The pericarditis of acute rheumatic fever is not a true infective pericarditis.It is more of inflammation .It is primarily T cell mediated reaction . Neutrophils rarely take part in this inflammation and hence no significant exudation . Hence , there is less sticky and adhesive molecules inside the pericardial space .The most inflamed layer is epicardium which a nothing but visceral pericardium .This layer lacks the tensile strength to constrict the underlying myocardium.
For constriction to occur the fibrinous ( thick ) layer of pericardium need to be involved . In rheumatic fever even though it is pancarditis , fibrous layer is not involved. Further the inflammatory gradient is thought to spread from within (Unlike tuberculosis )
Note : In chronic tuberculous pericarditis, diffuse inflammatory process invade from the exterior surface . Very often , one can not differentiate layers. In extreme cases even myocardium and pericardium can not be separated .
The peri-cardial effusion of acute rheumatic fever
- Is transient ,non infective and resolving (Unlike valvular inflammation !)
- Less of neutrophil activation (Less adhesion)
- It does not involve the thick , tensile fibrous layer of pericardium hence lacks the contractile force .
Other lingering questions
1.How common is tamponade in acute rheumatic fever ?
2.How important is the mass of the effusion (Viz a Viz Intra pericardial pressure !) in causing tamponade ?