Effusive–Constrictive Pericarditis
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《新英格兰医药杂志》
To the Editor: In their article on pericardial constriction, Sagristà-Sauleda et al. (Jan. 29 issue)1 note the critical contribution of the visceral layer of the pericardium to the pathogenesis of constrictive pericarditis. We fully agree with this point and would like to emphasize that constrictive cardiac physiology can develop even in the absence of a parietal pericardial layer. For example, a therapeutic option for the treatment of patients with mesothelioma is extrapleural pneumonectomy. If the disease is present in the left side of the chest, the lung, parietal pleura, parietal pericardium, and diaphragm are removed. Therefore, constrictive cardiac physiology due to pericarditis would seem unlikely in the absence of a parietal pericardium. In contrast, as recently reported, in about 5 percent of patients undergoing left-sided extrapleural pneumonectomy, constrictive physiology of a proliferative nature develops, with a cocoon of fibroblasts surrounding the myocardium and a need for surgical intervention.2 Cardiac decortication in such patients results in immediate vigorous contraction and expansion of the heart, suggesting the critical role of a diseased visceral pericardium in the development of cardiac constriction.
Holger K. Eltzschig, M.D.
University Clinic for Anesthesiology and Intensive Care Medicine
72076 Tübingen, Germany
David J. Sugarbaker, M.D.
Thomas W. Felbinger, M.D.
Harvard Medical School
Boston, MA 02115
felbinger@cbr.med.harvard.edu
References
Sagristà-Sauleda J, Angel J, Sánchez A, Permanyer-Miralda G, Soler-Soler J. Effusive-constrictive pericarditis. N Engl J Med 2004;350:469-475.
Byrne JG, Karavas AN, Colson YL, et al. Cardiac decortication (epicardiectomy) for occult constrictive cardiac physiology after left extrapleural pneumonectomy. Chest 2002;122:2256-2259.
To the Editor: Patients with effusive–constrictive pericarditis typically present with cardiac tamponade, but epicardial constriction is unmasked after pericardiocentesis.1,2 A hallmark of tamponade is nearly exact beat-by-beat equalization of right atrial pressure and intrapericardial pressure.2,3,4 In 11 of the 15 patients described by Sagristà-Sauleda et al., the right atrial pressure was at least 4 mm Hg greater than the intrapericardial pressure, so that tamponade was not initially predominant. This finding contrasts with the original description of this entity1 and may explain the small increase in the median cardiac index of 0.3 liter per minute per square meter after pericardiocentesis in the study by Sagristà-Sauleda et al.
Hancock, in his accompanying editorial,2 and the authors suggest that right atrial pressure and intrapericardial pressure be routinely measured during pericardiocentesis. However, as a practical matter, the diagnostic yield with respect to the detection of epicardial constriction was only 8 percent, and the need for visceral pericardiectomy was determined on the basis of the subsequent course and not simply on the basis of initial hemodynamics. Furthermore, it is likely that some patients who did not have constriction initially did have it later.
Chester M. Boltwood, Jr., M.D.
Valley Heart Associates Medical Group
Modesto, CA 95355
References
Hancock EW. Subacute effusive-constrictive pericarditis. Circulation 1971;43:183-192.
Hancock EW. A clearer view of effusive-constrictive pericarditis. N Engl J Med 2004;350:435-437.
Boltwood CM Jr. Ventricular performance related to transmural filling pressure in clinical cardiac tamponade. Circulation 1987;75:941-955.
Leimgruber PP, Klopfenstein HS, Wann LS, Brooks HL. The hemodynamic derangement associated with right ventricular diastolic collapse in cardiac tamponade: an experimental echocardiographic study. Circulation 1983;68:612-620.
To the Editor: Sagristà-Sauleda et al. and Hancock appropriately emphasize the importance of recognizing effusive–constrictive pericardial disease and the therapeutic implications of such recognition. In neither article, however, is there mention of the differentiation of constrictive pericardial disease from restrictive myocardial disease. Restrictive myocardial disease can mimic constrictive pericardial disease,1 and differentiation is important because surgical intervention in a patient who has restrictive disease is not only unwarranted but can also be fatal. One wonders whether the patient in the study who died from biventricular failure might have had restrictive myocardial disease.
Today, with the use of echocardiography2 and magnetic resonance imaging,3 differentiation between constrictive and restrictive disease is often possible and should always be pursued in cases such as those described by Sagristà-Sauleda et al. Nine of the 15 patients with effusive–constrictive disease had either idiopathic or radiation-induced pericarditis, both of which can involve the myocardium. As a result of these considerations, I think it is also important to consider and rule out restrictive myocardial disease when evaluating such patients.
Douglas R. Rosing, M.D.
National Institutes of Health
Bethesda, MD 20892-1650
rosingd@nhlbi.nih.gov
References
Kushwaha SS, Fallon JT, Fuster V. Restrictive cardiomyopathy. N Engl J Med 1997;336:267-276.
Rajagopalan N, Garcia MJ, Rodriguez L, et al. Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol 2001;87:86-94.
Giorgi B, Mollet NRA, Dymarkowski S, Rademakers FE, Bogaert J. Clinically suspected constrictive pericarditis: MR imaging assessment of ventricular septal motion and configuration in patients and healthy subjects. Radiology 2003;228:417-424.
The authors reply: Cardiac tamponade, as Dr. Boltwood reminds us, is classically defined by equal right atrial and intrapericardial pressures. However, in contrast to pure tamponade, effusive–constrictive pericarditis, in which additional cardiac compression is produced by constricting epicardium, may not always be characterized by equal right atrial and intrapericardial pressures. In fact, effusive–constrictive pericarditis is a mixed syndrome, in which one or the other of its components may predominate, as shown in Table 1 of our article. A reduction in intrapericardial pressure and an increase in transmural pressure after pericardiocentesis were apparent in our patients, indicating compression by pericardial effusion. Contrary to Dr. Boltwood's statement, in the original description by Hancock,1 intrapericardial pressure (mean, 14 mm Hg; range, 6 to 22) was lower than right atrial pressure (mean, 18 mm Hg; range, 11 to 25), which is in agreement with our findings.
We agree with Dr. Boltwood that in some patients who have tamponade without initial constriction, it may develop subsequently, and hemodynamic measurements during pericardiocentesis may not anticipate this development. However, our point is that as compared with pericardiocentesis performed at the bedside, pericardiocentesis performed in the catheterization laboratory, in addition to arguably greater safety, provides a greater amount of hemodynamic information, which is useful for the early detection of effusive–constrictive pericarditis.
Restrictive myocardial disease should indeed be considered in many instances of suspected cardiac constriction, as Dr. Rosing points out. This consideration may be particularly relevant in radiation-induced cases. In our series, a constricting epicardium was shown to be present in the seven patients who underwent surgery, including one of the patients with radiation-induced disease and the patient who died with biventricular failure. The latter patient had advanced disease, with severe congestive findings at the time of surgery. Whether the myocardium was involved as well is a matter of speculation. In addition, ruling out pericardial involvement in cases with suspected constriction by using imaging techniques is not straightforward, as shown by studies in which constricting pericardium was thin.2 This may be the case particularly when the epicardium is responsible for constriction.
The comment by Eltzschig et al. is a nice illustration of the concept that the epicardium can be responsible for cardiac constriction, as postulated in the case of effusive–constrictive pericarditis and other subacute cardiac constriction syndromes.
Jaume Sagristà-Sauleda, M.D.
Juan Angel, M.D.
Jordi Soler-Soler, M.D.
Hospital General Vall d'Hebron
08035 Barcelona, Spain
References
Hancock EW. Subacute effusive-constrictive pericarditis. Circulation 1971;43:183-192.
Talreja DR, Edwards WD, Danielson GK, et al. Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation 2003;108:1852-1857.
The editorialist replies: Differentiation of restrictive myocardial disease from constrictive pericarditis is a problem that must always be considered in patients who appear to have constrictive pericarditis. In effusive–constrictive disease, an associated restrictive myocardial disease, if present, would probably be an additional component, and the combination of the two would be particularly difficult to recognize. Combined constrictive pericarditis and restrictive myocardial disease is sometimes seen in radiation-related pericardial disease, but only rarely in pericardial disease with other causes.
Pericardial and right atrial pressures may be separated by a few millimeters of mercury in effusive–constrictive disease and also in some cases of pure tamponade, especially those that are not at the most severe end of the hemodynamic spectrum. The relative contributions of constriction and tamponade probably do vary in effusive–constrictive disease.
Even though constriction can be diagnosed later, and might even develop later, the advantage of a timely diagnosis is usually evident in clarifying the problem. The persistence of elevated venous pressure after pericardiocentesis can be mistakenly taken as an indication for repeated pericardiocentesis or for a surgical method of pericardial drainage, if it has not been demonstrated that the previous pericardiocentesis was actually successful in relieving the tamponade component (by lowering the intrapericardial pressure to a normal value). The diagnostic yield of measuring pericardial and right atrial pressures will be higher if the procedure is limited to patients with more severe clinical syndromes, those with a clinical evolution that is more subacute than acute, and those with causes such as previous radiotherapy or bacterial infection or with an idiopathic cause.
E. William Hancock, M.D.
Stanford University School of Medicine
Stanford, CA 94304
Holger K. Eltzschig, M.D.
University Clinic for Anesthesiology and Intensive Care Medicine
72076 Tübingen, Germany
David J. Sugarbaker, M.D.
Thomas W. Felbinger, M.D.
Harvard Medical School
Boston, MA 02115
felbinger@cbr.med.harvard.edu
References
Sagristà-Sauleda J, Angel J, Sánchez A, Permanyer-Miralda G, Soler-Soler J. Effusive-constrictive pericarditis. N Engl J Med 2004;350:469-475.
Byrne JG, Karavas AN, Colson YL, et al. Cardiac decortication (epicardiectomy) for occult constrictive cardiac physiology after left extrapleural pneumonectomy. Chest 2002;122:2256-2259.
To the Editor: Patients with effusive–constrictive pericarditis typically present with cardiac tamponade, but epicardial constriction is unmasked after pericardiocentesis.1,2 A hallmark of tamponade is nearly exact beat-by-beat equalization of right atrial pressure and intrapericardial pressure.2,3,4 In 11 of the 15 patients described by Sagristà-Sauleda et al., the right atrial pressure was at least 4 mm Hg greater than the intrapericardial pressure, so that tamponade was not initially predominant. This finding contrasts with the original description of this entity1 and may explain the small increase in the median cardiac index of 0.3 liter per minute per square meter after pericardiocentesis in the study by Sagristà-Sauleda et al.
Hancock, in his accompanying editorial,2 and the authors suggest that right atrial pressure and intrapericardial pressure be routinely measured during pericardiocentesis. However, as a practical matter, the diagnostic yield with respect to the detection of epicardial constriction was only 8 percent, and the need for visceral pericardiectomy was determined on the basis of the subsequent course and not simply on the basis of initial hemodynamics. Furthermore, it is likely that some patients who did not have constriction initially did have it later.
Chester M. Boltwood, Jr., M.D.
Valley Heart Associates Medical Group
Modesto, CA 95355
References
Hancock EW. Subacute effusive-constrictive pericarditis. Circulation 1971;43:183-192.
Hancock EW. A clearer view of effusive-constrictive pericarditis. N Engl J Med 2004;350:435-437.
Boltwood CM Jr. Ventricular performance related to transmural filling pressure in clinical cardiac tamponade. Circulation 1987;75:941-955.
Leimgruber PP, Klopfenstein HS, Wann LS, Brooks HL. The hemodynamic derangement associated with right ventricular diastolic collapse in cardiac tamponade: an experimental echocardiographic study. Circulation 1983;68:612-620.
To the Editor: Sagristà-Sauleda et al. and Hancock appropriately emphasize the importance of recognizing effusive–constrictive pericardial disease and the therapeutic implications of such recognition. In neither article, however, is there mention of the differentiation of constrictive pericardial disease from restrictive myocardial disease. Restrictive myocardial disease can mimic constrictive pericardial disease,1 and differentiation is important because surgical intervention in a patient who has restrictive disease is not only unwarranted but can also be fatal. One wonders whether the patient in the study who died from biventricular failure might have had restrictive myocardial disease.
Today, with the use of echocardiography2 and magnetic resonance imaging,3 differentiation between constrictive and restrictive disease is often possible and should always be pursued in cases such as those described by Sagristà-Sauleda et al. Nine of the 15 patients with effusive–constrictive disease had either idiopathic or radiation-induced pericarditis, both of which can involve the myocardium. As a result of these considerations, I think it is also important to consider and rule out restrictive myocardial disease when evaluating such patients.
Douglas R. Rosing, M.D.
National Institutes of Health
Bethesda, MD 20892-1650
rosingd@nhlbi.nih.gov
References
Kushwaha SS, Fallon JT, Fuster V. Restrictive cardiomyopathy. N Engl J Med 1997;336:267-276.
Rajagopalan N, Garcia MJ, Rodriguez L, et al. Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol 2001;87:86-94.
Giorgi B, Mollet NRA, Dymarkowski S, Rademakers FE, Bogaert J. Clinically suspected constrictive pericarditis: MR imaging assessment of ventricular septal motion and configuration in patients and healthy subjects. Radiology 2003;228:417-424.
The authors reply: Cardiac tamponade, as Dr. Boltwood reminds us, is classically defined by equal right atrial and intrapericardial pressures. However, in contrast to pure tamponade, effusive–constrictive pericarditis, in which additional cardiac compression is produced by constricting epicardium, may not always be characterized by equal right atrial and intrapericardial pressures. In fact, effusive–constrictive pericarditis is a mixed syndrome, in which one or the other of its components may predominate, as shown in Table 1 of our article. A reduction in intrapericardial pressure and an increase in transmural pressure after pericardiocentesis were apparent in our patients, indicating compression by pericardial effusion. Contrary to Dr. Boltwood's statement, in the original description by Hancock,1 intrapericardial pressure (mean, 14 mm Hg; range, 6 to 22) was lower than right atrial pressure (mean, 18 mm Hg; range, 11 to 25), which is in agreement with our findings.
We agree with Dr. Boltwood that in some patients who have tamponade without initial constriction, it may develop subsequently, and hemodynamic measurements during pericardiocentesis may not anticipate this development. However, our point is that as compared with pericardiocentesis performed at the bedside, pericardiocentesis performed in the catheterization laboratory, in addition to arguably greater safety, provides a greater amount of hemodynamic information, which is useful for the early detection of effusive–constrictive pericarditis.
Restrictive myocardial disease should indeed be considered in many instances of suspected cardiac constriction, as Dr. Rosing points out. This consideration may be particularly relevant in radiation-induced cases. In our series, a constricting epicardium was shown to be present in the seven patients who underwent surgery, including one of the patients with radiation-induced disease and the patient who died with biventricular failure. The latter patient had advanced disease, with severe congestive findings at the time of surgery. Whether the myocardium was involved as well is a matter of speculation. In addition, ruling out pericardial involvement in cases with suspected constriction by using imaging techniques is not straightforward, as shown by studies in which constricting pericardium was thin.2 This may be the case particularly when the epicardium is responsible for constriction.
The comment by Eltzschig et al. is a nice illustration of the concept that the epicardium can be responsible for cardiac constriction, as postulated in the case of effusive–constrictive pericarditis and other subacute cardiac constriction syndromes.
Jaume Sagristà-Sauleda, M.D.
Juan Angel, M.D.
Jordi Soler-Soler, M.D.
Hospital General Vall d'Hebron
08035 Barcelona, Spain
References
Hancock EW. Subacute effusive-constrictive pericarditis. Circulation 1971;43:183-192.
Talreja DR, Edwards WD, Danielson GK, et al. Constrictive pericarditis in 26 patients with histologically normal pericardial thickness. Circulation 2003;108:1852-1857.
The editorialist replies: Differentiation of restrictive myocardial disease from constrictive pericarditis is a problem that must always be considered in patients who appear to have constrictive pericarditis. In effusive–constrictive disease, an associated restrictive myocardial disease, if present, would probably be an additional component, and the combination of the two would be particularly difficult to recognize. Combined constrictive pericarditis and restrictive myocardial disease is sometimes seen in radiation-related pericardial disease, but only rarely in pericardial disease with other causes.
Pericardial and right atrial pressures may be separated by a few millimeters of mercury in effusive–constrictive disease and also in some cases of pure tamponade, especially those that are not at the most severe end of the hemodynamic spectrum. The relative contributions of constriction and tamponade probably do vary in effusive–constrictive disease.
Even though constriction can be diagnosed later, and might even develop later, the advantage of a timely diagnosis is usually evident in clarifying the problem. The persistence of elevated venous pressure after pericardiocentesis can be mistakenly taken as an indication for repeated pericardiocentesis or for a surgical method of pericardial drainage, if it has not been demonstrated that the previous pericardiocentesis was actually successful in relieving the tamponade component (by lowering the intrapericardial pressure to a normal value). The diagnostic yield of measuring pericardial and right atrial pressures will be higher if the procedure is limited to patients with more severe clinical syndromes, those with a clinical evolution that is more subacute than acute, and those with causes such as previous radiotherapy or bacterial infection or with an idiopathic cause.
E. William Hancock, M.D.
Stanford University School of Medicine
Stanford, CA 94304