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In this trial, patients with tuberculous pericarditis were randomly assigned to prednisolone or placebo and to Mycobacterium indicus pranii or placebo. Neither therapy reduced the risk of the composite outcome of death, cardiac tamponade, or constrictive pericarditis. Tuberculous pericarditis is a common cause of pericardial effusion, cardiac tamponade, and constrictive pericarditis in sub-Saharan Africa and parts of Asia. 1 – 3 Patients with tuberculous pericarditis often have concomitant human immunodeficiency virus (HIV) infection. 1 Despite antituberculosis therapy, pericardial drainage, or pericardiectomy, mortality and morbidity remain high. 4 Mortality is as high as 26% at 6 months but is even higher (approximately 40%) among persons with the acquired immunodeficiency syndrome. 5 The use of glucocorticoid therapy in patients with tuberculous pericarditis to attenuate the inflammatory response may improve outcomes and decrease the risk of death by reducing cardiac tamponade and pericardial constriction, 6 but . . .

Constrictive pericarditis is a result of chronic inflammation characterized by thickening and calcification of pericardial fibers, impaired diastolic filling, reduced cardiac output, and ultimately heart failure. The main objective of this multicenter trial is to evaluate whether conventional extracorporeal circulation pericardial resection has a better prognosis than pericardial resection without extracorporeal circulation. This study is a multicenter, randomized controlled, evaluator blinded, parallel group study with an advantageous framework. A total of 436 participants with constrictive pericarditis will be randomly assigned to either the extracorporeal circulation pericardial resection group or the non-extracorporeal circulation pericardial clearance group in a 1:1 ratio using a computer. Incomplete pericardial detachment is associated with low cardiac output syndrome after pericardial resection. The causes of low cardiac output syndrome are related to incomplete resection of thickened pericardium, unsatisfactory relief of left ventricular compression, excessive ventricular dilation after pericardial dissection, myocardial weakness, and heart failure. The relief of left ventricular compression is crucial for the postoperative recovery of cardiac function.

Despite the monumental advances in the diagnoses and therapeutics of malignancy, several cancer patients have presented with pericardial involvement, including acute pericarditis, constrictive pericarditis, and pericardial effusion. Multiple factors can contribute to acute pericarditis, including direct metastasis to the heart, pericardial hemorrhage, infections due to immunosuppression, and cancer therapies that include chemotherapy, immunotherapy, and radiation. Pericardial effusion, either due to cancer invasion or cancer treatment, is one of the most common incidental findings in cancer patients, which significantly worsens morbidity and mortality. If left untreated, pericardial effusion is known to cause complications such as pericardial tamponade. Constrictive pericarditis can be due to radiation exposure, chemotherapy, or is a sequela of a previous episode of acute pericarditis. In conclusion, early detection, prompt treatment, and understanding of pericardial diseases are necessary to help improve the quality of life of cancer patients, and we aim to summarize the knowledge of pericardial involvement in patients with cancer.

A 65-year-old male with chronic liver disease and refractory ascites was being evaluated for liver transplant, when constrictive pericarditis (CP) was suspected. Initial diagnostics were inconclusive due to overdiuresis. After suspension of diuretics, cardiac magnetic resonance confirmed CP, leading to successful pericardiectomy and normalization of liver function, emphasizing volume status and multimodality imaging role in CP diagnosis.

Summary Introduction Tuberculous (TB) pericarditis carries significant mortality and morbidity rates, not only during the primary infection, but also as part of the granulomatous scar-forming fibrocalcific constrictive pericarditis so commonly associated with this disease. Numerous therapies have previously been investigated as adjuvant strategies in the prevention of pericardial constriction. Colchicine is well described in the treatment of various aetiologies of pericarditis. The aim of this research was to investigate the merit for the use of colchicine in the management of tuberculous pericarditis, specifically to prevent constrictive pericarditis. Methods This pilot study was designed as a prospective, double-blinded, randomised, control cohort study and was conducted at a secondary level hospital in the Northern Cape of South Africa between August 2013 and December 2015. Patients with a probable or definite diagnosis of TB pericarditis were included (n = 33). Study participants with pericardial effusions amenable to pericardiocentesis underwent aspiration until dryness. All patients were treated with standard TB treatment and corticosteroids in accordance with the South African Tuberculosis Treatment Guidelines. Patients were randomised to an intervention and control group using a webbased computer system that ensured assignment concealment. The intervention group received colchicine 1.0 mg per day for six weeks and the control group received a placebo for the same period. Patients were followed up with serial echocardiography for 16 weeks. The primary outcome assessed was the development of pericardial constriction. Upon completion of the research period, the blinding was unveiled and data were presented for statistical analysis. Results TB pericarditis was found exclusively in HIV-positive individuals. The incidence of pericardial constriction in our cohort was 23.8%. No demonstrable benefit with the use of colchicine was found in terms of prevention of pericardial constriction (p = 0.88, relative risk 1.07, 95% CI: 0.46–2.46). Interestingly, pericardiocentesis appeared to decrease the incidence of pericardial constriction. Conclusion Based on this research, the use of colchicine in TB pericarditis cannot be advised. Adjuvant therapy in the prevention of pericardial constriction is still being investigated and routine pericardiocentesis may prove to be beneficial in this regard.

ObjectivesThis scoping review sought to summarise available data on the prevalence, aetiology, diagnosis, treatment and outcome of pericardial disease in Africa.MethodsWe searched PubMed, Scopus and African Journals Online from 1 January 1967 to 30 July 2017 to identify all studies published on the prevalence, aetiologies, diagnosis, treatment and outcomes of pericardial diseases in adults residing in Africa.Results36 studies were included. The prevalence of pericardial diseases varies widely according to the population of interest: about 1.1% among people with cardiac complaints, between 3.3% and 6.8% among two large cohorts of patients with heart failure and up to 46.5% in an HIV-infected population with cardiac symptoms. Tuberculosis is the most frequent cause of pericardial diseases in both HIV-uninfected and HIV-infected populations. Patients with tuberculous pericarditis present mostly with effusive pericarditis (79.5%), effusive constrictive pericarditis (15.1%) and myopericarditis (13%); a large proportion of them (up to 20%) present in cardiac tamponade. The aetiological diagnosis of pericardial diseases is challenging in African resource-limited settings, especially for tuberculous pericarditis for which the diagnosis is not definite in many cases. The outcome of these diseases remains poor, with mortality rates between 18% and 25% despite seemingly appropriate treatment approaches. Mortality is highest among patients with tuberculous pericarditis especially those coinfected with HIV.ConclusionPericardial diseases are a significant cause of morbidity and mortality in Africa, especially in HIV-infected individuals. Tuberculosis is the most frequent cause of pericardial diseases, and it is associated with poor outcomes.

Key Points The most-common aetiologies of constrictive pericarditis in developed countries are cardiac surgery and idiopathic pericarditis, whereas in developing countries with high tuberculosis prevalence, tuberculous pericarditis is most common Constrictive pericarditis should be suspected in any patient for whom the severity of heart failure is disproportional to the degree of myocardial dysfunction Echocardiography is the initial investigation of choice, with cardiac MRI and CT being alternative or complementary imaging modalities Cardiac catheterization can be used when echocardiography, cardiac MRI, and CT provide equivocal results or when a mixed cardiac pathology requires further evaluation Patients with ongoing pericardial inflammation should initially receive anti-inflammatory therapy; those with noncalcific tuberculous constrictive pericarditis should be treated with antituberculous antimicrobial and steroid therapy to reverse the condition Pericardiectomy is curative with symptomatic improvement in most patients, but some develop late recurrence of symptoms; mortality is highest in patients with radiation pericarditis and associated myocardial disease Constrictive pericarditis arises from a stiffening of the pericardium, which prevents complete or satisfactory diastolic filling of the heart. In this Review, Syed and colleagues discuss the pathophysiology of constrictive pericarditis and how to differentiate the disease from other causes of heart failure with preserved ejection fraction that have a similar presentation. Finally, the authors detail how best to treat patients with pericardial constriction, including by complete pericardiectomy. Constrictive pericarditis can result from a stiff pericardium that prevents satisfactory diastolic filling. The distinction between constrictive pericarditis and other causes of heart failure, such as restrictive cardiomyopathy, is important because pericardiectomy can cure constrictive pericarditis. Diagnosis of constrictive pericarditis is based on characteristic haemodynamic and anatomical features determined using echocardiography, cardiac catheterization, cardiac MRI, and CT. The Mayo Clinic echocardiography and cardiac catheterization haemodynamic diagnostic criteria for constrictive pericarditis are based on the unique features of ventricular interdependence and dissociation of intrathoracic and intracardiac pressures seen when the pericardium is constricted. A complete pericardiectomy can restore satisfactory diastolic filling by removing the constrictive pericardium in patients with constrictive pericarditis. However, if inflammation of the pericardium is the predominant constrictive mechanism, anti-inflammatory therapy might alleviate this transient condition without a need for surgery. Early diagnosis of constrictive pericarditis is, therefore, of paramount clinical importance. An improved understanding of how constrictive pericarditis develops after an initiating event is critical to prevent this diastolic heart failure. In this Review, we discuss the aetiology, pathophysiology, and diagnosis of constrictive pericarditis, with a specific emphasis on how to differentiate this disease from conditions with similar clinical presentations.

Constrictive pericarditis (CP) is a form of diastolic heart failure that arises because an inelastic pericardium inhibits cardiac filling. This disorder must be considered in the differential diagnosis for unexplained heart failure, particularly when the left ventricular ejection fraction is preserved. Risk factors for the development of CP include prior cardiac surgery and radiation therapy, but most cases are still deemed to be idiopathic. Making the diagnosis may be challenging and requires meticulous echocardiographic assessment, often supplemented by cross-sectional cardiac imaging and haemodynamic catheterisation. The key pathophysiological concepts, which serve as the basis for many of the diagnostic criteria, remain: (1) dissociation of intrathoracic and intracardiac pressures and (2) enhanced ventricular interaction. Complete surgical pericardiectomy is the only effective treatment for chronic CP. A subset of patients with subacute inflammatory CP, often identified by cardiac MRI, may respond to anti-inflammatory treatments.

Cardiac tamponade is a medical emergency caused by the progressive accumulation of pericardial fluid (effusion), blood, pus or air in the pericardium, compressing the heart chambers and leading to haemodynamic compromise, circulatory shock, cardiac arrest and death. Pericardial diseases of any aetiology as well as complications of interventional and surgical procedures or chest trauma can cause cardiac tamponade. Tamponade can be precipitated in patients with pericardial effusion by dehydration or exposure to certain medications, particularly vasodilators or intravenous diuretics. Key clinical findings in patients with cardiac tamponade are hypotension, increased jugular venous pressure and distant heart sounds (Beck triad). Dyspnoea can progress to orthopnoea (with no rales on lung auscultation) accompanied by weakness, fatigue, tachycardia and oliguria. In tamponade caused by acute pericarditis, the patient can experience fever and typical chest pain increasing on inspiration and radiating to the trapezius ridge. Generally, cardiac tamponade is a clinical diagnosis that can be confirmed using various imaging modalities, principally echocardiography. Cardiac tamponade is preferably resolved by echocardiography-guided pericardiocentesis. In patients who have recently undergone cardiac surgery and in those with neoplastic infiltration, effusive–constrictive pericarditis, or loculated effusions, fluoroscopic guidance can increase the feasibility and safety of the procedure. Surgical management is indicated in patients with aortic dissection, chest trauma, bleeding or purulent infection that cannot be controlled percutaneously. After pericardiocentesis or pericardiotomy, NSAIDs and colchicine can be considered to prevent recurrence and effusive–constrictive pericarditis. Cardiac tamponade is a potentially life-threatening emergency involving compression of the heart caused by accumulation of fluid in the pericardial sac. This Primer by Adler and colleagues provides an overview of the epidemiology, pathophysiology, diagnosis, treatment and effect on patient quality of life of cardiac tamponade as well as of areas requiring further research.

Effusive-constrictive pericarditis (ECP) is an increasingly recognized clinical syndrome. It has been best characterized in patients with tamponade who continue to have elevated intracardiac pressure after the removal of pericardial fluid. The disorder is due to pericardial inflammation causing constriction in conjunction with the presence of pericardial fluid under pressure. The etiology is diverse with similar causes to constrictive pericarditis and the condition is more prevalent with certain etiologies such as tuberculous pericarditis. The diagnosis is most accurately made using simultaneous intrapericardial and right atrial pressure measurements with pericardiocentesis, although non-invasive Doppler hemodynamic assessment can assess residual hemodynamic findings of constriction following pericardiocentesis. The clinical presentation has considerable overlap with other pericardial syndromes and as yet there are no biomarkers or non-invasive findings that can accurately predict the condition. Identifying patients with ECP therefore requires a certain index of clinical suspicion at the outset, and in practice, a proportion of patients may be identified once there is objective evidence for persistent atrial pressure elevation after pericardiocentesis. Although a significant number of patients will require pericardiectomy, a proportion of patients have a predominantly inflammatory and reversible pericardial reaction and may improve with the treatment of the underlying cause and the use of anti-inflammatory medications. Patients should therefore be observed for the improvement on these treatments for a period, whenever possible, before advocating pericardiectomy. Imaging modalities identifying ongoing pericardial inflammation such as contrast-enhanced magnetic resonance imaging or nuclear imaging may identify those subsets more likely to respond to medical therapies. Pericardiectomy, if necessary, requires removal of the visceral pericardium.