Case Study
Mitral regurgitation following pericardiectomy for constrictive pericarditis
Asian Cardiovascular & Thoracic Annals 0(0) 1–4 ß The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492315593695 aan.sagepub.com
Cheng He1, Reny Suryani2, Chin Hiew2, Andrew Cheng1 and Bo Zhang1
Abstract Pericardiectomy is the only definitive treatment option for patients with constrictive pericarditis. We present the case of a 67-year-old man who developed new moderate to severe mitral regurgitation following phrenic nerve-to-phrenic nerve pericardiectomy for constrictive pericarditis. The severity of the regurgitation was followed up by serial echocardiography which showed improvement 19 days later and complete resolution at 9 months after surgery. Potential mechanisms explaining the evolution of this mitral valve dysfunction in the setting of pericardiectomy are postulated.
Keywords Mitral valve insufficiency, Pericardiectomy, Constrictive pericarditis
Introduction Constrictive pericarditis is a chronic inflammatory process that results in a densely thickened pericardium that compresses the heart, limiting diastolic ventricular filling. The etiology is idiopathic in the majority of cases. Pericardiectomy is the only definitive treatment option, with most patients achieving symptomatic relief following the procedure. We report the unusual case of a 66-year-old man with new severe mitral regurgitation (MR) immediately following pericardiectomy for constrictive pericarditis. Spontaneous resolution of MR was observed on echocardiography 9 months after surgery. Potential mechanisms resulting in this self-reverting clinical entity are discussed.
Case report A 67-year-old man was admitted with a 3-day history of fever, central abdominal pain, and raised inflammatory markers, on the background of suspected recent pneumonia for which he had received oral antibiotics. No significant medical or surgical history was noted other than occupational asbestos exposure, depression, and previous heavy smoking. Computed tomography of the abdomen and pelvis (Figure 1) showed a small to moderate pericardial effusion and pericardial
enhancement suggestive of pericarditis, which were new compared to computed tomography 4 years earlier following a fall. Further history revealed exertional dyspnea with markedly decreased exercise tolerance over the preceding 12 months, occasional night sweats, and mild lethargy. There was no history of exposure to tuberculosis, radiotherapy treatment, autoimmune disorders, or malignancy. The patient was persistently febrile and his dyspnea continued to worsen during admission. Physical examination revealed jugular venous distension with no signs of ascites or peripheral edema. Cardiovascular examination demonstrated dual heart sounds with no audible murmur. Respiratory examination showed a widespread expiratory wheeze with no inspiratory crackles. Sinus tachycardia was noted on electrocardiography, and a chest radiograph was unremarkable. Aside from persistently raised inflammatory markers, further pathological investigations failed to find a focus of infection. 1 Department of Cardiothoracic Surgery, Barwon Health, Geelong, Victoria, Australia 2 Department of Cardiology, Barwon Health, Geelong, Victoria, Australia
Corresponding author: Cheng He, Department of Cardiology, Barwon Health, Geelong, Victoria, Australia. Email: [email protected]
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2
Asian Cardiovascular & Thoracic Annals 0(0)
Figure 1. Computed tomography showing thickening of the pericardium suggestive of pericarditis.
to ramus intermediate grafts) were performed on cardiopulmonary bypass via a median sternotomy. Intraoperative findings of a significantly thickened pericardium with extensive adherence to the heart were in keeping with the diagnosis of constrictive pericarditis. The postoperative recovery was uncomplicated. The cause of the patient’s constrictive pericarditis remained idiopathic. A pericardial biopsy was negative for infection (including tuberculosis) and neoplasm. Blood tests were negative for autoimmune disorders. Pericardial histopathology showed marked fibrous thickening and sclerosis without active inflammation, no signs of granulomas nor caseation, and appearances consistent with a nonspecific chronic fibrosing process. A followup transthoracic echocardiogram (Figure 4) on postoperative day 4 revealed new moderate to severe MR with a mildly dilated LV. Despite this, the patient continued to do well and was discharged 9 days postoperatively. A follow-up transthoracic echocardiogram 19 days postoperatively showed regression of MR to mild to moderate with concurrent normalization of LV dimensions. A further transthoracic echocardiogram at 9 months after surgery showed only trivial MR (Figure 5).
Discussion
Figure 2. Preoperative transthoracic echocardiogram showing mild mitral regurgitation (apical long axis view).
Preoperative transthoracic echocardiography (Figure 2) indicated thickened pericardium around the right heart border with very minimal pericardial fluid. There was also a septal bounce and > 25% variation of mitral inflow velocities. These changes were suggestive of constrictive pericarditis. The patient had mild MR with normal left ventricular (LV) size and function. A coronary angiogram revealed severe ostial left main stenosis with mild coronary artery disease elsewhere. Right heart catheterization (Figure 3) showed equalization of LV and right ventricular diastolic plateau pressures with increased right ventricular end-diastolic pressure, suggestive of constrictive pericarditis. A phrenic-tophrenic pericardiectomy and concomitant coronary artery bypass (left internal mammary artery to left anterior descending coronary artery, and radial artery
In patients with constrictive pericarditis, clinical and hemodynamic responses after pericardiectomy may not be immediately evident. For some patients, improvements occur over many months. In one echocardiography study, 43% of patients exhibited persistent abnormal LV diastolic filling years after pericardiectomy.1 This delayed recovery appeared to affect patients who had a longer duration of symptoms preoperatively. The mechanism of this impaired recovery is unclear but may relate to the degree of underlying myocardial atrophy and fibrosis as a result of prolonged pericardial compression.2 Some authors have suggested incomplete decortication as a reason for poor operative response.3 However, Senni and colleagues1 found a similar degree of abnormal LV findings on echocardiography following surgery, irrespective of whether the patient had a radical pericardiectomy or partial pericardiectomy. Therefore, a long period of myocardial compression arising from chronic constrictive pericarditis results in greater myocardial involvement. This may explain observations of better outcomes of early pericardiectomy.4 To date, there have been only two reports describing MR after pericardiectomy where the valve defect recovered conservatively with time.5,6 The etiology of MR in this context is not clear. Increased mobility of the lateral LV wall has been proposed by Buckingham and colleagues5 as a mechanism for postoperative MR,
Downloaded from aan.sagepub.com at University of New England on June 4, 2016
He et al.
3
Figure 3. Right heart catheterization showing equalization of left and right ventricular diastolic plateau pressures.
Figure 4. Transthoracic echocardiogram four days post-surgery showing new moderate to severe mitral regurgitation (parasternal long axis view).
Figure 5. Transthoracic echocardiogram 9 months after surgery showing trivial mitral regurgitation (apical long-axis view).
whereby increased inward movement of the lateral wall causes a functional lengthening of the anterolateral papillary muscle, thus disrupting mitral leaflet coaptation. A second hypothesis, involving shortening of the posteromedial papillary muscle due to a return to normal movement of the interventricular septum, was not supported by Terada and colleagues.6 Further, increased LV volume causing dilatation of the mitral annulus is another possible contributing factor to perioperative MR after pericardiectomy.
In our patient, the immediate postoperative findings showed new abnormalities in LV diastolic filling with the severe MR. The intravascular expansion associated with cardiopulmonary bypass would undoubtedly have exacerbated an already dilated ventricle following removal of the constrictive pericardium. Therefore, a significant increase in LV diastolic volume and shortening of the lateral LV wall may be contributing factors to the functional MR observed following pericardiectomy. By 9 months after pericardiectomy, resolution of
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4
Asian Cardiovascular & Thoracic Annals 0(0)
our patient’s MR occurred in conjunction with the return of LV dimensions to baseline measurements. It is plausible that compensation for the altered ventricular dynamics following removal of the constricting pericardium occurred with time, thus allowing spontaneous improvement of the initially observed MR after pericardiectomy.
2.
3.
Declaration of conflicting interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
4.
Funding
5.
The author(s) received no financial support for the research, authorship, and/or publication of this article. 6.
References 1. Senni M, Redfield MM, Ling LH, Danielson GK, Tajik AJ and Oh JK. Left ventricular systolic and diastolic
function after pericardiectomy in patients with constrictive pericarditis: Doppler echocardiographic findings and correlation with clinical status. J Am Coll Cardiol 1999; 33: 1182–1188. Levine HD. Myocardial fibrosis in constrictive pericarditis. Electrocardiographic and pathologic observations. Circulation 1973; 48: 1268–1281. Culliford AT, Lipton M and Spencer FC. Operation for chronic constrictive pericarditis: do the surgical approach and degree of pericardial resection influence the outcome significantly? Ann Thorac Surg 1980; 29: 146–152. Matsubara H, Beppu S, Koyama J, et al. Prediction of ineffective outcome of surgical treatment for constrictive pericarditis. J Cardiol 1995; 25: 89–94. Buckingham RE Jr, Furnary AP, Weaver MT, Floten HS and Davis RF. Mitral insufficiency after pericardiectomy for constrictive pericarditis. Ann Thorac Surg 1994; 58: 1171–1174. Terada Y, Mitsui T and Yamada S. Mitral regurgitation after pericardiectomy for constrictive pericarditis. Jpn J Thorac Cardiovasc Surg 1999; 47: 27–30.
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Mitral regurgitation following pericardiectomy for constrictive pericarditis
Asian Cardiovascular & Thoracic Annals 0(0) 1–4 ß The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492315593695 aan.sagepub.com
Cheng He1, Reny Suryani2, Chin Hiew2, Andrew Cheng1 and Bo Zhang1
Abstract Pericardiectomy is the only definitive treatment option for patients with constrictive pericarditis. We present the case of a 67-year-old man who developed new moderate to severe mitral regurgitation following phrenic nerve-to-phrenic nerve pericardiectomy for constrictive pericarditis. The severity of the regurgitation was followed up by serial echocardiography which showed improvement 19 days later and complete resolution at 9 months after surgery. Potential mechanisms explaining the evolution of this mitral valve dysfunction in the setting of pericardiectomy are postulated.
Keywords Mitral valve insufficiency, Pericardiectomy, Constrictive pericarditis
Introduction Constrictive pericarditis is a chronic inflammatory process that results in a densely thickened pericardium that compresses the heart, limiting diastolic ventricular filling. The etiology is idiopathic in the majority of cases. Pericardiectomy is the only definitive treatment option, with most patients achieving symptomatic relief following the procedure. We report the unusual case of a 66-year-old man with new severe mitral regurgitation (MR) immediately following pericardiectomy for constrictive pericarditis. Spontaneous resolution of MR was observed on echocardiography 9 months after surgery. Potential mechanisms resulting in this self-reverting clinical entity are discussed.
Case report A 67-year-old man was admitted with a 3-day history of fever, central abdominal pain, and raised inflammatory markers, on the background of suspected recent pneumonia for which he had received oral antibiotics. No significant medical or surgical history was noted other than occupational asbestos exposure, depression, and previous heavy smoking. Computed tomography of the abdomen and pelvis (Figure 1) showed a small to moderate pericardial effusion and pericardial
enhancement suggestive of pericarditis, which were new compared to computed tomography 4 years earlier following a fall. Further history revealed exertional dyspnea with markedly decreased exercise tolerance over the preceding 12 months, occasional night sweats, and mild lethargy. There was no history of exposure to tuberculosis, radiotherapy treatment, autoimmune disorders, or malignancy. The patient was persistently febrile and his dyspnea continued to worsen during admission. Physical examination revealed jugular venous distension with no signs of ascites or peripheral edema. Cardiovascular examination demonstrated dual heart sounds with no audible murmur. Respiratory examination showed a widespread expiratory wheeze with no inspiratory crackles. Sinus tachycardia was noted on electrocardiography, and a chest radiograph was unremarkable. Aside from persistently raised inflammatory markers, further pathological investigations failed to find a focus of infection. 1 Department of Cardiothoracic Surgery, Barwon Health, Geelong, Victoria, Australia 2 Department of Cardiology, Barwon Health, Geelong, Victoria, Australia
Corresponding author: Cheng He, Department of Cardiology, Barwon Health, Geelong, Victoria, Australia. Email: [email protected]
Downloaded from aan.sagepub.com at University of New England on June 4, 2016
2
Asian Cardiovascular & Thoracic Annals 0(0)
Figure 1. Computed tomography showing thickening of the pericardium suggestive of pericarditis.
to ramus intermediate grafts) were performed on cardiopulmonary bypass via a median sternotomy. Intraoperative findings of a significantly thickened pericardium with extensive adherence to the heart were in keeping with the diagnosis of constrictive pericarditis. The postoperative recovery was uncomplicated. The cause of the patient’s constrictive pericarditis remained idiopathic. A pericardial biopsy was negative for infection (including tuberculosis) and neoplasm. Blood tests were negative for autoimmune disorders. Pericardial histopathology showed marked fibrous thickening and sclerosis without active inflammation, no signs of granulomas nor caseation, and appearances consistent with a nonspecific chronic fibrosing process. A followup transthoracic echocardiogram (Figure 4) on postoperative day 4 revealed new moderate to severe MR with a mildly dilated LV. Despite this, the patient continued to do well and was discharged 9 days postoperatively. A follow-up transthoracic echocardiogram 19 days postoperatively showed regression of MR to mild to moderate with concurrent normalization of LV dimensions. A further transthoracic echocardiogram at 9 months after surgery showed only trivial MR (Figure 5).
Discussion
Figure 2. Preoperative transthoracic echocardiogram showing mild mitral regurgitation (apical long axis view).
Preoperative transthoracic echocardiography (Figure 2) indicated thickened pericardium around the right heart border with very minimal pericardial fluid. There was also a septal bounce and > 25% variation of mitral inflow velocities. These changes were suggestive of constrictive pericarditis. The patient had mild MR with normal left ventricular (LV) size and function. A coronary angiogram revealed severe ostial left main stenosis with mild coronary artery disease elsewhere. Right heart catheterization (Figure 3) showed equalization of LV and right ventricular diastolic plateau pressures with increased right ventricular end-diastolic pressure, suggestive of constrictive pericarditis. A phrenic-tophrenic pericardiectomy and concomitant coronary artery bypass (left internal mammary artery to left anterior descending coronary artery, and radial artery
In patients with constrictive pericarditis, clinical and hemodynamic responses after pericardiectomy may not be immediately evident. For some patients, improvements occur over many months. In one echocardiography study, 43% of patients exhibited persistent abnormal LV diastolic filling years after pericardiectomy.1 This delayed recovery appeared to affect patients who had a longer duration of symptoms preoperatively. The mechanism of this impaired recovery is unclear but may relate to the degree of underlying myocardial atrophy and fibrosis as a result of prolonged pericardial compression.2 Some authors have suggested incomplete decortication as a reason for poor operative response.3 However, Senni and colleagues1 found a similar degree of abnormal LV findings on echocardiography following surgery, irrespective of whether the patient had a radical pericardiectomy or partial pericardiectomy. Therefore, a long period of myocardial compression arising from chronic constrictive pericarditis results in greater myocardial involvement. This may explain observations of better outcomes of early pericardiectomy.4 To date, there have been only two reports describing MR after pericardiectomy where the valve defect recovered conservatively with time.5,6 The etiology of MR in this context is not clear. Increased mobility of the lateral LV wall has been proposed by Buckingham and colleagues5 as a mechanism for postoperative MR,
Downloaded from aan.sagepub.com at University of New England on June 4, 2016
He et al.
3
Figure 3. Right heart catheterization showing equalization of left and right ventricular diastolic plateau pressures.
Figure 4. Transthoracic echocardiogram four days post-surgery showing new moderate to severe mitral regurgitation (parasternal long axis view).
Figure 5. Transthoracic echocardiogram 9 months after surgery showing trivial mitral regurgitation (apical long-axis view).
whereby increased inward movement of the lateral wall causes a functional lengthening of the anterolateral papillary muscle, thus disrupting mitral leaflet coaptation. A second hypothesis, involving shortening of the posteromedial papillary muscle due to a return to normal movement of the interventricular septum, was not supported by Terada and colleagues.6 Further, increased LV volume causing dilatation of the mitral annulus is another possible contributing factor to perioperative MR after pericardiectomy.
In our patient, the immediate postoperative findings showed new abnormalities in LV diastolic filling with the severe MR. The intravascular expansion associated with cardiopulmonary bypass would undoubtedly have exacerbated an already dilated ventricle following removal of the constrictive pericardium. Therefore, a significant increase in LV diastolic volume and shortening of the lateral LV wall may be contributing factors to the functional MR observed following pericardiectomy. By 9 months after pericardiectomy, resolution of
Downloaded from aan.sagepub.com at University of New England on June 4, 2016
4
Asian Cardiovascular & Thoracic Annals 0(0)
our patient’s MR occurred in conjunction with the return of LV dimensions to baseline measurements. It is plausible that compensation for the altered ventricular dynamics following removal of the constricting pericardium occurred with time, thus allowing spontaneous improvement of the initially observed MR after pericardiectomy.
2.
3.
Declaration of conflicting interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
4.
Funding
5.
The author(s) received no financial support for the research, authorship, and/or publication of this article. 6.
References 1. Senni M, Redfield MM, Ling LH, Danielson GK, Tajik AJ and Oh JK. Left ventricular systolic and diastolic
function after pericardiectomy in patients with constrictive pericarditis: Doppler echocardiographic findings and correlation with clinical status. J Am Coll Cardiol 1999; 33: 1182–1188. Levine HD. Myocardial fibrosis in constrictive pericarditis. Electrocardiographic and pathologic observations. Circulation 1973; 48: 1268–1281. Culliford AT, Lipton M and Spencer FC. Operation for chronic constrictive pericarditis: do the surgical approach and degree of pericardial resection influence the outcome significantly? Ann Thorac Surg 1980; 29: 146–152. Matsubara H, Beppu S, Koyama J, et al. Prediction of ineffective outcome of surgical treatment for constrictive pericarditis. J Cardiol 1995; 25: 89–94. Buckingham RE Jr, Furnary AP, Weaver MT, Floten HS and Davis RF. Mitral insufficiency after pericardiectomy for constrictive pericarditis. Ann Thorac Surg 1994; 58: 1171–1174. Terada Y, Mitsui T and Yamada S. Mitral regurgitation after pericardiectomy for constrictive pericarditis. Jpn J Thorac Cardiovasc Surg 1999; 47: 27–30.
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