Pericarditis complicating acute myocardial infarction: incidence of complications and significance of electrocardiogram on admission

The records of 31 patients with pericarditis complicating acute myocardial infarction were reviewed and compared to a control group of 274 patients with infarction but without pericarditis. The cases of pericarditis all occurred within one week of myocardial infarction and were included only if a typical pericardial friction rub was heard by more than one observer.Sex distribution and age were similar in both groups. There was a higher incidence of anterior wall infarction in the group with pericarditis. The incidence of atrial arrhythmias was less than in controls, while the incidence of ventricular arrhythmias, significant congestive heart failure, and death was slightly greater in those with pericarditis.Maximum ST segment elevation on the day of admission in the group with pericarditis was compared with a control group. In those with anterior wall infarction and pericarditis, the average ST segment elevation in the anterior precordium was 5.6 mm. compared to 2.6 mm. in the controls. In those with inferior wall infarction and pericarditis, the average ST segment elevation was 3.6 mm. in Lead III compared to 1.7 mm. in a control group.It is concluded that patients who develop pericarditis within one week of acute myocardial infarction do not have an increased incidence of atrial arrhythmias. The incidence of ventricular arrhythmias, significant congestive heart failure, and death are slightly greater and may be due to more extensive myocardial infarction. The higher initial ST segment elevation in patients with pericarditis may indicate a greater amount of injury or may be a sign of pericardial involvement that is seen before clinical pericarditis is present.     

Clinical significance of PQ segment depression in acute Q wave anterior wall myocardial infarction

Objectives.This study was disigned to evaluate the clinical significance of PQ segment depression and to examine the frequency of PQ segment depression in infarction-associated pericarditis.Background. PQ segment deviation is almost as characteristic as the classic ST segment deviation and is detected in most patients with pericarditis. However, the incidence and clinical characteristics of PQ segment depression in acute myocardial infarction are not defined.Methods. Three hundred four consecutive patients with acute Q wave anterior wall myocardial infarction were examined carefully by auscultation, electrocardiogram, echocardiogram and chest roentgenogram. The diagnosis of pericarditis was made on the basis of pericardial rub detected by more than two observers during the 1st 3 days after hospital admission. At least 0.5 mm of PQ segment depression from the TP segment observed for >24 h in both limb and precordial loads was considered diagnostic of PQ segment depression.Results. A pericardial rub was present in 65 patients (21 %) and absent in 239 patients. PQ segment depression was detected in both limb and precordial loads in 30 patients (10%): 18 patients with pericardial rub and 12 patients without pericardial rub. On the basis of five clinical variables, multivariate analysis was performed to determine the important variables related to the occurrence of PQ segment depression. Pericardial rub was selected with left ventricular segments with advanced asynergy as a significant factor related to PQ segment depression. There were 31 in-hospital deaths, and a significantly higher hospital mortality rate was observed in patients with PQ segment depression (23% vs. 9%).Conclusions. Although PQ segment depression was observed in a minority of patients with infarction-associated pericarditis, it was one of the clinical signs of larger infarct size and increased hospital deaths.     

The role of infarction-associated pericarditis on the occurrence of atrial fibrillation

Aims Transient atrial fibrillation is a relatively common arrhythmiain the early phase of acute Q-wave myocardial infarction. However,the role of infarction-associated pericarditis on the genesisof atrial fibrillation is controversial. This study was designedto examine the relative importance of infarction-associatedpericarditis among other clinical variables on the genesis oftransient atrial fibrillation in patients with acute myocardialinfarction. Methods and results Three hundred and ninety-eight patients with acute Q-wave myocardialinfarction were examined carefully by means of auscultation,ECG, two-dimensional echocardiography and haemodynamic measurements.The diagnosis of pericarditis was made on the basis of pericardialrub detected during the first 3 days after admission. At least0·5mm of PQ-segment depression from a TP segment lastingmore than 24h in both limb and precordial leads was considereddiagnostic of PQ-segment depression. Atrial fibrillation waspresent in 76 patients (19%). Sixteen (42%) of 38 patients withPQ-segment depression had atrial fibrillation, whereas 23 (30%)of 77 patients with pericardial rub had atrial fibrillation.Based on ten clinical variables, multivariate analysis was performedto determine the important variables related to the occurrenceof atrial fibrillation. PQ-segment depression (chi-square=4·10,P<0·05) was selected with age (chi-square=10·52,P<0·005), the number of left ventricular segmentswith advanced asynergy (chi-square=7·73, P<0·01)and pericardial effusion (chi-square=7·95, P<0·005)as important factors related to atrial fibrillation. Patientswith PQ-segment depression had a significantly higher pulmonarycapillary wedge pressure than those without it. Conclusion Among patients with infarction-associated pericarditis, thosewith PQ-segment depression represent atrial involvement associatedwith extensive myocardial damage and hence, PQ-segment depressionis one of the clinical signs related to the occurrence of atrialfibrillation in acute Q-wave myocardial infarction.     

Pericarditis in acute myocardial infarction: characterization and clinical significance

To determine the significance of pericarditis following acute myocardial infarction, the hospital course and 12-month follow-up were analyzed in 703 patients enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Pericarditis, defined by the detection of a pericardial rub, occurred in 20% of the patients (n = 141) and was more likely to follow Q wave than non-Q wave infarction (25% vs 9%, p less than 0.001). Patients with pericarditis experienced more serious myocardial damage compared to those without pericarditis, as evidenced by a larger infarct size (25 +/- 1 vs 17 +/- 1 MB-CK gm-Eq/m2, p less than 0.001), a lower admission left ventricular ejection fraction (42 +/- 1% vs 48 +/- 1%, p less than 0.001), and a higher incidence of congestive heart failure (47% vs 26%, p less than 0.001) and atrial tachyarrhythmias (16% vs 10%, p less than 0.05). When patients were classified by the presence of Q or non-Q wave infarction, these differences persisted although statistical significance was not always achieved due to smaller sample size. Mortality at 12-month follow-up for patients with pericarditis was 18% compared with 12% for patients without pericarditis (p = 0.055). This mortality difference could be accounted for in part by the lower ventricular ejection fraction in patients with pericarditis (p = 0.20 after adjustment).     

不同指标诊断心肌梗死后心包炎的差异

目的　观察不同指标对诊断梗死后心包炎发生率的差异以及溶栓与 PTCA对梗死后心包炎发生率的影响。方法　 1 60例急性心肌梗死病人分为常规药物治疗组 75例、溶栓组 5 2例、 PTCA组 3 3例。于梗死后一周内每日常规检查病人且每 1 -2日记录心电图一次 ,部分常规药物治疗及溶栓的病人于梗死后 5 -7天行心脏超声检查。结果　以心包摩擦音、胸膜炎样胸痛、典型心包炎心电图、心电图不典型 T波演变、心包积液作为诊断标准 :梗塞后心包炎发生率在常规组分别为 8%、 2 9.3 %、 1 .3 %、 3 2 %、 2 0 % ;在溶栓组分别为 3 .8%、 1 5 .3 %、 0 %、 2 3 %、 1 7% ;在 PTCA组分别为 0 %、 6.7%、 0 %、 1 0 %。结论　不同指标诊断梗死后心包炎的发生率明显不同 ,其中以心电图不典型 T波改变最高。溶栓与 PTCA治疗可明显降低梗死后心包炎的发生率。     

Factors associated with pericardial effusion in acute Q wave myocardial infarction

To elucidate the clinical characteristics associated with pericardial effusion in the early phase of myocardial infarction, 330 patients with acute Q wave infarction were studied. According to echocardiography, 83 patients had pericardial effusion on the third day of hospitalization, and careful auscultation revealed that a pericardial rub was absent in 45 patients and was present in 38 patients. Based on seven clinical variables, multivariate analysis was performed to determine the important variables related to the occurrence of pericardial effusion with and without pericardial rub. Pulmonary capillary wedge pressure and left ventricular segments with advanced asynergy were the significant factors related to the occurrence of pericardial effusion without a pericardial rub. The presence of ventricular aneurysmal motion, left ventricular segments with advanced asynergy, and alveolar arterial oxygen difference were related to pericardial effusion with a pericardial rub. Therefore, a hemodynamic factor was the major mechanism associated with the increase in extravascular myocardial fluid and the consequent occurrence of hydropericardia in the absence of a pericardial rub, whereas an increase in the microvascular permeability in the myocardium with excessive fluid exudating through the irritated epicardial surface was the mechanism related to pericardial effusion with a pericardial rub in the early phase of acute myocardial infarction.     

Frequency and clinical significance of pericardial friction rubs in the acute phase of myocardial infarction

An early pericardial friction rub was noted in 23.4% of a population of 1264 consecutive patients admitted with acute myocardial infarction. The incidence of the rub did not vary with age, sex or past cardiac history. The pericardial rub, however, was more often a complication of Q- than non-Q-wave infarcts (25.5% vs 10.5%, P greater than 0.001) and of anterior than inferior infarcts (35.3% vs 20.8%, P greater than 0.001). In comparing the 297 patients with a pericardial rub to the 967 others, we noted that the former group had a higher CK peak (1706 +/- 1110 UI l-1 vs 1189 +/- 1038 UI l-1, P greater than 0.001) and a higher incidence of Killip class greater than 1 (47.5% vs 33.2%, P greater than 0.001), atrial flutter or fibrillation (22.2% vs 9.3%, P greater than 0.001), second or third degree atrioventricular blocks (16.8% vs 9.4%, P greater than 0.001) and complete bundle branch block (14.5% vs 7.1%, P greater than 0.001). In spite of this, the development of a pericardial rub did not increase the in-hospital mortality (10.8% in patients with pericardial rub; 11.3% in those without).     

Pericardial Effusion as a Consequence of Acute Myocardial Infarction

Pericarditis is a common complication of acute myocardial infarction (MI). Its incidence during the first few days after acute MI is 24%–43% when echocardiographic criteria are used, whereas the frequency of clinical pericarditis is much less (from 5% for all acute MIs to 21% for anterior Q wave MIs). Clinical, electrocardiographic findings are discussed. Effusions are mostly small, and the resolution is frequently slow, lasting 1–18 months. Tamponade is extremely rare in the absence of cardiac rupture. Q wave MIs (especially anterior) are more frequently accompanied by pericardial effusion. The prognostic significance of echocardiographically proved pericarditis is questionable.     

Incidence and significance of pericardial effusion in acute myocardial infarction as determined by two-dimensional echocardiography

To determine the incidence and clinical significance of pericardial effusion after acute myocardial infarction, two-dimensional echocardiography was serially performed in 66 consecutive patients. Pericardial effusion was observed in 17 (26%); the effusion was small in 13 patients, moderate in 3 and large with signs of cardiac tamponade in 1. In this patient, two-dimensional echocardiography strongly suggested myocardial rupture. The observation of pericardial effusion was not associated with age, sex, previous myocardial infarction, atrial fibrillation or treatment with heparin. It was more often a complication of anterior than of inferior acute infarction. Patients with pericardial effusion had higher peak levels of creatine kinase and lactic dehydrogenase and a higher wall motion score index. More patients with pericardial effusion had congestive heart failure or ventricular arrhythmias, developed a ventricular aneurysm or died within 1 year after their infarction. In conclusion, pericardial effusion is frequently visualized by two-dimensional echocardiography after acute myocardial infarction and its presence is associated with an increased occurrence of complications and cardiac death.     

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 postinfarclion 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.     

Atrial diastolic friction.

A typical triphasic pericardial rub was heard in a patient with acute myocardial infarction. Phonocardiograms during atrioventricular block demonstrated a fourth rub component in atrial diastole following every sufficiently isolated P wave.     

Akute und chronisch-konstriktive Perikarditis

Acute pericarditis is an inflammatory disease of the pericardium of variable etiology. A viral infection may sometimes preceede symptoms but frequently the etiology remains unknown (idiopathic pericarditis). The disease is typically associated with left-sided chest pain and ECG abnormalities mimicking acute myocardial infarction. At physical examination the characteristic finding is a pericardial friction rub. A pericardial effusion of varying extent may be present or develop in the course of the disease. Pericardial tamponade, which may develop insidiously, represents a life-threatening complication. Pathophysiologically, filling of the cardiac chambers is impeded resulting in orthopnea, tachycardia, and eventually shock. Emergency pericardiocentesis is the treatment of choice. Constrictive pericarditis is the result of a chronic inflammation of the pericardium. Clinically it is characterized by dyspnea during exercise, symptoms of right heart failure and typical hemodynamic findings. Treatment primarily includes surgical removal of the thickened pericardium.     

Arrhythmias in acute pericarditis. An endomyocardial biopsy study

It is still controversial whether the arrhythmias in acute pericarditis are of myocardial or pericardial origin. The aim of the present study was to investigate the occurrence of arrhythmias and conduction disorders in patients with acute pericarditis with no endomyocardial biopsy evidence of myocarditis (group 1: 40 patients, 65% males, mean age 45.6 +/- 15.7 years, mean heart rate [HR] 98.7 +/- 22.2 beats per minute) in comparison to endomyocardial biopsy proven acute myocarditis/perimyocarditis (group 2: 10 patients, 3/10 with perimyocarditis, 70% males, mean age 46.1 +/- 15.8 years, mean heart rate 76.7 +/- 33.1 beats per minute). At the initial assessment all patients underwent comprehensive clinical work-up including echocardiography, cardiac catheterization, and endomyocardial biopsy. In all patients biventricular endomyocardial biopsy was performed using standard femoral approach and Schikumed 7 F or 8 F bioptomes. Tissue samples were stained by H & E, v. Gieson and independently reviewed by two cardiac pathologists. In addition immunohistochemistry and immunocytochemistry were performed, and only patients fulfilling Dallas and World Heart Federation criteria were selected for group 2. Comparative analysis of electrocardiograms and 24-hour Holter recordings at initial presentation revealed in group 1 vs group 2 significantly less frequent paroxysmal supraventricular tachyarrhythmias (5% vs 40%), and ventricular fibrillation (0 vs 20%), in contrast to atrial fibrillation that occurred more often (20% vs 0) (all p < 0.05). Furthermore, in the group 2 one patient died due to VF and two patients underwent ICD implantation. Low voltage (40% vs 30%) and ST/T wave changes (47.5% vs 30%), as well as the incidence of the II degree AV block (5% vs 0) and complete AV block (2.5% vs 10%) were not significantly different between the groups. In conclusion, patients with pericarditis and no endomyocardial biopsy indications of myocarditis had significantly less often life threatening rhythm disorders in contrast to patients with endomyocardial biopsy proven acute myocarditis/perimyocarditis. On the contrary, incidence of transitory atrial fibrillation was higher in acute pericarditis, than in myocarditis.     

Diagnosis and management of pericardial effusion

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 elevationof 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.     

Acute and chronic-constrictive pericarditis

Acute pericarditis is an inflammatory disease of the pericardium of variable etiology. A viral infection may sometimes precede symptoms but frequently the etiology re-mains unknown (idiopathic pericarditis). The disease is typically associated with left-sided chest pain and ECG abnormalities mimicking acute myocardial infarction. At physical examination the characteristic finding is a pericardial friction rub. A pericardial effusion of varying extent may be present or develop in the course of the disease. Pericardial tamponade, which may develop insidiously, represents a life-threatening complication. Pathophysiologically, filling of the cardiac chambers is impeded resulting in orthopnea, tachycardia, and eventually shock. Emergency pericardiocentesis is the treatment of choice. Constrictive pericarditis is the result of a chronic inflammation of the pericardium. Clinically it is characterized by dyspnea during exercise, symptoms of right heart failure and typical hemodynamic findings. Treatment primarily includes surgical removal of the thickened pericardium.     

Frequency of pericardial effusion as determined by M-mode echocardiography in acute myocardial infarction

A pericardial friction rub occurs in 6 to 16% of patients after acute myocardial infarction (AMI), but the incidence of pericardial effusion (PE) is not known. M-mode echocardiography was done 1, 3 and 5 days after AMI in 43 consecutive patients admitted within 24 hours of AMI, and PE was detected in 16 (37%). The PE was small in 7 patients, moderate in 6 and large in 3. A pericardial friction rub developed in 8 (19%), of whom only 4 had PE. Pleuritic chest pain diminished by sitting up and relieved by antiinflammatory agents developed in 12 (28%), of whom only 5 had PE. The peak creatine kinase level was significantly higher in patients with PE (1,769 +/- 1,003 U) than in those without (1,181 +/- 838 units). More patients with PE were in Killip classification II, III or IV (11 of 16 [69%] vs 9 of 27 [33%]). The presence of PE was not associated with age, site of AMI, development of Q waves, use of heparin or previous AMI. In conclusion, PE as detected by M-mode echocardiography is frequently present after AMI, and its presence is not closely associated with the occurrence of a pericardial friction rub or typical pericardial pain.     

Factors associated with persistent and transient fascicular blocks in anterior wall acute myocardial infarction

To determine the factors associated with persistent and transient fascicular blocks, 144 patients with Q-wave anterior wall acute myocardial infarction (AMI) were studied. Thirty-three patients had new onset of fascicular block considered to be a consequence of AMI. Multivariate analysis using 16 clinical variables revealed that the number of asynergic segments, serum potassium level and pericardial rub were significant factors related to the occurrence of fascicular block. Among the 33 patients with fascicular block, 18 had persistent (group 1) and 15 had transient (group 2) fascicular blocks. When the 2 groups with fascicular block were compared, group 1 had significantly more asynergic segments than group 2 (4.7 +/- 1.2 vs 3.7 +/- 1.6, respectively), whereas pericardial rubs were observed significantly more in group 2 (67%) than in group 1 (28%). Therefore, the inflammatory process of AMI was 1 of the mechanisms related to the occurrence of a transient fascicular block and a more extensive myocardial necrosis was associated with a persistent fascicular block.     

Regional Pericarditis: A Review of the Pericardial Manifestations of Acute Myocardial Infarction

Regional pericarditis has been described in several settings, but occurs most frequently after transmural myocardial infarction. While the diagnosis remains elusive, it must be considered in all patients with recurrent chest pain following acute myocardial infarction (AMI). Pericarditis classically presents with positional chest pain, a pericardial friction rub, diffuse ST‐segment elevation, and PR depression, but regional ECG changes associated with infarction‐associated pericarditis sometimes exist. Given the magnitude and frequency of AMI, it is imperative to be aware of the myriad of pericardial manifestations of myocardial injury. An illustrative case and a comprehensive review of the literature will be provided. Copyright © 2009 Wiley Periodicals, Inc.     

Relationship between electrocardiographically estimated infarct size and clinical findings in anterior myocardial infarction

In 292 patients with anterior myocardial infarction (MI) and no previous MI the electrocardiographically estimated infarct size was correlated with clinical findings during hospitalization and 3-month follow-up. Patients with ECG-defined transmural MI had a higher incidence of different types of complications, such as congestive heart failure (CHF), hypotension, pericarditis, and a longer duration of hospitalization than patients with nontransmural MI. In a subgroup including 182 patients of the total series, a precordial map containing 24 electrodes was used. The sum of R waves (ΣR), the sum of Q waves (ΣQ), the number of Q waves, and ΣR-ΣQ were calculated 4 days after arrival in hospital to estimate the size of infarction. There was generally a correlation between these ECG variables and different clinical findings, such as incidence of CHF, hypotension, pericarditis, and the duration of hospitalization. It is concluded that the ECG determined infarct size in anterior MI in a majority of patients correlates with the incidence of different types of complications in acute myocardial infarction. In the individual patient, however, the risk of developing complications cannot be predicted by ECG changes.     

Pericardial involvement in acute myocardial infarction

The incidence of both early postinfarction pericarditis and post-myocardial infarction (Dressler's syndrome) appears to be declining. Pericardial pain and pericardial friction rub define early postinfarction pericarditis and usually develop on day 2 or 3 after a transmural myocardial infarction. The clinical course is benign, and the prognosis of the patient is not altered by development of this complication. Pericardial effusions have been found in as many as 28% of patients after acute MI. Asymptomatic pericardial effusions do not require specific therapy nor do they absolutely contraindicate the use of anticoagulation as was previously thought. The preferred form of therapy for early postinfarction pericarditis is aspirin. Avoidance of corticosteroids and NSAIDs must be considered carefully because of the reported complications of these agents. The post-myocardial infarction syndrome develops usually during the second or third week after acute MI but may be seen as early as 24 hours and as late as several months after the MI. Whether this syndrome is the result of autosensitization to myocardial antigens released into the circulation during infarction remains uncertain. Alternative hypotheses for the causation of the syndrome include the release of blood in the pericardial space and simply that the syndrome represents a prolonged and exaggerated form of early postinfarction pericarditis. Clinically, post-myocardial infarction syndrome is manifested by fever, malaise, chest pain, and the presence of a pericardial and possibly pleuropericardial friction rub. Pericardial effusion is frequently large, and, rarely, cardiac tamponade may develop and require pericardiocentesis. Treatment consists of aspirin, NSAIDs, or corticosteroids.(ABSTRACT TRUNCATED AT 250 WORDS)