Pericardite I: introduzione

Pericarditis is inflammation of the pericardium, a membranous sac covering and protecting the heart. The pericardium has two layers—an inner visceral layer and outer parietal layer—separated by fluid that reduces friction during heartbeats. This protective structure can become inflamed due to various infectious or noninfectious causes, leading to significant chest pain and other symptoms requiring medical intervention.

Infectious causes of pericarditis include viruses such as Coxsackievirus and Echovirus, bacteria like tuberculosis, fungi such as Histoplasmosis, and parasites like Toxoplasmosis. Viral infections are the most common infectious cause, while bacterial, fungal, and parasitic infections are less frequent but can be severe, particularly in immunocompromised individuals.

Noninfectious causes include cardiac surgery, autoimmune disorders like systemic lupus erythematosus and rheumatoid arthritis, trauma, radiation therapy, renal failure, cancer metastasis to the pericardium, certain medications including chemotherapeutic agents, and post-myocardial infarction inflammation. These diverse triggers highlight pericarditis as a multifaceted condition requiring careful diagnosis.

Pericarditis begins when immune cells including neutrophils, lymphocytes, and macrophages infiltrate the pericardium and release inflammatory mediators. Pericardial blood vessels become more permeable, allowing fluid and proteins to leak into the pericardial space, creating pericardial effusion. Over time, fibrin deposits on the epicardium, leading to a rough, thickened pericardial surface that restricts heart motion.

Pericarditis is classified into acute pericarditis lasting less than six weeks, chronic pericarditis lasting longer than three months, recurrent pericarditis occurring after initial episodes, constrictive pericarditis where thickening and scarring restrict heart function, and effusive-constrictive pericarditis combining fluid accumulation with constriction. Each type presents distinct clinical challenges and complications requiring specific management approaches.

Chronic inflammation causes fibrosis and scarring of the pericardium, where the tissue thickens and becomes rigid. This fibrotic tissue restricts the heart's normal movement and ability to fill and pump blood efficiently. Pressure changes from accumulated fluid or fibrotic development further impede cardiac function, making constrictive pericarditis a severe form requiring careful clinical management.

During pericarditis, increased vascular permeability allows proteins and cells to accumulate in the pericardial space, creating pericardial effusion. This fluid buildup, combined with fibrin deposition and potential fibrosis, increases pressure within the pericardial sac. To learn more about recognizing how pericarditis affects the heart's function, explore pericarditis clinical features and diagnostic tests for appropriate clinical interventions.