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Ann Thorac Surg 1995;60:1115-1116
© 1995 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery, Washington University School of Medicine, 3108 Queeny Tower, Barnes Hospital Plaza, St. Louis, MO 63110
This case report by Barrington and colleagues addresses an uncommon complication of thoracotomy defibrillator implantation, namely, constriction from the fibrous capsule that forms around the patch electrodes placed in the intrapericardial position.
Their literature review further documents that the reported incidence of constrictive ``pericarditis'' after thoracotomy defibrillator implantation is one-tenth that reported after other types of cardiac operations. Because postoperative constriction is itself rare [1], they conclude that constriction after intrapericardial placement of patch electrodes is probably underrecognized.
Although the other case reports documenting this complication are present in cardiology, medical, and radiology journals, this appears to be the first clinical report in a surgical journal. However, any cardiac surgeon who has had to perform an open heart operation on a patient with previously placed intrapericardial patches cannot have failed to notice the intense inflammatory response generated by these ''inert`` patches. In some cases this fibrous capsule has obliterated the underlying epicardial anatomy and tissues, including the epicardial coronary arteries. Because typically one patch was sewn to the epicardium overlying the left ventricle and one to the right ventricular epicardium, either left- or right-sided constriction could be possible. On the assumption that this complication could occur, some researchers advocated extrapericardial placement of patches, even at the time of concomitant revascularization [2, 3]. In the era when intrathoracic patches were a component of implantable cardioverter defibrillator systems, placement of these patches within the pericardium was reported to be associated with lower defibrillation thresholds [4].
Unbeknownst to Barrington and co-workers, studies by Spotnitz and colleagues [5, 6] have examined this complication experimentally. The effect of the combination of patches and related fibrosis was demonstrated in this chronic porcine model to result in diastolic changes consistent with restrictive pericardial disease, similar to the findings reported in this case report.
On the basis of these experimental findings and this literature review, the assumption by Barrington and colleagues that this complication is underrecognized is probably correct. This is important for several reasons. First, surgical decortication represents the only effective treatment for an otherwise progressive and relentless process. Second, the population of patients who were most likely to have intrapericardial patches placed at the incident operation were those with the worst ventricular function [6]; this population would be least likely to tolerate further impairment of function by the patches. Third, a number of these devices were placed in patients awaiting transplantation, as an ''electrophysiologic bridge to transplantation`` [7]. For obvious reasons, these patients would be unlikely to tolerate a further decline in function while awaiting transplantation.
With the advent of nonthoracotomy devices for implantation, the number of patients at risk for this complication will remain constant for a time, and then decline. At this time, however, the majority of the approximately 35,000 implantable cardioverter defibrillators implanted in the United States have been to date thoracotomy devices using patch electrodes. A significant percentage of these patients had intrapericardial patches placed at the time of the original implant, and therefore, the caution of Barrington and colleagues about recognizing this problem will remain important for the foreseeable future.
In those patients with implantable cardioverter defibrillators who are clinically asymptomatic, screening for this problem by transesophageal echocardiography can be performed at the time of generator and lead replacement. If necessary, invasive right-heart catheterization could also be performed in this setting. In patients who present with worsening failure, consideration of this circumstance as a cause for the declining clinical condition should be made. Again, transesophageal echocardiography to assess transmitral and transtricuspid flow velocity profiles [5, 8], as well as regional wall motion, would be the most useful screening test to differentiate constriction from worsening cardiomyopathy. As pointed out by Barrington and colleagues, however, a high index of suspicion is perhaps the most important factor in recognizing this underreported condition in implantable cardioverter defibrillator patients.
References
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  J. H. Lemmer Jr and T. B. Ferguson Jr Defibrillator Patch Constriction Ann. Thorac. Surg., March 1, 1996; 61(3): 1042 - 1042. [Full Text]
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