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PubMed1983

Constrictive pericarditis following coronary-artery bypass grafting in a patient with chronic asymptomatic pericardial disease.

Constrictive pericarditis is a rare complication of open-heart surgery. We describe a patient who was found at the time of coronary artery bypass surgery to have asymptomatic pericardial thickening and subsequently developed rapidly progressive constrictive pericarditis. At operation for pericardiectomy, the bypass graft to the posterior descending coronary artery was found to be strangled by fibrous tissue while the remaining two bypass grafts were patent. Following pericardiectomy, the patient made a good recovery.

Chronic Disease↗
PubMed1993

Pericardial color Doppler flow in postpericardiotomy effusive constrictive pericarditis.

A laminar color Doppler flow was discovered in the pericardial space in a 35-year-old man with postpericardiotomy effusive constrictive pericarditis. The flow was detected by transesophageal color Doppler echocardiography. A further pulsed Doppler study revealed a to-and-fro flow, which was synchronized with the cardiac rhythm. We hypothesized that this flow was generated by the rhythmic cardiac contraction. It was then augmented by hard fibrous pericardium and became detectable by color Doppler echocardiography. Pericardial effusion is a frequent echocardiographic finding but little attention has been paid to the flow in it. The laminar flow in the pericardial space in our patient is related to his hard pericardium and can aid in making the diagnosis of effusive constrictive pericarditis. We suggest that flow in the pericardial space deserves more attention and may provide valuable diagnostic aid.

Adult↗
PubMed2003

Constrictive pericarditis in 26 patients with histologically normal pericardial thickness.

BACKGROUND: Traditionally, increased pericardial thickness has been considered an essential diagnostic feature of constrictive pericarditis. Although constriction with a normal-thickness pericardium has been demonstrated clinically by noninvasive imaging, the details of clinicopathological correlates have not been described. METHODS AND RESULTS: A total of 143 patients with proven constriction underwent pericardiectomy at Mayo Clinic between 1993 and 1999. Their baseline characteristics, operative data, and pathological specimens were reviewed retrospectively. The pericardium was of normal thickness (< or =2 mm) in 26 patients (18%; group 1) and was thickened (>2 mm) in 117 (82%; group 2). The most common causes of constriction in group 1 included previous cardiac surgery, chest irradiation, previous infarction, and idiopathic disease. There was little difference in symptoms and findings on physical examination between the 2 groups. Microscopically, no patient had an entirely normal pericardium. Histopathological abnormalities in group 1 were mild and focal, including fibrosis, inflammation, calcification, fibrin deposition, and focal noncaseating granulomas. Pericardiectomy was equally effective in relieving symptoms regardless of the presence or absence of increased thickness. CONCLUSIONS: Pericardial thickness was not increased in 18% of patients with surgically proven constrictive pericarditis, although the histopathological appearance was focally abnormal in all cases. When clinical, echocardiographic, or invasive hemodynamic features indicate constriction in patients with heart failure, pericardiectomy should not be denied on the basis of normal thickness as demonstrated by noninvasive imaging.

Adult↗
PubMed1978

Echocardiographic features of the interventricular septum in chronic constrictive pericarditis.

Echocardiographic characteristics of the interventricular septum (IVS) have been studied in eight patients with chronic constrictive pericarditis (CP). Values of septal thickening (ST) were clearly below normal in all cases. Interventricular septal systolic motion (IVSSM) was normal in four cases, hypokinetic in three and paradoxical in one. In seven out of the eight patients, an early interventricular septal diastolic motion (IVSDM) consisting of a sudden anterior displacement followed by a brisk posterior rebound was recorded. The beginning of this anomalous movement was coincident with the pericardial knock in the phonocardiogram and its peak was coincident with the simultaneously recorded deep "y" trough in the jugular pulse tracing. The tendency toward normality of IVSDM observed after pericardiectomy in six out of seven patients suggests that this peculiar interventricular septal systolic motion may be a frequent and probably specific echocardiographic finding in constrictive pericarditis.

Adolescent↗
PubMed1978

Echocardiographic features of constrictive pericarditis.

The most characteristic echocardiographic features of 12 patients with constrictive pericarditis were compared with the findings in 10 normal volunteers. Left ventricular posterior wall (LVPW) "flatness" was quantified by measuring the diastolic change in distance from the crystal artifact to the LVPW endocardium. In 11 of 12 patients the net diastolic LVPW endocardial movement was less than 1 mm. In 10 normal volunteers LVPW endocardium moved posteriorly in diastole from 1.5 to 4 mm (mean 2.2 +/- 0.8). Abnormal septal motion was present in five of 12 patients with constriction. Pericardial thickness measured using standard damping techniques for both cnstriction and normal population did not distinguish the two groups. The "flattening" of the left ventricular endocardium as quantified above verifies earlier qualitative observations and was the most consistent finding in this series of patients with constrictive pericarditis.

Aged↗
PubMed1991

Circus movement atrial flutter in canine sterile pericarditis model. Activation patterns during entrainment and termination of single-loop reentry in vivo.

BACKGROUND: Recently, we used a custom designed "jacket" electrode with 127 bipolar electrodes in a flexible nylon matrix to map the total atrial epicardial surface in the in situ canine heart. Atrial flutter in dogs with sterile pericarditis was shown to be due to a single wave front circulating around a combined functional/anatomic obstacle, with the arc of functional conduction block contiguous with one or more of the atrial vessels. METHODS AND RESULTS: In the present study, this model was used to analyze the activation pattern during pacing-induced entrainment and termination of single reentrant loops in a syncytium without anatomically predetermined pathways. Sustained atrial flutter was induced in five dogs with 3-5-day-old sterile pericarditis. Atrial pacing at a cycle length 5-30 msec shorter than the spontaneous cycle length entrained the arrhythmia and could result in a "classical" activation pattern, characterized by an antidromic stimulated wave that collided with the reentrant orthodromic wave front of the previous beat at a constant site. However, two variations of this classical activation pattern were also observed: 1) Pacing at short cycle lengths could lead to localized conduction block in antidromic direction, forcing a change in the pathway of the antidromic wave front. This could prevent the expected shift of the site of collision in antidromic direction. 2) The stimulated orthodromic wave front could also use a pathway different from that of the original reentrant impulse, so that a different circuit was active during the pacing period. Termination of atrial flutter by rapid atrial stimulation was associated with progressive slowing and finally blocking of the paced orthodromic wave front and a progressive shift of the site of collision in antidromic direction. The occurrence of conduction block was determined by the cycle length of stimulation and the number of stimulated beats. A longer train at the critical cycle length or the critical number of beats at a shorter cycle length could reinduce the same reentrant circuit or a different reentrant circuit, respectively, during stimulated cycles following the beat that terminated reentry. CONCLUSIONS: The epicardial activation sequence during entrainment of reentrant arrhythmias does not necessarily follow a standard activation pattern. Instead, the stimulated orthodromic as well as the antidromic wave front might use a pathway different from that of the original reentrant wave front. The mechanisms of termination, failure of termination, and reinitiation of single-loop reentry are similar to those in the "figure-eight" reentrant circuit.

Animals↗
PubMed1993

Mechanism of spontaneous termination of stable atrial flutter in the canine sterile pericarditis model.

BACKGROUND: We tested the hypotheses that spontaneous termination of stable atrial flutter is directly related to spontaneous beat-to-beat cycle length oscillations and that block of the circulating reentrant wave front occurs in an area of slow conduction. METHODS AND RESULTS: We studied 30 episodes of spontaneous termination of stable atrial flutter induced by atrial stimulation in 11 conscious, nonsedated dogs with sterile pericarditis. Additionally, in 5 dogs, 14 episodes of spontaneous termination of stable atrial flutter were studied with a multisite mapping system to record simultaneously from 190 right atrial electrodes. In the conscious-state studies, atrial flutter cycle length oscillations began 6 +/- 1 (mean +/- SEM) beats before termination in 26 episodes, stable atrial flutter evolved into atrial fibrillation in 3 episodes, and no cycle length change occurred before termination in 1 episode. In the open-chest studies, in all instances, spontaneous oscillations began 7 +/- 1 beats before termination. The only consistent oscillation pattern occurred for the last two beats: a long cycle length (149 +/- 9 milliseconds) followed by a much shorter cycle length (110 +/- 6 milliseconds) (P < .01). Activation maps demonstrated that all cycle length oscillations were explained by changes of conduction in an area(s) of slow conduction in the reentrant circuit. In two instances, the last (short) cycle length was associated with disappearance of an area of slow conduction. In all episodes, the last circulating reentrant wave front blocked in an area of slow conduction in the reentrant circuit. Although not tested, during the last beat, the very early arrival of the circulating reentrant wave front at an area of slow conduction suggests an important role for refractoriness, with head and tail interactions, resulting in block. CONCLUSIONS: Spontaneous termination of stable atrial flutter in the sterile pericarditis model (1) is preceded by beat-to-beat cycle length oscillations that result from changes in conduction in areas of slow conduction in the reentrant circuit and (2) results from block of the circulating reentrant wave front in an area of slow conduction.

Animals↗
PubMed1994

Characterization of the excitable gap in a functionally determined reentrant circuit. Studies in the sterile pericarditis model of atrial flutter.

BACKGROUND: Single premature beats were introduced in the reentrant circuit during stable atrial flutter in the canine sterile pericarditis model to test the hypotheses that (1) despite the fact that the reentrant circuit is functionally determined, there is a fully excitable gap; (2) the excitable gap in the reentrant circuit is not uniform; and (3) inhomogeneities of conduction in the reentrant circuit explain the effects of premature beats. METHODS AND RESULTS: A multiplexing system was used to record 190 unipolar electrograms from the right atrial free wall during 18 atrial flutter episodes in 9 dogs. In all 18 episodes, premature stimuli captured the atrial flutter reentrant circuit. At the longest coupling intervals, the return cycle at the site closest to the pacing site did not prolong. As the coupling interval of the premature stimulus decreased, the return cycle then progressively increased, associated with changes in conduction in the reentrant circuit that were not uniform. The result was that coupling intervals associated with introduction of the premature beat also were not constant. The mean duration of the total (ie, fully plus partially) excitable gap was 12 +/- 4 ms in areas of slow conduction, and it was always shorter than the total excitable gap in other areas (22 +/- 6 ms, P < .001). The mean duration of the fully excitable gap based on analysis of the return cycle was 4 +/- 1 ms in the reentrant circuit. In 13 of 18 atrial flutter episodes, a premature stimulus terminated atrial flutter by causing block of the orthodromic wave front of the premature beat in an area of slow conduction. The mean coupling interval that caused orthodromic block was 113 +/- 5 ms (recorded at the site just proximal to the area of block), and it was always longer than the delivered stimulus coupling interval at the pacing site (96 +/- 8 ms, P < .001). CONCLUSIONS: We conclude that in this functionally determined atrial flutter reentrant circuit in the canine sterile pericarditis model, (1) a fully excitable gap is present in at least part of the reentrant circuit; (2) the duration of the excitable gap in the reentrant circuit is shortest in areas of slow conduction; and (3) when a premature beat encounters the partially excitable gap of the reentrant circuit, it results in changes in conduction such that the coupling intervals are not uniform throughout in the reentrant circuit.

Animals↗
PubMed1997

Simultaneous multisite mapping studies during induced atrial fibrillation in the sterile pericarditis model. Insights into the mechanism of its maintenance.

BACKGROUND: Chronic atrial fibrillation (AF) is thought to be due to multiple, simultaneously circulating wavelets. In the canine sterile pericarditis model, the mechanisms of maintenance of AF are not yet understood. METHODS AND RESULTS: During six induced AF episodes in six dogs with sterile pericarditis, 372 unipolar electrograms were recorded simultaneously from an electrode array placed around both atrial free walls, along with 10 to 24 electrodes from the atrial septum, by use of a multiplexing system. Activation maps during 12 consecutive 100-ms windows were analyzed from an episode of sustained AF in each dog (mean duration, 32 +/- 24 minutes). In two dogs, two such activation maps during the same episode of AF were analyzed. During AF, multiple unstable reentrant circuits (mean number, 1.4 +/- 0.1 per 100-ms analysis window) with very short cycle lengths (mean, 111 +/- 8 ms) present primarily in the atrial septum and right atrium were responsible for maintenance of AF. The unstable reentrant circuits frequently disappeared and re-formed. Wave fronts traveling from one atrium to the other and/or from the atrial septum play an important role in re-formation of unstable reentrant wave fronts. CONCLUSIONS: In this model of paroxysmal AF, unstable reentrant circuits of very short cycle length principally involving the atrial septum appear to be critical for maintenance of AF. Some reentrant circuits disappear as others re-form, so that at least one reentrant circuit is always present. Because the atria cannot follow their very short cycle lengths in a 1:1 manner, AF is maintained.

Animals↗
PubMed1997

Safety of transvenous atrial defibrillation: studies in the canine sterile pericarditis model.

BACKGROUND: It is recognized that a ventricular vulnerability period exists during which atrial shock delivery may induce a ventricular tachyarrhythmia. This study was designed to define the zone in which the ventricles are vulnerable to induction of ventricular tachyarrhythmia during delivery of atrial shocks in the sterile pericarditis canine model of atrial fibrillation. METHODS AND RESULTS: Two days after creation of sterile pericarditis, 24 dogs underwent either a four-part or five-part ventricular vulnerability protocol during which atrial shocks were delivered between transvenous catheters, one in the distal coronary sinus and one in the right atrial appendage. The protocol included part 1, shocks during induced atrial fibrillation; parts 2 through 4, shocks delivered synchronously with the last ventricular beat of one of the following three ventricular pacing protocols: constant ventricular rates (S1S1), short-long-short cycles (S1S2S3-V), and ventricular premature beats (S1); and part 5, shocks delivered synchronously with the last R wave resulting from an atrially paced short-long-short cycle (S1S2S3-A). Ventricular tachyarrhythmia was induced 122 times: 2 of 665 shocks in two dogs in part 1, 29 of 786 shocks in nine dogs in part 2, 67 of 734 shocks in 15 dogs in part 3, 24 of 919 shocks in five dogs in part 4, and none in part 5. All ventricular proarrhythmia resulted from shocks delivered during the T wave of a preceding ventricular beat. No episodes of ventricular tachyarrhythmia were induced by atrial shocks synchronized to R waves with the previous RR at intervals above the QT+60 ms interval (absolute interval >320 ms), with one exception, at the QT+100 ms interval (absolute interval 360 ms). CONCLUSIONS: With transvenous electrode catheters used to deliver atrial shocks, life-threatening ventricular rhythms were induced but were limited to a specific zone defined by the QT interval.

Animals↗
PubMed1980

Recurrent pericarditis due to cystic teratoma of the mediastinum: a case report.

A case of a benign cystic teratoma of the anterior mediastinum and recurrent pericarditis is presented. The clinical, angiocardiographic, surgical, and pathologic findings are described. The cardinal clinical picture of long-standing recurrent pericarditis and the excellent surgical results make this case noteworthy.

Dermoid Cyst↗
PubMed1985

Severe pericarditis as a presenting sign of bronchogenic carcinoma.

An exudative pericarditis was the only sign of an adenocarcinoma arising from the right main bronchus of the lung for two and a half months. No metastases were found at the time of diagnosis. Pericarditis relapsed quickly after repeated pericardiocenteses, and systemic chemotherapy did not influence its course. Cardiac tamponade caused the death of the patient.

Adenocarcinoma↗
PubMedDate not supplied

Pericardial infusion of tissue plasminogen activator in fibropurulent pericarditis.

A 61-year-old man developed a loculated fibropurulent pericarditis, a rare complication of bacteremia. This occurred as a complication of a Staphylococcal aureus bacteremia from a head and neck abscess following self-extraction of a tooth. Despite surgical intervention and placement of 2 pericardial drains, a refractory, inadequately drained infected pericardial effusion persisted. Although there is limited experience with thrombolytic therapy to dissolve a fibrin clot in the pericardium, break down loculated adhesions, and facilitate free drainage of infected material, lysis is well described in the management of exudative pleural effusions. After infusion of 30 mg of tissue plasminogen activator in 100 cc normal saline through the pericardial drain of the patient, a large amount of infected serosanginous material subsequently drained during the next 2 days. The patient became afebrile and culture negative, remained hemodynamically stable, and had resolution of his pericarditis and pericardial effusion on electrocardiogram and echocardiogram, respectively.

Abscess↗
PubMed1997

Acinetobacter pericarditis with tamponade in a patient with systemic lupus erythematosus.

We describe a case of active systemic lupus erythematosus (SLE) complicated with a large amount of pericardial effusion with diastolic collapse of right ventricle suggestive of tamponade. Isolates from surgical drainage of pericardial fluid showed Acinetobacter baumannii exhibiting multiple antibiotics resistance. Despite the high frequency of both pericardial involvement and of infection complications in SLE, septic pericarditis and tamponade is considered rare. Most of the reported cases of septic pericarditis in SLE were due to Staphylococcal aureus, and Acinetobacter baumannii has never been reported before.

Acinetobacter Infections↗
PubMed2026

Disseminated meningococcal infection presenting with constrictive pericarditis and bilateral septic arthritis without meningitis: A case report.

Invasive meningococcal disease is a life-threatening infection that classically presents as meningitis or meningococcemia. Extra-meningeal manifestations, including pericarditis and septic arthritis, are uncommon and may complicate diagnosis, particularly in the absence of meningeal involvement. A previously healthy vaccinated man in his 50s presented with acute bilateral knee pain and swelling following a short history of fever, productive cough, fatigue, and dyspnea. Blood cultures grew Neisseria meningitidis serogroup W, whereas cerebrospinal fluid, synovial fluid, and pericardial fluid cultures remained negative. Cardiac magnetic resonance imaging demonstrated constrictive pericarditis with circumferential pericardial enhancement and pericardial effusion. The patient was successfully treated with intravenous ceftriaxone, colchicine, ibuprofen, pericardiocentesis, and bilateral knee washout, followed by oral ciprofloxacin. This case adds to the limited literature describing concurrent cardiac and musculoskeletal manifestations of invasive meningococcal disease without meningitis and shows the importance of early recognition, comprehensive investigation and multidisciplinary management of these uncommon presentations.

Neisseria meningitidis↗
PubMed2005

Idiopathic recurrent acute pericarditis: familial Mediterranean fever mutations and disease evolution in a large cohort of Caucasian patients.

Idiopathic recurrent acute pericarditis (IRAP) is suspected to be an autoimmune phenomenon. We studied 46 consecutive patients. We looked for: 1) the occurrence of new diagnoses of autoimmune diseases during our follow up; 2) HLA typing; and 3) the presence of the most frequent mutations linked to familial Mediterranean fever (FMF gene or MEFV). HLA typing was done in 21 patients at loci B, DRB1, DQA1 and DQB1. MEFV gene was looked in 23 patients using specific primers. During the follow-up we made a new diagnosis of primary Sjögren's syndrome in four patients (8.7%) and of rheumatoid arthritis in one patient (2.2%). HLA B14, DRB1*01 and DQB1*0202 were significantly more prevalent, but we did not find a typical HLA typing. MEFV gene was searched: exon 10 was checked by sequence and the E148Q mutation by restriction site analysis. No mutations were found. In conclusion, the prevalence of definite immunorheumatological diseases and the absence of the mutations linked to FMF reinforce the notion that idiopathic acute recurrent pericarditis is an autoimmune condition.

Arthritis, Rheumatoid↗
PubMed1985

Septal myocardial abscess and infectious pericarditis in a case of bacterial endocarditis.

A case of acute aortic valve endocarditis is reported, in which the complications of pericarditis and myocardial abscess were diagnosed clinically. Two dimensional and M-mode echocardiography showed large echo-free spaces and a marked thickening of the interventricular septum which had not been detected previously, suggesting pericardial effusion and myocardial abscess. This is the first case in Japan to our knowledge, in which the pericarditis and myocardial abscess were detected preoperatively and successfully treated surgically.

Abscess↗
PubMed1994

Gallium-67 citrate scintigraphy in idiopathic pericarditis--report of a case.

We report a case of idiopathic pericarditis in a 71-year-old woman without a friction rub or electrocardiographic changes suggestive of pericardial inflammation. She noticed dyspnea and palpitation on exertion about 40 days before admission. After admission, pericardial effusion and inflammatory reactions, such as elevated C-reactive protein, were found. Moreover, gallium-67 citrate scintigraphy revealed abnormal isotope accumulation over the cardiac silhouette. Therefore, she was diagnosed as having "active" pericarditis. The finding with the gallium scan became negative with steroid therapy. In this case, a gallium scan was very useful in assessing and monitoring the course of pericardial inflammation.

Aged↗