Acta Cardiologica

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Pericardial involvement in systemic lupus erythematosus: current diagnosis and therapy Peter Kruzliak, Miroslav Novak, Pavel Piler & Gabriela Kovacova To cite this article: Peter Kruzliak, Miroslav Novak, Pavel Piler & Gabriela Kovacova (2013) Pericardial involvement in systemic lupus erythematosus: current diagnosis and therapy, Acta Cardiologica, 68:6, 629-633, DOI: 10.1080/AC.68.6.8000011 To link to this article: https://doi.org/10.1080/AC.68.6.8000011

Published online: 23 May 2017.

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Date: 12 January 2018, At: 08:07

Acta Cardiol 2013; 68(6): 629-633

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doi: 10.2143/AC.68.6.8000011

[ Review article ]

Pericardial involvement in systemic lupus erythematosus: current diagnosis and therapy

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Peter KRUZLIAK1,2, MD, MSc; Miroslav NOVAK1, MD, PhD; Pavel PILER3, MD; Gabriela KOVACOVA4, MD 1 Dept. of Cardiovascular Diseases, International Clinical Research Center, St. Anne´s Faculty Hospital and Masaryk University, Brno, Czech Republic; 2Institute of Normal and Pathological Physiology and Centre of Excellence for Regulatory Role of Nitric Oxide in Civilization Diseases, Slovak Academy of Sciences, Bratislava, Slovak Republic; 3Dept. of Cardio-thoracic and Transplant Surgery, International Clinical Research Center, St. Anne´s Faculty Hospital and Masaryk University, Brno, Czech Republic; 4 th 5 Dept. of Internal Medicine, University Hospital and Comenius University, Bratislava, Slovak Republic.

Abstract Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect almost any organ system. Cardiac involvement is common and has been acknowledged as a primary cause of morbidity and mortality in patients with SLE. Pericarditis is the most common cardiovascular manifestation in SLE. In this review we present the current diagnosis and treatment of SLE-related pericardial involvement.

Keywords Systemic lupus erythematosus – cardiovascular manifestations – pericarditis – pericardial effusions – diagnosis – treatment.

SYSTEMIC LUPUS ERYTHEMATOSUS Systemic lupus erythematosus (SLE) is an inflammatory multisystem disease associated with immune complex deposition, production of autoantibodies, and various laboratory abnormalities and clinical features1. Patients may present with virtually any organ-system involvement including arthritis, glomerulonephritis, skin rashes, serositis, and neurological symptoms. The disease prevalence is almost 1:2,500 as reported by Roman and Salmon and Lawrence et al.2,3, and almost 15 to 50/100,000 people as reported in the United States. Involvement of women is higher than men, in that almost 90% of the patients are women. SLE is more common in blacks and younger patients, but can occur at any age1.

Address for correspondence: Peter Kruzliak, MD, MSc, Dept. of Cardiovascular Diseases, International Clinical Research Center, St. Anne´s Faculty Hospital and Masaryk University, Pekarska 53, 656 91 Brno Czech Republic. E-mail: [email protected] Received 8 April 2013; revision accepted for publication 15 July 2013.

The diagnosis of SLE is based on clinical and laboratory features. Over 95% of patients with SLE have a positive antinuclear antibody (ANA); however, an isolated finding of a positive ANA is not diagnostic of SLE. Anti-double-stranded DNA is more specific for SLE but with lower sensitivity, occurring in only 50% to 70% of patients, more frequently in the presence of glomerulonephritis. Patients with SLE may have positive antiphospholipid antibodies (APLAs), which predispose to arterial and venous thrombosis, pulmonary hypertension, valvular dysfunction, and/or miscarriage. Frequent laboratory abnormalities include anaemia, thrombocytopenia, leucopenia or lymphopenia. Lupus can be induced by certain medications and both idiopathic and drug-induced lupus can have cardiac manifestations1.

CARDIAC INVOLVEMENT IN SLE Cardiac involvement is common and has been acknowledged as a primary cause of morbidity and mortality in SLE. Its prevalence has been estimated to be more than 50% 1. In the past, cardiac manifestations were severe, often leading to death and they were frequently found in post-mortem examinations.

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Nowadays, cardiac manifestations are often mild and asymptomatic and they can be recognized by echocardiography and other non-invasive tests. All three layers of the heart — pericardium, myocardium and endocardium — can be involved by lupus; this section will focus on pericarditis4.

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PERICARDIAL INVOLVEMENT IN SLE Pericarditis is the most common cardiovascular manifestation in SLE. Badui et al. reported that pericardial effusion was the most frequently observed cardiovascular complication (39%) in one hundred consecutive female patients with active systemic lupus erythematosus5.The pericardium can be involved by acute and chronic inflammatory changes; granular deposition of immunoglobulin and C3, demonstrated by direct immunofluorescence, support the role of immune complexes in the development of pericarditis6. SLE pericarditis may occur as part of a generalized serositis with ascites and pleural effusions1. In SLE the pericardial effusion is exudative in nature. It is usually clear or may be serosanguinous but is very rarely haemorrhagic7. Rudra et al. reported a case of SLE presenting with cardiac tamponade due to a haemorrhagic pericardial effusion in a 14-year-old girl8. On microscopy, polymorphonuclear leucocytes are most numerous and monocytes too may be present. Examination of the centrifuged specimen may reveal LE cells which are then diagnostic of SLE8,9. The pericardial fluid may also demonstrate anti-nuclear and anti-DNA antibodies4,6,10. On histopathology, small pericardial blood vessels were surrounded by an infiltrate of lymphocytes, plasma cells, macrophages, and rare polymorphonuclear leukocytes. On immunofluorescence, IgG was present in a predominantly granular pattern around small pericardial vessels. Thus, Bidani and colleagues concluded that immune complex deposition was the cause of pericarditis11. Pericardial involvement has been reported in between 33% and 72% of cases in necropsy series, and includes fibrinous pericarditis, chronic fibrous pericarditis, pericardial adhesions12-14. Pericarditis may remain clinically silent and evidence of previous pericardial disease is often observed on echocardiography. Large series have found echocardiographic features of pericarditis in 20% to 50% of patients with SLE15. Symptomatic pericarditis occurs in about 25% of the patients and asymptomatic pericardial involvement in more than half of the cases1. Sugiura et al. determined the frequency and clinical correlates of asymptomatic pericardial effusion (PE) in

patients with systemic lupus erythematosus (SLE)16. Among 50 patients with SLE, 12 patients (24%) had pericardial effusions and 17 patients (34%) had hypoalbuminaemia. Patients with PE had a significantly lower serum albumin (P < 0.001), higher incidence of proteinuria (P = 0.003), higher C-reactive protein (P = 0.036) and pulmonary artery systolic pressure (P = 0.011) and tended to have a higher incidence of PR-segment depression (P = 0.082) compared with those without PE. When four variables (PR-segment depression, C-reactive protein, serum albumin and pulmonary artery systolic pressure) were used in the multivariate analysis, serum albumin (P = 0.005, odds ratio = 0.016) and pulmonary artery systolic pressure (P = 0.010, odds ratio = 1.106) emerged as significant variables related to the occurrence of asymptomatic PE. Pericardial effusions are usually mild and although moderate to large effusions may occur, major complications such as cardiac tamponade are rare in patients without renal failure. In the setting of renal failure, it may be difficult to distinguish pericarditis due to uraemia from SLE1,17,18. Cervera et al. reported moderate to large pericardial effusions in 7% of patients with SLE19.Tamponade occurs in less than 2% of cases1,17,20,21. On the other hand, cardiac tamponade can be the first sign of SLE. Swinkels et al. described a case of cardiac tamponade as the initial manifestation of SLE in a 21-year-old female patient21. Weich et al. described the clinical, echocardiographic and laboratory characteristics of large pericardial effusions and cardiac tamponade secondary to SLE. All patients older than 13 years presenting with large pericardial effusions (> 10 mm) requiring pericardiocentesis were included. Eight cases (out of 258) were diagnosed with SLE. The mean (SD) age was 29.5 (10.7) years. Common clinical features were Raynaud‘s phenomenon, arthralgia and lupus nephritis class III/IV. Echocardiography showed Libman-Sacks endocarditis (LSE) in all the mitral valves. Two patients developed transient left ventricular dysfunction; both these patients had pancarditis. Typical serological findings included antinuclear antibodies, anti-double stranded DNA antibodies, low complement C4 levels and low C3 levels. CRP was elevated in six cases. Treatment consisted of oral steroids and complete drainage of the pericardial effusions. No repeat pericardial effusions or constrictive pericarditis developed amongst the survivors (3.1 years follow-up). This study concludes that large pericardial effusions due to SLE are rare, and associated with nephritis, LSE and myocardial dysfunction22. Rosenbaum et al. retrospectively reviewed the records of 71 patients with SLE, admitted to their hospital with the diagnosis of pericarditis, pericardial

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Pericardial involvement in systemic lupus erythematosus

effusion and tamponade23. Clinical features in the patients with tamponade were compared with those with pericardial effusions without tamponade. Pericardial effusion and SLE was confirmed in 41 patients. Pericardial tamponade occurred in nine of these patients (21.9%) at the time of presentation. All tamponade patients were women. Patients with pericardial effusions who developed tamponade had a statistically significant (P = 0.05) lower C4 level as compared with patients who did not develop tamponade. A low C4 level at presentation was predictive of the development of tamponade. Pericardial involvement appears more frequently at SLE onset or during SLE relapses, although it can occur at any time of the disease4. Pericarditis usually appears as an isolated attack or as recurrent episodes24. Kruzliak et al. reported a clinical case of recurrent pericarditis as the first clinical sign of SLE in a young patient18. Signs and symptoms of acute pericarditis include a typical precordial or substernal chest pain, usually positional (aggravated by lying down), often with a pleuritic quality, sometimes with dyspnoea; moreover, patients may have fever, tachycardia and decreased heart sounds; pericardial rubs can be heard but are usually rare, perhaps because they are present often for only a few hours and are missed. If a patient presents for the first time with pericarditis, it is usually impossible to invoke SLE as the cause until appropriate laboratory tests are available suggesting the diagnosis. However, patients with idiopathic pericarditis more often have a history of recent viral infection, and are more often male. In idiopathic pericarditis there is usually leukocytosis, whereas a finding of leucopenia would suggest SLE. A significant rise in jugular venous pressure is unusual25. Patients with pericardial effusion (as opposed to thickening) are more likely to have pericardial pain and active lupus elsewhere; when present, pericardial effusions are usually small and do not cause haemodynamic problems26. The diagnosis of pericarditis can be confirmed by ECG findings of elevated ST segments and tall T waves (although slight T-wave changes or transient elevation of ST segments are most characteristic), or by echocardiographic findings of pericardial effusion or thickened pericardium. Serial electrocardiograms may show a progression of changes in pericarditis. Initially, a diffuse elevation of ST segments (without reciprocal ST-segment depression) is found. This is followed by a lowering of ST segments back toward baseline and subsequent T-wave inversion. In most cases, T waves then return to normal25. Effusions may be accompanied by a drop in voltage. After severe attacks, the T waves may not recover to their original voltage27. Both effusion and thickening are frequent in echocardiographic studies. Most effusions are mild.

Echocardiography (two-dimensional and Doppler echocardiography) is the modality of choice in evaluating pericardial disease, because it is both non-invasive and sensitive. However, echocardiography may be an insensitive technique in diagnosing pericarditis when it is not accompanied by effusion or thickening or in cases with loculated pericardial effusions. Especially those in unusual locations can be difficult to diagnose with echocardiography4,16,18,25,28. Echocardiography is an excellent initial imaging tool for evaluating the pericardium, particularly pericardial effusion, but it can be limited by the intrinsic properties of the technique, such as small or limited field of view, occasionally poor acoustic windows, and problems related to anatomic factors, such as severe emphysema. Moreover, echocardiography cannot be used to evaluate associated abnormalities in the mediastinum, lungs, and adjacent structures29. Cross-sectional imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) offer distinct advantages in the imaging of the pericardium. Both modalities provide a larger field of view than does echocardiography, thus allowing the examination of the entire chest and detection of associated abnormalities in the mediastinum and lungs. CT has been found to be an excellent tool for detecting pericardial effusion and disease29,30. The normal pericardial sac is made up of an inner visceral and outer parietal layer with a serosal lining; the space in between constitutes the pericardial cavity. On CT this is seen as a thin line of fibrous tissue; the visceral pericardium cannot be visualized separately. The higherattenuation pericardium is distinguished in relation to the low-attenuation mediastinal fat anteriorly and epicardial fat posteriorly. Multidetector CT enables motionfree imaging of the pericardium, as well as multiplanar reformation of images for better visualization of any pericardial disease31. MRI can provide comprehensive depiction of the pericardium without the use of either iodinated contrast material or ionizing radiation. Though MRI is traditionally considered together with CT, as the preferred imaging modality to morphologically visualize the pericardium and pericardial space, MRI can substantially aid in clarifying the intricate relation between pericardial constraint and cardiac filling32. On MRI, the pericardium is depicted by a thin rim of low signal on both T1 and T2 weighted images31. Several studies have examined the normal thickness of the pericardium on CT and MRI and at autopsy. The pericardial thickness varies over different parts of the heart; it is at its thinnest over the left ventricle31. Bull et al. reported that when using 1-mm high-resolution CT (HRCT) the upper limit of the thinnest part of the

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pericardium was 0.7 mm and when using 10-mm CT slices it was 1.2 mm. The upper limit of normal for the thickest part of the pericardium is 2 mm31,33-35.

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TREATMENT OF PERICARDIAL INVOLVEMENT IN SLE Small, asymptomatic pericardial effusions may occur if there is cardiac involvement and should be observed4,18. Non-steroidal anti-inflammatory drugs are helpful for mild cases of pericarditis and pericardial effusions. NSAIDs drugs are the first choice in therapy of idiopathic and viral pericarditis. Failure to respond to NSAID therapy within one week (defined as persistence of fever, pericarditic chest pain, a new pericardial effusion, or worsening of general illness) suggests that a cause other than idiopathic or viral pericarditis is present. In the series of 254 patients deemed to be at low risk who were treated with aspirin as outpatients, 98 percent of the 221 who responded to aspirin were presumed to have idiopathic or viral disease, while 2 percent were diagnosed with an autoimmune disorder36. If the pericardial pain and inflammation do not respond to NSAIDs or if the acute pericarditis recurs, colchicine has been observed to be effective in relieving pain and preventing recurrent pericarditis. The routine use of colchicine is supported by recently reported results of the Colchicine for Acute Pericarditis (COPE) Trial. One hundred twenty patients with a first episode of acute pericarditis (idiopathic, acute, postpericardiotomy syndrome, and connective tissue disease) entered a randomized, open-label trial comparing aspirin plus colchicine (1.0 to 2.0 mg for the first day followed by 0.5 to 1.0 mg/d for 3 months) with treatment with aspirin alone. Colchicine reduced symptoms at 72 hours (11.7% versus 36.7%; P ≤ 0.03) and recurrence at 18 months (10.7% versus 36.7%; P = 0.004; number needed to treat = 5). Colchicine was discontinued in 5 patients because of diarrhea. No other adverse events were noted. Importantly, none of 120 patients developed cardiac tamponade or progressed to pericardial constriction37-39. In early studies, pericarditis usually responded quickly to corticosteroids, with serial chest x-rays showing rapid and radiologic evidence of resorption of fluid27.

However, many studies have noted pericardial effusion developing or persisting even with corticosteroid treatment, such as the autopsy study of Kong et al., in which 11 of 12 patients with pericardial effusion had taken corticosteroids40. Accordingly, systemic steroids should be considered only in patients with recurrent pericarditis unresponsive to NSAIDs and colchicine or as needed for treatment of an underlying inflammatory disease. If steroids are to be used, an effective dose (1.0 to 1.5 mg/kg of prednisone) should be given, and it should be continued for at least 1 month before slow tapering39,41. The intrapericardial administration of steroids has been reported to be effective in acute pericarditis without producing the frequent reoccurrence of pericarditis that complicates the use of systemic steroids, but the invasive nature of this procedure limits its utility. Very few patients with frequent, highly symptomatic recurrences of pericarditis despite intensive medical therapy may require surgical pericardiectomy. However, painful relapses can occur even after pericardiectomy, especially if the pericardium is not completely removed39. Patients presenting with pericardial tamponade may necessitate pericardiocentesis. Refractory cases of large pericardial effusions may benefit from a pericardial window23.

CONCLUSION Pericarditis/pericardial effusion is a frequent and clinically significant cardiovascular manifestation of SLE. Diagnosis is mainly based on echocardiography. According to the nature of the effusion and the patient‘s clinical condition we can choose adequate therapy based on NSAID, corticosteroids or pericardiocentesis in case of tamponade.

ACKNOWLEDGEMENT This work was supported by a grant of European Regional Development Fund – Project FNUSA-ICRC (No. CZ.1.05/1.1.00/02.0123).

CONFLICT OF INTEREST: none declared.

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Pericardial involvement in systemic lupus erythematosus: current diagnosis and therapy.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect almost any organ system. Cardiac involvement is common and has been...
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