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 and Pericardial Effusion: Management Update

Prompt recognition of the signs and symptoms of pericardial disease is critical so that appropriate treatments can be initiated. Acute pericarditis has a classical presentation, including symptoms, physical examination findings, and electrocardiography abnormalities. Early recognition of acute pericarditis will avoid unnecessary invasive testing and prompt therapies that provide rapid symptom relief. Non-steroidal anti-inflammatory drugs (NSAIDs) remain first-line therapy for uncomplicated acute pericarditis, although colchicine can be used concomitantly with NSAIDS as the first-line approach, particularly in severely symptomatic cases. Colchicine should be used in all refractory cases and as initial therapy in all recurrences. Aspirin should replace NSAIDS in pericarditis complicating acute myocardial infarction. Systemic corticosteroids can be used in refractory cases or in those with immune-mediated etiologies, although generally should be avoided due to a higher risk of recurrence. Pericardial effusions have many etiologies and the approach to diagnosis and therapy depends on clinical presentation. Pericardial tamponade is a life-threatening clinical diagnosis made on physical examination and supported by characteristic findings on diagnostic testing. Prompt diagnosis and management is critical. Treatment consists of urgent pericardial fluid drainage with a pericardial drain left in place for several days to help prevent acute recurrence. Analysis of pericardial fluid should be performed in all cases as it may provide clues to etiology. Consultation of cardiac surgery for pericardial window should be considered in recurrent cases and may be the first-line approach to malignant effusions, although acute relief of hemodynamic compromise must not be delayed. Constrictive pericarditis is associated with symptoms that mimic many other cardiac conditions. Thus, correct diagnosis is critical and involves identification of pericardial thickening or calcification in association with characteristic hemodynamic alterations using noninvasive and invasive diagnostic approaches. Constrictive physiology may occur transiently and resolve with medical therapy. In chronic cases, definitive therapy requires referral to an experienced surgeon for pericardiectomy.     

Cardiac tamponade complicating myocardial infarction in the era of thrombolytics and platelet IIb/IIIa: case report and literature review

Pericardial tamponade is a rare complication of acute myocardial infarction. The authors present the case of a patient with a large anterior myocardial infarction administered thrombolytics who developed postinfarction pericarditis. Because of a stuttering course with concomitant postinfarction angina, urgent angiography, leading to percutaneous transluminal coronary angioplasty and stent implantation, was performed. Administration of abciximab prior to percutaneous transluminal coronary angioplasty appears to have precipitated pericardial tamponade. The authors review the literature concerning numerous commonly utilized therapeutic options that could have contributed to the development of pericardial tamponade.     

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.     

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).     

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.     

Pericardial effusion diagnosed by echocardiography. Clinical and electrocardiographic findings in 171 patients

Clinical and electrocardiographic findings in 171 patients with pericardial effusion diagnosed by echocardiographic studies were reviewed. In 70 patients the effusion was unsuspected. There were 87 small, 50 moderate, and 31 large effusions. Cardiac tamponade was present in three patients. Congestive heart failure was the most common cause of pericardial effusion and occurred in 37 patients. Other frequently noted conditions included cardiac disease without congestive heart failure, neoplasms, acute nonspecific pericarditis, renal failure, and acute myocardial infarction. A pericardial friction rub was present in 23 patients, two-thirds of whom had moderate or large effusions. Atrial arrhythmias were common. Low voltage occurred in 31 of 136 patients and was more common with large effusions. The ability to distinguish between a small effusion and the quantity of pericardial fluid present normally is a problem requiring further clarification.     

Probable postcardiotomy syndrome following implantation of a transvenous pacemaker: report of the first case.

The syndrome of fever and pericarditis is reported following implantation of a transvenous pacemaker in a 72-year-old man. The pacemaker was placed for prophylactic reasons (i.e., presence of bifascicular block). The syndrome resolved spontaneously after over four weeks of fever and a pericardial friction rub. Perforation of the right ventricle, although not recognized in this patient, is a complication which occurs with passage of a transvenous pacemaker. There was no other antecedent events to explain the syndrome such as myocardial infarction or trauma to the chest.     

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 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.     

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.     

Early onset Dressler's syndrome--a study of fifteen cases

Fifteen out of 612 acute myocardial infarction patients who had onset of features of post-myocardial infarction (Dressler's) syndrome between the 3rd and 21st post-infarction days were studied. All had pericardial rub and raised ESR, 86.6% had fever, 73.3% had arthralgia and 66.7% had pleuro-pericardial pain. Early onset Dressler's syndrome (EODS) was found to be more common in anterior wall myocardial infarction, to occur earlier in second infarctions and in diabetics, and to occur most commonly between the 6th and 10th post-infarction days. It was concluded that EODS is an occasional cause for recurrent chest pain after acute myocardial infarction.     

Constrictive pericarditis after myocardial infarction. Sequela of anticoagulant-induced hemopericardium

Hemopericardium developed following adequate (and not excessive) anticoagulation in a patient with acute transmural anterior myocardial infarction and an early pericardial friction rub. Drainage of a bloody effusion by pericardiocentesis did not prevent progression to constrictive pericarditis within one year. The clinical features of this case and of the only two other similar occurrences reported in the medical literature are described and lead to a discussion of therapeutic and preventive measures.     

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.     

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.     

Transient syncope, left bundle branch block and first degree atrioventricular block after "pill-in-the-pocket" administration

Postcardiac injury syndrome (PCIS) is a common complication after cardiac surgery and myocardial infarction which is defined as a late developing pleuropericarditis accompanied by a friction rub, elevated inflammation markers and pericardial or pleural effusion. Although almost all of the cases follow a major cardiac operation or myocardial infarction, and are called as postpericardiotomy syndrome (PPS) and postmyocardial infarction syndrome (PMIS), unusual presentations after minor cardiac insults, have also been reported in the literature. We have described an unusual case of PCIS with typical clinical, laboratory, echocardiographic findings that occurred after a prolonged and complicated stent implantation procedure.     

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.     

Factors associated with atrial fibrillation in Q wave anterior myocardial infarction

To elucidate the role of inflammatory and hemodynamic factors in the genesis of atrial fibrillation in acute myocardial infarction, 228 patients with a first Q wave anterior myocardial infarction were studied. Forty-nine patients had pericarditis (detection of pericardial rub by careful auscultation), and 36 patients had echocardiographically demonstrated hydropericardium (presence of pericardial effusion without pericardial rub). During the first 3 days after admission, transient episodes of atrial fibrillation were observed in 10 patients (20%) with pericarditis (group 1), 15 patients (42%) with hydropericardium (group 2), and 20 patients (14%) without pericarditis and hydropericardium (group 3). Although there was no significant difference in the incidence of atrial fibrillation between groups 1 and 3, patients in group 2 had a significantly higher incidence of atrial fibrillation than those in groups 1 and 3. Pulmonary capillary wedge pressure and the number of advanced asynergic segments were found to be the important factors discriminating the three groups by multivariate analysis. Therefore atrial fibrillation after acute Q wave anterior infarction was not related to the inflammatory infiltration involving the atria but to the increase in atrial pressure resulting from hemodynamic change caused by more extensive myocardial damage.     

Pericardial disease in scleroderma (systemic sclerosis)

A review of the records of 210 patients with scleroderma seen between 1952 and 1972 revealed two clinical patterns of pericardial disease in 15 patients: (1) Chronic pericardial effusion (11 patients), confirmed by roentgenography and ultrasound, occurred in association with dyspnea, Raynaud's syndrome, cardiomegaly, congestive heart failure and pleural effusion in the absence of renal failure. In three patients hemodynamic signs of pulsus paradoxus, Kussmaul's sign or pulsus alternans developed. In six patients with chronic effusion renal failure developed within 6 months, an incidence severalfold higher than expected in the scleroderma population at large. (2) Acute pericarditis (four patients) was associated with dyspnea, chest pain, pericardial friction rub, fever, cardiomegaly and elevated latex fixation titers (in two of four patients).Pericardial disease is a recognizable clinical entity in scleroderma and should be considered in all patients with cardiomegaly, congestive heart failure or chest pain. In 34 autopsy studies, the incidence of pericardial involvement (62 per cent) exceeded the incidence of significant myocardial fibrosis (30 per cent); thus pericardial scleroderma represents a relatively common form of cardiac involvement in this diffuse connective tissue disease.