Severe hypocalcemia after denosumab treatment leading to refractory ventricular tachycardia and veno-arterial extracorporeal membrane oxygenation support: a case report.

BACKGROUND: Severe hypocalcemia may lead to life-threatening arrhythmias. Denosumab is an effective treatment for osteoporosis that allows long intervals between doses. However, there is a risk of hypocalcemia in some patients. Due to the long half-life of denosumab, emergency physicians caring for patients presenting with symptoms of hypocalcemia may not be aware of the medication, and adverse effects may last longer. CASE PRESENTATION: A 55-year-old woman with a history of systemic lupus erythematosus (SLE) and anxiety disorder called for an ambulance for symptoms of hyperventilation and muscle cramps. After evaluation at the local hospital, she developed pulseless ventricular tachycardia and was resuscitated by defibrillation by the hospital staff. After conversion to sinus rhythm, she was transported to a tertiary center. Upon arrival, pulseless ventricular tachycardia occurred again, and veno-arterial extracorporeal membrane oxygenation (ECMO) and intra-aortic balloon pumping (IABP) were implemented. Laboratory results showed severe hypocalcemia (corrected calcium level of 5.3 mg/dL) whereupon intravenous calcium supplementation was started. She had received the first dose of denosumab (60 mg) by subcutaneous injection 24 days prior to hospitalization. She was eventually weaned from ECMO and IABP support. CONCLUSION: Cardiac arrest due to hypocalcemia is relatively rare but can be fatal. In the present case, hyperventilation may have acutely exacerbated pre-existing hypocalcemia, leading to ventricular tachycardia. The patient had a slightly decreased serum calcium level prior to denosumab. Close monitoring may be preferable after the primary dose of denosumab in selected patients. Emergency physicians caring for patients who may be suffering from symptoms/signs of hypocalcemia must be mindful of medications that have long half-lives and affect electrolyte balance when treating fatal arrhythmia due to hypocalcemia.

Nitroglycerin improves left ventricular relaxation by changing systolic loading sequence in patients with excessive arterial load.

Nitroglycerin abbreviates left ventricular (LV) relaxation through improved hemodynamics as well as by direct actions on the myocardium. The aim of this study was to examine whether the changing systolic loading sequence during nitroglycerin administration affects LV relaxation in patients with excessive arterial load. By use of a conductance catheter with microtip manometer, the effects of intravenous nitroglycerin (0.3-0.5 microg/kg/min) on LV function and hemodynamics were examined in 39 patients with various degrees of LV contractility. Patients were divided into two groups according to LV-arterial coupling, the ratio of end-systolic elastance (Ees) to effective arterial elastance (Ea). In patients with Ees/Ea ratio > 1, nitroglycerin had no effect on the time to peak force or on the time constant of LV relaxation (tau). On the other hand, in patients with Ees/Ea < 1, which represented excessive arterial load, nitroglycerin significantly shortened the time to peak force, shifted the peak of the loading sequence from late to early systole, and significantly decreased tau without any changes in Ees. Thus, nitroglycerin improved LV relaxation in patients with excessive arterial load partly by changing the systolic loading sequence.