BACKGROUND: Cardiac sarcoidosis involves a significant but difficult-to-define risk of sudden cardiac death (SCD). Current guidelines recommend consideration of an implantable cardioverter defibrillator for patients with extensive or significant myocardial late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging. However, extensive/significant LGE is not defined. METHODS: A nationwide cardiac sarcoidosis registry was screened for patients entered before 2020 with cardiac magnetic resonance imaging done before or <3 months after diagnosis. Available studies were re-analyzed for LGE mass as a percentage of left ventricular (LV) mass and the number of LGE-positive LV segments in a 17-segment model. The occurrence of fatal or aborted SCD and ventricular tachycardia (VT) prompting therapy was recorded until the end of 2020 and subjected to cumulative incidence analyses, including competing events (LV assist device implantations, heart transplantations, and fatalities other than SCD). The predictors of SCD/VT were assessed using Fine and Gray modeling and time-dependent receiver operating characteristic analysis. RESULTS: Altogether, 305 patients (66% women, median age 51) with clinically manifest, definite (45%) or probable cardiac sarcoidosis (55%) were analyzed. On follow-up (median, 4.0 years), 21 SCDs, 60 VTs, and 14 competing events were noted. Both LGE mass and the number of LGE segments predicted the composite of SCD/VT ( P <0.001), with receiver operating characteristic analyses identifying LGE mass ≥9.9% and ≥6 LGE segments as discriminative thresholds. At presentation, 70 patients were free of class I and class IIa implantable cardioverter defibrillator indications unrelated to LGE. Their 5-year rate of SCD/VT was 6.3% (0.0–14.8%) with LGE mass <9.9% versus 21.5% (6.5–36.6%) with higher LGE mass, and 6.9% (0.0–16.3%) with <6 LGE segments versus 20.5% (5.9–35.2%) with ≥6 segments. CONCLUSIONS: In cardiac sarcoidosis, myocardial LGE making up ≥9.9% of LV mass or affecting ≥6 LV segments may suggest prognostically significant LV involvement and a high risk of SCD. However, prospective validation of the thresholds is needed.

Background: Inadequate myocardial glucose metabolism suppression (GMS) can hamper interpretation of cardiac [¹⁸F]fluorodeoxyglucose (FDG) positron emission tomography (PET/CT). Use of β-hydroxybutyrate (BHB) measurement before [¹⁸F]FDG injection has been proposed for predicting adequate GMS. However, limited information is available on BHB measurement in guiding preparations for [¹⁸F]FDG-PET/CT. The purpose of this study was to evaluate if point-of-care measured BHB is useful in guiding heparin premedication for cardiac [¹⁸F]FDG-PET/CT. Results: 155 patients (82 male) had followed a high-fat, low-carbohydrate diet and fasted for at least twelve hours. For the first 63 patients, BHB was measured, but it was not used to guide premedication. For the subsequent 92 patients, heparin 50 IU/kg was injected intravenously 15–20 min before [¹⁸F]FDG injection if the BHB level was low (< 0.35 mmol/l). Cardiac [¹⁸F]FDG uptake pattern was evaluated visually and [¹⁸F]FDG uptake in the myocardium and blood pool were measured. Median BHB level was 0.4 (range 0.1–5.8) mmol/l. Eighty-eight patients (57%) reached a BHB level higher than 0.35 mmol/l. 112 patients (72%) had adequate GMS. In the high BHB group, 74 patients (84%) had adequate GMS, whereas of those with low BHB, only 38 (57%) had adequate GMS (p < 0.001). In the low BHB group, the prevalence of inadequate GMS was comparable in patients with and without heparin (44% vs. 42%, p = 0.875). Conclusions: While high BHB predicts adequate GMS, unfractionated heparin does not improve GMS in patients with low BHB.

Background: Corresponding to impaired insulin response in skeletal muscle, insulin resistance may occur in the myocardium, suggesting a link between cardiometabolic disorders and cardiac glucose metabolism. We aimed to investigate whether cardiometabolic disorders predict myocardial [¹⁸F]fluorodeoxyglucose ([¹⁸F]FDG) uptake suppression in cardiac positron emission tomography / computed tomography (PET/CT) following a ketogenic diet and fasting. Results: The study included 100 patients undergoing [¹⁸F]FDG-PET/CT following a ketogenic diet of 1–2 days and a 12 h fast. Blood glucose, insulin, β-hydroxybutyrate (BHB), cholesterol, triglycerides and free fatty acid (FFA) levels were measured before [¹⁸F]FDG injection and later off-diet following overnight fast. The homeostatic model assessment–insulin resistance (HOMA-IR) value was calculated. Non-contrast computed tomography was used to assess the presence of fatty liver and visceral and subcutaneous fat areas. Suppression of myocardial [¹⁸F]FDG uptake was considered adequate if myocardial uptake was equal to or lower than the blood pool background. Compared to inadequate suppression, adequate suppression was associated with higher levels of BHB (median 0.26 mmol/l for inadequate and 0.43 mmol/l for adequate suppression, p = 0.004), FFA (0.58 mmol/l and 0.76 mmol/l respectively, p < 0.001), triglycerides (0.87 mmol/l and 1.12 mmol/l respectively, p = 0.028), and lower liver-spleen attenuation ratios (1.17 and 1.04 respectively, p = 0.013). Low HDL cholesterol, high triglycerides and off-diet HOMA-IR, as well as visceral adiposity, fatty liver and hypertension, predicted adequate suppression in men. Elevated BHB and FFA were significant predictors of adequate suppression in women. Conclusions: Cardiometabolic disorders are associated with lower myocardial [¹⁸F]FDG uptake. Insulin resistance and several other cardiometabolic risk factors are associated with attenuated uptake, especially in men. In women, factors reflecting metabolic response to a ketogenic diet and fasting have a more pronounced effect on myocardial [¹⁸F]FDG uptake.

Severe cases of heart failure (HF), both new onsets of HF and acute exacerbations of chronic HF, are frequently observed during infections. A potentially lethal complication of HF with very low left ventricular ejection fraction is thrombus formation within the heart chambers. A 67-year-old male was admitted to our hospital with shortness of breath after a COVID-19 infection. He was diagnosed with severe acute heart failure and a massive thrombus in the left ventricle. While the thrombus subsided quickly without any observable embolic events, the patient had a lengthy hospitalization stay complicated by tachyarrhythmias and secondary infections. Eventually, his heart failure improved, and he continued to recover post-hospital discharge. We present a case of severe heart failure and intraventricular thrombosis following COVID-19 infection. The patient required potent anti-inflammatory medication in addition to conventional heart failure medication to recover from his HF.