Prosthetic Valve Complications

1) immediate post op

• atrial arrhythmias; occlusion or damage to coronary arteries or conduction system during valve replacement —> dysrrhythmias; AMI
• Rupture of heart –> pericardial tamponade

2) Bleeding

• haemorrhage with warfarin

3) Infection [prosthetic valve endocarditis PVE]

4) Thromboembolism of prosthetic cardiac valves

• emboli may form on valve surfaces
• valve surface may become occluded by slowly developing thrombi
• Thromboembolic complications due to:

i) inherent thrombogenicity of materials used

ii) abnormalities of blood flow through valves

• Latest generation of valves made from porcine xenograft or bovine pericardium offer improved cardiac function with greatly reduced clotting risk and freedom from anticoagulant drugs
• Thromboembolism is a major cause of morbidity & death following implantation of prosthetic devices

• ‘Red thrombus’ [stasis thrombus]

- composed of red cells entrapped in fibrin strands

- seen around sewing rings of prosthetic heart valves (and in CPB reservoirs)

• ‘White thrombus’ [platelet thrombus]

- occurs in regions of brisk flow

- composed of platelets

- seen on cages and struts of prosthetic heart valves (& in tubing & cannulae of CPB)

• disintegration of ball-cage prothetic valve or tissue valves (porcine & cadaver)—> release of fragments

• Thrombus induced by artificial surfaces may be manifested in several ways:

i) gross thrombus may form on artificial surface facing blood —> impair movement of the ball, disc, leaflet

ii) bits of thrombus or all may break free & embolize down stream

- major cause of morbidity with nontissue prosthetic mitral & aortic valves

- in porcine tissue valves, peripheral embolization shares equal importance as a cause of morbidity as degeneration, calcification & infection

iii) repeated generation of microscopic platelet aggregates and cellular debris

iv) accelerated consumption of platelets and fibrinogen associated with foreign body stimulation of coagulation

v) activation of haemostatic mechanisms result in systemic effects:

- activation XII —> production of kinins —> vessel dilatation & increased permeability

- platelet activation —> release serotonin—> bronchoconstriction with pulmonary embolism —> cerebral vasoconstriction with haemorrhage

vi) exposure of blood to foreign surface has a deleterious effect on platelet function

5) Prosthetic valve failure

· Mechanical failure of valve due to (eg):

i) impingement of ends of sutures or chordal strands

ii) valve dehiscence

Prosthetic endocarditis

a) Pathological complications

• • Mechanical valves: may lead to mechanical complications (obstruction, regurgitation)
• • Tissue valves: may lead to total destruction of cusps or vegetations that stiffen and obstruct the valve
• • May cause annular infection & abscess formation

b) Untreated time course & prognosis

• • prosthetic valve endocarditis PVE
• • < 60 days post surgery (early PVE)
• organisms acquired perioperatively
• approx 1% of cases; mortality in this 1% of about 74%
• • > 60 days post surgery (late PVE)
• at 6 months incidence approx 1%
• at 5 years incidence increased to 5%
• mortality approx 45%
• pathogenesis with endocarditis occurring on native valves

c) Indications for surgery

• treatment include antibiotics ± replacement of infected valve
• decision to replace valve relate to factors that increase mortality including early PVE, nonstreptococcal aetiology, systemic embolisation, heart failure, paravalvular leaks
• medical therapy for late PVE, streptococcal with no evidence valvular mechanical failure or systemic emboli