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.     

Natural course of the S-T segment and QRS complex in patients with acute anterior myocardial infarction

Sums of the S-T segment elevation from the 35 lead precordial electrocardiographic map (∑ST₃₅) and Standard 6 lead precordial electrocardiogram (∑ST₆) were obtained from 20 patients after acute anterior myocardial infarction and the calculations repeated 2, 4, 12, 24, 48, 72 and 240 hours later. Q and R wave areas were summed (∑Q₃₅, ∑Q₆, ∑R₃₅ and ∑R₆). ∑ST₃₅ and ∑ST₆ values decreased significantly in patients without pericarditis 7 to 12 hours after the onset of symptoms (P < 0.02), but increased significantly from these reduced values 25 to 48 hours after the onset of symptoms. An increase in ∑ST₃₅ and ∑ST₆ (P < 0.05) occurred 13 to 24 hours after the onset of symptoms in four patients with pericarditis before a pericardial rub was heard. No significant change in ∑Q₃₅ occurred from the initial to the final map study; a decrease in ∑R₃₅ (P < 0.02) occurred only in a group of patients studied at or before 5 hours after initial symptoms. No correlation was found between the initial level of S-T segment elevation and subsequent change in Q or R wave areas except in two patients whose initial electrocardiographic studies were performed at or within 5 hours of initial symptoms. Good correlation was found between ∑ST₃₅ and ∑ST₆ (r = +0.906, P < 0.001), ∑Q₃₅ and ∑Q₆ (r = +0.864, P < 0.001), and ∑R₃₅ and ∑R₆ (r = +0.903, P < 0.001). The course of the S-T segment and QRS complex after anterior myocardial infarction depends on the time of study after initial symptoms. The Standard 6 lead precordial electrocardiogram may offer a practical alternative to the 35 lead map for patients with anterior myocardial infarction.     

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.     

Clinical characteristics of ST-segment elevation in lead V6 in patients with Q-wave acute inferior wall myocardial infarction

BACKGROUND: Precordial ST-segment depression in acute inferior infarction is well recognized, but few studies have evaluated ST-segment elevation in lateral precordial leads. The present study examined the clinical significance of ST-segment elevation in lead V6 in patients with acute Q-wave inferior myocardial infarction. METHODS: We studied the initial electrocardiography of 125 consecutive patients with acute Q-wave inferior myocardial infarction admitted to hospital within 12 h of the onset of chest pain. They were classified into two groups: group 1 = 34 patients with ST-segment elevation in lead V6; group 2 = 91 patients with no ST-segment elevation in lead V6. RESULTS: Among the seven clinical variables examined, the number of left ventricular asynergic segments (P < 0.001) and pulmonary capillary wedge pressure (P = 0.001) were related to ST-segment elevation in lead V6. The incidences of major arrhythmias (50% compared with 31%, P = 0.04), pericardial effusion (32% compared with 9%, P = 0.003), and pericardial rub (15% compared with 2%, P = 0.02) during the patients' stay in hospital were greater in group 1 than in group 2. Among the patients in group 1, the right coronary artery was the culprit artery in 22 of 24 patients (92%) with ST segment depression in lead I, whereas the circumflex artery was the culprit artery in nine of 10 patients (90%) with isoelectric or ST-segment elevation in lead I. CONCLUSION: The presence of ST-segment elevation in lead V6 in patients with acute Q-wave inferior myocardial infarction was associated with larger infarct size, and greater incidences of major arrhythmias and pericardial involvement during the patient's stay in hospital.     

Dressler-like syndrome after pulmonary embolism and infarction

Among 195 patients with pulmonary embolism admitted to our hospital, three men and three women, 16 to 65 years old, developed a pericardial syndrome five to 15 days after the onset of pulmonary embolism and infarction. Other known causes of pericarditis were ruled out by clinical history and ancillary methods. The six patients had a pericardial rub, fever, anemia, leukocytosis, and increasing sedimentation rate; four had a pericardial effusion; two had a pleural effusion. One patient, with coexisting heart disease, died after another episode of pulmonary embolism; in the other five, oral corticosteroids induced complete remission of the pericardial syndrome. This type of pericarditis deserves wider recognition.     

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.     

Coccidioidal pericarditis: a case presentation and review of the literature.

BACKGROUND: Pericardial involvement with Coccidioides immitis is an infrequent occurrence with a relatively unfavorable prognosis. METHODS: A case of coccidioidal pericarditis is presented along with a review of the medical literature on coccidioidal pericarditis to give the clinician a better understanding of the various presentations, complications and outcomes of this disease. Medline (National Library of Medicine, Bethesda) was electronically searched covering the years 1966-2003 using search words coccidioidomycosis and pericarditis. RESULTS: Sixteen patients were identified from the literature review and one new patient was added. All the patients were males with a mean age of 37.5 years. Chest pain, dyspnea and cough were the most common presenting symptoms. Five patients had evidence of pericardial tamponade, pulsus paradoxus was noted in three patients and three patients presented with pericardial constriction. One patient had Kussmaul's sign, one patient had pericardial frictional rub and another had pericardial knock. Cardiomegaly on chest x-ray was present in ten patients; EKG was noted to have low voltage in five and ST segment elevation in four patients. Delayed hypersensitivity to coccidioidal antigen was reported in nine patients and positive in eight patients. Complement fixation titers were positive in all 11 patients in whom it was assayed. Fifty-three percent of the patients with coccidioidal pericarditis died. CONCLUSION: Coccidioidal pericarditis is a rare disease entity that has a relatively unfavorable prognosis, yet many patients present with diagnostic clues to this disorder. An enhanced understanding of the clinical features of coccidioidal pericarditis may lead to improved outcomes.     

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.     

Outcome after thrombolytic therapy of nine cases of myopericarditis misdiagnosed as myocardial infarction

Anecdotal reports have suggested that cardiovascular complicationsmay occur if thrombolytic therapy is performed in cases of pericarditismisdiagnosed as acute myocardial infarction. From 1980 to 1993,47 cases of myopericarditis mimicking myocardial infarctionhave been admitted to our institution. The misdiagnosis wasmade because of clinical onset characterized by a typical chestpain, and/or localized ST segment elevation. Since 1987, nine(919 males, age 40±14 years) out of the 47 patients (19%)have been treated with a thrombolytic agent (streptokinase 419,rt-PA 519) followed by intravenous heparin. This treatment wasstarted during the pre-hospital pliase (2/9) and while in hospital(7/9). No pericardial rub was present; ST segment elevationwas mainly localized in inferior and lateral leads; no Q wavedeveloped; median creatine kinase rise was 268 units (range38 to 1280), and only one patient had a small pericardial effusion.The mean level of fibrinogen after thrombolysis was 1.72 g.l^–1 (range 0.10 to 4.50). In all cases, typical ECG cliangeswere present suggesting pericarditis with a subsequent returnto a normal ECG. No severe cardiac or pericardial complicationor arrhytlxmia occurred; only one patient developed a non-compressiveand resolvable pericardial effusion. Cardiac catheterizations(coronary and left ventricular angiographies) were normal whenperformed (5/9). Long-term follow-up (mean 46±29 months)was favourable without any coronary events. In conclusion, thrombolytictherapy was uncomplicated in our patients with myopericarditissimulating evolving myocardial infarction.     

Acute nonspecific pericarditis

In order to learn the natural history of nonspecific acute pericarditis in our environment, we studied retrospectively 50 patients seen at The Instituto Nacional de Cardiología Ignacio Chávez, between 1972-1985. The clinical history, electrocardiogram, chest x ray, laboratory findings, as well as the outpatient follow-up were analyzed. There was a history of a respiratory or gastrointestinal infection, probably viral in origin, in almost half of the cases (46%). Chest pain was present in 96% of the patients and was the most common symptom. In only half of the patients a pericardial friction rub was heard. A typical S-T elevation was found in 90% of the electrocardiograms. Arrhythmias and conduction disorders were unusual. The echocardiogram showed a pericardial effusion in seven patients and six had a pleural effusion. Only one patient developed signs of cardiac tamponade. None of the patients in this study developed a chronic constrictive pericarditis and there were no deaths. Before or after hospitalization, 14 patients (28%) had multiple episodes of chest pain suggestive of recurrent pericarditis. This study shows that nonspecific acute pericarditis seems to be a self-limited illness with a good prognosis, few recurrences and practically no complications.     

Pericardial disease in patients with cancer: The differentiation of malignant from idiopathic and radiation-induced pericarditis

Pericardial disease developed in 31 patients with a variety of malignancies. Half of the patients (58 percent) were found to have malignant pericardial involvement, 32 percent idiopathic pericarditis and 10 percent radiation-related pericarditis. Facial swelling, cardiac arrhythmias and pericardial tamponade occurred frequently in the patients with malignant pericardial disease. Fever, pericardial friction rub and improvement with nonsteroidal anti-inflammatory drugs characterized the patients with idiopathic pericarditis. Effusive-constrictive pericarditis requiring pericardiectomy was noted in patients with radiation-induced disease. Pericardiocentesis documented malignant pericardial disease in 85 percent of patients studied, while 15 percent required open biopsy for diagnosis. Specific therapy directed at malignant pericardial disease may contribute to survival up to one year in 25 percent of patients. In 40 percent of patients with idiopathic pericarditis and in the majority of patients with radiation-induced pericarditis, survival was one year with specific therapy. A systematic evaluation of pericardial disease will benefit a subset of cancer patients with idiopathic pericarditis and radiation-induced pericarditis who can be managed conservatively.     

尿毒症心包炎的临床研究

本文40例维持性血透尿毒症患者中,心包炎的发生率约为35％.除心包摩擦音外,来见其它特殊临床症状.约50％的患者无任何症状.诊断依靠超声心动图检查.查明患者有无心包积液、心包填塞、心包积液量以及心包炎及范围具有一定价值。该病需加强透析治疗,包括延长透析时间、缩短透析间隔,使用高效、高通透膜,加用血滤及血液灌流,减少肝素用量或改为腹透。本文也讨论了该病的病因.     

The normal and diseased pericardium: Current concepts of pericardial physiology,diagnosis and treatment

The past quarter century has seen remarkable contributions to understanding the role of the pericardium in health and disease and to diagnostic methods in the context of significant changes in the clinical spectrum of acute pericarditis, pericardial effusion and their sequelae. Anatomic studieshave demonstrated pericardial ultrastructure and its relation to function and delineated the pericardial lymphatics and their participation in inflammation and tamponade. Physiologic investigationshave revealed the pericardium's mechanical, membranous and ligamentous functions and its role in ventricular interaction, pericardial modification of cardiac responses during acute cardiocirculatory loading and effects on diastolic function (and, at high filling pressures, systolic function), including reduction by pericardial fluid of true filling pressure—the myocardial transmural pressure. The diastolic mean pressure plateau and phasic venoatrial pressure and flow during cardiac tamponade have been further characterized and the mechanisms producing pulsus paradoxus have been elucidated, including the importance of inspiratory increase in right ventricular filling. A far reaching compensatory response to tamponade has been revealed, particularly adrenergic stimulation, and, over time, blood volume expansion. Right heart tamponade and low pressure tamponade have been identified and the importance of the pericardium in the restrictive dynamics of right ventricular myocardial infarction has been demonstrated. Constrictive pericarditis,And the currently more common effusive-constrictive pericarditis,have been studied, in depth, clinically and hemodynamically.Cardiography in pericardial diseasenow includes M-mode and two-dimensional echographic studies, enabling rapid diagnosis and further physiologic study in cardiac tamponade and constriction. The four stages of typical electrocardiographic evolutionin acute pericarditis and atypical variants have been codified and characteristic PR segment deviations identified. The non-etiologic role of acute pericarditis in arrhythmiashas been clarified in prospective clinical and postmortem investigations. Electric alternation has been elucidated and its relation to cardiac "swinging" has been at least partly explained. Special roles now exist for contrast roentgenography, computed tomography(especially for cysts) and radionuclide imaging. Clinical advancesin pericardial disease include changes in the prevalence of established etiologies and identification of new etiologies, for example, immunopathic processes to explain recurrent pericarditis and the post-injury (including postoperative) pericardial syndromes. New forms of constriction—uremic, postoperative, radiation—have appeared in increasing numbers. The pericardial rubhas been characterized and codified, confirming a typical three-component structure (with frequent exceptions).     

Double blind randomised placebo controlled trial of adjunctive prednisolone in the treatment of effusive tuberculous pericarditis in HIV seropositive patients

OBJECTIVE—To determine the effect of adjunctive prednisolone on morbidity, pericardial fluid resolution, and mortality in HIV seropositive patients with effusive tuberculous pericarditis.
DESIGN—Double blind randomised placebo controlled trial.
SETTING—Two medical school affiliated referral hospitals in Harare, Zimbabwe.
PATIENTS—58 HIV seropositive patients aged 18-55 years with tuberculous pericarditis.
INTERVENTIONS—All patients received standard short course antituberculous chemotherapy and were randomly assigned to receive prednisolone or placebo for six weeks.
MAIN OUTCOME MEASURES—Clinical improvement, echocardiographic and radiologic pericardial fluid resolution, and death.
RESULTS—29 patients were assigned to prednisolone and 29 to placebo. After 18 months of follow up there were five deaths in the prednisolone treated group and 10 deaths in the placebo group. Mortality was significantly lower in the prednisolone group (log rank χ² = 8.19, df = 1, p = 0.004). Resolution of raised jugular venous pressure (p = 0.017), hepatomegaly (p = 0.007), and ascites (p = 0.015), and improvement in physical activity (p = 0.02), were significantly more rapid in the prednisolone treated patients. However, there was no difference in the rate of radiologic and echocardiographic resolution of pericardial effusion.
CONCLUSIONS—Adjunctive prednisolone for effusive tuberculous pericarditis produced a pronounced reduction in mortality. It is suggested prednisolone should be added to standard short course chemotherapy to treat HIV related effusive tuberculous pericarditis.


Keywords: tuberculous pericarditis; HIV infection; echocardiography; prednisolone     

Purulent pneumococcal pericarditis. A continuing problem in the antibiotic era

The clinical findings in five patients with purulent pneumococcal pericarditis are presented. Predisposing factors were untreated pneumococcal pneumonia and empyema in three patients and congenital hypogammaglobulinemia in one patient. The three patients, in whom the diagnosis was established by pericardiocentesis, recovered without sequelae after surgical drainage of the pericardium and systemic antibiotic therapy. The two remaining patients had unsuspected purulent pericarditis demonstrated postmortem.A review of 113 cases of purulent pneumococcal pericarditis since 1900 was made. A preceding pneumonia was present in 93.1 per cent of the patients; 66.6 per cent had pneumonia with empyema. Signs frequently associated with pericarditis such as a pericardial friction rub, pulsus paradoxus and an enlarged cardiac silhouette may be absent although circulatory embarrassment exists. Pericardiocentesis is mandatory to establish the diagnosis of purulent pneumococcal pericarditis. Although mortality in untreated patients was 100 per cent, the 10 patients treated with both systemic antibiotics and surgical drainage survived.     

Clinical significance of pericardial rub with regional ventricular dilatation

To elucidate the clinical characteristics associated with regional ventricular dilatation in the early phase of myocardial infarction (MI), 228 patients with acute Q-wave anterior MI were studied. Forty-nine patients (21 percent) had echocardiographically demonstrated regional ventricular dilatation (an abnormal bulge in the left ventricular contour during both systole and diastole) on the third hospital day. Careful auscultation revealed that a pericardial rub was present in 49 patients (21 patients with and 28 patients without regional ventricular dilatation) during the first three days after hospital admission. Multivariate analysis was performed to determine the relative importance of pericardial rub with six other clinical variables related to regional ventricular dilatation. Pericardial rub and cardiac output were the significant factors related to the presence of regional ventricular dilatation. Thus, a pericardial rub, in concert with impaired left ventricular function, is a physical sign associated with regional ventricular dilatation, and anatomically transmural infarction is the possible factor explaining their association.     

Pericarditis and acquired immunodeficiency syndrome

In order to evaluate the frequency and clinical features of pericarditis caused by the HIV virus, 17 patients (mean age 28 years) presenting with pericarditis were investigated at the University Clinics of Mont-Amba (Za?re), between January, 1985 and December, 1986. The clinical diagnosis of AIDS had been made on the basis of the WHO criteria. An ELISA test, a tuberculin test and a T4-lymphocyte count were performed in all patients. Cardiovascular explorations were limited to electrocardiography, radiography of the chest, echocardiography and pericardial needle aspiration. HIV pericarditis accounted for 50 p. 100 of all cases of pericarditis. It was either dry or effusive with little fluid, and its clinical signs at the early stage of AIDS were retrosternal pain and pericardial friction rub. A search for anti-HIV antibodies may be negative at that stage. Diagnostic errors can be avoided if the tuberculin test is negative and if an ELISA test is performed repeatedly at 3 weeks' intervals. Pericarditis should be counted among the minor signs of AIDS.     

Post-myocardial infarction pericarditis

Opinion statement Post-myocardial infarction pericarditis occurs in approximately 5% to 6% of patients who receive thrombolytic agents. It should be suspected in any patient with pleuropericardial pain. A pericardial friction rub may or may not be present. Differentiation of pericarditis from recurrent angina may be difficult, but a careful history and evaluation of serial electrocardiograms can help distinguish the two entities. Dressler’s syndrome, pericarditis that occurs at least 1 week following myocardial infarction, is now exceedingly rare. Most cases of pericarditis have a benign course; however, because pericarditis is associ-ated with larger infarcts, overall long-term mortality rate is increased. Rare complications include hemopericardium, cardiac tamponade, and constrictive pericarditis. Therapy is directed toward relief of pain, which usually responds well to nonsteroidal anti-inflammatory agents (eg, aspirin or ibuprofen).