Non-ischemic cardiomyopathy (NICM) consists of a heterogeneous group of disorders that result from diverse underlying processes - including infectious, autoimmune, infiltrative, genetic, and otherwise idiopathic. We present a case of inflammatory cardiomyopathy diagnosed by multimodal imaging, including cardiac magnetic resonance (CMR) and positron emission scan with 18F-fluorodeoxyglucose (FDG-PET). A 68-year-old Caucasian male with history of hypertension, hyperlipidemia, chronic kidney disease (stage II), and recent diagnoses of NICM and non-sustained ventricular tachycardia 6 months ago presented to our heart failure clinic to be evaluated for advanced heart failure therapies. CMR showed evidence of non-coronary disease late gadolinium enhancement (LGE) in the basal and mid interventricular septum as well as in both papillary muscles. The LGE extent was 14% of the myocardium. Given results of CMR and rising suspicion for sarcoidosis, our patient underwent FDG-PET, which showed persistent inflammation involving 37% of the left ventricle. The patient underwent endomyocardial biopsy (EMB) of both ventricles at a total of 9 sites using electroanatomic voltage mapping which can identify diseased tissues with low voltage signals. The biopsy results showed minimal focal interstitial edema, but no granulomas or active inflammation. Given the degree of active inflammation on FDG-PET the patient was treated with 3 months of oral prednisone. Subsequent FDG-PET demonstrated complete resolution of inflammation in addition to recovery of ejection fraction from 25% to 49%. This case illustrates the role of FDG-PET resulting in a timely diagnosis even when EMB results were inconclusive. Future studies are needed to determine the outcomes of immunosuppression in these patients. Figure 1. CMR demonstrating late gadolinium enhancement (LGE) in the septum, lateral wall, and the papillary muscles. The yellow arrows point to the areas of LGE. Figure 2. FDG-PET image demonstrating significant active inflammation, correlating to SUV (max) = 3.3 involving 37% of the left ventricle. The yellow arrows point to the areas of increased FDG uptake. Non-ischemic cardiomyopathy (NICM) consists of a heterogeneous group of disorders that result from diverse underlying processes - including infectious, autoimmune, infiltrative, genetic, and otherwise idiopathic. We present a case of inflammatory cardiomyopathy diagnosed by multimodal imaging, including cardiac magnetic resonance (CMR) and positron emission scan with 18F-fluorodeoxyglucose (FDG-PET). A 68-year-old Caucasian male with history of hypertension, hyperlipidemia, chronic kidney disease (stage II), and recent diagnoses of NICM and non-sustained ventricular tachycardia 6 months ago presented to our heart failure clinic to be evaluated for advanced heart failure therapies. CMR showed evidence of non-coronary disease late gadolinium enhancement (LGE) in the basal and mid interventricular septum as well as in both papillary muscles. The LGE extent was 14% of the myocardium. Given results of CMR and rising suspicion for sarcoidosis, our patient underwent FDG-PET, which showed persistent inflammation involving 37% of the left ventricle. The patient underwent endomyocardial biopsy (EMB) of both ventricles at a total of 9 sites using electroanatomic voltage mapping which can identify diseased tissues with low voltage signals. The biopsy results showed minimal focal interstitial edema, but no granulomas or active inflammation. Given the degree of active inflammation on FDG-PET the patient was treated with 3 months of oral prednisone. Subsequent FDG-PET demonstrated complete resolution of inflammation in addition to recovery of ejection fraction from 25% to 49%. This case illustrates the role of FDG-PET resulting in a timely diagnosis even when EMB results were inconclusive. Future studies are needed to determine the outcomes of immunosuppression in these patients. Figure 1. CMR demonstrating late gadolinium enhancement (LGE) in the septum, lateral wall, and the papillary muscles. The yellow arrows point to the areas of LGE. Figure 2. FDG-PET image demonstrating significant active inflammation, correlating to SUV (max) = 3.3 involving 37% of the left ventricle. The yellow arrows point to the areas of increased FDG uptake.