[Constrictive pericarditis associated with combined valvular diseases--etiology of constrictive pericarditis and echocardiography].
Explore the source record for details and available documents.
Adult↗
SEARCH · Search PubMed
Results for “Pericarditis”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Effect of definition on incidence of postinfarction pericarditis: is it time to redefine postinfarction pericarditis?
Explore the source record for details and available documents.
Electrocardiography↗
The changing spectrum of pericardiectomy for chronic pericarditis: occult constrictive pericarditis.
Explore the source record for details and available documents.
Adolescent↗
[Considerations on extra-pericardic dislocations of the heart (so-called pericardic hernias)].
Explore the source record for details and available documents.
Aged↗
Clonal Hematopoiesis and Risk of New-Onset Myocarditis and Pericarditis.
IMPORTANCE: Clonal hematopoiesis of indeterminate potential (CHIP) is the age-related clonal expansion of hematopoietic stem cells with leukemia-associated mutations. Certain CHIP mutations promote atherosclerosis and heart failure through immune-related pathways. OBJECTIVE: To test whether CHIP is associated with the development of myocarditis and pericarditis. DESIGN, SETTING, AND PARTICIPANTS: This observational population-based cohort study used data from the UK Biobank. Enrollment occurred between 2006 and 2010. Participants with whole-exome sequencing, no prevalent cardiovascular disease or hematological malignancy, and complete covariate data were included. Follow-up occurred for a median of 13.6 (IQR, 12.8-14.2) years. Analyses were conducted from November 2024 to July 2025. EXPOSURES: Any CHIP (variant allele frequency [VAF] ≥2%) and large CHIP (VAF ≥10%) constituted coprimary study exposures. Secondary analyses considered DNMT3A and TET2 CHIP as separate exposures. MAIN OUTCOMES AND MEASURES: The primary outcome was a composite of incident myocarditis and pericarditis. Cox regression tested associations of CHIP with myocarditis and pericarditis, adjusting for age, sex, race and ancestry, and cardiovascular risk factors. Secondary analyses considered myocarditis and pericarditis as separate outcomes. Additional analyses compared associations of CHIP with myocarditis and pericarditis with those with other cardiovascular diseases, and tested the bidirectional associations between CHIP and noncardiac immune-mediated inflammatory diseases. RESULTS: Among 335 426 participants (mean age, 56.1 years; 185 429 female [55.3%] and 149 997 male [44.7%]), 11 057 had any CHIP (3.3%), 7271 had large CHIP (2.2%), and 382 developed myocarditis or pericarditis (0.11%). Any and large CHIP were associated with multivariable-adjusted hazard ratios of 1.75 (95% CI, 1.14-2.68; P = .01) and 2.07 (95% CI, 1.28-3.33; P = .003), respectively, for the primary composite outcome of incident myocarditis and pericarditis. Increased risks were observed for DNMT3A and TET2 CHIP, with hazard ratios of 2.22 (95% CI, 1.17-4.21; P = .01) for DNMT3A with pericarditis and 3.65 (95% CI, 1.16-11.49; P = .03) for TET2 with myocarditis. CHIP associated with myocarditis and pericarditis more strongly than with other cardiovascular diseases (eg, coronary artery disease and heart failure). Any CHIP was also associated with 1.27-fold risk (95% CI, 1.16-1.39; P < .001) of developing noncardiac immune-mediated inflammatory diseases, without evidence for reverse causation. CONCLUSIONS AND RELEVANCE: In this study, CHIP was a strong risk factor for myocarditis and pericarditis among middle-aged adults. Targeting CHIP and its downstream pathways may represent a strategy for preventing or treating pericarditis and myocarditis.
Adult↗
Postpacemaker implant pericarditis: incidence and outcomes with active-fixation leads.
Pericarditis has been noted as a potential complication of pacemaker implantation. This study evaluated the risk of developing pericarditis following pacemaker implantation with active-fixation atrial leads. Included were 1,021 consecutive patients (mean age 73.4+/-0.4 years, range 16-101 years; 45.2% women) undergoing new pacemaker system implantation between 1991 and 1999 who were reviewed for the complication of pericarditis. The incidence and outcomes of postimplantation pericarditis in patients receiving active-fixation atrial leads were compared to those not receiving these leads. Of 79 patients who received active-fixation atrial leads, 4 (5%) developed pericarditis postpacemaker implantation. Of 942 patients with passive-fixation atrial leads or no atrial lead (i.e., a ventricular lead only), none developed pericarditis postoperatively (P < 0.001). Of patients receiving active-fixation ventricular leads only (n = 97), none developed pericarditis. No complications were apparent at the time of implantation in patients who developed pericarditis. Pleuritic chest pain developed between 1 and 28 hours postoperatively. Three patients had pericardial rubs without clinical or echocardiographic evidence of tamponade. They were treated conservatively with acetylsalicylic acid or ibuprofen and their symptoms resolved without sequelae in 1-8 days. One patient (without pericardial rub) died due to cardiac tamponade on postoperative day 6. Postmortem examination revealed hemorrhagic pericarditis with no gross evidence of lead perforation. Pericarditis complicates pacemaker implantation in significantly more patients who receive active-fixation atrial leads. It may be precipitated byperforation of the atrial lead screw through the thin atrial wall. Patients developing postoperative pericarditis should befollowed closely due to the risk of cardiac tamponade.
Adolescent↗
Recurrent pericarditis.
The most common background for recurrent pericarditis is that of acute nonspecific pericarditis. Relapsing pericarditis also may follow cardiac trauma, cardiac operations, myocardial infarction, and intrapericardial bleeding. The exact recurrence rate after initial attacks of idiopathic pericarditis is unknown but appears to be in the range of 15% to 32%. The mechanism of recurrent pericarditis is uncertain. An autoimmune response has been proposed, but this concept is unproved. Yoneda and coworkers, in a case of pericarditis due to coxsackie B virus, found no rise in antibody titer to this virus during recurrences. The prognosis, except for disabling pain and malaise, is good, and constrictive pericarditis, chronic myocardial disease, and cardiac tamponade are unusual complications. Although constrictive pericarditis may follow an initial attack of idiopathic pericarditis, it was reported in neither two other series of patients with relapsing pericarditis nor in this series. Cardiac tamponade has been reported as an occasional complication of relapses but did not occur in our patients. None of our patients died. Most patients with recurrent pericarditis respond to adrenal steroid therapy, but many times there is difficulty in weaning the patient from the drug. Because it is suspected that adrenal steroids may prolong attacks and promote tendency to further recurrences, initial therapy should be offered with aspirin or NSAIDs, and adrenal steroid therapy should be used only when there is no response to these agents. Recurrences may take place over a period lasting as long as 15 years, and patients with as many as 19 recurrences have been described.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
A new classification for pericarditis associated with meningococcal infection.
UNLABELLED: Acute meningococcal pericarditis is a rare clinical disorder. Our review of the literature disclosed that current classifications are confusing since they fail to differentiate between two distinct criteria: time and causality. We suggest a new classification of the various states of meningococcal pericarditis on the basis of the pathophysiological process: disseminated meningococcal disease with pericarditis (purulent, culture-positive, associated with meningococcal bacteraemia); isolated meningococcal pericarditis (purulent, culture-positive but without signs of meningeal or other clinical systemic involvement); and reactive meningococcal pericarditis (immunological, late-onset, culture-negative, resembling post-viral pericarditis). It is essential that clinicians recognize the various states of the disease, since they differ in natural history, treatment and prognosis. CONCLUSION: From personal experience and a literature review it emerges that meningococcal pericarditis should be classified as: (1) Pericarditis as local manifestation of disseminated meningococcal disease; (2) isolated meningococcal pericarditis; (3) reactive (immunopathic) meningococcal pericarditis.
Adolescent↗
Constrictive pericarditis and restrictive cardiomyopathy: evaluation with MR imaging.
Twenty-nine patients who were referred with the possible diagnosis of constrictive pericarditis underwent electrocardiographically gated transverse spin-echo magnetic resonance (MR) imaging to determine the accuracy of spin-echo MR imaging for the diagnosis of constrictive pericarditis and to compare the morphologic features of constrictive pericarditis with those of restrictive cardiomyopathy as seen on spin-echo MR images. Constrictive pericarditis was verified by means of surgery and/or catheterization in 17 patients. The sensitivity, specificity, and accuracy of MR imaging in the diagnosis of constrictive pericarditis were 88%, 100%, and 93%, respectively. Thickened pericardium was observed in 88% of patients with proved constrictive pericarditis. Pericardial thickening was not identified in patients with restrictive myocarditis (n = 4). The most frequent site of pericardial thickening was over the right ventricle. In constrictive pericarditis, the signal intensity of the thickened pericardium was similar or decreased compared with that of the myocardium. Indirect findings of impaired right ventricular diastolic filling (eg, dilatation of the inferior vena cava and right atrium) were identified in constrictive pericarditis and restrictive cardiomyopathy. MR imaging can serve as a noninvasive examination for the definitive diagnosis of constrictive pericarditis and can help distinguish between constrictive pericarditis and restrictive cardiomyopathy on the basis of pericardial thickness.
Cardiomyopathy, Restrictive↗
Diagnosis of tuberculous pericarditis and treatment without corticosteroids at a tertiary teaching hospital in Taiwan: a 14-year experience.
Tuberculous (TB) pericarditis is a rare but life-threatening form of extrapulmonary tuberculosis. The diagnostic strategy and optimal therapy for TB pericarditis are not well established. We retrospectively analyzed the diagnostic data, clinical characteristics, treatment and outcome in a total of 19 patients with TB pericarditis treated from January 1988 to July 2002. Based on the finding of echocardiography, 8 of these patients were classified as having early stage and 11 as having advanced-stage disease. There were 15 men and 4 women, with a mean age of 65 years (range, 34 to 80 years). All patients received antituberculosis chemotherapy, and all but 2 underwent at least 1 of the following procedures: pericardiocentesis and biopsy, pericardial window placement, and pericardiectomy. None of the patients received corticosteroids concurrently. Of the 8 patients with early-stage TB pericarditis, 3 (37.5%) developed constrictive pericarditis, while of the 7 patients with advanced-stage disease (excluding 4 who had already developed TB constrictive pericarditis at diagnosis), 6 (85.7%) subsequently developed constriction. These findings underscore the importance of pericardiectomy in patients with advanced-stage TB pericarditis. To avoid potentially lethal cardiac tamponade and constrictive cardiomyopathy, clinicians should have a high index of suspicion of TB pericarditis when encountering a patient with pericardial effusion. Histopathologic study of pericardial tissue sample is the key to timely diagnosis of TB pericarditis. The favorable outcomes of patients in this series suggest that a combination of antituberculosis chemotherapy and timely pericardiectomy may be the optimal therapy for patients with TB pericarditis.
Adrenal Cortex Hormones↗
[Diagnosis, etiology and clinical course of acute and chronic pericarditis].
Between 1976 and 1982 18 patients with acute and 13 with chronic pericarditis (excluding constrictive pericarditis) were seen at the Medical Outpatient Clinic, University Hospital, Zürich. The prominent symptom in acute pericarditis was chest pain (15/18 patients versus 0/13 in chronic pericarditis, p less than 0.001) and in chronic pericarditis dyspnea (7/13 patients versus 1/18 in acute pericarditis, p less than 0.005). Pericardial friction rub and ST elevation were significantly more frequent in acute than in chronic pericarditis. In contrast, elevation of venous pressure occurred more often in the chronic than in the acute form. During the follow-up of 3.2 years the NYHA class decreased from 2.5 to 1.2 (p less than 0.001) in the group with acute pericarditis although 7 recurrences occurred in 3 patients within the first two years. The follow-up in the patients with chronic pericarditis was 4.4 years and the NYHA class decreased from 2.4 to 1.4 (p less than 0.05). There were, however, two deaths in the group with chronic pericarditis and pericardiocentesis and/or pericardiectomy had to be performed in 8/13 patients.
Adult↗
Immune reactions in tuberculous and chronic constrictive pericarditis. Clinical data and diagnostic significance of antimyocardial antibodies.
Humoral immune reactions were analyzed in 12 patients with exudative tuberculous pericarditis, 10 patients with constrictive pericarditis due to former tuberculosis, 10 patients with viral pericarditis, 20 patients with pulmonary tuberculosis, and 98 healthy donors. Pericarditis occurred in 12.5% of the patients with tuberculosis, whereas the incidence of tuberculosis in the 149 patients with pericarditis was 8%. Repeated pericardial puncture and pericardial effusions of greater than 500 ml with impending cardiac tamponade had to be performed in 4 patients. Clinical data indicated probable myocardial involvement in 4 of 12 patients. Antimyolemmal antibodies, which are a muscle-specific subtype of antisarcolemmal antibodies, were found in all patients with exudative tuberculous pericarditis and viral perimyocarditis, in only 1 of 12 patients with constrictive pericarditis, and in no patients with pulmonary tuberculosis. Antifibrillary antibodies--primarily of the antimyosin type--were missed in patients with viral heart disease but were demonstrated in 75% of patients with tuberculous pericarditis. Only sera with complement-fixing antimyolemmal antibodies of the IgG type in titers greater than 1:40 induced cytolysis of vital adult heterologous cardiocytes isolated and enriched by silica sol gradient centrifugation. These findings suggest not only that antimyolemmal antibodies are diagnostic indicators of perimyocardial involvement in tuberculous pericarditis, but also that they may play a significant role in its pathogenesis.
Antibody Specificity↗
Differentiation of constrictive pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow.
OBJECTIVES: The purpose of this study was to test the utility of measuring respiratory variation in pulmonary venous flow by transesophageal echocardiography. BACKGROUND: Respiratory variation of atrioventricular and central venous flow velocities by Doppler echocardiography has been used to differentiate constrictive pericarditis from restrictive cardiomyopathy. METHODS: We performed pulsed wave Doppler transesophageal echocardiography of the left or right pulmonary veins in 31 patients with diastolic dysfunction. Fourteen patients had constrictive pericarditis, and 17 had restrictive cardiomyopathy. We measured the pulmonary venous peak systolic and diastolic flow velocities and the systolic/diastolic flow ratio with transesophageal echocardiography during expiration and inspiration. The percent change in Doppler flow velocity from expiration to inspiration (%E) was calculated. RESULTS: Pulmonary venous peak systolic flow in both inspiration and expiration was greater in constrictive pericarditis than in restrictive cardiomyopathy. The %E for peak systolic flow tended to be higher in constrictive pericarditis (19% vs. 10%, p = 0.09). In contrast, pulmonary venous peak diastolic flow during inspiration was lower in constrictive pericarditis than in restrictive cardiomyopathy. The %E for peak diastolic flow was larger in constrictive pericarditis (29% vs. 16%, p = 0.008). The pulmonary venous systolic/diastolic flow ratio was greater in constrictive pericarditis in both inspiration and expiration. The combination of pulmonary venous systolic/diastolic flow ratio > or = 0.65 in inspiration and a %E for peak diastolic flow > or = 40% correctly classified 86% of patients with constrictive pericarditis. CONCLUSIONS: The relatively larger pulmonary venous systolic/diastolic flow ratio and greater respiratory variation in pulmonary venous systolic, and especially diastolic, flow velocities by transesophageal echocardiography can be useful signs in distinguishing constrictive pericarditis from restrictive cardiomyopathy.
Blood Flow Velocity↗
T wave changes consistent with epicardial involvement in acute myocardial infarction. Observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis.
OBJECTIVES: This study was designed to evaluate the presence or absence of atypical T wave evolution in patients with a postinfarction pericardial effusion but without clinically recognized postinfarction pericarditis. A second purpose was to evaluate the frequency of atypical T wave evolution in a previous study of postinfarction pericarditis. BACKGROUND: Electrocardiographic (ECG) criteria involving the evolution of the T wave after an acute myocardial infarction were recently described in patients with regional postinfarction pericarditis. Atypical T wave evolution was found to have a sensitivity of 100% and a specificity of 77% for clinically recognized regional postinfarction pericarditis with or without a pericardial effusion. METHODS: The hospital records and serial ECGs of 20 patients with clinically recognized postinfarction pericarditis (Group I) were reviewed. The records and serial ECGs of 20 additional patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis (Group II) were also examined. The type of postinfarction T wave pattern, typical or atypical, was recorded in both groups. RESULTS: All 20 patients in Group I had atypical T wave evolution. Among the 20 patients in Group II, every patient also had atypical T wave evolution. Fifteen percent of all 40 patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred postinfarction pericarditis. CONCLUSIONS: The high sensitivity of atypical T wave evolution in diagnosing regional postinfarction pericarditis was confirmed. However, similar T wave alterations were also observed when a postinfarction pericardial effusion existed in the absence of clinically recognized pericarditis. Fifteen percent of patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred pericardial involvement. Thus, the presence of atypical T wave evolution may be a more sensitive indicator of a transmural infarction than the development of a Q wave.
Electrocardiography↗
Diagnosis of constrictive pericarditis by two-dimensional echocardiography: studies in a new experimental model and in patients.
The purpose of this study was to determine the value of two-dimensional echocardiography in detecting constrictive pericarditis. Serial two-dimensional echocardiography was performed in eight closed chest conscious dogs with experimental constrictive pericarditis, using a new model that creates constrictive pericarditis by the introduction of a pericardial irritant mixture. Constrictive pericarditis was confirmed in these dogs by cardiac catheterization and pathologic examination. Four patients with constrictive pericarditis and three patients with restrictive cardiomyopathy (amyloidosis) were also studied. Analysis of short-axis two-dimensional echocardiograms was performed to determine the frame by frame change in left ventricular cavity areas throughout diastole. Curves of diastolic left ventricular cavity area change versus percent duration of diastole were constructed for each animal and human subject. Pericardial thickness was measured at various gain settings on two-dimensional and M-mode echocardiograms and at post-mortem examination. In dogs with constrictive pericarditis, the echocardiograms seriously overestimated and correlated poorly with pathologic measurements of pericardial thickness. In dogs after constrictive pericarditis developed, 69 +/- 11% (mean +/- SD) (range 50 to 84) of cavity area change occurred in the initial 30% of diastole compared with 35 +/- 7% (range 20 to 45) in control two-dimensional echocardiograms (p less than 0.001). Four patients with constrictive pericarditis showed similar accelerated cavity expansion in early diastole, but three patients with cardiac amyloidosis showed more variable left ventricular diastolic expansion rates. It is concluded that two-dimensional echocardiograms can demonstrate characteristic diastolic filling abnormalities in constrictive pericarditis, but cannot accurately measure pericardial thickness.
Amyloidosis↗
The electrocardiographic diagnosis of regional pericarditis in acute inferior myocardial infarction.
The diagnosis of postinfarction localized (regional) pericarditis has remained elusive. During the course of a recent study of patients with fatal free-wall rupture, an atypical pattern of T-wave evolution was observed during the days preceding death. It was learned, from autopsy examination, that these electrocardiographic changes were due to the associated localized pericarditis, rather than the rupture, per se. Therefore, this investigation was undertaken to ascertain if the same atypical T-wave changes occur in patients with postinfarction localized pericarditis, but without free-wall rupture, and to determine if the frequency of those changes differs between those patients with inferior and those with anterior postinfarction pericarditis. Forty-three patients with regional postinfarction pericarditis were identified clinically. They were divided into three groups, anterior (17), inferior (17) and lateral or posterior (9) myocardial infarction. In this report those patients with anterior regional postinfarction pericarditis are compared with those with inferior postinfarction pericarditis. It was found that an atypical T-wave evolution pattern--either persistently positive T-waves after 48 h or reversal of initially inverted T-waves after 48 h--existed in every patient irrespective of infarct location. However, the two atypical patterns of T-wave evolution occurred with distinctly different frequencies between the two sites of infarction. With inferior postinfarction pericarditis, gradual reversal of initially inverted T-waves occurred in 14 patients (82%) while only three (18%) had persistently positive T-waves. Conversely, among patients with anterior postinfarction pericarditis, reversal after inversion occurred in five of 17 patients (29%) while 12 of 17 patients (71%) had persistently positive deflections (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Electrocardiography↗
Constrictive pericarditis in chronic ulcerative colitis.
Acute pericarditis has been described as an extraintestinal manifestation of inflammatory bowel disease (IBD), as well as a consequence of IBD treatment, specifically sulfasalazine and mesalamine. Until now, there have been no reported cases of constrictive pericarditis associated with IBD or its treatment. A 37-year-old woman with a 24-year history of chronic ulcerative colitis (CUC) presented with a 3-month history of fevers, palpitations, dyspnea, syncope, and retrosternal chest pain. Two weeks before symptoms, she had initiated oral mesalamine for an ongoing CUC flare. Physical examination suggested constrictive pericarditis. An echocardiogram revealed a thickened pericardium with a nearly circumferential fibrinous effusion, with Doppler confirming diastolic compromise. The patient proceeded to radical pericardectomy. Pathological examination showed grossly hemorrhagic acute and chronic pericarditis, with cultures and cytology negative. To date, only 104 cases of IBD with acute pericarditis have been reported, with fewer than 10 cases of mesalamine-induced acute pericarditis reported. This is the first reported case of constrictive pericarditis related to IBD or its treatment. Although our patient may have had IBD-associated constrictive pericarditis, her mesalamine use raises the possibility of a drug-induced constrictive pericarditis.
Adult↗
Phasic coronary flow characteristics in patients with constrictive pericarditis: comparison with restrictive cardiomyopathy.
BACKGROUND: Phasic coronary flow characteristics have been reported in patients with aortic valve disease and hypertrophic cardiomyopathy. The purpose of this study was to assess the differences in coronary flow characteristics between patients with constrictive pericarditis and those with restrictive cardiomyopathy. METHODS AND RESULTS: The study populations consisted of 7 case patients with constrictive pericarditis, 8 with restrictive cardiomyopathy, and 11 control subjects with chest pain and normal coronary arteries. Five minutes after injection of 3 mg of isosorbide dinitrate, phasic coronary flow velocity patterns were analyzed in the proximal segment of the angiographically normal left anterior descending coronary artery at rest using a 0.014-in, 15-MHz Doppler guidewire. Coronary flow reserve was obtained from the ratio of adenosine-induced (0.14 mg x kg(-1) x min(-1) I.V.) hyperemic/baseline time-averaged peak velocity. Although in case patients with constrictive pericarditis and restrictive cardiomyopathy maximal hyperemic time-averaged peak velocity (21+/-8 and 31+/-17 versus 60+/-19 cm/s, respectively; P<.001) and coronary flow reserve (1.3+/-0.4 and 1.6+/-0.6 versus 3.6+/-0.4, respectively, P<.001) were significantly lower than in control subjects, there were no significant differences in these indexes between the two groups of case patients. Velocity half-time of diastolic flow velocity corrected by square root(RR), which indicates deceleration of diastolic flow, in the groups of case patients with constrictive pericarditis and restrictive cardiomyopathy was significantly less than that in control subjects (6.2+/-2.6 and 10.6+/-1.5 versus 16.9+/-2.7, respectively; P<.001); this was also significantly smaller in constrictive pericarditis than restrictive cardiomyopathy (P<.001). This index <9.5 could distinguish constrictive pericarditis from restrictive cardiomyopathy with a sensitivity of 86% and a specificity of 88%. Furthermore, time from the beginning of diastole to diastolic peak velocity corrected by square root(RR) indicating acceleration of diastolic flow velocity in constrictive pericarditis was significantly less than that in restrictive cardiomyopathy and control subjects (2.8+/-1.2 versus 4.8+/-0.8 and 4.4+/-0.6, respectively; P<.001). CONCLUSIONS: Although coronary flow reserve is limited in both constrictive pericarditis and restrictive cardiomyopathy because of restriction of hyperemic response, rapid acceleration and more rapid deceleration of diastolic flow velocity are more characteristic in constrictive pericarditis than in restrictive cardiomyopathy.
Adult↗