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Sarcoidosis is a systemic disease and recognition of cardiac involvement remains challenging. We report a case and illustrate the integral role of cardiac PET perfusion-metabolic imaging in evaluating various stages of cardiac sarcoidosis. A 61-year-old African-American male presented with a 6-month history of progressive exertional dyspnea, cough, palpitations, and atypical chest pain. Physical exam was consistent with acute heart failure and his baseline EKG showed sinus rhythm with frequent premature ventricular contractions. Chest x-ray showed bilateral hilar adenopathy and telemetry monitoring was significant for multiple runs of nonsustained ventricular tachycardia. Echocardiography showed ejection fraction of 30% with global biventricular hypokinesis. Patient underwent coronary angiogram revealing minimal coronary atherosclerosis. A gadolinium-enhanced cardiac MRI was obtained (Figure 1), and a diagnosis of pulmonary and cardiac sarcoidosis was made following which a dual chamber defibrillator was implanted. Prednisone 20 mg daily and methotrexate 12.5 mg weekly was planned. However, given that treatment response and disease progression assessment could not be achieved with serial cardiac MRI (ICD placed), a baseline rest Rubidium 82/F-18 flourodeoxyglucose (Rb-82/18-FDG) cardiac PET was obtained prior to treatment to be used to then assess treatment response with serial scans as indicated showing pattern consistent with active cardiac sarcoidosis (Figure 2). Treatment was initiated and methotrexate titrated up to 15 mg weekly. He was seen in the clinic five months after medical therapy was initiated. Subjectively reported minimal to no symptoms. A repeat cardiac PET was done (Figure 3) using same protocol to assess response to therapy showed marked improvement. His dose of prednisone was decreased to 10 mg daily and then discontinued. Few months later, amiodarone and methotrexate were discontinued due to early development of interstitial lung disease. Seven months after discontinuation of medical therapy, he developed recurrent heart failure symptoms. Echocardiogram EF was 30%-35%. Repeat cardiac PET was done (Figure 4) showing recurrence of active cardiac sarcoidosis. He was reinitiated on prednisone at 50 mg but refused to take it due to weight gain and did not return for follow-up appointments. This case highlights the role of cardiac PET not only in situations where MRI cannot be used but also following treatment response and disease reactivation which is challenging to assess with cardiac MRI. The emerging importance of cardiac PET in cardiac sarcoidosis is now acknowledged in the recent consensus documents and nuclear societies recommendations 1,2 as an indicator of cardiac sarcoidosis in contrast to prior older imaging criteria for CS which included on SPECT or MRI abnormalities. 3 Whole body imaging to evaluate sarcoid activity in other extra cardiac organs apart from the heart and quantitation of standardized uptake values (SUVmax) to enhance diagnosis of disease activity and response to therapy were not available in our study but are key methods to better evaluate and assess sarcoidosis as shown in recent studies. 4

Regadenoson (REG), a selective adenosine A2a receptor agonist, is becoming the preferred pharmacologic agent for stress myocardial perfusion imaging (MPI). Hemodynamic and stress variables, immediate safety and use of aminophylline when using REG combined with low-level exercise (REG WALK MPI) compared with REG MPI, have not been well studied and formed the basis of our study. Retrospective evaluation of patients who underwent REG MPI (n = 887) was compared to patients undergoing REG WALK MPI (n = 485) from January to November 2009. Patient demographics, hemodynamic parameters, REG MPI data, side effects, immediate major clinical events, and use of aminophylline were evaluated. Patients in REG WALK MPI group tended to be younger, male and obese compared to patients in REG MPI group. REG WALK MPI patients had higher stress heart rate (103 ± 20.5 vs 84 ± 19 bpm, P = .001), higher heart rate reserve (36.3 ± 19 vs 14.7 ± 15.5 bpm, P

Background. Abnormal stress myocardial perfusion imaging studies (SMPI) with angiographically insignificant coronary artery disease (ICAD) have often been labeled “false positive” scans. We evaluated the prognostic predictors and outcomes in an unselected patient population having abnormal SMPI and ICAD (study group) over a 24 month period of follow-up. Methods. Retrospective study of consecutive patients who had SMPI and subsequent coronary angiography showing ICAD within 6 months of index scan with matched control group with normal scans. Major Adverse Cardiac Events (MACE) were defined as the first occurrence of death or myocardial infarction (MI). Patients were followed up to 24 months from the time of their SMPI to identify the development of MACE. Results. One hundred and twenty five patients formed the study group and one hundred and thirty six patients formed the control group. Over a two-year follow up, approximately 13% of the study group had MACE as compared to 4.2% in the control group (P=022). Abnormal SMPI, EF