Introduction: Allergic contact dermatitis to cardiac rhythm devices (CRD) has been reported sporadically from the early 1980s to present. Most of these cases involve allergic reactions to direct contact agents such as nickel, silicone, titanium, cobalt, epoxy resin, mercury, polysulfone, polyurethane and polychloroparaxylene. Our case is unique in that the strongest allergic reaction was with thiuram and P-phenylenediamine (PPD), which has only been documented once since the advent of permanent pacemakers (PPM) Case: 58-year old male with history of hypertension and coronary artery disease presented with palpitations and fatigue. Holter monitoring demonstrated tachybrady syndrome and he underwent dual chamber PPM implantation (L331 Accolade TM MRI - Boston Scientific Inc). Eight weeks later he presented with new onset rash around his neck and the surgical site. PPM allergy was suspected, as patient did not respond to empiric antibiotics. He underwent PPM and lead extraction. Decision was made to observe patient without immediate re-implantation of PPM. Skin patch testing was strongly positive to thiuram and PPD. Final diagnosis of allergic contact dermatitis was made and patient’s condition improved. Discussion: Thiuram and PPD, the raw materials used in the production of silicone rubber, encase pacemaker headers and leads. Individuals typically get sensitized to PPD by using hair dyes or temporary henna tattooing. The device used in our patient contained the same compounds. No studies to date document the true incidence and/or prevalence of allergic reactions to pacemaker components. One non-randomized retrospective trial reported benefits of skin patch testing before CRD implantation in patients who had a history of allergy to metals. Future trials are warranted to further evaluate the efficacy and benefits of pre-implantation skin testing and if it would benefit the population as a whole.
Brugada syndrome is a congenital cardiac channelopathy characterized by ST-segment elevation (≥2 mm) and subsequent inverted T wave in a minimum of two right precordial leads (Brugada type 1 ECG [electrocardiogram] pattern) on ECG. Brugada syndrome is estimated to be responsible for 4%-12% of all sudden cardiac deaths and up to 20% in patients with structurally normal hearts. Development of a temporary Brugada pattern, known as Brugada phenocopy, has been observed in individuals presenting with reversible underlying conditions such as hyperkalemia, hyponatremia, acidosis, ischemia, and pulmonary embolism, among others. Herein we present a case of Brugada phenocopy seen in a patient in diabetic ketoacidosis, which resolved after the electrolyte abnormalities were corrected.
Introduction: 1. In contemporary practice, implantation of Cardiovascular Implantable Electronic Devices (CIED) is associated with low complication rate peri-procedurally. 2. However, in some patients these complications can have high morbidity and mortality; namely pneumothorax, pericardial tamponade, pacemaker syndrome, and rarely tricuspid regurgitation (TR) secondary to lead impingement. 3. TR secondary to RV lead impingement is not uncommon but infrequently lead to severe TR and worsening heart failure symptoms. 4. We present a case of severe TR secondary to RV lead impingement leading to splanchnic congestion and recurrent ascites, worsening renal failure leading to hemodialysis (HD), all of which resolved with lead extraction. Case: A 77-year-old woman with known CAD with prior PTCA, paroxysmal AF, and prior watchman implantation, evaluated in our clinic for severe TR. She had recurrent admissions for ascites needing paracentesis. Her liver function and ultrasound was normal. Her renal function worsened and HD was initiated. ECHO showed normal LVEF, severe TR with RVSP of 74mmHg, and mild RV dysfunction. Pericardial physiology was normal. The lead was noted to be impinging on the septal leaflet, and adherent. Normal pulmonary valve function. Follow up: We proceeded to perform RV lead extraction and implanted a new leadless pacemaker [MICRA-AV, Medtronic Inc]. Her follow up ECHO in 2 weeks showed mild TR and normal RV function. RVSP had dropped significantly to 34mmHg. Surprisingly, her needs for paracentesis came down and by 3 months follow up she did not need paracentesis anymore. Her renal function improved, and her HD needs stopped. Conclusions: 1. CIED implantations are associated with low complication rate (less than 5% in total) in most patient cohorts but in some patients it can be associated with significant complications increasing their morbidity and sometimes mortality. 2. Severe TR is a well-recognized complication of pacemaker implantation. It led to recurrent ascites needing paracentesis, ESRD requiring HD and multiple hospital admissions and thus increasing the morbidity. 3. It is important to recognize the uncommon complications of such commonly used intracardiac devices for electrophysiologists, cardiologists and PCPs.
BACKGROUND: Acute pericarditis is the most common disorder affecting the pericardium. It accounts for less than 1% of patients who are admitted to the hospital for non-ischemic chest pain and 5% who present to the emergency department with non-ischemic chest pain. The most common etiology of acute pericarditis in developed countries is idiopathic although a pre-disposing viral illness has also been recognized as a common cause. Infectious etiologies in developed countries have been seen with commonly occurring viruses such as coxsackievirus, echovirus, adenovirus and less frequently EBV. CASE: We present a 41-year-old man who came in with fevers, rigors, shortness of breath and chest pain. Transthoracic echocardiogram was (TTE) demonstrated a large pericardial effusion without evidence of tamponade. He underwent a diagnostic pericardiocentesis followed by a pericardial window during his initial hospitalization without any complications and was discharged home on NSAIDs and colchicine. Serology results demonstrated positive EBV IgG and Nuclear Antigen, concerning for active EBV pericarditis. Pathology resulted as necrotizing pericardial tissue with diffuse inflammation. The patient was readmitted within 48 hours with worsening shortness of breath and leg edema. Repeat TTE revealed a large recurrent pericardial effusion with right ventricular collapse concerning for tamponade. The patient was ultimately transferred to a tertiary care center for pericardiectomy evaluation. DISCUSSION: Ebstein-Barr virus is rarely an etiology of acute pericarditis, much less necrotizing pericarditis. When identified it should raise concern for long term complications such as recurrent pericarditis and tamponade. We believe patients who have evidence of necrotizing pericarditis are at a high risk for constrictive pericarditis and should not only have closer follow while maintaining a low clinical threshold for definitive treatment with pericardiectomy.
BACKGROUND: Immune checkpoint inhibitors (ICI) have changed the treatment scope for malignancies. The mechanism of ICIs is targeting of immune checkpoints that can suppress a response to a stimulus which can effect any organ. Adverse effects are usually mild but myocarditis, although rare, is becoming more recognized as a life threatening entity. The increase in mortality seen with ICI-induced myocarditis is more frequent with combination therapy. Most cases of ICI-induced myocarditis are limited to direct myocardial injury but there is a lack of evidence regarding conduction disease. CASE DESCRIPTION: We present a 74-year-old man with known metastatic malignancy recently started on ICI with ipilimumab and nivolumab who presented with complaints of abdominal pain, SOB and chest pain. His ED workup was consistent with colitis and acute PE without RV strain. Troponins and BNP were elevated and his ECG showed 3rd degree AV block. A coronary angiogram was negative for obstructive CAD and a temporary trans-venous pacemaker was placed. Cardiac MR showed LGE with active inflammation of the mid-myocardium. The patient had complex presentation as a side effect of ICI leading to myocarditis, 3rd degree AV block, colitis and PE. He was started on high dose methylprednisolone 1gm daily. Within 24 hours there was improvement evidenced by intermittent return of intrinsic conduction. At 48 hours there was marked improvement with restoration of sinus rhythm without evidence of AV block and/or use of the temporary pacemaker. Discussion: Early recognition of disease processes is difficult when there is minimal data to support a cause and effect. Increasing clinical awareness regarding adverse effects of ICI is paramount in decreasing the risk for unnecessary therapies, in our case, placement of a permanent pacemaker. Although there have been case reports of ICI-induced myocarditis, there has not been expert consensus regarding management of conduction pathway abnormalities.
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