Optimizing Pulmonary Artery Pressures with use of Ivabradine in Cardiomyopathy

Abstract

Case reportPatient is a 42 yr old male with past medical history of chronic systolic heart failure, nonischemic cardiomyopathy since 2011, felt to be secondary to chronic prescription anabolic steroid use, EF 10-15%, history of cardiac arrest due to hyperkalemia, ICD single-chamber, hypertension, and chronic kidney disease stage III. Based on right heart cath and cardiopulmonary stress test, the patient is too good for advanced heart failure therapies. He is a NYHA II and is managed on carvedilol 25mg po BID, lisinopril 5 mg po daily, ivabradine 7.5mg po BID. On 2/13/18, patient ran out of his ivabradine. The following day his heart rate started to increase to the mid 90s from a baseline of 70s . It took two days for his diastolic pulmonary artery pressure (PAd) to increase above his set threshold of 15-20mmHg after stopping the ivabradine. He was able to restart ivabradine on 2/20/18 and his heart rate came back to the 70s and his PAd dropped back below 20 mmHg.ConclusionOptimizing PAd can be influenced by many factors including hypervolemia, hypovolemia, blood pressure, and heart rate. In many cases, optimizing heart failure medications such as the betablockers and angiotension converting enzyme inhibitors can help optimize PAd, however controlling blood pressure and heart rate are important also. In this case study, using ivabradine to reduce heart rate shows a significant improvement in PAd without adjusting diuretics or other heart failure medications. Patient is a 42 yr old male with past medical history of chronic systolic heart failure, nonischemic cardiomyopathy since 2011, felt to be secondary to chronic prescription anabolic steroid use, EF 10-15%, history of cardiac arrest due to hyperkalemia, ICD single-chamber, hypertension, and chronic kidney disease stage III. Based on right heart cath and cardiopulmonary stress test, the patient is too good for advanced heart failure therapies. He is a NYHA II and is managed on carvedilol 25mg po BID, lisinopril 5 mg po daily, ivabradine 7.5mg po BID. On 2/13/18, patient ran out of his ivabradine. The following day his heart rate started to increase to the mid 90s from a baseline of 70s . It took two days for his diastolic pulmonary artery pressure (PAd) to increase above his set threshold of 15-20mmHg after stopping the ivabradine. He was able to restart ivabradine on 2/20/18 and his heart rate came back to the 70s and his PAd dropped back below 20 mmHg. Optimizing PAd can be influenced by many factors including hypervolemia, hypovolemia, blood pressure, and heart rate. In many cases, optimizing heart failure medications such as the betablockers and angiotension converting enzyme inhibitors can help optimize PAd, however controlling blood pressure and heart rate are important also. In this case study, using ivabradine to reduce heart rate shows a significant improvement in PAd without adjusting diuretics or other heart failure medications.