Different aetiological agents either infectious or non-infectious (see chapter on the aetiology of pericardial diseases) interact with the pericardium in a rather non-specific way causing inflammation of the pericardium (pericarditis) with possible increased production of pericardial fluid or in some cases reduced reabsorption (pericardial effusion) [1–3]. The pericardium is rather rigid, and sudden changes of its volume may occur only with sudden increase of intrapericardial pressure generating a compressing effect on cardiac chambers and impairing diastolic filling during the entire diastole, thus causing a reduced cardiac output (cardiac tamponade) [3]. On the contrary, slowly accumulating pericardial fluid may occur without the development of cardiac tamponade in other cases (isolate chronic large pericardial effusion) [3]. The final stage of any pathological process affecting the pericardium is represented by fibrosis with possible thickening and calcification leading to a loss of pericardial elasticity and a constrictive effect of the pericardium on cardiac chambers, thus impairing diastolic filling in mid-late diastole (constrictive pericarditis).

In clinical practice, all these manifestation of pericardial disease can be grouped in specific presentations including signs and symptoms and having peculiar diagnostic, therapeutic and prognostic features. Such distinct clinical presentations are usually named “pericardial syndromes” [4–6]. The main pericardial syndromes include: