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)     

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.     

The postcardiac injury syndromes.

Late pericarditis following myocardial infarction, cardiac surgery, or trauma is referred to as postmyocardial infarction syndrome (PMIS) or postcardiotomy syndrome (PCS), respectively. The term postcardiac injury syndrome (PCIS) is used to encompass both these entities. PCIS is characterized by fever, pleuropericardial pain, pericarditis, and pulmonary involvement. Abnormal laboratory findings include leukocytosis, high sedimentation rate, and chest x-ray abnormalities of pleural effusion with or without pulmonary infiltrates. Evidence supports an immunopathic etiology; viruses may play a contributing role. The course is benign but rare complications include tamponade, constriction, anemia, and coronary bypass graft occlusion. Anti-inflammatory agents are helpful; indo-methacin and steroids are preferably avoided. Rarely, PMIS-like syndrome may occur following pulmonary embolism. Anticoagulation and steroids have been used successfully in the latter situation.     

Right ventricular infarction

Right ventricular infarction commonly occurs in association with acute inferior left ventricular infarction, but is uncommon when infarction involves other areas of the left ventricle. Evidence of right ventricular infarction often can be detected by physical examination, electrocardiography, echocardiography, or radionuclide ventriculography. However, hemodynamically significant infarction (i.e., hypotension or shock) is much less frequent, occurring in approximately 10% of patients with other evidence of right ventricular infarction. Right ventricular infarction increases ventricular stiffness, thereby impeding diastolic filling. This results in hemodynamic changes similar to those found in constrictive pericarditis: elevated systemic venous pressure, a Y descent greater than the X descent, and an inspiratory increase in venous pressure. The increase in venous pressure generally equals or even exceeds left atrial pressure. When hypotension or shock occurs, expansion of vascular volume is generally employed as initial therapy. In nonresponders, dobutamine or similar inotropic agents may be helpful. The prognosis during the acute phases is guarded, but, in survivors, prognosis is favorable and generally related to the extent of left ventricular involvement.     

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)     

Inadvertent thrombolytic therapy for cardiovascular diseases masquerading as acute coronary thrombosis

We report three cases of inadvertent thrombolytic administration to patients with cardiovascular diagnoses masquerading as acute coronary thrombosis presenting to a tertiary care private hospital. Despite a final diagnosis of myocarditis, aortic dissection, and pericarditis, the initial presentation and electrocardiogram were believed to indicate an acute myocardial infarction due to coronary thrombosis. Intravenous thrombolytic agents were administered early in their presentation. Cardiac catheterization in two of the patients revealed normal coronary arteriography and in the third patient confirmed an aortic dissection. The patient with an aortic dissection died while the other two recovered without adverse consequences of the thrombolytic agents. Prior reports of five patients, treated with intravenous thrombolytic agents for suspected coronary thrombosis, who proved to have a final diagnosis of pericarditis or aortic dissection are reviewed. Death or tamponade occurred in four of five. The consequences of inadvertently administering intravenous thrombolytic agents to patients with nonthrombotic cardiac disorders can be serious. If the diagnosis of acute myocardial infarction due to coronary thrombosis is uncertain, serial electrocardiograms, bedside echocardiography, or urgent cardiac catheterization may be appropriate before administering these agents.     

Recurrent delayed pericarditis after pacemaker implantation: a post-pericardiotomy-like syndrome?

INTRODUCTION: Pacemaker implantation is a usual technique in cardiology which may be followed by acute pleural effusion and delayed unusual pericarditis. CASE REPORT: We reported the case of a 67 year-old man hospitalized for faintness. Rhythmical auricular disease was diagnosed and pacemaker was implanted without immediate complication. Though pericarditis with tamponade at the day 21 will require emergency pericardiotomy surgery. A recurrent pericarditis at day 45 was treated with anti-inflammatory drugs without relapse at the end of the treatment. DISCUSSION: Repeated delayed pericarditis after pacemaker surgery may be compared to the Dressler syndrome which occurs after myocardial infarction.     

Myocardial infarction caused by Aspergillus embolization in a patient with aplastic anemia

A 38-year-old Japanese man with severe aplastic anemia had invasive pulmonary aspergillosis as a complication. He was treated with amphotericin B for six weeks, but the aspergillosis did not improve. Then he experienced a fatal myocardial infarction. An autopsy revealed disseminated aspergillosis involving pericarditis and Aspergillus embolization to the coronary arteries. This led to the acute myocardial infarction. Cardiac aspergillosis is rare, but should be included within the differential diagnosis when chest pain of unknown origin occurs in an immunosuppressed patient.     

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。     

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.     

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.     

Pericarditis

Pericarditis is a common but frequently subclinical entity. There are a number of causes, including infection, systemic illness, cardiac disease, trauma, and neoplasm. Iatrogenic causes include surgery, cardiac instrumentation, irradiation, and medications. The clinical presentation varies, depending on the cause. Chest pain and dyspnea are characteristic complaints. A typical progression of ECG changes occurs during the course of acute pericarditis. These changes occasionally require differentiation from those of acute myocardial infarction or normal variant ST segment elevation. Echocardiography is the most sensitive technique for detecting the presence of pericardial effusion. In addition, a number of echocardiographic findings are characteristic of larger effusions and cardiac tamponade. Any form of pericarditis may lead to the development of cardiac tamponade. Malignant effusion is probably the most common single cause.     

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.     

Recurrent pericarditis

Recurrent pericarditis is the most troublesome complication of pericarditis occurring in 15 to 30% of cases. The pathogenesis is often presumed to be immune-mediated although a specific rheumatologic diagnosis is commonly difficult to find. The clinical diagnosis is based on recurrent pericarditis chest pain and additional objective evidence of disease activity (e.g. pericardial rub, ECG changes, pericardial effusion, elevation of markers of inflammation, and/or imaging evidence of pericardial inflammation by CT or cardiac MR). The mainstay of medical therapy for recurrent pericarditis is aspirin or a non-steroidal anti-inflammatory drug (NSAID) plus colchicine. Second-line therapy is considered after failure of such treatments and it is generally based on low to moderate doses of corticosteroids (e.g. prednisone 0.2 to 0.5 mg/kg/day or equivalent) plus colchicine. More difficult cases are treated with combination of aspirin or NSAID, colchicine and corticosteroids. Refractory cases are managed by alternative medical options, including azathioprine, or intravenous human immunoglobulins or biological agents (e.g. anakinra). When all medical therapies fail, the last option may be surgical by pericardiectomy to be recommended in well-experienced centres. Despite a significant impairment of the quality of life, the most common forms of recurrent pericarditis (usually named as “idiopathic recurrent pericarditis” since without a well-defined etiological diagnosis) have good long-term outcomes with a negligible risk of developing constriction and rarely cardiac tamponade during follow-up. The present article reviews current knowledge on the definition, diagnosis, aetiology, therapy and prognosis of recurrent pericarditis with a focus on the more recent available literature.     

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.     

Cardiovascular complications of thrombolytic therapy in patients with a mistaken diagnosis of acute myocardial infarction

Thrombolytic drugs given to patients with a mistaken diagnosis of acute myocardial infarction could produce adverse effects, although no such cases have been reported. Two patients treated with intravenous streptokinase for presumed but nonexistent acute myocardial infarction are described. Pericardial tamponade developed in both patients, in one after aortic dissection and in the other after pericarditis. Both required surgery; one died. Symptoms and electrocardiographic abnormalities mimicking acute myocardial infarction may be caused by non-coronary syndromes. In such cases, treatment with thrombolytic agents may exacerbate the underlying disease process and produce cardiovascular complications.     

Acute pleurisy revealing post-myocardial infarction syndrome

We report a case of Dressler's syndrome in which the diagnosis was made following an investigation of pleurisy which the laboratory data revealed as inflammatory. A myocardial infarction which had occurred two months earlier had passed unnoticed. The principal value of this case was to draw attention to the syndrome which may initially be a pleurisy but also clinically the picture may mimic pneumonia, both alone or together may be associated with classical pericarditis. Pleurisy occurs in Dressler's syndrome but it is rarely the presenting diagnosis as the cardiac picture tends to predominate.     

Technetium-99m stannous pyrophosphate myocardial scintigrams in pericardial disease

Technetium-99m stannous pyrophosphate (^99mTc-PYP) myocardial scintigrams were obtained in 35 acute pericarditis and in three chronic constrictive pericarditis patients. Thirteen of 35 acute pericarditis patients (37%) and one of three chronic constrictive pericarditis patients (33%) had abnormal scintigrams (a diffuse pattern in eight patients and a regional pattern in six patients). Of the 17 acute pericarditis patients with classic ST-segment changes of acute pericarditis, 10 (56%) had abnormal scintigrams compared to three of 17 patients (18%) without these ECG change (P < 0.02). These data indicate that pericardial disease may cause an abnormal scintigram. Therefore, one must rule out pericardial disease before concluding that a positive scintigram is due to acute myocardial infarction.     

Pericardial involvement in end-stage renal disease

Pericardial involvement in end-stage renal disease (ESRD) is manifested most commonly as acute uremic or dialysis pericarditis and infrequently as chronic constrictive pericarditis. The causes of uremic and dialysis pericarditis remain uncertain. The clinical and laboratory manifestations of acute pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis in patients with chronic renal failure are similar to those observed in nonuremic patients with similar pericardial involvement, except that chest pain occurs less frequently in those with ESRD. Therapeutic interventions for acute uremic or dialysis pericarditis with or without pericardial effusion include intensive hemodialysis, pericardiocentesis (infrequently used), pericardiostomy with or without instillation of intrapericardial glucocorticoids, pericardial window, and pericardiectomy. Chronic constrictive pericarditis is treated with pericardiectomy.