Ann Thorac Surg 1995;59:684-688
© 1995 The Society of Thoracic Surgeons
Right Atrial Compression Related to Defibrillator Patches
Jeffrey M. Piehler, MD,
Duncan A. Killen, MD,
A. Michael Borkon, MD,
William A. Reed, MD,
Michael E. Gorton, MD,
George M. Gura, Jr, MD,
Amy H. Kragel, MD
Department of Cardiovascular Diseases, Sections of Cardiovascular Surgery and Cardiology, and Department of Pathology, Mid-America Heart Institute of Saint Luke's Hospital, Kansas City, Missouri
Accepted for publication November 19, 1994.
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Abstract
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Acceptable function of an internal defibrillator can be achieved with different patch orientations. For patients requiring defibrillator patches concomitant with a cardiac procedure requiring extracorporeal circulation, application of one of the patches within the pericardium adjacent to the right atrium has provided excellent defibrillation thresholds. We describe 4 such patients in whom a compressing thrombus subsequently developed between the patch and the atrium. The thrombus was small and asymptomatic in 1 patient, but caused localized tamponade requiring reexploration in 2 patients and a fatal superior vena caval obstruction in 1. The precise etiology of this serious complication remains unclear, but its occurrence argues against the application of intrapericardial defibrillator patches in this orientation.
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Introduction
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Implantable defibrillators are an effective means of treating malignant ventricular arrhythmias that are not amenable to antiarrhythmic medications or ablative surgical interventions [1–6]. There are several surgical approaches that can be used successfully to implant the necessary patches and leads, including median sternotomy, bilateral anterior thoracotomies, and left anterior thoracotomy, as well as the left subcostal and subxiphoid approaches [1, 6–8]. Although initially advocated by some for all implantations [7, 9], the median sternotomy approach is currently only used in patients undergoing concomitant cardiac procedures requiring extracorporeal circulation. In these patients, the defibrillation patches are sutured within the opened pericardium in an orientation that permits satisfactory defibrillation thresholds, avoiding contact with any constructed coronary artery bypass conduits. Our practice has been to use a two-patch or three-patch system, often with one patch sutured to the lateral pericardium overlying the right atrium, a second generous-sized patch placed slightly posterolaterally around the left ventricular apex, and a third patch placed, as needed, over the diaphragmatic or anterior surface of the right ventricle. We have frequently utilized such a three-patch system because of the occurrence of consistently low defibrillation thresholds and the belief that three patches offer greater flexibility should future modifications of the system be required. All patches are sutured to the overlying pericardium, not to the epicardium. The left ventricular patch and the sensing and pacing leads are applied before weaning from extracorporeal circulation when manipulation of the heart is well tolerated. The remaining patches are applied after decannulation and heparin reversal. The ends of the implanted leads and patches are capped and placed in a subcutaneous pocket in the left upper quadrant of the abdomen. We usually have implanted and activated the defibrillator generator at a second procedure during the same hospitalization, when we are confident that the patient has recovered without evidence of infection, coagulopathy, or other problems that might compromise the operation of the generator.
In this report we describe 4 patients who underwent implantation of defibrillator patches made by a single manufacturer (Medtronic, Minneapolis, MN) at the same time as other cardiac procedures that required extracorporeal circulation. In each patient, a large or medium-sized patch was sutured to the pericardium overlying the right atrium. In each instance, a localized thrombus subsequently developed between the patch and the right atrium, which was apparently asymptomatic in 1 patient, but which caused early postoperative hemodynamic compromise in 2 and contributed to the death of the final patient. Constrictive pericarditis [10, 11], epicardial vessel erosion [9, 12, 13], and postoperative bleeding with tamponade [14] necessitating reexploration have all been observed as complications of defibrillator patches, but we describe here the formation of a localized thrombus compressing the right heart. We believe it important to describe this potentially serious complication of defibrillator patches applied adjacent to the right atrium.
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Case Reports
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Patient 1
A 61-year-old man underwent cardiac catheterization and electrophysiologic study after suffering two episodes of out-of-hospital cardiac arrest; these revealed the presence of coronary artery disease and easily inducible sustained ventricular tachycardia. On June 10, 1992, he underwent triple coronary artery bypass grafting and the implantation of three defibrillator patches, one of which was placed adjacent to the right atrium. His postoperative course was complicated by a low cardiac output syndrome. Despite intravenous inotropic support, progressive cardiogenic shock with unrelenting metabolic acidosis developed. His rhythm remained sinus. Findings from transthoracic echocardiography, performed on the second postoperative day, did not suggest the presence of tamponade. Nonetheless, because of the progressive deterioration in his condition and the fact that tamponade could not be absolutely excluded, transesophageal echocardiography was performed. This revealed right atrial compression from a mass between the defibrillator patch and the heart (Fig 1
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Fig 1. . (Patient 1.) Transesophageal echocardiographic view of localized thrombus (TH) interposed between the defibrillator patch and the right atrium (RA).
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The patient was returned to the operating room, where a firm oval mass consisting of multilaminated clot (10 x 9 x 5.5 cm) was found interposed precisely between the defibrillator patch and the right atrium with compression of the right atrium. No other clots were present in the pericardial space, and there was no active bleeding from the heart. Removal of the clot resulted in immediate hemodynamic improvement. Recovery was slowed by transient hepatic dysfunction. On July 1, 1992, a defibrillator generator was implanted. He was discharged from the hospital 25 days after his original operation, and continues to do well.
Patient 2
A 72-year-old man had undergone aortic valve replacement in 1976. On June 24, 1992, he suffered an episode of out-of-hospital tachycardia (with associated loss of consciousness). After hospitalization and stabilization of his condition, cardiac electrophysiologic studies revealed him to have inducible, sustained, ventricular tachycardia. Cardiac catheterization revealed a left ventricular ejection fraction of 0.25, moderate mitral regurgitation, and an aortic prosthetic valve peak gradient of 65 to 75 mm Hg. Coronary angiography revealed no notable coronary artery disease.
On July 7, 1992, the patient underwent repeat aortic valve replacement, together with aortic root enlargement aortoplasty (using a pericardial patch) and the placement of three defibrillator patches, one being placed over the right atrium. His early postoperative course was complicated by recurrent supraventricular and ventricular tachycardia, low cardiac output, congestive heart failure, respiratory failure, and moderate renal insufficiency. He later suffered a sternotomy wound infection, recurring pneumonia, episodes of upper and lower gastrointestinal bleeding, and sepsis. The wound infection was superficial and did not involve the patches or mediastinum. An attempt was made to maintain anticoagulation; however, this was periodically discontinued during episodes of gastrointestinal bleeding. On October 20, 1992, transthoracic echocardiography revealed a left ventricular ejection fraction of 0.30 to 0.35 with no evidence of intrapericardial thrombus. Over time, his cardiac rhythm stabilized in a sinus mechanism with normal cardiac output. However, despite treatment, he continued to suffer recurrent sepsis from pulmonary origin and died on the 113th postoperative day.
Autopsy revealed a localized 1.0-cm-thick thrombus that adhered to the epicardium beneath the right atrial defibrillator patch. The coil pattern of the defibrillator patch was imprinted onto the thrombus; histologic examination confirmed a regular arrangement of alternating plateaus and valleys (Fig 2). The plateaus were composed of fibrotic epicardial tissue expanded by fresh hemorrhage (red blood cells and fibrin), and the valleys corresponded to the locations of the defibrillator coils. There was also a small (2 x 2 x 3–cm) thrombus beneath the right ventricular patch without chamber compression; changes similar to those described for the atrial patch were seen in the epicardium beneath the right ventricular patch.
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Fig 2. . (Patient 2.) (A) Section of the atrial epicardium beneath the defibrillator patch showing a regular arrangement of plateaus and valleys. The fibrous epicardium is expanded by fresh hemorrhage. (Hematoxylin and eosin; original magnification, x2.) (B) Epicardium expanded by accumulation of red blood cells and fibrous tissue. (Hematoxylin and eosin; original magnification, x10.)
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Patient 3
A 65-year-old man with a history of myocardial infarction was admitted to his local hospital because of recurrent ventricular tachycardia and hypotension requiring multiple cardioversions. Cardiac catheterization revealed severe mitral regurgitation, a left ventricular ejection fraction of 0.45 to 0.50, subtotal occlusion of the circumflex coronary artery, and a moderately severe stenotic lesion in the anterior descending coronary artery. He then underwent successful balloon angioplasty of the circumflex coronary artery, and this produced clinical improvement.
The patient was later transferred to our institution and on September 30, 1992, underwent two-vessel coronary artery bypass grafting and mitral valve repair. Three defibrillator patches were implanted, one sutured to the pericardium over the right atrium. His recovery was uneventful, with the exception of episodic atrial flutter and fibrillation that converted to sinus rhythm with antiarrhythmic agents. Transthoracic echocardiography performed 1 week postoperatively revealed a left ventricular ejection fraction of 0.25 to 0.30 with only a trace of mitral regurgitation. A defibrillator generator was implanted on October 13, 1992. His subsequent course was uneventful; sodium warfarin was prescribed for anticoagulation, and he was discharged from the hospital in sinus rhythm 19 days after his initial operation.
The patient was readmitted emergently to his local hospital on October 29, 1992, complaining of chest pain and shortness of breath. Thrombolytic therapy was empirically administered, although there was no firm electrocardiographic evidence of myocardial infarction. Transthoracic echocardiography was performed and was believed to reveal anterior left ventricular segmental wall hypokinesis; mitral valve function was thought to be satisfactory. A computed tomographic scan of the chest was obtained, which revealed occlusion of the superior vena cava and a non-contrast-enhancing mass adjacent to the right atrium, possibly causing compression. Shortly thereafter, refractory cardiogenic shock developed, and the patient died on the day of admission.
Autopsy confirmed the presence of a large (15 cm in the longest diameter) fresh thrombus between the right-sided defibrillator patch and the heart. The patch and the thrombus were enclosed in a fibrous pocket that was adherent to the right atrium and superior vena cava, both of which were extensively compressed. Histologic examination of the pocket wall revealed fibrin, chronic inflammatory infiltrate, and foreign body giant cells.
Patient 4
A 67-year-old man presented with a long-standing history of mitral regurgitation, aortic regurgitation, and ventricular ectopy. He had been documented to have nonsustained episodes of ventricular tachycardia, and recently class IV congestive heart failure had developed. Cardiac electrophysiologic studies revealed inducible monomorphic ventricular tachycardia. Cardiac catheterization documented the presence of severe aortic and mitral regurgitation, and coronary angiography revealed normal coronary arteries. The left ventricular ejection fraction was 0.40.
On October 9, 1992, the patient underwent aortic and mitral valve replacement and the implantation of three defibrillator patches, one patch being placed over the right atrium. His early postoperative course was unremarkable, except for junctional rhythm and the need for moderate inotropic support. On the first postoperative day, after tracheal extubation, progressive dyspnea developed, leading to respiratory arrest. He underwent cardiopulmonary resuscitation and was placed on mechanical ventilation. Because of a persistently low cardiac output, an intraaortic balloon pump was inserted. Although his condition remained stable for 24 hours while he was on the intraaortic balloon pump with inotropic support, profound hemodynamic deterioration subsequently developed, marked by oliguria, hypotension, elevated right-sided and left-sided filling pressures, and low cardiac output despite increasing the dosage of inotropic agents.
The patient was emergently returned to the operating room on October 12, 1992, where exploration revealed a firm oval clot measuring 11.5 x 8 x 5 cm interposed precisely between the overlying defibrillator patch and the right atrium. The clot was severely compressing the right atrium. Removal of the clot brought about immediate hemodynamic improvement. There was no other significant clot in the pericardial sac, and there was no evidence of atrial bleeding. The clot was composed of many thin pancaked layers, with each layer showing an impression of the defibrillator patch electrode (Fig 3). Hematoxylin-eosin–stained sections of the thrombus revealed a typical lamellar thrombus composed predominantly of red blood cells and fibrin with basophylic bands of fibrin corresponding to the location of the defibrillator coils.
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Fig 3. . (Patient 4.) Frontal (A) and lateral (B) views of thrombus removed from beneath the right atrial defibrillator patch. In view (A), one of the pancakelike layers of thrombus has been removed, revealing the regular imprint of the defibrillator coil throughout successive layers of thrombus.
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Postoperatively, the patient's respiratory and left ventricular function progressively improved; he was discharged from the hospital 24 days after his original operation and has subsequently done well.
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Comment
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The transsternal route is not our currently preferred approach for isolated implantation of a defibrillation system. Nevertheless, if a median sternotomy is used or is required because concomitant cardiac procedures are planned, application of one of the defibrillation patches adjacent to the right atrium is both accepted and associated with good defibrillator performance [8]. Unfortunately, our experience described here suggests that positioning a patch on the pericardium overlying the right atrium could spawn thrombus formation between the patch and the atrium, which can lead to life-threatening cardiac compression. In 2 of our patients (patients 1 and 4), removal of the thrombus led to dramatic and immediate improvement in their hemodynamic state, which had been compatible with right-sided flow compromise. Patient 3 experienced superior vena cava syndrome resulting from external compression and caused by a clot documented at postmortem examination. The compression in this patient certainly contributed to the low cardiac output and probably to his death as well. The clot appeared to be relatively thin and asymptomatic in patient 2, although its presence was also clearly identified at autopsy.
The explanation for the localized thrombus formation in these patients is not entirely clear: a source of blood and an environment conducive to thrombus formation beneath the patch are obvious prerequisites. Regarding the source of blood, no active cardiac bleeding sites were found in the 2 patients (patients 1 and 4) who underwent reoperation in the early postoperative period, and the patches had all been secured to the pericardium, not to the heart. Nevertheless, epicardial erosion from intrapericardial defibrillator patches has been reported [12–14], and this explanation might be supported by the histologic findings in the two hearts examined at autopsy (patients 2 and 3), in which red blood cells and hemosiderin-laden macrophages were identified in the myocardial wall. Certainly a full-thickness atrial erosion from the patch would appear unlikely in our patients, as this would probably not spontaneously seal or evade detection upon removal of the overlying thrombus at early reoperation.
It may be important that all of the patients in our series had been subjected to extracorporeal circulation. Early in our defibrillator experience we utilized the transsternal route for all defibrillator implantations, and placed a variety of patches in the same locations. We are not aware of any instances of thrombus formation between the right atrial patches and the heart in any of these 42 patients who were not placed on extracorporeal circulation. Conceivably the coagulation perturbations associated with cardiopulmonary bypass could have provided a source of intrapericardial blood in the 2 patients (patients 1 and 4) requiring early reexploration, although the explanation for the localization of the thrombotic process solely beneath the atrial patches remains uncertain. Similarly, the 2 patients (patients 2 and 3) in whom the thrombi were detected late postoperatively had been anticoagulated with warfarin, and 1 (patient 3) received systemic thrombolytic therapy, potentially providing a cause for intrapericardial or epicardial bleeding.
Regardless of the source of blood, the atrial patch surface appears to be an environment conducive to localized thrombosis. All 4 of these patients received patches made by a single manufacturer (Medtronic). We have used a competing defibrillator system (CPI; St. Paul, MN) under similar circumstances (with a patch applied opposite the right atrium after a cardiac procedure requiring extracorporeal circulation) in 38 patients without encountering this complication; the 4 cases reported here arose from a similar cohort of 14 patients with Medtronic patches. If epicardial erosion were the primary source of blood beneath the patch, one would expect a greater incidence of this complication with the CPI patches, which have a stiffer and rougher surface than the Medtronic patches. Because this has not been seen, it would appear that the surface of the Medtronic patch is more thrombogenic. In the 2 patients who underwent early reoperation, the thrombi demonstrated a peculiar laminated appearance, suggesting multiple episodes of thrombosis adjacent to the patch surface, and separation of the intact thrombus from the patch, followed by the redeposition of a new layer of thrombus. This process would appear to have occurred repetitively, leading to the laminations, each of which maintained an impression of the patch electrode contour. Such impressions would probably not be seen if the primary site of thrombosis were the smooth atrial wall. Laminations were not seen in patient 2, whose thrombus was discovered later at postmortem examination, although the pattern of the defibrillator coil was imprinted on the outer surface of the clot. Conceivably the interior architecture of the thrombus could have deteriorated in the interim. In patient 3, the findings suggest an acute hemorrhage within a chronic fibrous pocket around the patch, perhaps related to thrombolytic therapy. The fact that minimal thrombus formation was noted beneath patches placed adjacent to a ventricular surface is obviously important, and suggests that the less mobile right atrial wall may contribute to thrombus formation or perhaps be more susceptible to epicardial vessel erosion. Three of these patients had atrial fibrillation, atrial flutter, or junctional rhythm before the thrombus was discovered, potentially creating an area of stasis between the patch and the heart that could contribute to thrombus formation. No discharges of the defibrillator occurred in any of these patients (the generator was not yet implanted in 3), eliminating electrical causes as a source of thrombus development.
Our experience should be contrasted with a recent case report published by Feng and others [12] in which they describe localized thrombosis beneath a defibrillator patch that had eroded the adjacent ventricular surface; active bleeding was encountered at reexploration. In our 2 patients undergoing early reoperation, we saw no evidence of atrial or epicardial bleeding. On the other hand, both the patient described by Feng's group and our own received patches made by the same manufacturer, and it is interesting that the acute thrombus pictured in the Feng report also had a surface imprint of the patch, although laminations were not described [12]. This further emphasizes the thrombogenic properties of this patch surface, which can lead to life-threatening cardiac compression if the patches are placed adjacent to a compliant chamber.
Our data do not permit an accurate estimate of the risk for this complication. Most patients with defibrillator patches do not undergo specific investigation for such a thrombus, which can apparently be asymptomatic, as in patient 2. Nevertheless, we believe that this experience should cause surgeons to be cautious about placing Medtronic defibrillator patches within the pericardium adjacent to the right atrium, especially in patients requiring extracorporeal circulation, as we observed a 29% (4/14) incidence of this complication under these circumstances. Experience with other operative approaches has documented that satisfactory defibrillation thresholds can be obtained with patches applied to pericardial surfaces over the right and left ventricles [1, 6–9] or in an extrapericardial location [15], and we recommend that this practice be extended to those patients undergoing defibrillator implantation through the median sternotomy route.
For those patients with such patches already in place over the right atrium, we recommend careful echocardiographic surveillance, especially if there is a clinical suspicion of cardiac compression. Unfortunately, even in retrospect, we are not able to identify the compressing hematomas by transthoracic echocardiography in 3 of our 4 patients. Whether a higher success rate would have been achieved with transesophageal echocardiography is uncertain, although in patient 1 transesophageal echocardiography did reveal a thrombus that was not seen transthoracically. Nevertheless, if a patient with a defibrillator patch applied over the right atrium exhibits symptoms of right heart tamponade or constriction, the possibility of a localized compressing hematoma should be considered and would probably be best evaluated by transesophageal echocardiography or radiographic techniques that visualize the lateral right atrial wall, such as computed tomography, magnetic resonance imaging, or contrast-enhanced cavography.
At our institution, most defibrillators are now implanted without thoracotomy [16], and thus we anticipate the incidence of this potentially severe complication to decline. Nevertheless, this experience is of relevance to those patients who may still undergo defibrillator patch implantation during the correction of other cardiac problems.
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Footnotes
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Address reprint requests to Dr Piehler; Medical Plaza II, Suite 50, 4320 Wornall Rd, Kansas City, MO 64111.
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References
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Abstract
Introduction
