest pain (worse on reclining) High pitch friction rub. Significant exudate  cardiac tamponade  faint distant heart sounds, distended neck veins, declining cardiac output and shock Chronic constrictive pericarditis  venous distension and low cardiac output.