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Resumen Introduccion y objetivos Algunos estudios han descrito un cambio en el espectro etiologico de la pericarditis constrictiva. Ademas, no hay datos sobre la relacion entre la forma de presentacion clinica y la etiologia. El objetivo de este estudio es describir las etiologias de la enfermedad, su relacion con la forma de presentacion clinica y los hallazgos quirurgicos, asi como identificar los factores predictivos de una mala evolucion. Metodos Se analizo a un total de 140 pacientes consecutivos a los que se practicaron intervenciones quirurgicas por pericarditis constrictiva en un mismo centro en un periodo de 34 anos. Resultados La etiologia fue idiopatica en 76 pacientes (54%) y tras pericarditis aguda idiopatica en 24 (17%), pericarditis tuberculosa en 15 (11%), pericarditis purulenta en 10 (7%) y cirugia cardiaca en 5 (4%), radioterapia en 3 (2%) y uremia en 2 (1%). La duracion media de los sintomas antes de la pericardiectomia fue de 19 meses (desviacion estandar: 44 meses); la forma de presentacion clinica mas aguda fue la de las pericarditis purulentas (26 [intervalo, 7-60] dias) y la mas cronica, la de los casos idiopaticos (29 meses [4 dias-360 meses]). La mortalidad perioperatoria fue del 11%. No hubo diferencias en la mortalidad segun etiologias. La mediana de seguimiento fue de 12 (0,1-33,0) anos, durante los cuales fallecieron 50 pacientes. En un analisis de regresion de Cox, la edad en el momento de la operacion, la clase funcional de la New York Heart Association avanzada (III–IV) y los antecedentes de pericarditis aguda idiopatica se asociaron a una mayor mortalidad durante el seguimiento. Conclusiones La mayoria de los casos de pericarditis constrictiva son idiopaticas. La cirugia cardiaca y la radioterapia causan una minoria de los casos. Las presentaciones aguda y subaguda merecen un estudio etiologico. La edad, la clase funcional avanzada y la pericarditis aguda idiopatica previa se asocian a mayor mortalidad.

Introduction and objectives There is a paucity of information about the real benefit of colchicine administration in the first episode of acute idiopathic pericarditis (AIP). The main objective of the present study was to assess the real efficacy of colchicine in patients with AIP who did not receive corticosteroids. Methods Randomized multicenter open-label study. Patients with a first episode of AIP (not secondary to cardiac injury or connective tissue disease) were randomized into 2 groups: group A received conventional anti-inflammatory treatment plus colchicine for 3 months, and group B received conventional anti-inflammatory treatment only. None of the patients received corticosteroids. The primary endpoint was the appearance of recurrent episodes of pericarditis. The secondary endpoint was the time to first recurrence. Follow-up was extended to 24 months. Results A total of 110 patients (83.6% men, age 44 ± 18.3 years) were randomized to group A (n = 59) and group B (n = 51). No differences were found in baseline demographics or in the clinical features of the index episode or in the type of anti-inflammatory treatment administered in both groups. The follow-up was completed by 102 patients (92.7%). No differences were found in the rate of recurrent pericarditis between groups (12 patients [10.9%]; group A vs group B, 13.5% vs 7.8%; P = .34). The time to first recurrence (group A vs group B, 9.6 ± 9.0 vs 8.3 ± 10.5 months; P = .80) did not differ between groups. Conclusions Among patients with a first episode of AIP who had not received corticosteroids, the addition of colchicine to conventional anti-inflammatory treatment does not seem to reduce the recurrence rate. Clinical trial registration: URL: https://www.clinicaltrialsregister.eu . Identifier: EudraCT 2009-011258-16

Background— Volume expansion has been proposed as an alternative treatment for cardiac tamponade; however, the scientific evidence for this recommendation is very poor. Methods and Results— Forty-nine unselected patients (23 males; age 55±16 years) with large pericardial effusion and hemodynamic tamponade underwent fluid overload with intravenous administration of 500 mL of normal saline over 10 minutes. Cardiac index and intrapericardial, left ventricular end-diastolic, right atrial, and right ventricular end-diastolic pressures were measured during basal state (tamponade), after fluid overload, and after pericardiocentesis. Twenty-eight patients (57%) had physical signs of tamponade, and 10 (20%) were hypotensive. Size of pericardial effusion was 31±13 mm. Initial mean arterial pressure was 88±21 mm Hg, and cardiac index was 2.46±0.80 L · min −1 · m −2 . Intrapericardial pressure was 8.31±5.98 mm Hg. Volume expansion caused a significant increase in mean arterial pressure (from 88±21 to 94±23 mm Hg, P =0.003) and cardiac index (from 2.46±0.80 to 2.64±0.68 L · min −1 · m −2 , P =0.013), as well as in intrapericardial pressure (from 8.31±5.98 to 11.02±6.27 mm Hg, P =0.0001), right atrial pressure (from 9.76±5.91 to 12.82±6.34 mm Hg, P =0.0001), and left ventricular end-diastolic pressure (from 14.21±5.97 to 19.48±6.19 mm Hg, P =0.0001). Cardiac index increased by >10% in 23 patients (47%), remained unchanged in 11 (22%), and decreased in 15 (31%). No patient developed clinical complications. Predictors of this favorable response were systolic blood pressure Conclusions— Approximately one half of patients with cardiac tamponade develop a significant increase in cardiac output after volume overload. Low systolic blood pressure (

Cardiac tamponade is a life-threatening condition that may require the urgent removal of pericardial fluid. Therefore, the pericardiocentesis procedure should be part of the skills of physicians treating critically ill patients. The pericardiocentesis technique has evolved from a blind and unguided procedure, prone to complications, to a safer and more effective guided technique by using echocardiography or fluoroscopy. However, as in any invasive procedure, complications still occur. Therefore, indications should be restricted to patients with cardiac tamponade or a high suspicion of specific aetiologies when performed for diagnostic purposes. Accurate indications, optimal imaging assessment, knowledge of materials required, familiarization with different techniques, and rapid recognition of complications are key for a successful procedure.

Background— Low-pressure cardiac tamponade is a form of cardiac tamponade in which a comparatively low pericardial pressure results in cardiac compression because of low filling pressure. This syndrome is poorly characterized because only isolated cases have been reported. We conducted a study of its clinical and hemodynamic profiles. Methods and Results— From 1986 through 2004, we evaluated all patients at our institution with combined pericardiocentesis and cardiac catheterization. We identified those patients who fulfilled catheterization-based criteria of low-pressure cardiac tamponade and compared their clinical and catheterization data with those of patients with classic tamponade. A total of 1429 patients with pericarditis were evaluated, 279 of whom underwent combined pericardiocentesis and catheterization. Criteria of low-pressure cardiac tamponade were met in 29, whereas 114 had criteria of classic cardiac tamponade. Patients with low-pressure tamponade less frequently had clinical signs of tamponade, but the rate of constitutional symptoms, use of diuretics, and echocardiographic findings of tamponade were similar in both groups. Patients with low-pressure tamponade showed a significant increase in cardiac output after pericardiocentesis, but they usually had less severe cardiac tamponade compared with patients with classic tamponade. Prognosis was related mainly to the underlying disease. Conclusions— Low-pressure cardiac tamponade was identified in 20% of patients with catheterization-based criteria of tamponade. Clinical recognition may be difficult because of the absence of typical physical findings of tamponade in most patients. Although some patients are critically ill, most show a stable clinical condition. However, these patients obtain a clear benefit from pericardiocentesis.

Los sindromes pericardicos agudos incluyen basicamente la pericarditis aguda y el taponamiento cardiaco. El presente trabajo esta dedicado fundamentalmente al manejo diagnostico y terapeutico de la pericarditis aguda. En nuestro medio, la gran mayoria de pericarditis cuya causa no es evidente en la presentacion clinica inicial corresponde a pericarditis idiopaticas o virales, que tienen un curso benigno y autolimitado (aunque algunos pacientes pueden desarrollar taponamiento cardiaco). Esta nocion de prevalencia es fundamental para establecer un protocolo de manejo logico que evite, por un lado, el excesivo uso de procedimientos invasivos del pericardio, pero que permita, por otro lado, diagnosticar los casos de pericarditis especificas (tuberculosa, purulenta y neoplasica). Segun estas consideraciones y nuestra propia experiencia proponemos un protocolo de estudio y manejo de las enfermedades agudas del pericardio que difieren sustancialmente de las recientes «Guias de practica clinica para el diagnostico y tratamiento de las enfermedades del pericardio» de la Sociedad Europea de Cardiologia. Tambien se comentan aspectos del taponamiento cardiaco y de las formas de constriccion aguda y subaguda que se pueden presentar en la fase de resolucion de las pericarditis agudas.

Background Effusive–constrictive pericarditis is an uncommon pericardial syndrome characterized by concomitant tamponade, caused by tense pericardial effusion, and constriction, caused by the visceral pericardium. We conducted a prospective study of its clinical evolution and management. Methods From 1986 through 2001, all patients with effusive–constrictive pericarditis were prospectively evaluated. Combined pericardiocentesis and cardiac catheterization were performed in all patients, and pericardiectomy was performed in those with persistent constriction. Follow-up ranged from 1 month to 15 years (median, 7 years). Results A total of 1184 patients with pericarditis were evaluated, 218 of whom had tamponade. Of these 218, 190 underwent combined pericardiocentesis and catheterization. Fifteen of these patients had effusive–constrictive pericarditis and were included in the study. All patients presented with clinical tamponade; however, concomitant constriction was recognized in only seven patients. At ca...

Echocardiography, thoracic computed tomography, and magnetic resonance imaging are three valuable imaging techniques for the management and pathophysiological understanding of cardiac tamponade and constrictive pericarditis. However, these techniques should not be used independently from clinical findings. In this article we describe the findings that can be obtained with these imaging techniques, emphasizing how they should be integrated in the clinical context of the patient. Only the proper use of these imaging techniques can optimize the management of patients with pericardial disease.

Introduction and objectives Some reports have described a change in the etiologic spectrum of constrictive pericarditis. In addition, data on the relationship between its clinical presentation and etiology are lacking. We sought to describe the etiologies of the disease, their relationship with its clinical presentation and surgical findings, and to identify predictors of poor outcome. Methods We analyzed 140 consecutive patients who underwent surgery for constrictive pericarditis over a 34-year period in a single center. Results The etiology was idiopathic in 76 patients (54%), acute idiopathic pericarditis in 24 patients (17%), tuberculous pericarditis in 15 patients (11%), purulent pericarditis in 10 patients (7%), and cardiac surgery, radiation and uremia in 5, 3 and 2 patients respectively (4%, 2% and 1%). Mean duration of symptoms before pericardiectomy was 19 months (standard deviation, 44 months), the most acute presentation being for purulent pericarditis (26 days [range, 7-60 days]) and the most chronic for idiopathic cases (29 months [range, 4 days-360 months]). Perioperative mortality was 11%. There was no difference in mortality between etiologies. Median follow-up was 12 years (range, 0.1-33.0 years) in which 50 patients died. In a Cox-regression analysis, age at surgery, advanced New York Heart Association functional class (III to IV) and previous acute idiopathic pericarditis were associated with increased mortality during follow-up. Conclusions Most cases of constrictive pericarditis are idiopathic. Cardiac surgery and radiation accounted for a minority of cases. Etiologic investigations are warranted only in acute or subacute presentations. Age, advanced functional class, and previous acute idiopathic pericarditis are associated with increased mortality.

Pericardial effusion is a common finding in everyday practice. Sometimes, its cause is obviously related to an underlying general or cardiac disease, or to a syndrome of inflammatory or infectious acute pericarditis. On other occasions, pericardial effusion is an unexpected finding that requires specific evaluation. In these cases, the main issues are aetiology, the clinical course, and the possibility of evolution to haemodynamic embarrassment. This is especially relevant in cases of large pericardial effusions, in which echocardiographic recordings not infrequently show findings suggestive of subclinical haemodynamic derangement, mainly right atrial or right ventricular wall collapse. These uncertainties have led to a heterogeneous approach to the management of the syndrome of pericardial effusion by different groups of investigators. The main goal of this article is to give a comprehensive review of aetiology, haemodynamic findings, and management of pericardial effusion. In addition, some comments on the management of neoplastic pericardial effusion are also provided. In an asymptomatic patient, a pericardial effusion of less than 10 mm on the echocardiogram may be an incidental finding, especially in elderly women, as shown in the Framingham study.1 In these patients, neither invasive studies nor treatment are required. A follow up echocardiogram is probably warranted to see if the echocardiographic findings are unchanged. Further investigation or treatment of these patients is not necessary if the echo findings are stable. A wide variety of conditions may result in pericardial effusion. All types of acute pericarditis (inflammatory, infectious, immunologic or of physical origin) can be associated with pericardial effusion.2 In addition, pericardial effusion of varying degrees can be seen in other conditions such as neoplasia (with or without direct pericardial involvement), myxoedema, renal insufficiency, pregnancy, aortic or cardiac rupture, trauma, chylopericardium, or in the setting of chronic salt and water retention of many causes, including chronic heart …

Introduccion y objetivos . El objetivo de este estudio es valorar si existen diferencias en el espectro etiologico y el curso clinico del derrame pericardico en pacientes ancianos, como se ha sugerido, lo que implicaria un manejo clinico distinto en funcion de la edad del paciente. Metodos . Todos los ecocardiogramas practicados en nuestro hospital entre 1990 y 1996 fueron revisados para seleccionar aquellos con derrame pericardico moderado o severo. Los pacientes con edad inferior a 66 anos fueron incluidos en el grupo I, y aquellos con edad superior a 65 anos fueron asignados al grupo II. Resultados . Se seleccionaron 322 pacientes con derrame moderado (122) o severo (200). En el grupo I fueron incluidos 221 pacientes (edad 15-65 anos; media, 47) y 101 pacientes fueron asignados al grupo II (edad 66-88 anos; media, 72,5). El derrame era severo en el 60% del grupo I y en el 66% del grupo II (p = NS), y se produjo taponamiento en 36% del grupo I y 38,6% del grupo II (p = NS). Las infecciones pericardicas especificas (pericarditis tuberculosa y purulenta) fueron mas frecuentes en el grupo I (el 5,9 frente al 0,9%; p Conclusiones . Este estudio sugiere que el derrame pericardico tiene, en general, una etiologia, curso clinico y pronostico similares en pacientes ancianos respecto a los de la poblacion general. Por tanto, su manejo deberia ser similar y cualquier posibilidad etiologica debe ser considerada en el diagnostico diferencial, con independencia de la edad del paciente.

El test de mesa basculante (TMB) permite realizarel diagnostico de sincope vasovagal en pacientescon sincope de causa desconocida. Diversos autoreshan propuesto su utilizacion para el manejoterapeutico de estos pacientes. Si bien existen limitacionespara su uso en el manejo terapeutico,en este articulo se analizan aquellas situaciones enlas que puede ser util. Por un lado, dado que parael tratamiento correcto de cualquier patologia esimprescindible realizar el diagnostico, en la medidaen la que el TMB permite realizar el diagnosticoetiologico del sincope, puede ser util para su tratamiento.Por otro lado, permite caracterizar loscomponentes cardioinhibidor y vasodepresor de larespuesta vasovagal, lo que puede ser de ayuda enla seleccion inicial del tratamiento. Se ha sugeridoque la propia realizacion de un TMB podria tenerun efecto beneficioso sobre las recidivas de los sincopesvasovagales en pacientes con sincopes recurrentesy refractarios a otros tratamientos. Por ultimo,la realizacion de ensayos clinicos controladoscon el TMB puede permitir conocer la efectividadreal de los distintos farmacos en pacientes con sincopevasovagal. Se ha considerado, sin embargo,que existen importantes limitaciones para su usoen el manejo clinico de pacientes individuales

Otras entidades de la ESC que han participado en la elaboracion de este documento: Asociaciones: Acute Cardiovascular Care Association (ACCA), European Association for Cardiovascular Prevention and Rehabilitation (EACPR), European Association of Cardiovascular Imaging (EACVI), European Association of Percutaneous Cardiovascular Interventions (EAPCI), Heart Failure Association (HFA). Consejos: Council for Cardiology Practice (CCP), Council on Cardiovascular Nursing and Allied Professions (CCNAP), Council on Cardiovascular Primary Care (CCPC). Grupos de Trabajo: Farmacoterapia Cardiovascular, Cirugia Cardiovascular, Cardiopatias Congenitas en el Adulto, Enfermedades del Miocardio y del Pericardio, Circulacion Pulmonar y Funcion Ventricular Derecha, Valvulopatias. El contenido de esta Guia de Practica Clinica de la Sociedad Europea de Cardiologia (ESC) se publica exclusivamente para uso personal y educativo. No se autoriza su uso comercial. No se autoriza la traduccion o reproduccion de ningun fragmento de esta guia sin la autorizacion escrita de la ESC. La autorizacion se solicitara por escrito a Oxford University Press, editorial de European Heart Journal y representante autorizado de la ESC para gestionar tales permisos. Descargo de responsabilidad. Esta guia recoge la opinion de la ESC y se ha elaborado tras el estudio minucioso de los datos y la evidencia disponibles hasta la fecha. La ESC no es responsable en caso de que haya alguna contradiccion, discrepancia o ambiguedad entre la guia de practica clinica (GPC) de la ESC y cualquier otra recomendacion oficial o GPC publicada por autoridades relevantes de la sanidad publica, particularmente en lo que se refiere al buen uso de la atencion sanitaria y las estrategias terapeuticas. Se espera que los profesionales de la salud tengan en consideracion esta GPC a la hora de tomar decisiones clinicas, asi como al implementar estrategias medicas preventivas, diagnosticas o terapeuticas. No obstante, esta guia no anula la responsabilidad individual de cada profesional al tomar las decisiones oportunas relativas a cada paciente, de acuerdo con dicho paciente y, cuando fuera necesario, con su tutor o representante legal. Ademas, las GPC de la ESC no eximen al profesional medico de su obligacion etica y profesional de consultar y considerar atentamente las recomendaciones y las GPC actualizadas emitidas por autoridades sanitarias competentes. Es tambien responsabilidad del profesional verificar la normativa y la legislacion sobre farmacos y dispositivos medicos a la hora de prescribirlos. Los formularios de autorizacion de todos los autores y revisores se encuentran en la pagina web de la ESC: www.escardio.org/guidelines

A transthoracic echocardiogram of a 72-year-old woman who was admitted to the hospital complaining of dyspnea at rest and peripheral edema showed severe pericardial effusion with right chamber and left atrial collapse, as well as left ventricular hypertrophy with systolic anterior movement of the septal mitral leaflet and systolic gradient through the left ventricular outflow tract (peak gradient of 70 mm Hg; online-only Data Supplement Movie I and Figure 1). A grade 3/6 systolic murmur was heard. The ECG showed sinus rhythm and respiratory phasic changes in QRS amplitude (Figure 2). The patient was referred to the …

This article focuses on syndromes associated with cardiac constriction (i.e., constrictive pericarditis). These include classic chronic constrictive pericarditis, subacuteelasticconstriction including effusive-constrictive pericarditis, transient cardiac constriction, and occult constrictive pericarditis, all of which have their own clinical and developmental peculiarities. Establishing clinical suspicion is the basic first step in making a diagnosis, which can subsequently be confirmed by careful interpretation of imaging studies. With pericardial calcification, a simple chest radiograph may be sufficient; in other cases, Doppler echocardiography or chest computed tomography are necessary. The diagnosis of effusive-constrictive pericarditis requires cardiac catheterization combined with pericardiocentesis and the recording of intracavitary and intrapericardial pressures both before and after pericardiocentesis. It should be remembered that spontaneous regression is possible in some forms of constrictive pericarditis, particularly those that appear during the resolution of acute idiopathic pericarditis with effusion or that develop after cardiac surgery. Finally, there are only a few reports in the literature about occult constrictive pericarditis and its diagnosis is problematic.

Essentially, acute pericardial syndromes include acute pericarditis and cardiac tamponade. This article focuses on the diagnosis and management of acute pericarditis. In Spain, most cases of acute pericarditis whose etiology is not apparent at initial clinical presentation are either idiopathic or viral pericarditis, which follow a benign or self-limiting clinical course (although tamponade may develop in some patients). Knowledge of this basic epidemiologic fact is essential for the development of a rational management protocol that, on the one hand, avoids the unnecessary use of invasive pericardial diagnostic procedures in patients with idiopathic pericarditis and that, on the other hand, correctly identifies most cases of specific pericarditis, which mainly comprise purulent, tuberculous or neoplastic pericarditis. In accordance with this rationale and on the basis of our own experience, we have proposed a protocol for the management of acute pericardial disease that differs markedly from the "Guidelines on the Diagnosis and Management of Pericardial Disease" recently produced by the European Society of Cardiology. In addition, we have made some comments on the cardiac tamponade and the acute and subacute constrictive pericarditis that can occur during the resolution of acute pericarditis.

Aims To assess the reproducibility of the response to sequential head-up tilt tests. Methods and Results A head-up tilt test was performed early after syncope in 127 patients with a normal ECG and no structural heart disease. Patients with a positive response (82 patients) were randomized to two (1 week and 2 weeks later) or one (2 weeks later) additional head-up tilt tests, and patients with a negative response (45 patients) were randomized to a second head-up tilt test 1 or 2 weeks after the first. The reproducibility of a positive response in the second head-up tilt test was 80% after 1 week and 53% after 2 weeks ( P

Aims To assess the diagnostic yield of the head-up tilt test and electrophysiology in different groups of patients with syncope of unknown origin established according to simple clinical criteria. Methods and Results Six hundred consecutive patients with syncope of unknown origin submitted to a tilt test. Two hundred and forty seven of them also underwent electrophysiology. Patients were divided into groups according to age at the time of first syncope, ECG findings and the presence of organic heart disease. Positive responses to the tilt test were more common in patients who had suffered their first syncope at an age equal to or below 65 years (group I) than in older patients (group II) (47% vs 33%, P

To examine whether the size of the effusion, the presence of tamponade, and inflammatory signs are useful in determining the causes of moderate or severe pericardial effusions.All echocardiograms performed at a general hospital between January 1990 and April 1996 were screened for pericardial effusion. Patients with moderate (echo-free space of 10 to 20 mm during diastole) or severe (echo-free space20 mm) effusions were studied.We identified 322 patients (166 [52%] men, mean [+/- SD] age 56 +/- 17 years [range 15 to 88 years]), 132 (41%) with moderate and 190 (59%) with severe pericardial effusion. The most frequent etiologic diagnoses were acute idiopathic pericarditis (n = 66 [20%]), iatrogenic effusions (n = 50 [16%]), cancer (n = 43 [13%]), and chronic idiopathic pericardial effusion (n = 29 [9%]). In 192 (60%) of the patients, the cause of the effusion was a known medical condition. In the 130 other patients, inflammatory signs were associated with acute idiopathic pericarditis (likelihood ratio = 5. 4, P0.001), severe effusions without inflammatory signs or tamponade were associated with chronic idiopathic pericardial effusion (likelihood ratio = 20, P0.001), and tamponade without inflammatory signs was associated with malignant effusions (likelihood ratio = 2.9, P0.01).In many patients, pericardial effusions are due to a known underlying disease or condition. In patients without underlying diseases, inflammatory signs, the size of effusion, and the presence or absence of cardiac tamponade can be helpful in establishing cause.

A large idiopathic chronic pericardial effusion can be defined as a collection of pericardial fluid that persists for more than three months and has no apparent cause. We conducted a prospective study of the natural history and treatment of this disorder.Between 1977 and 1992, we prospectively evaluated and enrolled patients with large idiopathic chronic pericardial effusion. We performed pericardiocentesis in most of the patients. We performed pericardiectomy when large pericardial effusion reappeared after pericardiocentesis. Follow-up ranged from 18 months to 20 years (median, 7 years).During the study period, we evaluated a total of 1108 patients with pericarditis, 461 of whom had large pericardial effusion. Twenty-eight of these patients (age range, 7 to 85 years; median, 61) had large idiopathic chronic effusion and were included in the study. The duration of effusion ranged from 6 months to 15 years (median, 3 years). At the initial evaluation, 13 patients were asymptomatic. Overt tamponade was found in eight patients (29 percent). Therapeutic pericardiocentesis, performed in 24 patients, was followed by the disappearance of or marked reduction in the effusion in 8. Five of the 24 patients underwent early pericardiectomy, and in 11 large pericardial effusion reappeared. Cardiac catheterization, performed in 16 patients, showed elevated intrapericardial pressure (4.75+/-3.79 mm Hg) and reduced transmural pressure (1.0+/-2.50 mm Hg) before pericardiocentesis. Both of these abnormalities in pressure improved significantly after pericardiocentesis. Pericardiectomy, performed in 20 patients, yielded excellent long-term results. At the end of the follow-up period, 10 patients had died, but none had died from pericardial disease.Large idiopathic chronic pericardial effusion is well tolerated for long periods in most patients, but severe tamponade can develop unexpectedly at any time. Pericardiocentesis alone frequently results in the resolution of large effusions, but recurrence is common and pericardiectomy should be considered whenever a large effusion recurs after pericardiocentesis.

Background Clinical data are of unquestionable value for management purposes in cardiac tamponade, whereas the precise value of Doppler echocardiographic findings is not yet fully understood. We aimed to prospectively assess the correlation between clinical and Doppler echocardiographic signs in the diagnosis of cardiac tamponade in a large series of patients with pericardial effusion. Methods During a 2-year period, all patients with moderate and large pericardial effusion were prospectively assessed. The presence of clinical findings suggesting cardiac tamponade, right cardiac chamber collapse on the echocardiogram, and Doppler venous flow pattern were simultaneously evaluated. Results One hundred ten patients were included (49 with moderate and 61 with large effusions). Thirty-eight patients showed clinical features suggestive of cardiac tamponade and 72 did not. In patients with clinical tamponade, 90% had collapse of one or more right cardiac chambers, but 4 (10%) did not have any collapse. Venous flow was analyzable in 63%, suggesting tamponade in 75% of the patients. In patients without clinical tamponade, 34% showed collapse of one or more cardiac chambers. Venous flow pattern was normal in 80%, inconclusive in 11%, and only suggestive of tamponade in 9% of patients. If clinical features of tamponade were considered the diagnostic standard, sensitivity and specificity would be 90% and 65% for the presence of any collapse, 68% and 66% for right atrial collapse, 60% and 90% for right ventricular collapse, and 45% and 92% for simultaneous collapse of both chambers. Sensitivity and specificity of venous flow analysis would be 75% and 91%, respectively. Conclusions There is a good correlation between absence of collapse and absence of tamponade, but the correlation is poor between collapse and tamponade. Abnormal venous flow has a good correlation with clinical features of tamponade, with a higher sensitivity than right ventricular collapse and a much higher specificity than right atrial collapse. (Am Heart J 1999;138:759-64.)

PURPOSE: To assess whether drainage of pericardial effusion by pericardiocentesis or surgery is justified as a routine measure in the initial management of patients with large pericardial effusion without tamponade or suspected purulent pericarditis. SUBJECTS AND METHODS: All patients with large pericardial effusion without tamponade or suspected purulent pericarditis who were seen at our institution during a span of 6 years (1990 to 1995) were retrospectively (46) or prospectively (25) reviewed. Large pericardial effusion was defined as a sum of echo-free pericardial spaces in diastole exceeding 20 mm. RESULTS: Large pericardial effusion was diagnosed in 162 patients, 71 of whom fulfilled criteria for inclusion. Of these, 26 underwent a pericardial drainage procedure. Diagnostic yield was 7%, as only 2 specific diagnoses were made using these procedures. During follow-up (95% of patients, median 10 months), no patient developed cardiac tamponade or died as a result of pericardial disease, nor did any new diagnoses become manifest in the 45 patients who did not have pericardial drainage initially. Moderate or large effusions persisted in only 2 of 45 patients managed conservatively. CONCLUSIONS: Routine pericardial drainage procedures have a very low diagnostic yield in patients with large pericardial effusion without tamponade or suspected purulent pericarditis, and no clear therapeutic benefit is obtained with this approach. Clinical outcomes depend on underlying diseases, and do not appear to be influenced by drainage of pericardial fluid.

Pericardial effusion is a common finding in everyday clinical practice. The first challenge to the clinician is to try to establish an etiologic diagnosis. Sometimes, the pericardial effusion can be easily related to a known underlying disease, such as acute myocardial infarction, cardiac surgery, end-stage renal disease or widespread metastatic neoplasm. When no obvious cause is apparent, some clinical findings can be useful to establish a diagnosis of probability. The presence of acute inflammatory signs (chest pain, fever, pericardial friction rub) is predictive for acute idiopathic pericarditis irrespective of the size of the effusion or the presence or absence of tamponade. Severe effusion with absence of inflammatory signs and absence of tamponade is predictive for chronic idiopathic pericardial effusion, and tamponade without inflammatory signs for neoplastic pericardial effusion. Epidemiologic considerations are very important, as in developed countries acute idiopathic pericarditis and idiopathic pericardial effusion are the most common etiologies, but in some underdeveloped geographic areas tuberculous pericarditis is the leading cause of pericardial effusion. The second point is the evaluation of the hemodynamic compromise caused by pericardial fluid. Cardiac tamponade is not an “all or none” phenomenon, but a syndrome with a continuum of severity ranging from an asymptomatic elevation of intrapericardial pressure detectable only through hemodynamic methods to a clinical tamponade recognized by the presence of dyspnea, tachycardia, jugular venous distension, pulsus paradoxus and in the more severe cases arterial hypotension and shock. In the middle, echocardiographic tamponade is recognized by the presence of cardiac chamber collapses and characteristic alterations in respiratory variations of mitral and tricuspid flow. Medical treatment of pericardial effusion is mainly dictated by the presence of inflammatory signs and by the underlying disease if present. Pericardial drainage is mandatory when clinical tamponade is present. In the absence of clinical tamponade, examination of the pericardial fluid is indicated when there is a clinical suspicion of purulent pericarditis and in patients with underlying neoplasia. Patients with chronic massive idiopathic pericardial effusion should also be submitted to pericardial drainage because of the risk of developing unexpected tamponade. The selection of the pericardial drainage procedure depends on the etiology of the effusion. Simple pericardiocentesis is usually sufficient in patients with acute idiopathic or viral pericarditis. Purulent pericarditis should be drained surgically, usually through subxiphoid pericardiotomy. Neoplastic pericardial effusion constitutes a more difficult challenge because reaccumulation of pericardial fluid is a concern. The therapeutic possibilities include extended indwelling pericardial catheter, percutaneous pericardiostomy and intrapericardial instillation of antineoplastic and sclerosing agents. Massive chronic idiopathic pericardial effusions do not respond to medical treatment and tend to recur after pericardiocentesis, so wide anterior pericardiectomy is finally necessary in many cases.

The possible effect of amiodarone administration on the effectiveness and complications of electrical cardioversion of supraventricular tachyarrhythmias has not been properly assessed. To investigate the effects of amiodarone on cardioversion, we performed 130 electrical cardioversion procedures in 116 patients who were receiving long-term amiodarone therapy (group I) and 44 cardioversion procedures in 43 patients who were receiving intravenous infusions of amiodarone (group II). All patients in groups I and II had atrial fibrillation or flutter. In group I, there was a higher incidence of ventricular premature beats than in a control group of patients who underwent 100 cardioversions; one patient had severe bradycardia with asystole, which was resolved satisfactorily. In group II there was a higher incidence of sinus bradycardia and ventricular premature beats. It was concluded that electrical cardioversion of supraventricular arrhythmias can be safely performed in patients who are receiving long-term oral or intravenous amiodarone therapy if the usual precautions are observed.

Background Effusive–constrictive pericarditis is an uncommon pericardial syndrome characterized by concomitant tamponade, caused by tense pericardial effusion, and constriction, caused by the visceral pericardium. We conducted a prospective study of its clinical evolution and management. Methods From 1986 through 2001, all patients with effusive–constrictive pericarditis were prospectively evaluated. Combined pericardiocentesis and cardiac catheterization were performed in all patients, and pericardiectomy was performed in those with persistent constriction. Follow-up ranged from 1 month to 15 years (median, 7 years). Results A total of 1184 patients with pericarditis were evaluated, 218 of whom had tamponade. Of these 218, 190 underwent combined pericardiocentesis and catheterization. Fifteen of these patients had effusive–constrictive pericarditis and were included in the study. All patients presented with clinical tamponade; however, concomitant constriction was recognized in only seven patients. At ca...

Contributors PART I. Introduction Improving Patient Adherence: State of the Art, With A Special Focus on Medication Taking for Cardiovascular DisordersR. Brian Haynes, MD, PhDPART II. Factors and Interventions Affecting Compliance Chapter 1. Predicting ComplianceDeborah J. Bowen, PhD, Almut Helmes, MS, and Erika Lease, BA Chapter 2. Strategies to Increase Adherence to TreatmentJudith K. Ockene, PhD, MEd Chapter 3. Behavioral Strategies to Improve Medication-Taking ComplianceElizabeth A. Schlenk, PhD, RN, Lora E. Burke, PhD, RN, and Cynthia Rand, PhD, PART III. Multi-Level Organizational Approaches to Compliance Chapter 4. Provider Approaches to Improve ComplianceIra S. Ockene, MD Chapter 5. Organizational Approaches to Improve ComplianceThomas E. Kottke, MD, Leif Solbert, MD, and Milo Brekke, PhD, PART IV. Measurement of ComplianceChapter 6. Conceptual and Methodological ProblemsJacqueline Dunbar-Jacob, PhD, RN, FAAN and Susan Sereika, PhD Chapter 7. Biological MeasuresJohn Urquhart, MD, FRCP (Edin) Chapter 8. Electronic MeasuresLora E. Burke, PhD, MPH, RN Chapter 9. Analysis of Electronic Event Monitored AdherenceSusan M. Sereika, PhD and Jacqueline Dunbar-Jacob, PhD, RN, FAAN Chapter 10. Self-Report DataJames R. Hebert, ScD, Yunsheng Ma, MD, MPH, Cara B. Ebbeling, PhD, Charles E.Matthews, PhD, and Ira S. Ockene, MD PART V. Issues in Special Populations Chapter 11. ChildrenTom Baranowski, PhD, Janice C. Baranowski, MPH, RD, LD, and Karen Cullen, DrPH, RD, LDChapter 12. Minority PopulationsShiriki K. Kumanyika, PhD, MPH, RD Chapter 13. Obese PopulationsMichael G. Perri, PhD PART VI. Issues Across Settings Chapter 14. Clinical TrialsEleanor Schron, MS, RN and Susan M. Czajkowski, PhD Chapter 15. Treatment TargetsHarlan M. Krumholz, MD, Mohsen Davoudi, MD, Joan M. Amatruda, RN, and Sarah A.Roumanis, RN PART VII. Special Topics Chapter 16. Analysis of Clinical Trials and Treatment NonadherenceSusan M. Sereika, PhD and Ed Davis, MD Chapter 17. Compliance of Providers to GuidelinesThomas A. Pearson, MD, PhD and Laurie A. Kopin, ANP Chapter 18. Impact of Compliance on Clinical OutcomesMichel Burnier, MD and Hans R. Brunner, MD Chapter 19. Managed CareThomas H. Lee, MD, MSc PART VIII. Future Directions Chapter 20. Innovative Approaches to ComplianceDeborah J. Aaron, PhD, MSIS, Kimberly A. Morris, PhD, Patricia A. Nixon, PhD, JeffreyP. Martin, MBA, Deborah Echement, BA, and Ronald E. LaPorte, PhD Chapter 21. Future Directions: What Paths Do Researchers Need to Take? What Needs to be Done to Improve Multi-Level Compliance?Neil B. Oldridge, PhD

Twenty-nine consecutive spontaneous attacks of paroxysmal supraventricular tachycardia (PSVT) in 14 infants (mean age 4.4 months) were treated with verapamil. No infant had associated heart disease. Verapamil 1-2 mg i.v was administered over 30 seconds. The dosage varied according to the weight of the infant. Within 60 seconds sinus rhythm was obtained in 28 instances (96.5%). No significant complications were observed. The high effectiveness, rapid action and lack of undesirable side effects observed in this series suggest that verapamil is the drug of choice in the treatment of PSVT in infants without underlying heart disease.

Two patients who had a huge pericardial effusion of at least 9 and 14 years' duration caused by cardiac toxoplasmosis are reported. Toxoplasma gondii were seen in the pericardial fluid, and serologic evidence also demonstrated the activity of the infection. These cases illustrate both the need to exclude toxoplasmosis in chronic pericardial effusion of unknown cause and the possibility of seeing toxoplasma in the pericardial fluid of patients with active toxoplasmic pericarditis. Moreover, in endemic areas, cardiac toxoplasmosis may not be an exceptional cause of chronic pericardial effusion.

Forty-nine consecutive patients (44 with atrial fibrillation and five with atrial flutter) received 10 mg of verapamil five to seven minutes before elective electroversion, to evaluate the feasibility of the latter while verapamil effects were present. Excluded were patients with moderate-to-severe heart failure, acute myocardial infarction, mean ventricular rate lower than 70 beats/minute, those receiving any antiarrhythmic drug other than digoxin, and those in whom sinus node dysfunction was suspected. In six patients, eight complications took place: four instances of hypotension (systolic blood pressure below 80 mm Hg), two instances of junctional escape rhythm (47 and 63 beats/minute) and two instances of junctional tachycardia. In all four instances of hypotension, return to normal values of blood pressure was spontaneous (within five minutes in three patients). Rhythm disturbances were transient, without clinical relevance. This study suggests that electroversion can be safely carried out during clinical action of verapamil in properly selected patients, and that occasional, self-limited hypotension is the only complication of clinical significance to be expected.

A series of 231 patients with "primary" acute pericardial disease (acute pericarditis or tamponade presenting without an apparent cause) were studied according to the following protocol: general clinical and laboratory studies (stage I), pericardiocentesis (stage II), pericardial biopsy (stage III) and blind antituberculous therapy (stage IV). In 32 patients (14%) a specific etiologic diagnosis was obtained (13 with neoplasia, 9 with tuberculosis, 4 with collagen vascular disease, 2 with toxoplasmosis, 2 with purulent pericarditis and 2 with viral pericarditis). "Diagnostic" pericardiocentesis (32 patients) was performed when clinical activity and effusion persisted for longer than 1 week or when purulent pericarditis was suspected, whereas "therapeutic" pericardiocentesis (44 patients) was performed to treat tamponade; their diagnostic yield was 6% and 29%, respectively. "Diagnostic" biopsy (20 patients) was carried out when illness persisted for longer than 3 weeks, whereas "therapeutic" biopsy was performed whenever pericardiocentesis failed to relieve tamponade; their diagnostic yield was 5% and 54%, respectively. The diagnostic yield difference between "diagnostic" and "therapeutic" procedures was significant (p less than 0.001); in contrast, the global diagnostic yield of pericardiocentesis (19%) and biopsy (22%) was similar. At the end of follow-up (1 to 76 months, mean 31 +/- 20), no patient in whom a diagnosis of idiopathic pericarditis had been made showed signs of pericardial disease. It is concluded that a "diagnostic" procedure is not warranted as a routine method, a choice between "therapeutic" pericardiocentesis and biopsy is circumstantial and must be individualized, and only through a systematic approach can a substantial diagnostic yield be reached in primary acute pericardial disease.

In 16 of 177 patients with effusive acute idiopathic pericarditis (10 men, 6 women, mean age 38 years), features of cardiac constriction were detected (by physical examination in 6 patients and by noninvasive recordings in all) between 5 and 30 days after an echocardiogram had shown pericardial effusion, at a time when signs of activity had abated and effusion was already minimal or had altogether disappeared. Cardiac catheterization was performed in 5 patients, showing either overt (3 patients) or occult (2 patients) cardiac constriction. Two patients had clinical signs of cardiac failure. After a mean of 2.7 months, the features of constriction had spontaneously disappeared In all patients in the clinical examination and noninvasive recordings, and remained so In subsequent control studies (mean follow-up 31 months). Repeat cardiac catheterization in the 5 patients in whom it had been previously performed showed normal features both in the basal state and after fluid overload. The results of the present study show that some patients may go through a transient phase of cardiac constriction at the end of the effusive period of acute idiopathic pericarditis. Features of constriction are, in most cases, subtle and can go unrecognized if not specifically sought. However, they may have clinical relevance in some patients. These findings provide insight into the resolution phase of effusive acute idiopathic pericarditis, and an unneccesary pericardiectomy may be avoided.

Background: Some series have shown changes in the etiologic spectrum of Constrictive Pericarditis (CP). Data is lacking about the chronology of the disease depending of the etiology. Objectives: To describe the clinical presentation of CP emphasizing the timing of symptoms and the etiologic spectrum of a contemporary series of CP. Methods: Retrospective analysis of all cases of operated CP in our institution. Results: From 1978 to 2012, 140 cases of operated CP could be reviewed (99 males (71%), Mean age=54 years (y) (ranging from 19 to 80y)). Mean time of symptoms among all patients was 19.5months (m), ranging from 8 days to 30y. An acute presentation ( 6m) in 55 patients (39%). Table: Time of symptoms per etiology. The etiology of CP was Idiopatic in 76p (54%), post-Acute Idiopatic Pericarditis in 24p (17%), Tuberculous in 15p (11%), Purulent in 10p (7%), post-Cardiac surgery in 5p (3.6%), post-Radiotherapy in 3p (2%), uremia in 2p (1%). Figure 1: Distribution of etiologies in relation with its chronology of symptoms. View this table: Table 1. Etiology and time of symptoms ![Figure][1] Etiologies and timing of symptoms Conclusions: Post-Cardiac surgery and Radiotherapy are still an uncommon cause of CP. The vast majority of cases of chronic CP are idiopatic. The most acute presentation of CP is for patients with purulent CP (less than 1 months of symtoms), followed by uremic CP (1.4m) and Neoplasmic CP (1.7m). [1]: pending:yes

Objectives and methods: 1. To describe the clinical presentation, etiology, diagnostic tecniques, surgical findings and long-term follow-up of patients operated of Constrictive Pericarditis (CP). 2. To identify independent predictors of poor outcome after pericardiectomy. Retrospective analysis of all operated cases of CP: Clinical data, surgical findings and follow-up (FU) were recorded. Results: Between 1978 and 2012, 140 patients underwent pericardiectomy for CP (Male = 99 (71%), age=54 years-old, range (17-80y). Clinical presentation: Congestive heart failure (124p, 87%), chest pain (46p, 33%) or fever (33, 23.4%). Forty-nine patients (35%) were in an advanced NYHA class (III or IV) before surgery. The most frequent etiology of CP was idiopatic (71%). In patients with a specific cause of CP, tuberculosis (11%) was the most frequent diagnosis. Sixteen patients (11%) died perioperatively. Predictors of perioperative mortality were age (66±11 vs 53±16 years, p=0.002), NYHA status III or IV (31% vs 62%, p=0.014) and presence of pericardial effusion (27% vs 60%, p=0.01). Overall mortality during FU (12 years (range 0.1 to 34.5y)) was 39%. Long-term FU analysis (124 patients) showed that independent predictors of death were age at surgery (HR 1.05, 95% CI: 1.017-1.088), a previous episode of acute pericarditis (HR 2.93, 95% CI 1.26-6.81) and a preoperative NYHA status III or IV (HR 4.03, 95% CI 1.79-9.05). Etiology did not have an impact neither in perioperative survival nor in the long-term FU. View this table: Use of diagnostic procedures Conclusions: Idiopatic pericarditis is the most frequent cause of CP. Perioperative mortality is high. Factors associated with a poor perioperative outcome are age, advanced NYHA status and moderate or severe pericardial effusion. Long-term FU shows that independent predictors of poor outcome are age at surgery, advanced NYHA status and a previous episode of acute pericarditis.