A Clearer View of Effusive–Constrictive Pericarditis
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《新英格兰医药杂志》
In the 1920s and 1930s, when pericardiectomy first became an established therapy for constrictive pericarditis, surgeons recognized the condition in which pericardial effusion coexists with a visceral constrictive pericarditis (or constrictive epicarditis) (see Figure). In 1971, clinical and hemodynamic features were described that allowed the diagnosis to be made before an operation or autopsy had been performed. Since that time, individual cases have been reported nearly every year. Many of these cases, including at least one reported in the Case Records of the Massachusetts General Hospital,1 occurred in the United States. Others have been reported in at least 26 countries in Europe, Asia, Africa, and South America. However, the cases reported in this issue of the Journal by Sagristà-Sauleda et al. from Barcelona, Spain (pages 469–475), represent the first substantial series reported since 1971. The report provides new information on the prevalence of effusive–constrictive pericarditis, its causation, clinical and hemodynamic features, natural history, and response to medical and surgical therapy.
Figure. Effusive–Constrictive Pericarditis.
As illustrated in Panel A, the presence of pericardial fluid causes tamponade, and a thickened visceral pericardium (epicardium) causes constriction. Pressure tracings (Panel B) show marked and equal elevations of the pericardial and right atrial pressures before the removal of fluid; after fluid removal, the pericardial pressure is normal (increasing and decreasing with respiration), but the right atrial pressure remains elevated, indicating that there is still constriction caused by the visceral pericardium.
The most important reason for recognizing effusive–constrictive pericarditis clinically is to determine whether a visceral pericardiectomy is indicated. Drainage of the pericardial fluid or removal of only the parietal pericardium is ineffective when a visceral pericardial constriction is present. Noninvasive imaging studies provide an insufficient basis for the treatment decision, because the epicardial layer may be scarcely a millimeter thick and because increased thickness does not in itself prove the presence of constriction. Even the appearance at the time of surgery may be misleading, because the thickness of the epicardial layer may be deceptively unimpressive on visual inspection. Visceral pericardiectomy is a much more difficult and hazardous procedure than parietal pericardiectomy, but it is necessary for a good clinical result in cases of effusive–constrictive pericarditis.
The clinical diagnosis of this condition rests on the demonstration, in a patient with pericardial effusion and tamponade, that a clinical and hemodynamic picture consistent with pericardial constriction persists after the removal of enough pericardial fluid to lower the intrapericardial pressure to normal. Such a demonstration requires that pericardiocentesis be performed in a setting in which suitable recordings can be obtained of the pressures in the right heart chambers and in the pericardial space, before and after the removal of the fluid (see Figure). Such a procedure is not routine in most hospitals, a fact that probably accounts for the paucity of series in the medical literature. Indeed, many of the reported cases have been inferred by the authors on the basis of less-than-complete documentation. The report by Sagristà-Sauleda et al. is remarkable in that the requisite measurements were made routinely over a period of 16 years in patients in whom pericardiocentesis was performed in the cardiac catheterization laboratory.
It appears that any of the many causes of pericarditis may at least occasionally lead to an effusive–constrictive condition. Radiation therapy stands out as a factor that causes effusion–constriction with relative frequency, whereas cardiac surgery may cause this condition relatively less frequently. Cases of pericarditis caused by tuberculosis or another infectious disease have been relatively infrequent in reports from the United States and Europe, but such cases have been reported more frequently in other countries. Infective pericarditis is often observed to evolve over a period of days or weeks, from a stage of acute pericarditis with effusion and tamponade, through a stage of organizing exudates, and eventually to a stage of constrictive pericarditis without effusion. The effusive–constrictive condition appears to be a middle stage in this evolution. Such an evolution probably also follows other causes in which there may be a less flagrant, or even a clinically silent, initial stage of active pericarditis. Thus, the monitoring of intracardiac and intrapericardial pressures as part of a pericardiocentesis procedure is most relevant in patients who present with a subacute course of pericardial tamponade, particularly those in whom the condition is idiopathic or is related to infection, neoplasm, or rheumatologic disease.
Studies of effusive–constrictive pericarditis have provided insight into the pathophysiology of pericardial diseases. Cardiac tamponade and constrictive pericarditis are basically similar in restricting the filling of the heart and raising the systemic and pulmonary venous pressures. The venous-pressure waveforms differ, however, reflecting a single wave of forward flow (during systole) in tamponade, as compared with a biphasic pattern (a lesser wave in systole and a greater wave in early diastole) in constrictive conditions. Removing the pericardial fluid from a patient with effusive–constrictive pericarditis tends to change the pattern from one more like that found in tamponade to one more like that associated with constriction.
The recognition of effusive–constrictive pericarditis should attract the attention of physicians in many specialties. The treatment options for the management of pericardial effusion range from conservative medical management, through less invasive procedures such as pericardiocentesis or balloon pericardiostomy, to more invasive procedures such as subxiphoid surgical pericardiostomy or thoracoscopic parietal pericardiectomy, to full-scale pericardiectomy by means of thoracotomy. Varying clinical circumstances, such as the presence of metastatic neoplasm, previous radiation therapy, previous cardiac surgery, and the presence of end-stage renal disease or rheumatologic disease, will affect treatment decisions. The timely recognition of the effusive–constrictive condition enables physicians to choose the most appropriate therapy.
Source Information
From the Stanford University School of Medicine, Stanford, Calif.
References
Case Records of the Massachusetts General Hospital (Case 19-1997). N Engl J Med 1997;336:1812-1819.(E. William Hancock, M.D.)
Figure. Effusive–Constrictive Pericarditis.
As illustrated in Panel A, the presence of pericardial fluid causes tamponade, and a thickened visceral pericardium (epicardium) causes constriction. Pressure tracings (Panel B) show marked and equal elevations of the pericardial and right atrial pressures before the removal of fluid; after fluid removal, the pericardial pressure is normal (increasing and decreasing with respiration), but the right atrial pressure remains elevated, indicating that there is still constriction caused by the visceral pericardium.
The most important reason for recognizing effusive–constrictive pericarditis clinically is to determine whether a visceral pericardiectomy is indicated. Drainage of the pericardial fluid or removal of only the parietal pericardium is ineffective when a visceral pericardial constriction is present. Noninvasive imaging studies provide an insufficient basis for the treatment decision, because the epicardial layer may be scarcely a millimeter thick and because increased thickness does not in itself prove the presence of constriction. Even the appearance at the time of surgery may be misleading, because the thickness of the epicardial layer may be deceptively unimpressive on visual inspection. Visceral pericardiectomy is a much more difficult and hazardous procedure than parietal pericardiectomy, but it is necessary for a good clinical result in cases of effusive–constrictive pericarditis.
The clinical diagnosis of this condition rests on the demonstration, in a patient with pericardial effusion and tamponade, that a clinical and hemodynamic picture consistent with pericardial constriction persists after the removal of enough pericardial fluid to lower the intrapericardial pressure to normal. Such a demonstration requires that pericardiocentesis be performed in a setting in which suitable recordings can be obtained of the pressures in the right heart chambers and in the pericardial space, before and after the removal of the fluid (see Figure). Such a procedure is not routine in most hospitals, a fact that probably accounts for the paucity of series in the medical literature. Indeed, many of the reported cases have been inferred by the authors on the basis of less-than-complete documentation. The report by Sagristà-Sauleda et al. is remarkable in that the requisite measurements were made routinely over a period of 16 years in patients in whom pericardiocentesis was performed in the cardiac catheterization laboratory.
It appears that any of the many causes of pericarditis may at least occasionally lead to an effusive–constrictive condition. Radiation therapy stands out as a factor that causes effusion–constriction with relative frequency, whereas cardiac surgery may cause this condition relatively less frequently. Cases of pericarditis caused by tuberculosis or another infectious disease have been relatively infrequent in reports from the United States and Europe, but such cases have been reported more frequently in other countries. Infective pericarditis is often observed to evolve over a period of days or weeks, from a stage of acute pericarditis with effusion and tamponade, through a stage of organizing exudates, and eventually to a stage of constrictive pericarditis without effusion. The effusive–constrictive condition appears to be a middle stage in this evolution. Such an evolution probably also follows other causes in which there may be a less flagrant, or even a clinically silent, initial stage of active pericarditis. Thus, the monitoring of intracardiac and intrapericardial pressures as part of a pericardiocentesis procedure is most relevant in patients who present with a subacute course of pericardial tamponade, particularly those in whom the condition is idiopathic or is related to infection, neoplasm, or rheumatologic disease.
Studies of effusive–constrictive pericarditis have provided insight into the pathophysiology of pericardial diseases. Cardiac tamponade and constrictive pericarditis are basically similar in restricting the filling of the heart and raising the systemic and pulmonary venous pressures. The venous-pressure waveforms differ, however, reflecting a single wave of forward flow (during systole) in tamponade, as compared with a biphasic pattern (a lesser wave in systole and a greater wave in early diastole) in constrictive conditions. Removing the pericardial fluid from a patient with effusive–constrictive pericarditis tends to change the pattern from one more like that found in tamponade to one more like that associated with constriction.
The recognition of effusive–constrictive pericarditis should attract the attention of physicians in many specialties. The treatment options for the management of pericardial effusion range from conservative medical management, through less invasive procedures such as pericardiocentesis or balloon pericardiostomy, to more invasive procedures such as subxiphoid surgical pericardiostomy or thoracoscopic parietal pericardiectomy, to full-scale pericardiectomy by means of thoracotomy. Varying clinical circumstances, such as the presence of metastatic neoplasm, previous radiation therapy, previous cardiac surgery, and the presence of end-stage renal disease or rheumatologic disease, will affect treatment decisions. The timely recognition of the effusive–constrictive condition enables physicians to choose the most appropriate therapy.
Source Information
From the Stanford University School of Medicine, Stanford, Calif.
References
Case Records of the Massachusetts General Hospital (Case 19-1997). N Engl J Med 1997;336:1812-1819.(E. William Hancock, M.D.)