In a 70-year-old woman with wild-type transthyretin cardiac amyloidosis, upgrading to a CRT-D and initiating tafamidis stabilized functional symptoms and improved left ventricular ejection fraction to 31%.
Case Report (n=1)
No
This case highlights the limitations of conventional heart failure therapy in amyloid cardiomyopathy and the importance of early imaging-based diagnosis for timely disease-directed treatment.
Wild-type transthyretin cardiac amyloidosis (ATTRwt) is an underrecognized cause of heart failure that often mimics hypertensive or nonischemic cardiomyopathy. A 70-year-old woman with hypertension, diabetes, and chronic kidney disease presented with dyspnea, reduced left ventricular ejection fraction, and a 2:1 block requiring dual-chamber pacemaker implantation. Despite guideline-directed medical therapy, her heart failure worsened with further decline in systolic function. Ischemic etiology was excluded. Cardiac magnetic resonance demonstrated diffuse subendocardial late gadolinium enhancement consistent with amyloidosis. Negative monoclonal protein studies and genetic testing confirmed ATTRwt. Her device was subsequently upgraded to a cardiac resynchronization therapy-defibrillator due to persistent ventricular dysfunction and high pacing burden. Tafamidis was then initiated. This case highlights the limitations of conventional heart failure therapy in amyloid cardiomyopathy and the importance of early imaging-based diagnosis for timely disease-directed treatment.
Richard et al. (Tue,) conducted a case report in Wild-Type Transthyretin Cardiac Amyloidosis (n=1). Tafamidis and CRT-D upgrade was evaluated on Left ventricular ejection fraction. In a 70-year-old woman with wild-type transthyretin cardiac amyloidosis, upgrading to a CRT-D and initiating tafamidis stabilized functional symptoms and improved left ventricular ejection fraction to 31%.
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