**1. Introduction**

Constrictive pericarditis (CP), firstly described by Richard Lower in "*Tractatus de Corde*" (1669), is the end-stage evolution of chronic inflammation and fibrosis of pericardium. Many of the causes of acute pericarditis listed in previous chapters have been associated with the development of pericardial constriction weeks to months after the acute episode. Nonetheless, the appearance of progressive dyspnea and peripheral edema are not promptly addressed to CP and are frequently considered of unknown origin because of the diagnostic challenge that CP poses [1]. As a matter of fact, diagnosis of CP can be challenging because of the low prevalence (<1% of acute pericarditis, 0.2–0.4% of patients submitted to cardiac surgery) and subsequent detraining of echocardiography specialists. Moreover, constrictive hemodynamics can be difficult to distinguish from restrictive cardiomyopathy (RCM) physiology, a primary myocardial disease, and finally, pericardium could present a normal thickness in almost 20% of CP cases with calcifications present in less than half of patients [2].
