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.     

Pulmonary edema following pericardiotomy for cardiac tamponade

A 57-year-old man with a history of a previous myocardial infarction presented with acute cardiac tamponade due to malignant pericardial effusion. Immediately following emergency surgical drainage of the pericardium by subxiphoid window, acute pulmonary edema developed. The sudden increase in venous return following the release of cardiac compression may result in this rare complication. Gradual removal of pericardial fluid under hemodynamic monitoring is advisable, particularly in patients with preexisting heart disease.     

Successful invasive management and surgical repair of subacute ventricular rupture complicating myocardial infarction

We describe a patient following acute myocardial infarction with a protracted clinical course presenting transient episodes of hypotension, who eventually developed cardiac tamponade. Echocardiography demonstrated pericardial effusion and emergency pericardiocentesis revealed blood. The patient's condition was stabilized and she underwent emergency thoracotomy with successful repair of left ventricular rupture. We discuss the literature and suggest an approach for management of patients with suspected ventricular rupture after myocardial infarction.     

Subacute rupture of the free left ventricular wall following acute myocardial infarction. Successful surgery in a case

Free left ventricular wall rupture following acute myocardial infarction usually results in cardiac tamponade and sudden death. Occasionally, the bleeding into the pericardial sac is arrested by the surrounding pericardial tissue causing formation of a pseudoaneurysm. The case herein reported presented with a refractory pericardial effusion 1 month after an anterior myocardial infarction. While echocardiography failed to reveal a pseudoaneurysm or to localize a rupture, cineventriculography disclosed the diagnosis of a minimal rupture of the left ventricular free wall. The patient was successfully treated by surgery.     

Diagnosis of subacute ventricular wall rupture after acute myocardial infarction: sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria.

When ventricular free wall rupture after acute myocardial infarction is not followed by sudden death, it is referred to as subacute ventricular rupture. The sensitivity and specificity of clinical, hemodynamic and echocardiographic diagnostic variables obtained at bedside are unknown and were therefore prospectively studied in 1,247 consecutive patients with acute myocardial infarction including 33 patients with subacute ventricular rupture diagnosed at operation (group A) and 1,214 patients without ventricular rupture (at operation, postmortem study or at discharge) (group B). The incidence of syncope, recurrent chest pain, hypotension, electromechanical dissociation, cardiac tamponade, pericardial effusion, high acoustic intrapericardial echoes, right atrial and right ventricular wall compression identified in two-dimensional echocardiograms and hemopericardium demonstrated during pericardiocentesis was higher in group A than in group B (p less than 0.00001). The presence of cardiac tamponade, pericardial effusion greater than 5 mm, high density intrapericardial echoes or right atrial or right ventricular wall compression had a high diagnostic sensitivity (greater than or equal to 70%) and specificity (greater than 90%). The number of false positive diagnoses was always high for each diagnostic variable alone (greater than 20%), but the combination of clinical (hypotension), hemodynamic (cardiac tamponade) and echocardiographic variables allowed a sensitivity of greater than or equal to 65% with a small number of false positive diagnoses (less than 10%) and provided useful information for therapeutic decisions. The diagnosis of subacute ventricular rupture requires a surgical decision. Twenty-five (76%) of the 33 patients with subacute ventricular rupture survived the surgical procedure and 16 (48.5%) are long-term survivors. Thus, subacute ventricular wall rupture is a relatively frequent complication after acute myocardial infarction that can be accurately diagnosed and successfully treated.     

Free-wall rupture during the acute phase of myocardial infarction. Apropos of 2 cases surgically treated with success

The authors report two cases of cardiac rupture during acute myocardial infarction successfully treated surgically. In the first case, rupture occurred 7 days after hospital admission for anteroseptal myocardial infarction. The patient developed sudden cardiogenic shock with signs of venous hypertension without left ventricular failure. The second patient was admitted for syncopal chest pain with transient hypotension which regressed after volume repletion and pressor amine therapy. On admission, the patient had signs of cardiac tamponade. The ECG showed recent inferolaterobasal myocardial infarction. In both cases the diagnosis was made by 2D echocardiography which showed voluminous circumferential pericardial effusions probably due to haemorrage, with an image very suggestive of a blood clot in the effusion of the second patient. The two patients underwent emergency cardiac surgery and both survived with a 4 and 1.5 month follow-up respectively. These two cases confirm the value of 2D echocardiography as an emergency bedside procedure for the diagnosis of cardiac rupture, especially when images of intrapericardial thrombosis are observed, as in our second patient. In addition, the first case raises once again the question of the role of late thrombolysis as a predisposing factor of cardiac rupture at a time when this technique is proposed up to 24 hours after the onset of symptoms.     

Cardiac tamponade early after thrombolysis for acute myocardial infarction: a rare but not reported hemorrhagic complication

Among 392 consecutive patients admitted for acute myocardial infarction and treated with thrombolytic drugs, 4 patients (1%) developed an early hemorrhagic pericardial effusion (without ventricular wall rupture) evolving within 24 h to cardiogenic shock consequent to cardiac tamponade. They all suffered from a large anterior myocardial infarction treated within 4 h after onset of symptoms with intravenous anisoylated plasminogen streptokinase activator complex (one case), recombinant tissue-type plasminogen activator (rt-PA) (two cases) or streptokinase (one case), anticoagulation with heparin (all cases) and aspirin (three cases). As soon as pericardial effusion was established by echocardiography, emergency percutaneous pericardiocentesis was performed at the bedside 20 +/- 6 h after thrombolytic therapy was started. This corrected immediately the clinical and hemodynamic status of each patient and a catheter was left in the pericardial space for 34 +/- 18 h. Thus, in the presence of unexplained clinical and hemodynamic deterioration occurring during the first 24 h after thrombolytic treatment of a large myocardial infarction, cardiac tamponade should be suspected. Immediate percutaneous pericardiocentesis followed by continuous drainage is a simple and definitive treatment for this complication.     

Right ventricular infarction. Clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction.

Twelve patients with a clinical diagnosis of right ventricular infarction are described. All had acute inferior wall myocardial infarction associated with the bedside findings of jugular venous distension, clear lungs on auscultation, and arterial hypotension. Hemodynamically, there was elevation of right-sided filling pressures not explained by normal or minimally elevated pulmonary wedge pressures. Four patients had an incorrect diagnosis of acute cardiac tamponade. However, a review of the data showed that the hemodynamic features of right ventricular infarction more closely resemble those of pericardial constriction, a point that may be helpful in distinguishing right ventricular infarction from cardiac tamponade. Invasive and noninvasive techniques that exclude the presence of pericardial fluid and suggest enlargement and abnormal contractility of the right ventricle were helpful in establishing the diagnosis of right ventricular infarction in several patients.     

Pericardial effusion and tamponade

Pericardial effusion may occur as a result of a variety of clinical conditions, including viral, bacterial, or fungal infections and inflammatory, postinflammatory, autoreactive, and neoplastic processes. More common causes of pericardial effusion and tamponade include malignancy, renal failure, viral and bacterial infectious processes, radiation, aortic dissection, and hypothyroidism. It can also occur after trauma or acute myocardial infarction (as in postpericardiotomy syndrome following cardiac or thoracic surgery) or as an idiopathic pericardial effusion. Although pericardial effusion is common in patients with connective tissue disease, cardiac tamponade is rare. Among medical patients, malignant disease is the most common cause of pericardial effusion with tamponade. Table 1 shows the causes of pericardial tamponade. The effusion fluid may be serous, suppurative, hemorrhagic, or serosanguineous. The pericardial fluid can be a transudate (typically occurring in patients with congestive heart failure) or an exudate. The latter type, which contains a high concentration of proteins and fibrin, can occur with any type of pericarditis, severe infections, or malignancy. Once the diagnosis of pericardial effusion has been made, it is important to determine whether the effusion is creating significant hemodynamic compromise. Asymptomatic patients without hemodynamic compromise, even with large pericardial effusions, do not need to be treated with pericardiocentesis unless there is a need for fluid analysis for diagnostic purposes (eg, in acute bacterial pericarditis, tuberculosis, and neoplasias). The diagnosis of pericardial effusion/tamponade relies on a strong clinical suspicion and is confirmed by echocardiography or other pericardial imaging modalities. Alternatively, when the diagnosis of cardiac tamponade is made, there is a need for emergency drainage of pericardial fluid by pericardiocentesis or surgery to relieve the hemodynamic compromise. Following pericardiocentesis, it is necessary to prevent recurrence of tamponade. Intrapericardial injection of sclerosing agents, surgical pericardiotomy, and percutaneous balloon pericardial window creation are techniques used to prevent reaccumulation of pericardial fluid and recurrence of cardiac tamponade.     

Oozing type cardiac rupture repaired with percutaneous injection of fibrin-glue into the pericardial space: case report

Two patients, a 56-year-old man and an 81-year-old woman who were admitted to hospital because of anteroseptal acute myocardial infarction, were initially treated successfully with direct percutaneous transluminal coronary angioplasty. However, both patients later developed sudden cardiogenic shock due to cardiac tamponade caused by left ventricular free wall rupture (LVFWR). Prompt, life-saving pericardiocentesis was performed, then fibrin-glue was percutaneously injected into the pericardial space. After the procedure, there was no detectable pericardial effusion on echocardiography and the hemodynamic state became stable. The surgical treatment was the standard procedure for LVFWR, but percutaneous fibrin-glue therapy can also be considered for oozing type LVFWR.     

Survival of an octogenarian after rupture of the left ventricular free wall caused by myocardial infarction

Left ventricular free wall rupture is an uncommon complication after a myocardial infarction that is associated with a high mortality rate from pericardial tamponade, especially in the elderly. Early recognition and management of this clinical entity affects the outcome; therefore, a high index of suspicion is imperative. We present a case of an 80-year-old man admitted with myocardial infarction, who had subsequent findings of left ventricular free wall rupture complicated by pericardial tamponade. Emergent surgical repair led to successful recovery. A brief overview of the clinical presentation, diagnosis, and management of this challenging and potentially fatal complication is presented.     

Oozing-type of left ventricular rupture treated under percutaneous cardiopulmonary support without surgical repair.

A 65-year-old man was admitted to the National Defense Medical College Hospital for acute anterolateral myocardial infarction and cardiogenic shock. Emergency coronary angiography demonstrated occlusion of the proximal left anterior descending artery. Primary percutaneous transluminal coronary angioplasty (PTCA) was successfully performed with the support of intra-aortic balloon pumping (IABP) and medical treatment to stabilize the patient's blood pressure. On the second hospital day, the patient suffered cardiac tamponade. Pericardiocentesis showed bloody fluid and revealed that an oozing-type of left ventricular rupture had occurred after the myocardial infarction. Cardiogenic shock persisted after successful removal of the pericardial effusion. Although the heparinization required during percutaneous cardiopulmonary support (PCPS) can increase pericardial effusion, PCPS was initiated to correct the systemic hypoperfusion; a surgical team was on standby in case massive pericardial effusion resulted, but fortunately that did not occur, and cardiac function recovered. The patient was weaned successfully from PCPS and IABP and has remained in a satisfactory condition for over 1 year. PCPS contributed to the patient's recovery from cardiac shock and may have decreased the effusion from the oozing-type rupture by reducing ventricular wall tension.     

Repair of post-infarct left ventricular rupture with pericardial patch]

The devolpment of a left ventricular rupture after myocardial infarction is not a rare complication. We report a case of 70-year-old male patient with clinical and instrumental signs of cardiac tamponade after left ventricular rupture. We repaired this lesion with pericardial patch and biological Glue without extracorporeal circulation and sutureless.     

Prompt Recognition of Left Ventricular Free-Wall Rupture Aided by the Use of Contrast Echocardiography

In the modern period of reperfusion, left ventricular free-wall rupture occurs in less than 1% of myocardial infarctions. Typically, acute left ventricular free-wall rupture leads to sudden death from immediate cardiac tamponade. We present the case of a 59-year-old woman who sustained a posterior-wall myocardial infarction and subsequent cardiac arrest with pulseless electrical activity. A bedside transthoracic echocardiogram showed pericardial effusion with cardiac tamponade. Emergency pericardiocentesis yielded 500 mL of blood, and spontaneous circulation returned. Contrast-enhanced echocardiograms revealed inferolateral akinesis and a new, small myocardial slit with systolic extrusion of contrast medium, consistent with left ventricular free-wall rupture. During immediate open-heart surgery, a small hole in an area of necrotic tissue was discovered and repaired. This case highlights the usefulness of bedside contrast-enhanced echocardiography in confirming acute left ventricular free-wall rupture and enabling rapid surgical treatment.     

Case Report: Cardiac Tamponade Resembling an Acute Myocardial Infarction as the Initial Manifestation of Metastatic Pericardial Adenocarcinoma

Pericardial malignancies are uncommon, usually metastatic, linked to terminal oncology patients, and rarely diagnosed premortem. A very small number of patients will develop signs and symptoms of malignant pericardial effusion as initial clinical manifestation of neoplastic disease. Among these patients, a minority will progress to a life-threatening cardiac tamponade. It is exceedingly rare for a cardiac tamponade to be the unveiling clinical manifestation of an unknown malignancy, either primary or metastatic to pericardium. We present the case of a 50-year-old male who was admitted to the emergency department with an acute myocardial infarction diagnosis that turned out to be a cardiac tamponade of unknown etiology. Further studies revealed a metastatic pericardial adenocarcinoma with secondary cardiac tamponade. We encourage considering malignancies metastatic to pericardium as probable etiology for large pericardial effusions and cardiac tamponade of unknown etiology.     

Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990s?

STUDY OBJECTIVES: The decrease in incidence of tuberculosis, along with the increase in invasive cardiovascular procedures, may have changed the frequency of causes of bloody pericardial effusion associated with cardiac tamponade, although this is not yet recognized by medical textbooks. We analyzed the causes of bloody pericardial effusion in the clinical setting of cardiac tamponade in the 1990s; patients' survival; the effect of laboratory results on discharge diagnosis; and how often bloody pericardial effusion is a presenting manifestation of a new malignancy or tuberculosis. DESIGN: Retrospective, observational, single-center study. SETTING: A community hospital. PATIENTS: The charts of all patients who underwent pericardiocentesis for cardiac tamponade and had bloody pericardial effusion were retrospectively reviewed. RESULTS: Of 150 patients who had pericardiocentesis for relieving cardiac tamponade, 96 patients (64%) had a bloody pericardial effusion. The most common cause of bloody pericardial effusion was iatrogenic disease (31%), namely, secondary to invasive cardiac procedures. The other common causes were malignancy (26%), complications of atherosclerotic heart disease (11%), and idiopathic disease (10%). Tuberculosis was detected as a cause of bloody pericardial effusion in one patient and presumed to be the cause in another patient. Bloody pericardial effusion was found to be a presenting manifestation of a newly diagnosed malignancy in two patients. The patients in the idiopathic and iatrogenic groups were all alive and had no recurrence of pericardial effusion at 24 +/- 27 and 33 +/- 21 months after hospital discharge, respectively, whereas 80% of patients with malignancy-related bloody effusions died within 8 +/- 6 months. CONCLUSIONS: In a patient population that is reasonably representative of that in most community hospitals in the United States, the most common cause of bloody pericardial effusion in patients with signs or symptoms of cardiac tamponade is now iatrogenic disease. Of the noniatrogenic causes, malignancy, complications of acute myocardial infarction, and idiopathic disease predominated. Hemorrhagic tuberculous pericardial effusions are uncommon and may likely reflect a low incidence of cardiac tuberculosis in community hospitals in the United States.     

Contrast echocardiography for detection of incomplete rupture of the left ventricle after acute myocardial infarction

Myocardial rupture is a major complication after acute myocardial infarction. With complete rupture of the free left ventricular wall cardiac tamponade occurs with fatal outcome in most cases. With partial rupture, however, hemorrhage is slower, allowing days or weeks for diagnosis. Survival of these patients strongly depends on early recognition of this complication followed by immediate surgical intervention. Echocardiography is the diagnostic tool of choice to detect myocardial rupture with consecutive hemopericardium but diagnosis remains difficult even if suspected.We describe the case of a patient with inferior infarction who presented with cardiogenic shock, echocardiographic signs of pericardial effusion and abnormal motion and myocardial irregularities of the inferior wall. With Doppler echocardiography no flow across the wall was detected. Left heart contrast echocardiography confirmed the diagnosis of suspected myocardial rupture by clear deliniation of the defect. Immediate surgical repair was successfully performed in this patient with favorable long-term outcome. Thus, echocardiography early after acute myocardial infarction is useful in detecting subsequent complications and the use of contrast echocardiography should be considered in suspected myocardial rupture.     

Ventricular free wall rupture following acute myocardial infarction: a two-dimensional echocardiographic assessment

To assess the usefulness of two-dimensional echocardiography (2DE) in diagnosing ventricular free wall rupture following acute myocardial infarction, we studied the 2DE findings and the clinical pictures of seven consecutive patients with ventricular free wall rupture confirmed at the time of surgery or autopsy. Three patients had acute rupture; four, subacute rupture. All patients apparently had circulatory collapse despite continuing electrical activity at the onset of cardiac rupture. Four patients with subacute rupture recovered. In all patients, mild pericardial effusion was imaged by 2DE; however, this was not characteristic for cardiac rupture. In the patients with acute rupture, active left ventricular contractions were not observed after each QRS complex of the electrocardiogram. However, weak mitral valve motion was recorded at the time of cardiopulmonary resuscitation. The interesting and constant finding in acute rupture was the right ventricular collapse observed throughout the cardiac cycle. Diastolic right ventricular collapse was consistently observed in patients with subacute rupture, immediately after recovery from cardiogenic shock. Subacute cardiac rupture is a potentially curable lesion, and the clinical features and quick 2DE confirmation of cardiac tamponade allowed immediate surgery which saved two of the four patients.     

Factors in myocardial rupture An analysis of two hundred and four cases at Los Angeles County Hospital between 1924 and 1959

The total analysis of 204 cases of myocardial rupture which occurred in the Los Angeles County Hospital was reported. Myocardial rupture rarely occurs under the age of 50 years. Although the incidence of myocardial infarction invariably is reported to be higher among men than women our material indicates that cardiac rupture is somewhat more likely to develop in women [110 women (53.9 per cent), ninety-four men (46.1 per cent)]. Myocardial rupture is relatively rare in Negro patients.

In our material reasonably good correlation was obtained between electrocardiographic indication of acute myocardial infarction and necropsy incidence of myocardial necrosis. As was anticipated, myocardial rupture occurred at or immediately adjacent to the site of necrosis. Ordinarily, myocardial ruptures occur in the left ventricle. In our series the most frequent site of rupture was in the anterior wall, especially at the junction of the anterior wall and the septum.

Average survival time for twenty-one patients admitted to the hospital within 6 hours of the clinical onset of myocardial infarction was 9 days, whereas average survival time for twentyone patients hospitalized 7 hours or longer after the myocardial infarction was only 2.6 days. The longer survival time for patients hospitalized within the first 6 hours may be due to greater restriction of their activity in the immediate postinfarction period. Death usually is immediate in ventricular rupture, whereas in the interventricular septal rupture most of the patients survive a few days.

In the final 8 years and 3 months of our survey, the incidence of rupture following myocardial infarction has undergone a sharp decrease at the Los Angeles County Hospital. This decrease is presumably due to better management of the acute episode of myocardial infarction and more particularly to the use of vasopressor drugs and anticoagulants. Anticoagulants did not increase the incidence of the rupture but cardiac tamponade is relatively frequent in patients with myocardial rupture maintained on anticoagulants. The physician must be alert for signs of tamponade (i.e., pulsating neck veins, increase in cardiac dullness) because tamponade can be managed surgically. Except for the reduced incidence of myocardial rupture in the period of survey, the findings are in agreement with earlier reports from the same hospital.     

Images of magnetic resonance and computerized axial tomography in a case of subacute post-myocardial infarct heart rupture

In a patient with clinical and hemodynamic criteria of cardiac tamponade, during the acute phase of myocardial infarction, a two dimensional echocardiographic study showed pericardial effusion with an echo-dense mass in the pericardial space. Subacute ventricular free-wall rupture diagnosis was suspected. A cardiac computerized tomography (CT) and magnetic resonance (MR) study was made. CT showed an elevated density (32 HU) of pericardial effusion suggesting hemopericardium. RM imaging showed a very high and homogeneous signal in the pericardial space consistent with a methemoglobin phase clot. Anatomic confirmation was not possible.