Case Study
Acute pericarditis with cardiac tamponade induced by pacemaker implantation
Asian Cardiovascular & Thoracic Annals 2015, Vol. 23(9) 1093–1095 ß The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492314534250 aan.sagepub.com
Masami Shingaki, Yutaka Kobayashi and Haruo Suzuki
Abstract An 87-year-old woman was diagnosed with third-degree atrioventricular block and underwent pacemaker implantation. On postoperative day 12, she experienced cardiac tamponade that was suspected on computed tomography to be caused by lead perforation; therefore, we performed open-heart surgery. However, we could not identify a perforation site on the heart, and drained a 400-mL exudative pericardial effusion. Subsequently, we diagnosed the pericardial effusion as due to pericarditis induced by pacemaker implantation. It is sometimes difficult to distinguish pericarditis from pacemaker lead perforation, so both should be included in the differential diagnosis.
Keywords Cardiac tamponade, drainage, electrodes, implanted, pacemaker, artificial, pericardial effusion, pericarditis
Introduction Pericarditis after permanent pacemaker implantation (PMI) was recently recognized as a post-cardiac injury syndrome.1,2 Post-cardiac injury syndrome includes post-myocardial infarction pericarditis, postpericardiotomy syndrome, and post-traumatic pericarditis; pericarditis after PMI is classified as a type of post-traumatic pericarditis. We describe a rare case of acute life-threatening pericarditis with cardiac tamponade induced by PMI.
Case report An 87-year-old woman with a history of hypertension was referred to another hospital for general fatigue and diagnosed with bradycardia and third-degree atrioventricular block. She immediately underwent PMI with a VVI pacemaker via the left subclavian vein. The pacemaker lead was screwed in and placed at the apex of the right ventricle. One day after the operation, she had a high fever and a high white blood cell count; therefore, intravenous antibiotics were introduced to treat a suspected device infection. Nonsteroidal antiinflammatory drugs and aspirin were simultaneously introduced for treatment of suspected pericarditis. On postoperative
day (POD) 12, chest radiography showed cardiomegaly and bilateral pleural effusions (Figure 1). Echocardiography showed a massive pericardial effusion with signs of cardiac tamponade. Computed tomography (CT) demonstrated evidence of right ventricle perforation by the pacemaker lead (Figure 2), and the patient was transferred to our hospital for surgical intervention. With the patient under general anesthesia, we performed a full sternotomy and pericardiotomy and confirmed a slightly bloody but exudative 400mL pericardial effusion. The pericardium was thickened and part of it had adhered to the heart, but there was no sign of infection such as an abscess. We inspected the surface of the heart but saw neither a bleeding site nor a lead perforation. We diagnosed the etiology of cardiac tamponade as acute pericarditis due to PMI. The pathology of the pericardium specimens, which revealed inflammatory cell infiltration and Department of Cardiovascular Surgery, Uji Tokushukai Medical Center, Uji City, Japan Corresponding author: Masami Shingaki, MD, Department of Cardiovascular Surgery, Uji Tokushukai Medical Center, 86, Oguracho Kasugamori, Uji City, Kyoto Prefecture, 611-0042 Japan. Email: [email protected]
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Asian Cardiovascular & Thoracic Annals 23(9)
fibrous proliferation, supported this diagnosis. The pericardial effusion also contained inflammatory cells. Cultures of the blood and pericardial effusion were negative. We placed a drainage tube into the pericardial sac and removed the permanent pacemaker lead from the left subclavian vein. We then placed a temporary epicardial pacemaker lead on the right ventricle instead of a new permanent epicardial pacemaker lead because we were afraid that the latter lead might induce pericarditis again. The operation time was 106 min, and no blood transfusion was required. The patient was extubated on POD 1, started oral intake on POD 2, and was discharged in good health on POD 29. The drainage tube was removed on POD 3. Echocardiography showed no pericardial effusion on POD 8, and no atrioventricular block or bradycardia was detected after the operation; thus we decided not to reimplant a permanent pacemaker.
Figure 1. Chest radiograph showing cardiomegaly and bilateral pleural effusions with congestion.
Discussion The mechanism of post-cardiac injury syndrome is not yet clear, but an autoimmune response to intimal injury is considered the key mechanism of pericardial inflammation.1 Pericarditis after PMI is not a common complication, and some studies have reported an incidence of 1.5–2.0%.3,4 Among these cases, pericarditis requiring pericardiocentesis or surgical drainage is much less frequently seen in clinical situations. Ohlow and colleagues4 studied 968 consecutive cases of PMI and found that only 4 (0.4%) resulted in pericarditis requiring pericardiocentesis or surgical intervention. In our case, intervention was necessary for the cardiac tamponade due to hemodynamic collapse in addition to the suspicion of pacemaker lead perforation on CT. Methods for diagnosing lead perforation are not yet well established. CT is a useful modality, but an accurate diagnosis can be difficult to obtain in some cases due to pacemaker lead artifacts. In fact, no reports have indicated the diagnostic accuracy of CT for lead perforation, although CT is a useful adjunct to other modalities such as echocardiography.5 The etiology of pericarditis after PMI is not well understood, but some case reports have stressed the importance of the active fixation (screw tip) lead.6,7 They hypothesized that myocardial perforation was one cause of pericarditis in addition to the autoimmune response to intimal injury; that is, direct injury to the epicardium and blood pericardial effusion might induce pericardial inflammation. Our patient had an active fixation lead, but we could not macroscopically identify a point of screw tip penetration and suspected that this patient had an autoimmune response to the myocardial intimal injury but not the epicardial injury. This suspicion was supported by the fact that she had a high fever immediately after PMI, without pericardial effusion. It is sometimes difficult to distinguish pericarditis from pacemaker lead perforation, so both should be included in the differential diagnosis.
Figure 2. (A, B) Computed tomography showing massive pericardial effusion and suggesting a lead perforation.
Downloaded from aan.sagepub.com by guest on November 17, 2015
Shingaki et al.
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Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest statement None declared.
References 1. Imazio M and Hoit BD. Post-cardiac injury syndromes. An emerging cause of pericardial diseases. Int J Cardiol 2013; 168: 648–652. 2. Cevik C, Wilborn T, Corona R, Schanzmeyer E and Nugent K. Post-cardiac injury syndrome following transvenous pacemaker insertion: a case report and review of the literature. Heart Lung Circ 2009; 18: 379–383.
3. Levy Y, Shovman O, Granit C, et al. Pericarditis following permanent pacemaker insertion. Isr Med Assoc J 2004; 6: 599–602. 4. Ohlow MA, Lauer B, Brunelli M and Geller JC. Incidence and predictors of pericardial effusion after permanent heart rhythm device implantation: prospective evaluation of 968 consecutive patients. Circ J 2013; 77: 975–981. 5. Mak GS and Truong QA. Cardiac CT: imaging of and through cardiac devices. Curr Cardiovasc Imaging Rep 2012; 5: 328–336. 6. Kono K, Todoroki M, Karasawa T, et al. Delayed pericarditis associated with an implantable cardioverter defibrillator implantation using an active-fixation atrial lead. Pacing Clin Electrophysiol 2008; 31: 621–623. 7. Panaich SS, Cardozo S, Jacob S and Afonso L. Device lead screw tip induced pericarditis—a subtle complication in need of wider recognition. Int J Cardiol 2013; 167: e76–e77.
Downloaded from aan.sagepub.com by guest on November 17, 2015
Acute pericarditis with cardiac tamponade induced by pacemaker implantation
Asian Cardiovascular & Thoracic Annals 2015, Vol. 23(9) 1093–1095 ß The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492314534250 aan.sagepub.com
Masami Shingaki, Yutaka Kobayashi and Haruo Suzuki
Abstract An 87-year-old woman was diagnosed with third-degree atrioventricular block and underwent pacemaker implantation. On postoperative day 12, she experienced cardiac tamponade that was suspected on computed tomography to be caused by lead perforation; therefore, we performed open-heart surgery. However, we could not identify a perforation site on the heart, and drained a 400-mL exudative pericardial effusion. Subsequently, we diagnosed the pericardial effusion as due to pericarditis induced by pacemaker implantation. It is sometimes difficult to distinguish pericarditis from pacemaker lead perforation, so both should be included in the differential diagnosis.
Keywords Cardiac tamponade, drainage, electrodes, implanted, pacemaker, artificial, pericardial effusion, pericarditis
Introduction Pericarditis after permanent pacemaker implantation (PMI) was recently recognized as a post-cardiac injury syndrome.1,2 Post-cardiac injury syndrome includes post-myocardial infarction pericarditis, postpericardiotomy syndrome, and post-traumatic pericarditis; pericarditis after PMI is classified as a type of post-traumatic pericarditis. We describe a rare case of acute life-threatening pericarditis with cardiac tamponade induced by PMI.
Case report An 87-year-old woman with a history of hypertension was referred to another hospital for general fatigue and diagnosed with bradycardia and third-degree atrioventricular block. She immediately underwent PMI with a VVI pacemaker via the left subclavian vein. The pacemaker lead was screwed in and placed at the apex of the right ventricle. One day after the operation, she had a high fever and a high white blood cell count; therefore, intravenous antibiotics were introduced to treat a suspected device infection. Nonsteroidal antiinflammatory drugs and aspirin were simultaneously introduced for treatment of suspected pericarditis. On postoperative
day (POD) 12, chest radiography showed cardiomegaly and bilateral pleural effusions (Figure 1). Echocardiography showed a massive pericardial effusion with signs of cardiac tamponade. Computed tomography (CT) demonstrated evidence of right ventricle perforation by the pacemaker lead (Figure 2), and the patient was transferred to our hospital for surgical intervention. With the patient under general anesthesia, we performed a full sternotomy and pericardiotomy and confirmed a slightly bloody but exudative 400mL pericardial effusion. The pericardium was thickened and part of it had adhered to the heart, but there was no sign of infection such as an abscess. We inspected the surface of the heart but saw neither a bleeding site nor a lead perforation. We diagnosed the etiology of cardiac tamponade as acute pericarditis due to PMI. The pathology of the pericardium specimens, which revealed inflammatory cell infiltration and Department of Cardiovascular Surgery, Uji Tokushukai Medical Center, Uji City, Japan Corresponding author: Masami Shingaki, MD, Department of Cardiovascular Surgery, Uji Tokushukai Medical Center, 86, Oguracho Kasugamori, Uji City, Kyoto Prefecture, 611-0042 Japan. Email: [email protected]
Downloaded from aan.sagepub.com by guest on November 17, 2015
1094
Asian Cardiovascular & Thoracic Annals 23(9)
fibrous proliferation, supported this diagnosis. The pericardial effusion also contained inflammatory cells. Cultures of the blood and pericardial effusion were negative. We placed a drainage tube into the pericardial sac and removed the permanent pacemaker lead from the left subclavian vein. We then placed a temporary epicardial pacemaker lead on the right ventricle instead of a new permanent epicardial pacemaker lead because we were afraid that the latter lead might induce pericarditis again. The operation time was 106 min, and no blood transfusion was required. The patient was extubated on POD 1, started oral intake on POD 2, and was discharged in good health on POD 29. The drainage tube was removed on POD 3. Echocardiography showed no pericardial effusion on POD 8, and no atrioventricular block or bradycardia was detected after the operation; thus we decided not to reimplant a permanent pacemaker.
Figure 1. Chest radiograph showing cardiomegaly and bilateral pleural effusions with congestion.
Discussion The mechanism of post-cardiac injury syndrome is not yet clear, but an autoimmune response to intimal injury is considered the key mechanism of pericardial inflammation.1 Pericarditis after PMI is not a common complication, and some studies have reported an incidence of 1.5–2.0%.3,4 Among these cases, pericarditis requiring pericardiocentesis or surgical drainage is much less frequently seen in clinical situations. Ohlow and colleagues4 studied 968 consecutive cases of PMI and found that only 4 (0.4%) resulted in pericarditis requiring pericardiocentesis or surgical intervention. In our case, intervention was necessary for the cardiac tamponade due to hemodynamic collapse in addition to the suspicion of pacemaker lead perforation on CT. Methods for diagnosing lead perforation are not yet well established. CT is a useful modality, but an accurate diagnosis can be difficult to obtain in some cases due to pacemaker lead artifacts. In fact, no reports have indicated the diagnostic accuracy of CT for lead perforation, although CT is a useful adjunct to other modalities such as echocardiography.5 The etiology of pericarditis after PMI is not well understood, but some case reports have stressed the importance of the active fixation (screw tip) lead.6,7 They hypothesized that myocardial perforation was one cause of pericarditis in addition to the autoimmune response to intimal injury; that is, direct injury to the epicardium and blood pericardial effusion might induce pericardial inflammation. Our patient had an active fixation lead, but we could not macroscopically identify a point of screw tip penetration and suspected that this patient had an autoimmune response to the myocardial intimal injury but not the epicardial injury. This suspicion was supported by the fact that she had a high fever immediately after PMI, without pericardial effusion. It is sometimes difficult to distinguish pericarditis from pacemaker lead perforation, so both should be included in the differential diagnosis.
Figure 2. (A, B) Computed tomography showing massive pericardial effusion and suggesting a lead perforation.
Downloaded from aan.sagepub.com by guest on November 17, 2015
Shingaki et al.
1095
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest statement None declared.
References 1. Imazio M and Hoit BD. Post-cardiac injury syndromes. An emerging cause of pericardial diseases. Int J Cardiol 2013; 168: 648–652. 2. Cevik C, Wilborn T, Corona R, Schanzmeyer E and Nugent K. Post-cardiac injury syndrome following transvenous pacemaker insertion: a case report and review of the literature. Heart Lung Circ 2009; 18: 379–383.
3. Levy Y, Shovman O, Granit C, et al. Pericarditis following permanent pacemaker insertion. Isr Med Assoc J 2004; 6: 599–602. 4. Ohlow MA, Lauer B, Brunelli M and Geller JC. Incidence and predictors of pericardial effusion after permanent heart rhythm device implantation: prospective evaluation of 968 consecutive patients. Circ J 2013; 77: 975–981. 5. Mak GS and Truong QA. Cardiac CT: imaging of and through cardiac devices. Curr Cardiovasc Imaging Rep 2012; 5: 328–336. 6. Kono K, Todoroki M, Karasawa T, et al. Delayed pericarditis associated with an implantable cardioverter defibrillator implantation using an active-fixation atrial lead. Pacing Clin Electrophysiol 2008; 31: 621–623. 7. Panaich SS, Cardozo S, Jacob S and Afonso L. Device lead screw tip induced pericarditis—a subtle complication in need of wider recognition. Int J Cardiol 2013; 167: e76–e77.
Downloaded from aan.sagepub.com by guest on November 17, 2015
