top of page

Case Study 1: Mike
Existing HCM with AFib, Rheumatoid Arthritis and Worsening Shortness of Breath


Existing HCM with AFib, Rheumatoid Arthritis and Worsening Shortness of Breath

Mike is a 54-year-old man who came in for evaluation due to increased breathlessness since his last AFib ablation. He was diagnosed with obstructive HCM around age 35 after he had a murmur found on exam. He was intermittently followed by cardiology, but there were never significant concerns regarding his HCM as he had overall been stable. His echocardiogram at diagnosis showed an interventricular septal wall thickness of 2 cm, a left ventricular posterior wall thickness of 1.0 cm, and a peak LVOT gradient of 40 mmHg with Valsalva. He was managed with 50 mg of metoprolol and 120 mg of verapamil for many years.


At age 50, he presented to the emergency room with chest pain and was found to be in rapid AFib. He was started on amiodarone and soon underwent ablation. He remained in sinus rhythm until about a year ago, at which time he started having recurrent bouts of AFib.

His echocardiogram at an outside institution prior to cardioversion showed an LVEF of 30% in the setting of rapid AFib. He has now undergone a second AFib ablation and is maintained on sotalol, metoprolol, and apixaban. He is treated for RA with methotrexate and has mildly abnormal renal function with a creatinine of 1.4.


He came in for outpatient follow-up today, as it has been three months since his ablation. His HR is 65, BP 102/76, RR 12, oxygen saturation 98% on room air. He describes being less active than he was a year ago, now getting short of breath when climbing a flight of stairs. An echocardiogram was completed today in sinus rhythm showing an EF of 45%, left ventricular end diastolic dimension of 5.6 cm, IVS 1.3 cm, LVPW 0.9 cm, and LA volume index of 48 ml/m2. He also underwent cardiac MRI, which showed an EF of 45% and extensive delayed gadolinium enhancement comprising 30% of the left ventricular myocardium. He is wondering if his progressive symptoms are due to bradycardia or worsening rheumatoid arthritis. He has been told his cardiac hypertrophy has improved and his rhythm is now controlled.

Case Study 1:

bottom of page