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Ann Thorac Surg 1995;60:1112-1115
© 1995 The Society of Thoracic Surgeons
Section of Cardiology, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska
Accepted for publication April 12, 1995.
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Abstract |
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Introduction |
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During the past 10 years, more than 35,000 patients have had a new cardiac surgical procedure, implantation of an epicardial cardioverter/defibrillator system for the treatment of life-threatening cardiac arrhythmias. Intuitively, this procedure should have the same type of complications as other cardiac surgical procedures, but reports of defibrillator-associated pericardial constriction are exceedingly rare. We report a case of defibrillator patch-associated constriction as the starting point in a discussion of why this debilitating, but potentially curable, entity is less frequently reported in the defibrillator population.
A 35-year-old woman with a history of sick sinus syndrome went to her local hospital in May 1993 complaining of palpitations and profound dizziness. While sitting in the waiting room, she lost consciousness and became pulseless and apneic. A ``sternal thump'' was administered by the physician in attendance and cardiopulmonary resuscitation was begun with the patient regaining consciousness 15 to 20 seconds later. Initial electrocardiographic recordings showed sinus tachycardia without evidence of myocardial injury or infarction. She was transferred to our institution for further evaluation.
Both serial electrocardiograms and cardiac enzymes failed to demonstrate evidence of a myocardial infarction and her baseline electrocardiogram was entirely normal without evidence of Wolff-Parkinson-White or long QT syndrome. Her 2-year-old pacemaker (placed for treatment of sick sinus syndrome) was interrogated and found to be functioning properly. Continuous ambulatory monitoring showed several episodes of nonsustained ventricular tachycardia, the longest episode being 12 beats in duration. A signal averaged electrocardiogram was normal and a two-dimensional echocardiogram showed normal wall motion and chamber size without evidence of mitral valve prolapse or right ventricular abnormalities. She was able to exercise for 9 minutes 41 seconds on a standard Bruce protocol, achieving a maximum heart rate of 191 beats/min (the pacemaker was inhibited by her intrinsic sinus rhythm) without evidence of angina, hypotension, or ventricular tachycardia. Subsequent cardiac catheterization demonstrated normal left and right heart pressures, no significant coronary disease, and an ejection fraction of 0.60 with normal wall motion. An invasive electrophysiology study was performed and failed to induce any significant dysrhythmias.
These results indicated that she was a survivor of sudden cardiac death with a negative electrophysiology study and no obviously reversible cause for her cardiac arrest. On the basis of this conclusion, she opted for treatment with an automatic defibrillator. A CPI (Cardiac Pacemakers International, St. Paul, MN) model 1600 defibrillator was subsequently implanted using two CPI model L67 epicardial patches (placed inside the pericardium) as the defibrillating electrodes.
One month after defibrillator implantation she developed a postpericardiotomy syndrome that was successfully treated with nonsteroidal antiinflammatory therapy. Over the ensuing months, however, she was plagued by an ill-defined epigastric discomfort, fatigue, and shortness of breath. She gained more than 20 pounds by December 1993 and was experiencing nightly orthopnea. Physical examination at that time demonstrated hepatic congestion, marked peripheral edema, and jugular venous abnormalities suggestive of pericardial constriction. Cardiac catheterization documented constrictive physiology with right atrial, right ventricular diastolic, pulmonary arterial diastolic, pulmonary capillary wedge, and left ventricular end-diastolic pressures all being equal at 22 to 24 mm Hg (Fig 1
). Left ventriculography showed restricted movement of the left ventricle in the region covered by the epicardial defibrillator patches.
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She was not a candidate for a transvenous defibrillating system because of her dual chamber pacer and previous subclavian vein thrombosis. Consequently, two new CPI L67 patches were placed outside the pericardium and the model 1600 pulse generator was replaced in the subcutaneous pocket.
She recovered uneventfully from operation and more than 1 year later, has no evidence of constriction, either clinically, in her jugular venous waveform or by Doppler echocardiography.
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Comment |
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A Medline (National Library of Medicine) literature review uncovered only 6 published cases of defibrillator patch-associated constriction [5–9]. Cardiac Pacemakers, Inc (the largest worldwide supplier of defibrillators) is aware of only 1 other unpublished case of constriction (Michael Flanagan, Cardiac Pacemakers, Inc, St. Paul, MN; personal communication). This means that, including the current case report, there are only 8 recognized cases of defibrillator patch-associated constriction, which is about one-tenth of the expected incidence. Two possible explanations for this discrepancy between the expected and reported incidence of constriction come to mind.
First, the incidence of constriction may truly be lower with epicardial defibrillating patch placement than with coronary artery bypass grafting. Singer and colleagues [10] found that all of the intrapericardial electrode patches they examined at postmortem exhibited pericarditis with dense adhesions similar to the operative findings in this report. Their one example of extrapericardial electrode placement, however, showed no evidence of pericarditis at postmortem examination suggesting that extrapericardial placement may eliminate the nidus for the inflammatory reaction that leads to constriction. The finding that the patient in this report has remained free of clinical constriction 1 year after extrapericardial patch electrode placement suggests that this may be part of the explanation. The vast majority of epicardial systems, however, have been placed inside the pericardium to avoid damage to the phrenic nerve [11]; therefore the lower reported incidence of constriction cannot be explained entirely by this operative technique.
A second, and more disturbing, explanation for the low reported incidence of constriction may be our failure to recognize pericardial constriction. Because the majority of defibrillator patients also have depressed ejection fractions and New York Heart Association functional class II to IV heart failure [12, 13], worsening right heart failure is frequently interpreted as worsening systolic function. The patient in this report was known to have normal systolic function, therefore other causes of right heart failure were considered. In the typical patient with abnormal systolic function, however, we may not be so quick to look for other causes. What ``clues'' then should lead us to investigate the possibility of constriction and what type of testing might be beneficial in establishing this diagnosis?
``Crumpling'' of the epicardial patches on a plain chest radiograph has been suggested by some investigators as a clue to changes in the patch electrodes that may lead to constriction. This finding did not appear to be clinically useful in the Wisconsin series [6], however, where 21% of the patients had crumpled patches and only 1 patient had clinical constriction. Visualization by computed tomographic scanning did not improve the diagnostic yield either as 25% of the patients (in the same series) had an abnormally thickened pericardium by computed tomographic scan.
Doppler evaluation of ventricular filling and central venous flow patterns [14] is a useful tool for evaluating the presence of constriction, but the difficulty of obtaining adequate echocardiagraphic windows in the presence of the electrode patches is a practical limitation of this technique.
Arriving at the diagnosis of constriction then still appears to require a high index of suspicion as well as invasive hemodynamic assessment to document the equalization of diastolic pressures in the setting of the characteristic diastolic ``dip and plateau,'' such as was seen in this patient.
Although the diagnosis of constriction can be difficult to establish in this population, arriving at the correct diagnosis is important because untreated pericardial constriction has a poor prognosis and surgical pericardiectomy appears to be the only effective treatment [15]. Five of the 8 known cases of defibrillator patch-associated constriction did well after patch removal and decortication. The outcome in 2 of the remaining cases is unknown [8] and the only patient with infected electrode patches [5] died without leaving the hospital after the patches were surgically removed.
With the increasing availability of transvenous defibrillating systems, fewer epicardial electrode systems will be implanted, so this problem will become less of a concern. In the meantime, however, because the majority of the current defibrillator population uses epicardial patch electrodes, we should consider the possibility that any defibrillator patient with worsening fatigue, shortness of breath, and edema may not have worsening systolic myocardial function but defibrillator patch-associated pericardial constriction.
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