A Case of Nitinol Allergy Causing Pericardial Tamponade

ABSTRACT: Nickel hypersensitivity has been reported in up to 15% of the general population. However, there are few reported cases of patients developing nickel allergy after cardiac device implantation. This phenomenon is generally not well understood and many authorities believe that these devices are safe. Most reported cases of nickel allergy have presented with non-specific symptoms such as chest pain, palpitations, or pericarditis and the majority of patients have undergone atrial septal defect closure with devices containing nickel, such as the Amplatzer septal occluder device (St Jude Medical). Herein, we describe a case of hypersensitivity pericarditis complicated with cardiac tamponade that responded dramatically to anti-inflammatory therapy. We hypothesize that this hypersensitivity was secondary to nickel allergy.

J INVASIVE CARDIOL 2013;25(9):E180-E182

Key words: atrial septal defect, nickel allergy, pericardial tamponade

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Nickel hypersensitivity has been reported in up to 15% of the general population.¹ However, there are few reported cases of patients developing nickel allergy (NA) after cardiac device implantation.^2-6 This phenomenon is generally not well understood and many authorities believe that these devices are safe.^7,8 Most reported cases of NA have presented with non-specific symptoms, such as chest pain, palpitations, or pericarditis, and the majority have been in patients who have undergone atrial septal defect (ASD) closure with devices containing nickel, such the Amplatzer septal occluder device (St Jude Medical). Systemic toxicity is rare, despite evidence to suggest a 2- to 5-fold elevation in blood nickel level, which can be seen from a few months to years after device implantation.9,10 Herein, we describe a case of hypersensitivity pericarditis complicated with cardiac tamponade that responded dramatically to anti-inflammatory therapy. We hypothesize that this hypersensitivity was secondary to nickel allergy.

Case Report. A 66-year-old Caucasian woman presented to the emergency department with 1-week history of non-specific complaints of nausea, vomiting, diarrhea, headaches, and sharp chest pain. Her admission electrocardiogram (ECG) was unremarkable and cardiac biomarkers were negative. White blood cell count was 15.7 x 103 cells/mm3 (87% neutrophils, 6% lymphocytes, and 1% eosinophils). Work-up to identify a source of infection was started and the patient was admitted to the general medical floor with initiation of empiric antibiotics. Six months prior to this admission, she had suffered a cerebrovascular accident. Investigations revealed an atrial septal defect (ASD), which was treated percutaneously using a 25 mm Amplatzer septal occluder device (St Jude Medical). The procedure was uncomplicated and she was discharged on dual-antiplatelet therapy. 

During her current admission, she developed refractory shock. Cardiac biomarkers became positive, with a peak troponin-I of 24.6 ng/mL in 24 hours (99th centile <0.08 ng/mL). ECG demonstrated low QRS voltage, but was otherwise unremarkable. Physical examination showed a 35 mm Hg pulsus paradox. Bedside echocardiogram revealed a large anterior pericardial effusion with late diastolic collapse of the right ventricle suggestive of cardiac tamponade (Figure 1). There were no wall-motion abnormalities seen and the ASD device was intact. The patient was taken emergently to the catheterization lab, where cardiac tamponade was confirmed and pericardiocentesis was performed with evacuation of 100 cc of serous fluid. Coronary angiography was unremarkable for obstructive coronary disease. Pericardial fluid analysis was unrevealing, with a white cell count of 6375 cells/mm3 (1% eosinophils). All microbiological culture data remained negative. Despite successful pericardiocentesis, her clinical course remained unfavorable. Over the next 48 hours, she developed progressive multi-organ dysfunction requiring high-dose vasopressors, mechanical ventilation, and renal replacement therapy. A right heart catheterization was repeated (Table 1), showing elevated right-sided filling pressures. Repeat echocardiogram did not show reaccumulation of pericardial fluid and a concern for a restrictive cardiomyopathy was raised. Heart failure service was consulted for possibility of heart transplantation. Pathological and laboratory work-ups for restrictive cardiomyopathy were unrevealing. 

Retrospective history obtained from the family confirmed that the patient had not felt well since the ASD closure, complaining of fatigue, dyspnea, and frequent headaches. Furthermore, she had been allergic to nickel-containing jewelry prior to presentation. Treatment with intravenous methylprednisolone 80 mg every 8 hours was initiated without skin patch testing for NA given her serious clinical condition. Interestingly, within the next 24 hours her cardiac filling pressure began to improve with dramatic improvement in her systemic vascular resistance. She was maintained on the same dose of intravenous steroids for the next 5 days, during which she was successfully extubated and weaned off all support.  Steroid taper was begun on eay 6 and switched to oral therapy on day 8. Over the next 3 weeks, she made a complete recovery and was discharged to a nursing facility on oral prednisone 20 mg daily. Over the next 3 months, prednisone dose was tapered to 5 mg daily without incident. Serial follow-up echocardiography did not show reaccumulation of pericardial effusion. She was rehospitalized on several occasions subsequently for various issues, including clostridium difficle septicemia and eventually the family elected to pursue comfort care. She died 3 months after the index admission. 

Discussion. There are several devices available for ASD closure, including the popular Amplatzer closure device made from nitinol, which is a highly malleable, biologically inert alloy with tremendous elastic properties, making it an ideal choice for medical devices. The issue of NA and its effects remains controversial. Several case reports and series have reported non-serious reactions to device implantations. Most patients improved with medical management, while only a few required device removal. Information regarding correlation of history of NA and adverse patient outcomes remains obscure. An online survey from experienced congenital cardiac interventionists showed that the majority (80%) believed NA exists, while only 44% inquired about it before the procedure and none performed skin patch testing. All patients who had a reaction had undergone ASD closure and all reactions occurred within 1 month of device implantation.¹¹

Optimal treatment and prevention strategies of nickel-hypersensitivity related complications are not well defined. In a series of 6 patients with confirmed NA, none developed complications.¹² Nickel avoidance strategies using a platinum-coated device preventing the release of nickel while maintaining the same elasticity have been proposed.¹³ Further studies are warranted to answer these questions.

In our patient, we cannot claim a proven causal association between her clinical presentation and hypersensitivity to nickel; her clinical course, coupled with an unusual dramatic improvement following administration of high-dose steroids, is suggestive of such an association. We hypothesize that NA could have been responsible for this patient’s clinical challenge and it should be considered in the presence of vasodilatory shock when other more common causes, such as systemic infection, auto-immune disorders, or collagen vascular diseases, have been ruled out (especially in a patient with a nickel-containing ASD closure device).

Conclusion. NA should be considered in the differential diagnosis for patients who have undergone ASD closure with nickel-containing devices presenting with non-specific symptoms, pericardial effusion, or unexplained distributive shock.

References

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From ¹the Department of Cardiology, Bridgeport-Yale Hospital, Bridgeport, Connecticut, ²the Department of Cardiology, University of Alabama at Birmingham, Birmingham, Alabama, and ³the Department of Medicine, Division of Cardiovascular Disease, University of California Los Angeles, Los Angeles, California.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted March 26, 2013, provisional acceptance given April 10, 2013, final version accepted June 13, 2013. Address for correspondence: Mohit Jain, MD,

Department of Cardiology, Bridgeport-Yale Hospital, 267 Grant Street, Bridgeport, CT 06610. Email: mohitjainmd@gmail.com