Potential proarrhythmic side effect of high dose and prolonged infusion of sodium nitroprusside through calcium ion reduction: a case report

Abstract

Abstract Background Sodium nitroprusside (SNP) is an excellent drug in acute decompensated heart failure (HF) patients with high vascular peripheral resistance. Its prolonged administration may cause thiocyanate accumulation and toxicity. A proarrhythmic side effect has never been reported. Case summary Herein, we report a case of an adult male affected by advanced HF due to a valvular cardiomyopathy admitted to our intensive cardiology unit with severe decompensation and waiting for a heart transplant. He was treated for several weeks with high-dose SNP, due to severe pulmonary hypertension and an extremely labile haemodynamic profile. He progressively developed high thiocyanate levels and, concomitantly, free calcium ion depletion, despite normal total calcium levels, with iterative ventricular arrhythmias. Calcium ion depletion was not responsive to calcium supplementation. We suspected a causative role of thiocyanate since the negatively charged sulfur atom of the thiocyanate molecules could bind the positively charged free calcium ions, leading to a free calcium ion depletion. Thus, we cautiously reduced SNP dosage, according to the patient's haemodynamic profile, with concomitant progressive free calcium ion normalization, thus reducing the arrhythmic burden of the patient, being able to finally perform heart transplantation. Conclusion We describe for the first time a proarrhythmic side effect of prolonged SNP administration, namely, calcium ion depletion, likely related to thiocyanate toxicity. Despite aggressive calcium supplementation, the only way to reduce the arrhythmic burden was SNP down titration.