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This study investigated the association between left ventricular ejection fraction (LVEF) and the risk of ventricular arrhythmias (VA), heart transplantation, and death in cardiac sarcoidosis (CS). We identified 110 CS patients meeting 2014 Heart Rhythm Society (HRS) diagnostic criteria with baseline LVEF35% (n = 32) or ≥35% (n = 78). The primary end point was sustained VA or sudden cardiac death (SCD), and secondary end points included risk of heart transplantation, death, or a composite. Logistic regression determined risk factors for VA/SCD, and Cox proportional hazards regression analysis was performed for secondary end points. Receiver operating curve analysis determined the best discrimination point of LVEF for each end point; sensitivity analyses evaluated the effects of higher LVEF on each end point. Over a follow-up of 2.6 (range 1.0 to 5.8) years, 49 (44.5%) CS patients experienced VA/SCD, including 19 of 32 (59.4%) with LVEF35%, and 30 of 78 (38.5%) with LVEF ≥35%. After adjustment, LVEF35% was not significantly associated with an increased risk of VA/SCD compared with LVEF ≥35% (odds ratio 1.3, 95% confidence intervals 0.5 to 3.7). Although LVEF35% was associated with an increased risk of heart transplantation and death (28.1% vs 12.8%, p = 0.05), this was not significant after adjustment (hazard ratio 1.7, 95% confidence intervals 0.5 to 9.0, p = 0.53). In conclusion, patients with CS experience high rates of VA, SCD, and heart transplantation, even when LVEF is mildly impaired or normal. Patients with LVEF35% are at particularly elevated risk of VA/SCD. Our findings highlight the imperative to investigate arrhythmia risk in all patients with CS, even in the setting of an otherwise reassuring LVEF.

Despite efforts at early revascularization in acute coronary syndrome and advancing technologies in the field of temporary mechanical circulatory support (TMCS), the mortality from cardiogenic shock (CS) remains very high. Treatment of these patients involves understanding the trajectory of the condition and making complex decisions regarding the appropriate selection of medical and device therapies. The current definition of CS is not universally applicable and defines shock in absolute terms. CS should be thought of as a continuum rather than a binary diagnosis and is best defined as a clinical syndrome of tissue hypoperfusion resulting from cardiac dysfunction. Early intervention with appropriate timing and selection of apposite TMCS device may be the key to improving outcomes. TMCS device selection is a complex process requiring consideration of the severity of CS, patient-specific risks, technical limitations, overall goals of care, and assessment of futility of care. In this review, we discuss identification and pathophysiology of CS, and critically review acute management strategies, both medical and mechanical therapies and outline areas that need further investigation.