Delayed-onset eptifibatide-induced thrombocytopenia.

PURPOSE: We present a unique case of delayed-onset, profound eptifibatide-induced thrombocytopenia that occurred 5 days after initiation of the drug. SUMMARY: Eptifibatide is a platelet glycoprotein IIb/IIIa receptor inhibitor with indications for use in patients with acute coronary syndromes. Eptifibatide-induced thrombocytopenia is uncommon but well studied and typically occurs within 24 hours of initiation of the drug. In the case described here, a 62-year-old male with a past history of coronary artery disease (including percutaneous coronary intervention within the past 12 months) was started on eptifibatide at a dosage of 2 µg/kg per minute for management of significant thrombus burden prior to a planned cardiac revascularization procedure; heparin for anticoagulation was also initiated. About 5 days after initiation of eptifibatide, the patient developed severe thrombocytopenia, with the platelet count dropping precipitously from 249 × 103/µL on admission to less than 1 × 103/µL. After eptifibatide and heparin therapy were discontinued and the patient was switched to argatroban, the platelet count recovered to 38 × 103/µL over the next 2 days. An eptifibatide platelet antibody assay was positive for IgG-mediated reactions consistent with eptifibatide-induced thrombocytopenia. Scoring of this case with the Naranjo scale yielded a score of 4, suggesting a possible adverse reaction to eptifibatide. CONCLUSION: This is the first published case report of profound eptifibatide-induced thrombocytopenia occurring more than 24 hours after eptifibatide initiation and serves to bring awareness that a delayed reaction can occur.

Chordal Systolic Anterior Motion of the Mitral Valve in Dextro-Looped Transposition of the Great Vessels After Mustard Procedure.

BACKGROUND D-transposition of the great vessels (D-TGA) was once a fatal diagnosis within the first year of life. The Mustard and Senning procedures were invented to redirect the blood flow via intra-atrial baffles. The complicated nature of the clinical course and presence of chordal systolic anterior motion of the mitral valve in a patient with D-TGA and prior subpulmonic resection and Alfieri stitching is presented. CASE REPORT A 41-year-old man presented to the clinic with a chief concern of dyspnea on exertion and chronic chest pain. Diagnosed with D-TGA as an infant, he underwent balloon septostomy and later a Mustard procedure at 3 months of age and subpulmonic resection and Alfieri stitching as an adolescent. The patient now presented with transthoracic echocardiogram-revealed severe turbulence in native left ventricular outflow tract to the pulmonary circulation. Doppler velocities indicated this was originating from chordal systolic anterior motion of the mitral valve. CONCLUSIONS This case reinforces the need for practitioners caring for such patients to become familiarized with and educated in the field of adult congenital heart disease, as patients once plagued with shorter life expectancies are living longer. Repeat surgical intervention or catheter-based therapies may be considered in the future should medical therapy fail to control our patient's symptoms. A multidisciplinary approach and further monitoring of these patients for best practice guidelines would be ideal and beneficial for the patients and practitioners alike.

Twinning: Coronary Artery Disease in Monozygotic Twins.

We present the case of a patient whose monozygotic twin brother suffered a fatal myocardial infarction at the age of 40. The patient presented with similar symptoms as his brother. Given the family history, ischemic evaluation was undertaken and revealed similar coronary anatomy and severe coronary artery disease (CAD). We review the current literature regarding genetic and environmental factors regarding coronary anatomy, locations of atherosclerotic lesions, and screening in twins.

Anticoagulation in a Patient With Mechanical Prosthetic Valves and Calcific Uremic Arteriolopathy on Warfarin.

Calciphylaxis, or calcific uremic arteriolopathy (CUA), is a rare vascular calcific disease that is most often associated with renal dysfunction and warfarin, particularly end-stage renal disease (ESRD). This condition causes debilitatingly painful skin lesions, oftentimes plaques, throughout areas of cutaneous and subcutaneous adiposity. The progression of these lesions to black eschar with ulceration is the hallmark of CUA. In this report, we present the case of a Caucasian female with a past medical history of nephrogenic systemic fibrosis (NSF), ESRD, and mechanical aortic and mitral valves, anticoagulated with warfarin, who developed CUA. In the setting of mechanical prosthetic valves, vitamin K antagonists (VKA) and aspirin are the only evidence-based antithrombotic therapies. This case presents challenging decision-making when managing anticoagulant therapy in the absence of applicable guidelines.

Acute Refractory Hypocalcemia in a 51-Year-Old Male With a History of 1,1-Difluoroethane Inhalation.

Hypocalcemia is a common electrolyte derangement that is most associated with parathryoid hormone or vitamin D abnormalities. Less common causes that most providers are aware of include hyperphosphatemia, acute pancreatitis, chronic kidney disease, and sepsis. However, certain populations are at risk for less common, but no less dangerous, causes. One such cause is 1,1-difluoroethane, an organofluorine that is used as a propellant in aerosol sprays and is commonly abused. 1,1-Difluoroethane has been noted to cause severe hypocalcemia by accumulation of the metabolite fluorocitrate in tissues. Here, we present the case of a 51-year-old male with severe hypocalcemia and multiple rib fractures following a fall, with recent history of tibial fracture. The patient had a medical history of osteoporosis with numerous fractures and chronic steroid use. He admitted to using keyboard cleaner as an inhalant for the previous month, which was found to contain 1,1-difluoroethane. Previous case reports on 1,1-difluoroethane inhalation have not reported a patient with preexisting osteoporosis or refractory hypocalcemia.