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The patient reported no history of tuberculosis and had a negative tuberculin test&#46; He had remained asymptomatic until three months before the current hospitalization&#44; when progressive and disabling global heart failure began&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">On physical examination at admission to the cardiology department&#44; the patient was hemodynamically stable &#40;blood pressure 120&#47;70<span class="elsevierStyleHsp" style=""></span>mmHg&#41;&#44; tachypneic &#40;24<span class="elsevierStyleHsp" style=""></span>cpm&#41;&#44; not cyanotic &#40;94&#37; oxygen saturation in room air&#41; but pale&#46; His pulse was strong&#44; irregular and symmetrical&#46; Cardiac and pulmonary auscultation revealed a low intensity arrhythmia&#44; an early third sound&#44; a holosystolic mitral murmur radiating to the axilla and diminished breath sounds in the both lung bases&#44; accompanied by pulmonary rales&#46; There was marked jugular venous distension up to the mandibular angle&#44; painless hepatomegaly &#40;liver palpable 10<span class="elsevierStyleHsp" style=""></span>cm below the right costal margin on the mid-clavicular line&#41;&#44; positive hepatojugular reflux and lower limb edema up to the knee &#40;&#43;&#43;&#43;&#47;&#43;&#43;&#43;&#43;&#41;&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The electrocardiogram revealed atrial flutter with variable atrioventricular block and normal voltage&#46; Laboratory tests showed marked elevation of erythrocyte sedimentation rate &#40;ESR&#41; &#40;98<span class="elsevierStyleHsp" style=""></span>mm&#41; with no leukocytosis or neutrophilia&#44; and low C-reactive protein &#40;3<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46; Liver enzymes presented a pattern of passive congestion &#40;alkaline phosphatase and gamma-glutamyl transferase higher than aminotransferase&#41;&#46; NT-proBNP was normal &#40;142<span class="elsevierStyleHsp" style=""></span>pg&#47;ml&#41;&#46; The chest X-ray&#44; in posteroanterior view&#44; showed a normal cardiothoracic index and a small bilateral pleural effusion&#44; and in profile view&#44; a linear image located at the left ventricular &#40;LV&#41; lateral wall&#44; of whitish appearance&#46; Echocardiography performed at admission showed the entire pericardium to be thickened and hyperechogenic&#44; no ventricular dilatation&#44; moderately impaired LV global systolic function &#40;ejection fraction &#91;EF&#93; 38&#37; by Simpson&#39;s biplane method&#41; and biatrial dilatation&#46; There was mild mitral and tricuspid regurgitation&#44; and tricuspid valve flow showed respiratory variation of around 30&#37;&#46; Mitral valve flow did not present significant respiratory variation&#59; E-wave deceleration time was 120<span class="elsevierStyleHsp" style=""></span>ms &#40;mean of five complexes&#41;&#46; Echocardiographic study also documented severe pulmonary hypertension &#40;pulmonary artery systolic pressure &#91;PASP&#93; 70<span class="elsevierStyleHsp" style=""></span>mmHg&#41; and dilatation of the inferior vena cava &#40;28<span class="elsevierStyleHsp" style=""></span>mm&#41;&#44; with reduced respiratory variation &#40;&#60;50&#37;&#41;&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">The main diagnostic hypothesis was constrictive pericarditis &#40;CP&#41;&#46; Concomitant coronary artery disease was also considered&#44; since the patient had multiple cardiovascular risk factors and presented depressed left ventricular systolic function&#44; as was pulmonary disease &#40;in a former smoker with pleural thickening&#41;&#44; which would explain the elevated PASP&#46; Combined constrictive&#47;restrictive cardiomyopathy could not be ruled out&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Complementary diagnostic exams included the latest echocardiographic modalities&#44; notably assessment of LV strain and longitudinal early diastolic mitral annular velocity &#40;E&#8217;&#41;&#46; LV longitudinal strain was preserved&#44; as was early diastolic mitral annular velocity &#40;septal E&#8217;&#58; 8&#46;4<span class="elsevierStyleHsp" style=""></span>cm&#47;s&#59; E&#47;E&#8217;&#58; 8&#46;3&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#44; with a respiratory variation of &#62;25&#37;&#46; However&#44; circumferential strain was reduced&#44; a finding that supported a diagnosis of CP&#46; As in the exam performed 11 years previously&#44; chest CT showed diffuse pericardial thickening&#44; but this time focal pericardial calcification was also observed&#46; There were no significant parenchymal lung lesions &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; Cardiac magnetic resonance imaging &#40;MRI&#41; confirmed mild pericardial thickening in the basal and mid ventricular walls&#44; reaching 3<span class="elsevierStyleHsp" style=""></span>mm in the lateral LV wall &#40;normal &#60;2<span class="elsevierStyleHsp" style=""></span>mm&#41;&#46; Ventricular volumes and right ventricular EF were normal &#40;LVEF 40&#37;&#44; moderately impaired&#41;&#44; and there was mild mitral regurgitation&#46; No delayed enhancement study was performed&#44; as the patient did not wish to continue the exam&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">On the 6th day of hospital stay&#44; hemodynamic assessment showed elevated LV end-diastolic pressure &#40;22<span class="elsevierStyleHsp" style=""></span>mmHg&#41; and pulmonary artery wedge pressure &#40;22<span class="elsevierStyleHsp" style=""></span>mmHg&#41; despite six days of diuretic therapy&#44; a slightly diminished cardiac index &#40;1&#46;87<span class="elsevierStyleHsp" style=""></span>l&#47;min&#47;m<span class="elsevierStyleSup">2</span>&#41;&#44; and persistent pulmonary hypertension &#40;mean pulmonary artery pressure 38<span class="elsevierStyleHsp" style=""></span>mmHg&#41;&#46; Although the LV pressure curve presented a dip-and-plateau pattern&#44; the right ventricular curve did not&#46; Furthermore&#44; end-diastolic pressures in the left chambers showed a difference of &#62;5 mmHg compared to the right chambers &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#44; which did not support a diagnosis of CP&#46; Coronary angiography excluded significant lesions and ventriculography showed impaired global systolic function &#40;EF 45&#37;&#41; and generalized LV hypokinesia&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">We arrived at a diagnosis of CP in the light of the clinical picture&#44; laboratory tests &#40;normal NT-proBNP&#41; and noninvasive imaging studies &#40;chest X-ray and CT and cardiac MRI&#41;&#46; Some Doppler echocardiographic findings supported the diagnosis &#40;restrictive pattern and tricuspid flow with respiratory variation &#62;25&#37;&#41;&#44; while others did not &#40;mitral flow without respiratory variation&#41;&#59; the new echocardiographic modalities &#40;2D strain and tissue Doppler of the mitral annulus&#41; favored the principal hypothesis&#44; unlike the hemodynamic study&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">After clinical discussion&#44; a diagnosis of CP prevailed and the patient was accordingly referred for surgical pericardial decortication&#44; which was performed 19 days after admission&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">During the procedure&#44; the thickened pericardial membrane was completely removed &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#44; and pleural and pulmonary biopsy specimens were taken&#46; Anatomopathological study of the specimens showed marked fibrous thickening of the pericardium with focal congestion and nonspecific chronic inflammatory infiltrate&#44; and several focal dystrophic calcifications&#59; areas of pleural fibrous thickening with anthracotic pigment&#59; and areas of emphysema and interstitial fibrosis&#44; congestion and mild nonspecific chronic focal inflammatory infiltrate in pulmonary tissue&#46;</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">Etiological studies performed during hospitalization &#40;blood cultures&#44; tuberculin testing&#44; serum adenosine deaminase levels&#44; and viral serology&#41; were negative&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">The postoperative period was uneventful and the patient was discharged from our hospital one month after admission&#44; significantly improved&#44; and was in NYHA functional class I after 29 months&#46; The patient&#39;s echocardiogram &#40;<a class="elsevierStyleCrossRef" href="#fig0025">Figure 5</a>&#41;&#44; in sinus rhythm&#44; showed improved global systolic function &#40;EF 50&#37; by Simpson&#39;s biplane method&#41; and LV circumferential strain&#46; E-wave deceleration time was 191<span class="elsevierStyleHsp" style=""></span>ms &#40;higher than initially&#41; and the E&#47;A ratio was 1&#46;3&#44; confirming improved diastolic function&#46; There was no significant respiratory variation in valve flows and PASP was 42<span class="elsevierStyleHsp" style=""></span>mmHg &#40;right atrium&#47;right ventricle gradient&#58; 37<span class="elsevierStyleHsp" style=""></span>mmHg&#41;&#44; significantly lower than on initial assessment&#44; probably due to improved LV systolic and diastolic function&#46; The inferior vena cava presented normal caliber and respiratory variation&#46; A month and a half after this last cardiovascular evaluation&#44; the patient first presented rheumatoid arthritis&#46;</p><elsevierMultimedia ident="fig0025"></elsevierMultimedia></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Discussion</span><p id="par0060" class="elsevierStylePara elsevierViewall">Constrictive pericarditis is a rare but serious consequence of chronic inflammation of the pericardium that results in a rigid fibrotic shell that constricts the cardiac chambers&#46; The hemodynamic repercussions of this structural change include severe dysfunction of ventricular diastolic filling&#44; which can be additionally aggravated by systolic dysfunction due to secondary myocardial fibrosis and atrophy&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> In the case presented&#44; the patient had systolic and diastolic dysfunction due to the prolonged evolution of CP&#46; There is usually a long interval between the initial pericardial lesion and the onset of constriction&#44;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> which in our patient was 11 years&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">A diagnosis of CP should always be considered in patients presenting with predominantly right heart failure symptoms&#44; such as increased jugular venous pressure&#44; pleural effusion&#44; hepatomegaly&#44; ascites and peripheral edema&#46; Besides these systemic features&#44; another characteristic of CP is the presence of an early third sound &#40;pericardial knock&#41;&#44; which results from a sudden cessation of ventricular filling due to pericardial constriction&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> In more severe cases&#44; there is hypotension and circulatory collapse&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">Conventional and Doppler echocardiography play an important role in diagnosing this entity&#44; and in differential diagnosis with other causes of right ventricular &#40;RV&#41; failure&#44;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> of which restrictive cardiomyopathy &#40;RCM&#41; is the most challenging to differentiate&#44; since it has similar features on Doppler and hemodynamic study&#46; The presence of LV systolic dysfunction in our patient&#44; which is more common in RCM than in CP&#44; made differential diagnosis essential&#46; Dynamic respiratory variation in flow and enhanced ventricular interaction&#44; which are found in CP but not RCM&#44; are the most important pathophysiological processes for differential diagnosis&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> In CP&#44; there is a dissociation of intrathoracic and intracardiac pressures&#44; which results in a decrease in LV filling during inspiration&#46; A rigid and noncompliant pericardium leads to enhanced ventricular interaction and hence increased RV filling during inspiration&#46; Doppler and tissue Doppler echocardiography play a crucial role in analysis of these respiratory changes&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> When doubts remain&#44; new echocardiographic modalities can help in diagnosis&#46; Since in CP&#44; the mechanical and elastic properties of the myocardium are relatively preserved longitudinally but attenuated circumferentially and&#44; while rotation of the basal and mid segments is preserved&#44; apical rotation is markedly reduced&#44; it is assumed that longitudinal strain and early diastolic mitral annular velocity &#40;E&#8217;&#41; will be normal or increased &#40;unlike in RCM&#41;&#44; and that circumferential strain and the net twist angle &#40;difference between apical and basal rotation&#41; will be reduced &#40;as in RCM&#41;&#46; The net twist angle was not assessed in our patient&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">Mitral E&#8217; of &#62;8<span class="elsevierStyleHsp" style=""></span>cm&#47;s differentiates CP from RCM with a sensitivity of 89&#37; and specificity of 100&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Conventional&#44; Doppler and 2D strain echocardiography were crucial for differential diagnosis between CP and RCM in our patient&#44; and were also used to assess changes in cardiac morphology and function following pericardial decortication&#46; Postoperative improvement in LVEF supports the hypothesis that systolic dysfunction was secondary to chronic inflammation and myocardial fibrosis arising from prolonged pericardial constriction&#44; which is uncommon and thus makes our case somewhat unusual&#46; Delayed enhancement cardiac MRI&#44; which was not performed in our case due to the patient&#39;s refusal&#44; would have detected any areas of intramyocardial fibrosis&#46; Nevertheless&#44; normal initial values for longitudinal strain and improved EF after surgery point to the absence of severe intramyocardial fibrosis&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">Chest CT and cardiac MRI will detect a thickened pericardium in CP&#44; but the information they provide is merely anatomical and does not necessarily reflect pathophysiological changes&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> In the case presented&#44; these two exams supported our principal diagnostic hypothesis by documenting pericardial thickening with focal calcification&#46; However&#44; it should be remembered that 18&#37; of patients with surgically proven CP present normal pericardial thickness and so the absence of thickening does not exclude CP&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Measurement of NT-proBNP can also help in diagnosis&#44; as patients with CP present normal &#40;as in our case&#41; or slightly elevated values&#44; while those with RCM present very high levels&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> The fact that our patient recently developed rheumatoid arthritis may explain his elevated ESR&#44; since alterations in laboratory analyses frequently precede symptoms in this type of disease&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">With regard to hemodynamic findings&#44; the patient&#39;s LV systolic and diastolic dysfunction explained his reduced cardiac index and elevated LV end-diastolic&#44; pulmonary wedge&#44; and pulmonary artery pressures&#44; the latter probably exacerbated by concomitant lung disease &#40;emphysema&#41; documented on pulmonary biopsy&#46; Various possibilities were considered to explain the absence of equalization of ventricular end-diastolic pressures in our patient&#44; the most likely being volume depletion at the time of cardiac catheterization after six days of diuretic therapy&#46; A bolus of additional fluid should be administered to confirm the presence of constriction&#44; but this was not done as the patient had an episode of acute pulmonary edema in the context of hypertensive crisis the day before the hemodynamic study&#46; Although cardiovascular catheterization&#44; which can identify the typical hemodynamic behavior of CP&#44; is considered the gold standard diagnostic method&#44; in a recent study using high-fidelity&#44; micromanometer-tipped catheters to differentiate between CP and RCM&#44; the predictive power of conventional CP criteria was only 75&#37;&#46; The same study found that a new criterion &#8211; the systolic area index &#40;which assesses the change in ventricular pressure area during inspiration and expiration and considers a ratio of more than 1&#46;1 to be indicative of enhanced ventricular interaction&#41; &#8211; had 97&#37; sensitivity and 100&#37; predictive accuracy for identifying patients with surgically proven CP&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> However&#44; while the use of micromanometers may confer greater accuracy in assessing intracavitary pressures&#44; they do not appear preferable to new cardiac imaging modalities&#44; which are easier&#44; quicker&#44; noninvasive and reliable&#44; and should be used in the diagnosis of doubtful cases of constrictive pericarditis&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Conflicts of interest</span><p id="par0095" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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        "titulo" => "Abstract"
        "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Constrictive pericarditis is a rare clinical entity that can pose diagnostic problems&#46; The gold standard for diagnosis is cardiac catheterization with analysis of intracavitary pressure curves&#44; which are high and&#44; in end-diastole&#44; equal in all chambers&#46; The diastolic profile in both ventricles presents the classic dip-and-plateau pattern and the difference between the diastolic pressures of both ventricles should not exceed 3&#8211;5<span class="elsevierStyleHsp" style=""></span>mmHg&#46; Unfortunately&#44; these traditional criteria are not always present and in fact the sensitivity and specificity of equalization of diastolic pressures are relatively low and of limited value in individual patients&#46; This highlights the need to use new cardiac imaging techniques to resolve any doubts&#46; The case described here is a good example&#46;</p>"
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        "resumen" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">A pericardite constritiva &#233; uma entidade cl&#237;nica rara que pode colocar problemas diagn&#243;sticos&#46; O m&#233;todo padr&#227;o para a confirma&#231;&#227;o do seu diagn&#243;stico &#233; o cateterismo card&#237;aco&#44; com an&#225;lise das curvas de press&#227;o intracavit&#225;rias&#44; as quais est&#227;o elevadas e&#44; em teledi&#225;stole&#44; s&#227;o iguais em todas as cavidades&#46; O seu perfil diast&#243;lico em ambos os ventr&#237;culos apresenta o cl&#225;ssico aspeto <span class="elsevierStyleItalic">dip-plateau</span> e a diferen&#231;a entre as press&#245;es telediast&#243;licas ventriculares n&#227;o deve exceder 3-5<span class="elsevierStyleHsp" style=""></span>mmHg&#46; Infelizmente estes crit&#233;rios cl&#225;ssicos nem sempre se verificam e&#44; na verdade&#44; a sensibilidade e a especificidade da igualiza&#231;&#227;o das press&#245;es telediast&#243;licas dos ventr&#237;culos &#233; relativamente baixa e de valor limitado no doente individualmente considerado&#46; Esta realidade evidencia a necessidade de utilizar as novas t&#233;cnicas de imagem card&#237;aca&#44; que podem tornar claro o que &#233; duvidoso&#46; O caso cl&#237;nico aqui descrito &#233; um bom exemplo&#46;</p>"
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        "nota" => "<p class="elsevierStyleNotepara">Please cite this article as&#58; Silvia D&#44; et al&#46; Pericardite constritiva &#8211; novos m&#233;todos no diagn&#243;stico de uma velha doen&#231;a&#58; a prop&#243;sito de um caso cl&#237;nico&#46; Rev Port Cardiol&#46; 2012&#46; <span class="elsevierStyleInterRef" href="doi:10.1016/j.repc.2012.07.004">doi&#58;10&#46;1016&#47;j&#46;repc&#46;2012&#46;07&#46;004</span>&#46;</p>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Normal early diastolic mitral annular velocity &#40;E&#8217;&#41; supporting a diagnosis of constrictive pericarditis&#46;</p>"
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          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Postoperative echocardiography&#46; Top&#58; left ventricular ejection fraction &#40;50&#37; by Simpson&#39;s biplane method&#41;&#59; middle&#58; mitral flow &#40;in sinus rhythm&#59; deceleration time&#58; 191<span class="elsevierStyleHsp" style=""></span>ms&#59; E&#47;A ratio&#58; 1&#46;3&#41;&#59; bottom&#58; tricuspid flow &#40;right ventricle&#47;right atrium gradient&#58; 37<span class="elsevierStyleHsp" style=""></span>mmHg&#41;&#46;</p>"
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                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Guidelines on the diagnosis and management of pericardial diseases&#46; The Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
                          "autores" => array:3 [
                            0 => "B&#46; Maisch"
                            1 => "P&#46; Seferovic"
                            2 => "A&#46; Ristic"
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                      "doi" => "10.1016/j.ehj.2004.02.002"
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                        "tituloSerie" => "Eur Heart J"
                        "fecha" => "2004"
                        "volumen" => "25"
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                        "paginaFinal" => "610"
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                      "titulo" => "Pericardial diseases"
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                        0 => array:2 [
                          "etal" => false
                          "autores" => array:1 [
                            0 => "M&#46;M&#46; LeWinter"
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                      "LibroEditado" => array:4 [
                        "titulo" => "Braunwald&#39;s heart disease&#58; a textbook of cardiovascular medicine"
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