Constrictive pericarditis is a morbid condition, with a challenging diagnosis. Because constrictive pericarditis is generally considered a treatable cause of heart failure, evaluating for and distinguishing constrictive pericarditis from other causes of heart failure is key. This image vignette demonstrates a multimodality approach in the diagnosis of constrictive pericarditis, with emphasis on invasive hemodynamic assessment.
A 59-year-old woman with a history of chemo-radiation therapy for Hodgkin’s lymphoma presented with worsening dyspnea and edema. Computed tomography (CT) of the chest showed post-radiation fibrosis, bilateral pleural effusions, and incidental patchy pericardial calcifications (Figure 1). Echocardiography showed moderately reduced left ventricular systolic function and was non-diagnostic for constrictive pericarditis. Cardiac magnetic resonance imaging (MRI) revealed a small pericardial effusion with mild thickening of the pericardium, and a septal bounce, suggesting ventricular interdependence (Video).
Given the inconclusive findings on non-invasive imaging, an invasive hemodynamic assessment was performed. Elevated and equalized left ventricular and right ventricular pressures were noted, with respiratory discordance consistent with constrictive pericarditis (Figure 2). Due to her pulmonary co-morbidity, she was not a candidate for pericardial stripping. She was ultimately transitioned to hospice care.
Differentiating restrictive cardiomyopathy from constrictive pericarditis is challenging. Non-invasive imaging of the pericardium (looking for calcification or thickening), and for signs of ventricular interdependence (eg, septal bounce), is usually considered the first step. This, however, is not definitive.1 Invasive hemodynamic assessment is the gold standard to differentiate restrictive cardiomyopathy from constrictive pericarditis. The hallmarks are dissociation of intracardiac and intrathoracic pressure, and ventricular interdependence.2 Constrictive pericarditis results from rigid pericardial encasement of the cardiac chambers, resulting in elevation and equalization of ventricular diastolic pressures. Furthermore, changes in intrathoracic pressure are not transmitted to the heart.3 During inspiration, the reduction in intrathoracic pressure decreases pulmonary venous pressures, and consequently the gradient for blood to move from the pulmonary veins into the left ventricle, thereby reducing left ventricular volume. Conversely, this causes an increase in right ventricular volume and movement of the interventricular septum leftward.3 The opposite changes occur during expiration.
Constrictive pericarditis is considered a treatable cause of heart failure. Although the definitive diagnosis of constrictive pericarditis can only be established through surgery, a comprehensive diagnostic assessment, including an invasive hemodynamic assessment, is paramount.
Disclosures: The authors report no conflicts of interest regarding the content herein.
The authors can be contacted via Faris G. Araj, MD, at email@example.com.
- Vaitkus PT, Kussmaul WG. Constrictive pericarditis versus restrictive cardiomyopathy: a reappraisal and update of diagnostic criteria. Am Heart J. 1991; 122(5): 1431-1441. doi:10.1016/0002-8703(91)90587-8
- Goldstein JA, Kern MJ. Hemodynamics of constrictive pericarditis and restrictive cardiomyopathy. Catheter Cardiovasc Interv. 2020; 95(6): 1240-1248. doi:10.1002/ccd.28692
- Geske JB, Anavekar NS, Nishimura RA, Oh JK, Gersh BJ. Differentiation of Constriction and Restriction: Complex Cardiovascular Hemodynamics. J Am Coll Cardiol. 2016; 68(21): 2329-2347. doi:10.1016/j.jacc.2016.08.050