Constrictive pericarditis is a condition characterized by decreased elasticity and an increased thickening of thepericardium.[1] These changes reduce the ability of the heart to fill with blood and can lead to symptoms of heart failure.[1]
This condition may result from various disease processes which can have similar symptoms, and has been historically difficult to diagnose.[2] Understanding the differing etiologies and disease processes is important as it can lead to a timely diagnosis and appropriate treatment.[3]
Constrictive pericarditis can present with symptoms such as difficulty breathing, fatigue, abdominal swelling, or swelling of legs.[1] Physical examination findings can include elevatedJugular venous pressure (JVP),Kussmaul's sign,Peripheral edema,Ascites,Hepatomegaly.[1]Auscultation of the heart may reveal a high-pitched sound during the heart's relaxation phase (Diastole) known as a pericardial knock.
In areas of the world whereTuberculosis is endemic, it is the most common cause of constrictive pericarditis.[4] Outside of these areas the next most common cause is typically idiopathic or viral in nature.[3] Causes of constrictive pericarditis can include:
The pathophysiological characteristics of constrictive pericarditis are due to a thickened, fibroticpericardium that forms a non-compliant shell around the heart. This shell prevents the heart from expanding when blood enters it. As pressure on the heart increases, theStroke volume decreases as a result of a reduction in the ability of the heart to fill blood duringDiastole.[7] This results in significant changes in blood flow based on the stage of respiration.[8]
During inspiration, pressure in thethoracic cavity decreases but is not relayed to theleft atrium which can lead to a reduced flow to the left atrium and ventricle. During diastole, less blood flow in the left ventricle allows for more room for filling in right ventricle and therefore a septal shift occurs.[9]
During expiration, the amount of blood entering the left ventricle will increase, allowing theinterventricular septum to bulge towards the right ventricle, decreasing the right heart ventricular filing.[10]
Constrictive pericarditis can be categorized into general syndromes that reflect the nature of the disease development and course.[11]
Transient (subacute) constrictive pericarditis: constrictive pathophysiology may be reversible due to a transient inflammatory state that resolves without significant fibrosis.[3]
Advanced (chronic) constrictive pericarditis: constrictive pathophysiology may be irreversible due to significant fibrosis and loss of elasticity over a longer period of time (often 3-6 months).[3]
Effusive-constrictive pericarditis: similar yet distinct disease process to constrictive pericarditis characterized by a constrictive pathophysiology and the presence of a pericardial effusion.[3]
The diagnosis of constrictive pericarditis is often difficult to make. In particular,restrictive cardiomyopathy has many similar clinical features to constrictive pericarditis, and differentiating them in a particular individual is often a diagnostic dilemma.[12]
Chest X-Ray - pericardial calcification (common but not specific), pleural effusions are common findings.[13]
Echocardiography - the principal echographic finding is changes in cardiac chamber volume.[13]
CT andMRI - CT scan is useful in assessing the thickness of pericardium, calcification, and ventricular contour. Cardiac MRI may find pericardial thickening and pericardial-myocardial adherence. Ventricular septum shift during breathing can also be found using cardiac MRI.Late gadolinium enhancement can show enhancement of the pericardium due to fibroblast proliferation and neovascularization.[10]
BNP blood test - tests for the existence of the cardiac hormonebrain natriuretic peptide, which is only present in restrictive cardiomyopathy but not in constrictive pericarditis[14]
Transient or subacute constrictive pericarditis is treated with anti-inflammatory medication and can resolve without surgical intervention in many cases.[3] Cases that do not resolve with medication may be treated similar to chronic constrictive cases which often require surgical intervention.[3] In these cases the outcome of surgery may be improved as the pericardial inflammation would be decreased due to the medication trial.[3]
The definitive treatment for advanced or chronic constrictive pericarditis is a radicalPericardiectomy, which is a surgical procedure in which the entire pericardium is peeled away from the heart. This procedure has significant risk involved,[16] with mortality rates of 6% or higher in major referral centers.[17]
A poor outcome is often the result after a pericardiectomy is performed for radiation-induced constrictive pericarditis, and some patients may develop heart failure post-operatively.[18]
Constrictive pericarditis is a rare complication of many pericardial diseases.[11] It seen as a complication in approximately 1% of idiopathic pericarditis cases, and even fewer cases post cardiac surgery.[11]
The geographic distribution of constrictive pericarditis can be categorized based on etiology, with idiopathic or viral pericarditis considered to be the leading cause in Western countries.[11]In Western countries the remaining causes tend to be post-surgical, post-radiation, infectious, and connective tissue disorders.[11] In some developing countries Tuberculosis has been noted as the leading cause of constrictive pericarditis.[4]
^Cinar B, Enc Y, Goksel O, Cimen S, Ketenci B, Teskin O, Kutlu H, Eren E (2006). "Chronic constrictive tuberculous pericarditis: risk factors and outcome of pericardiectomy".Int J Tuberc Lung Dis.10 (6):701–6.PMID16776460.
