PERICARDIAL DISEASEThe pericardium acts as a protective covering for the heart. It consists of two separate layers, the inner visceral pericardium and the outer parietal pericardium. The visceral pericardium reflects back upon itself at the level of the great vessels to join the parietal pericardium, thus forming a sac. The pericardial sac contains up to 50 mL of pericardial fluid in the normal heart, although this is a potential space for fluid to collect. The pericardium serves to lubricate the surface of the heart, prevents deformation and dislocation of the heart and acts as a barrier to the spread of infection.Presentations of pericardial disease include:■acute pericarditisa pericardial effusion and cardiac tamponade■constrictive pericarditis.
Acute pericarditisThis refers to inflammation of the pericardium. Classically, fibrinous material is deposited into the pericardial space and pericardial effusion often occurs. Acute pericarditis has numerous aetiologies . The most common viral causes are Coxsackie B virus and echovirus. Viral pericarditis is usually painful but has a short time course and rarely long-term effects. Post-myocardial infarction pericarditis occurs in about 20% of patients in the first few days following MI. It may be difficult to differentiate this pain from recurrent angina when it occurs early (day 1-2 post- infarct) but a good history of the pain and serial ECG monitoring is helpful.Pericarditis may also occur later on in the recovery phase after infarction. This usually occurs as a feature of Dressler's syndrome, an autoimmune response to cardiac damage occurring 2-10 weeks post- infarct. Autoimmune reaction to myocardial damage is the main aetiology, andantimyocardial antibodies can often be found. Uraemic pericarditis is due to irritation of the pericardium by accumulating toxin s. It can occur in 6-10% of patients with advanced renal failure if dialysis is delayed. It is an indication for urgent dialysis as it continues to be associated with significant morbidity and mortality.
Bacterial pericarditis may rarely occur with septicaemia or pneumonia or it may stem from an early postoperative infection after thoracic surgery or trauma or may complicate endocarditis.Staphylococcus aureus is a frequent cause of purulent pericarditis in HIV patients. This form of pericarditis, especially staphylococcal, is fulminant and often fatal.Other endemic infectious pericarditis includes mycoplasmosis and Lyme pericarditis which are often effusive and require pericardial drainage. Tuberculous pericarditis usually presents with chronic low-grade fever, particularly in the evening, associated with features of acute pericarditis, dyspnoea, malaise, night sweats and weight loss. Pericardial aspiration isoften required to make the diagnosis. Constrictive pericarditis is a frequent outcome. " Fungal pericarditis is especially in immunocompromised patients, drug addicts or after cardiac surgery.Malignant pericarditis. Carcinoma of the bronchus, carcinoma of the breast and Hodgkin's lymphoma are the most common causes of malignant pericarditis. Leukaemia and malignant melanoma are also associated with pericarditis.
Clinical featuresPericardial inflammation produces sharp central chest pain exacerbated by movement, respiration and lying down. The main differential diagnoses are angina and pleurisy.The classical clinical sign is a pericardial friction rub occurring in three phases corresponding to atrial systole, ventricular systole and ventricular diastole. It may also be heard as a biphasic 'to and fro' rub. There is usually a fever, leucocytosis or lymphocytosis when pericarditis is due to viral or bacterial infection, rheumatic fever or myocardial infarction.Features of a pericardial effusion may also be present. Large pericardial effusion can compress adjacent bronchi and lung tissue and may cause dyspnoea.
InvestigationsECG is diagnostic. There is concave-upwards (saddle shaped) ST elevation . PR interval depression is a very specific indicator of acute pericarditis These changes evolve over time, with resolution of the ST elevation.The early ECG changes must be differentiated from ST elevation found in myocardial infarction .Cardiac enzymes should be assayed as they may be elevated if there is associated myocarditis .Chest X ray, echocardiograms and radionucleotide scans are of little value in uncomplicated acutepericarditis.
TreatmentIf a cause is found, this should be treated. Bed rest and oral NSAIDs In the few days following a myocardial infarction, NSAID use is associated with a higher rate of myocardial rupture and these drugs should not be used. Corticosteroids have been used when the disease does not subside rapidly, but they are associated with side-effects. In resistant cases, oral corticosteroids are again used to provide symptomatic relief. Numerous other treatments have been studied including azathioprine, colchicine, intravenous corticosteroids and pericardiectomy. Current data tend to favour the use of colchicine to prevent recurrent attacks of pericarditis.
If pericarditis persists for 6-12 months following the acute episode, it is considered chronic. If the pericardium thickens and restricts ventricular filling, constrictive pericarditis is said to have developed.Pericardial effusion and cardiac tamponadeA pericardial effusion is a collection of fluid within the potential space of the serous pericardial sac , commonly accompanying an episode of acute pericarditis. When a large volume collects in this space, ventricular filling is compromised leading to embarrassment of the circulation. This is known as cardiac tamponade.
Clinical featuresSymptoms of a pericardial effusion commonly reflect the underlying pericarditis. On examination:■ Heart sounds are soft and distant.■ Apex beat is commonly obscured.■ A friction rub maybe evident due to pericarditis in the early ■ base of the left lung, producing an area of dullness to percussion below the angle of the left scapula (Ewart's sign).■ As the effusion worsens, signs of cardiac tamponade may become evident:- raised jugular venous pressure with sharp rise and y descent (Friedreich's sign)- Kussmaul's sign (rise in JVP/increased neck vein distension during inspiration)- pulsus paradoxus- reduced cardiac output
Investigations■ ECG reveals low-voltage QRS complexes.■ ChestX-ray shows large globular or pear shaped heart with sharp outlines. Typically, the pulmonary veins are not distended.■ Echocardiography is the most useful technique for demonstrating the effusion and looking for evidence of tamponade.■ MRI should be considered if haemopericardium (blood in thepericardial space) or loculated pericardial effusions are suspected.■ Pericardiocentesis is the removal of pericardial fluid with aseptic technique under echocardiographic guidance. It is indicated when a tuberculous, malignant or purulent effusion is suspected.■ Pericardial biopsy may be needed if tuberculosis is suspected and pericardiocentesis not diagnostic.Other tests include looking for underlying causes, e.g. blood cultures, autoantibody screen.
TreatmentAn underlying cause should be sought and treated if possible. Most pericardial effusions resolve spontaneously.However, when the effusion collects rapidly, tamponade may result. Pericardiocentesis is then indicated to relieve the pressure - a drain may be left in temporarily to allow sufficient release of fluid.Pericardial effusions may reaccumulate, most commonly due to malignancy (in the UK). This may require pericardial fenestration, i.e. creation of a window in the pericardium to allow the slow release of fluid into the surrounding tissues. This procedure may either be performedtranscutaneously under local anaesthetic or using a conventional surgical approach.
Constrictive pericarditisCertain causes of pericarditis such as tuberculosis, haemopericardium, bacterial infection and rheumatic heart disease result in the pericardium becoming thick, fibrous andopen-heart surgery. In many cases these pericardial changes do not cause any symptoms. If, however, the pericardium becomes so inelastic as to interfere with diastolic filling of the heart, constrictive pericarditis is said to have developed. As these changes are chronic, allowing the body time to compensate, this condition is not as immediately life-threatening as cardiac tamponade, in which the circulation is more acutely embarrassed. Constrictive pericarditis should be distinguished from restrictive cardiomyopathy . The two conditions are very similar in their presentation, but the former is fully treatable, whereas most cases of the latter are not. In the later stages of constrictive pericarditis the subepicardial layers of myocardium may undergo fibrosis, atrophy and calcification.
Clinical featuresThe symptoms and signs of constrictive pericarditis occur due to:■reduced ventricular filling (similar to cardiac tamponade, i.e. Kussmaul's sign, Friedreich's sign, pulsus paradoxus)■systemic venous congestion (ascites, dependent oedema, hepatomegaly and raised JVP)■pulmonary venous congestion (dyspnoea, cough, orthopnoea, PND)lesscommonly■reduced cardiac output (fatigue, hypotension, reflex tachycardia)■rapid ventricular filling ('pericardial knock' heard in early diastole at the lower left sternal border)■atrial dilatation (30%of cases have atrial fibrillation).
Investigations■ChestX-ray : shows a relatively small heart in view of the symptoms of heart failure.Pericardial calcification is present in up to 50%.■ECG reveals low-voltage QRS complexes with generalized T wave flattening or inversion.■Echocardiography shows thickened calcified pericardium, and small ventricular cavities with normal wall thickness. Doppler studies may be useful.■CT and MRIare used to assess pericardial anatomy and thickness (3 mm or greater).■Endomyocardial biopsy may be helpful in distinguishing constrictive pericarditis from restrictive cardiomyopathy in difficult cases.■Cardiac catheterization.End-diastolic pressuresin the left and right ventricles measured during this procedure are usually equal, owing to pericardial constriction.Restrictive cardiomyopathy is a close mimic of constrictive pericarditis and all the above tests may not help to distinguish the two conditions.
TreatmentThe treatment for chronic constrictive pericarditis is complete resection of the pericardium. This is a risky procedure with a high complication rate due to the presence of myocardial atrophy in many cases at the timeof surgery. Thus early pericardiectomy is suggested in non-tuberculous cases, before severe constriction and myocardial atrophy have developed.In cases of tuberculous constriction, the presence of pericardial calcification implies chronic disease. Current evidence tends to favour early pericardiectomy with antituberculous drug cover in these cases. If there is no calcification, a course of antituberculous therapy shouldbe attempted first. If the patient's haemodynamic state remains static or deteriorates after 4—6 weeks of therapy, pericardiectomyis recommended.