Constrictive pericarditis


Constrictive pericarditis occurs when scarring and calcification of the pericardium result in loss of normal elasticity. This limits diastolic relaxation of the heart and causes congestive heart failure.


Constrictive pericarditis can be caused by any entity that can trigger pericarditis. These include:

  1. Tuberculosis, which is the most common cause worldwide.
  2. Viral infection.
  3. Radiation therapy. This occurred frequently in the late 1970s and early 1980s when high doses were given for non-Hodgkin's lymphoma. Constrictive pericarditis can present decades later.
  4. Trauma.
  5. Post-cardiac surgery.


Diagnosing constrictive pericarditis can be challenging. The main disorder that constrictive pericarditis must be distinguished from is restrictive cardiomyopathy, which has a similar clinical presentation and echocardiographic findings.

Invasive hemodynamic assessment can be helpful, yet challenging. Multiple parameters have been investigated to help distinguish these two entities and are summarized in the table below. The most helpful appears to be RV-LV discordance due to the “ventricular interdependence” seen in constrictive pericarditis.

Since the ventricles in the setting of constrictive pericarditis are unable to expand, the variation in intracardiac pressure during the respiratory cycle exerts changes only between the right and left ventricles. This does not occur in restrictive cardiomyopathy.

With inspiration, intrathoracic pressure decreases and the right ventricle fills. This causes the right ventricular pressure to increase, pushing the interventricular septum towards the left ventricle and impairing left ventricular filling.

With expiration, intrathoracic pressure increases and right ventricular filling is decreased. The left ventricle fills and pushes the interventricular septum towards the right and impairs right ventricular filling.


Measuring the b-type natriuretic peptide (BNP) level can help distinguish between constrictive pericarditis and restrictive cardiomyopathy. In constrictive pericarditis the BNP level is normal to very minimally elevated, while in restrictive cardiomyopathy the BNP level is significantly elevated. This was initially described by Leya and colleagues in 2005. BNP is released in response to myocardial wall stretch. In constrictive pericarditis, the scarred pericardium probits wall stretch, and thus the levels are low. In restrictive cardiomyopathy, the walls indeed do stretch from the increased cardiac pressures resulting in high serum levels of BNP.

A summary of the differences is below:

Restrictive Cardiomyopathy

Constrictive Pericarditis

RV and LV pressure concordance with respiratory cycle

RV and LV pressure discordance with respiratory cycle “ventricular interdependence”

No square root sign

Square root sign on LV pressure tracing

No ventricular interdependence

Ventricular interdependence

LV end-diastolic pressure higher than RV

RV and LV end-diastolic pressures elevated and equal

High BNP level

Low or normal BNP level



There is no medical therapy that works well to treat constrictive pericarditis. Since the stroke volume is relatively fixed, avoiding bradycardia can be helpful. The mainstay of therapy is surgical pericardiectomy, which is a tedious surgery to perform.