Frog sign and AV nodal reentrant tachycardia: A case report.

Supraventricular tachycardia is one the most frequent cardiac arrhythmias seen in patients, with AVNRT being the most common subtype. Two subgroups of AVNRT have been reported, that of typical and atypical. "Frog Sign," long considered a classic physical exam sign, albeit rare, is associated with typical AVNRT. We present a case of a patient who presented with frog sign and ultimately was determined to have AVNRT. Knowledge of "frog" sign aids clinical diagnosis and correct treatment.

Infective Endocarditis Manifesting as Severe Elevation in Serum Aminotransferases in the Absence of Severe Tricuspid Regurgitation, Heart Failure, or Shock: A Diagnostic Challenge.

Infective endocarditis (IE) is a challenging condition to diagnose, given its protean clinical signs and symptoms, Elevation in serum aminotransferases in IE is associated with valvular regurgitation, acute heart failure, or congestive hepatopathy. Studies show co-existing liver failure portends worsening outcomes in IE and poses a challenge for successful surgical management. Here we report a diagnostic challenge in a 35-year-old man with IE presenting predominantly with gastrointestinal symptoms and severe elevation in serum aminotransferase. The degree of aminotransferase elevation in our patient prompted consideration of alternative causes like acetaminophen toxicity. Severe elevation in aminotransferases as an initial presentation in the absence of significant valvular regurgitation, acute right heart failure, or shock is uncommon. A high degree of suspicion is required to diagnose IE when patients present with atypical signs and symptoms to avoid delay in initiation of antibiotics and improve overall morbidity and mortality.

Renal Phosphate Wasting Due to Tumor-Induced (Oncogenic) Osteomalacia.

Osteomalacia is a widely prevalent bone disorder that is caused by an imbalance in body calcium and phosphate. Tumor-induced osteomalacia (TIO) is a rare form of osteomalacia that is associated with mesenchymal tumors. It is caused by overproduction of fibroblast growth factor 23 (FGF-23), a hormone involved in phosphate regulation. A 59-year-old male with a history of factor V Leiden mutation, pulmonary embolism, and deep vein thrombosis was diagnosed with oncogenic osteomalacia in 2008 following laboratory findings significant for low phosphorus and elevated FGF-23 levels. He underwent a resection of a right suprascapular notch mass with the biopsy confirming a phosphaturic mesenchymal tumor. He was maintained on oral phosphorus and calcitriol replacements with a regular follow-up with oncology and nephrology. Eight years later, the patient's phosphorus levels started declining despite replacement. A repeat test showed FGF-23 levels once again elevated. A whole-body magnetic resonance imaging (MRI) scan showed no significant findings. The patient was continued on oral replacement therapy with a close follow-up. Two years later, urine phosphorus excretion was elevated at 2494 mg per 24 hours with low plasma phosphorus (1.2 mg/dL) and an elevated FGF-23 level of 1005 relative units (RU)/mL. A repeat MRI of the right shoulder revealed a mass in the supraspinatus muscle and another in the spinal glenoid notch. The masses were resected and the biopsy was consistent with a recurrence of the phosphaturic mesenchymal tumor. Follow-up serum phosphate levels remained in the normal range. FGF-23 plays a critical role in bone mineralization through the regulation of phosphate levels. Overproduction, as seen in mesenchymal tumors, results in hyperphosphaturia, hypophosphatemia, and low calcitriol levels. While the definitive treatment of TIO involves the resection of the mesenchymal tumor, localization of the tumor is often challenging given its small size and slow growth. This leads to delayed diagnosis and treatment. For individuals whose tumor cannot be resected or detected, burosumab is the preferred form of therapy. Interestingly, FGF-23 is shown to have a potential cardiovascular (CV) morbidity and mortality through various mechanisms like activation of myocardial FGF-23 receptors, endothelial dysfunction, inflammation, and altered phosphorus and vitamin D metabolisms. While studies have shown possible FGF-23 effects on CV outcomes in patients with chronic kidney disease, this has not been proven in cases of TIO.

A Rare Thrombophilic Occurrence: Dural Venous Sinus Thrombosis in a Patient with Significant Family History of Protein S Deficiency.

Protein S is a potent anticoagulant that downregulates thrombin formation and is a vitamin K-dependent glycoprotein which is primarily synthesized in the liver. A deficiency in this protein or decreased activity, as seen in hereditary protein S deficiency, can lead to life-threatening thrombosis. Hereditary protein S deficiency is a rare disease as listed by the National Organization for Rare Disorders (NORD). It is known to cause venous as well as arterial thromboembolic events commonly occurring in the deep leg and pelvic veins. Dural venous sinus thrombosis is a rare consequence of protein S deficiency and is associated with a risk of increased morbidity and mortality. We report a case of dural venous sinus thrombosis in a patient with a family history of protein S deficiency in nine family members. A 53-year-old female presented to the ED with a three-day history of persistent left-sided headache, left facial numbness with tingling, and photophobia. She denied any visual disturbances, slurring of speech, and/or unilateral weakness. Some 10 years prior to this episode, she was placed on warfarin therapy for deep vein thrombosis (DVT) of lower extremity, but she discontinued it after three years of treatment without consulting her treating physician. She was taking oral contraceptive pills (OCPs) for two years and discontinued one month ago. She has nine family members with protein S deficiency, but the patient was never screened for a hypercoagulable state. On admission, her vital signs were within normal limits. Pupils were round and reactive to light, neck was supple, there was a sensory deficit for pinprick on the left V2-V3 distribution, and remainder of the cranial nerves and neurologic examination was unremarkable. CT scan of the head demonstrated a hyper-density within the left transverse and sigmoid sinus suspicious for dural venous sinus thrombosis. This was confirmed by CT angiogram showing a filling defect throughout the transverse sinus and sigmoid sinus extending below the jugular bulb into the superior aspect of the jugular vein. Intravenous heparin and warfarin were initiated. As the patient had severe trypanophobia and IV heparin required frequent activated partial thromboplastin time (APTT) monitoring, this was later changed to subcutaneous low-molecular-weight heparin and warfarin. Subsequent thrombosis panel showed a reduced protein S activity of 15% and low levels of total and free protein S antigens. She was discharged home with life-long warfarin therapy. In conclusion, cerebral dural venous sinus thrombosis is a rare and potentially life-threatening condition that can be seen in hereditary protein S deficiency. A high degree of suspicion in young females with worsening headache and neurologic signs and symptoms will help with timely diagnosis and management avoiding serious consequences. In a patient with a family history of thrombophilia, as seen in our patient, screening is important in order to confirm an underlying thrombophilic state. Such testing may have helped our patient regarding education on avoiding potential risk factors for thrombophilia and importance of treatment adherence.

Bradycardia in Patients With COVID-19: A Calm Before the Storm?

Cardiac manifestations of coronavirus disease 19 (COVID-19), including arrhythmia, have been described in the literature. However, to our knowledge, association of COVID-19 with bradycardia has not been reported. This case study describes sinus bradycardia as a potential manifestation of COVID-19. This is a retrospective case series of four patients with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, admitted to St. Luke's University Health Network ICU between 24 March 2020 and 5 April 2020. Medical records of these patients were reviewed using the EPIC electronic health record system. Demographic, clinical, laboratory, and treatment data were reviewed against periods of bradycardia in each patient. The patient group comprised two males and two females. Two patients had pre-existing cardiovascular (CV) comorbidities but no history of arrythmias. Heart rates ranged between 66 and 88 beats/min on admission. The lowest rates during bradycardia were between 42 and 49 beats/min. The onset of sinus bradycardia in patients 1, 2, and 3 were day nine, 15, and five of illness, respectively. Patient 4 had three episodes of bradycardia, starting on day 10 of illness. Patients' bradycardia episodes lasted one to 14 days. During bradycardia, maximum body temperatures ranged between 99.9 and 100.2 degree Fahrenheit. Patients 2, 3, and 4 required vasopressors to maintain mean arterial pressure > 65 mmHg during episodes. All four patients were on propofol at some point during bradycardia with patients 1, 2, and 3 also receiving dexmedetomidine. There was no consistent correlation of these medications with bradycardia. Electrocardiogram (ECG) findings included sinus bradycardia. Prolonged QTc interval observed in patient 2 on admission improved during bradycardia. Transient sinus bradycardia is a possible manifestation of COVID-19 and is important for close CV surveillance. Etiology can be multifactorial, but severe hypoxia, inflammatory damage of cardiac pacemaker cells, and exaggerated response to medications are possible triggers. High levels of pro-inflammatory cytokines may act directly on the sinoatrial (SA) node contributing to the development of bradycardia. This may be a warning sign of the onset of a serious cytokine storm. An increased awareness of possible exaggerated bradycardia response is important to consider with the use of empiric medications which have arrhythmogenic effects.