Faculty Bibliography

BACKGROUND/UNASSIGNED:Previous studies have provided evidence of reduced recurrence of atrial fibrillation (AF), all-cause mortality, and heart failure (HF) hospitalizations after catheter ablation (CA) in both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Aggregate data comparing the efficacy of AF ablation and clinical endpoints in HF with mildly reduced ejection fraction (HFmrEF) to HFrEF and HFpEF are lacking. METHODS/UNASSIGNED:We conducted a systematic review and meta-analysis aimed at determining any differences in AF recurrence rate, all-cause mortality, and HF hospitalizations among patients with HFrEF, HFmrEF, and HFpEF who underwent AF ablation. A systematic search of PubMed/MEDLINE, Embase, and Cochrane Library databases was performed until October 31, 2023. RESULTS/UNASSIGNED:A total of seven studies comprising 3,795 patients were retained: HFrEF 1,281 (33.8%), HFmrEF 870 (22.9%), and HFpEF 1,644 (43.3%). After median follow-up of 24 months, there was no significant difference in rate of AF recurrence between the three HF categories: HFrEF 40% (30-49%), HFmrEF 35% (28-43%); and HFpEF 35% (25-45%). Only two studies which included outcomes in the three HF categories were identified. Pooled hazard ratio (HR) of all-cause mortality and HF hospitalization combined after ablation or other rhythm control compared to other conservative management were: HFrEF 0.77 (0.63 - 0.94); HFmrEF 0.81 (0.55 - 1.20); and HFpEF 0.74 (0.55 - 1.00). CONCLUSIONS/UNASSIGNED:CA has similar efficacy in the long-term resolution of AF among patients with HFrEF, HFmrEF, and HFpEF. Further studies are needed to provide a robust analysis on the potential impact of CA on all-cause mortality.

BACKGROUND:Low levels of high-density lipoprotein cholesterol (HDL-C) are clearly associated with atherosclerotic cardiovascular disease (ASCVD), but the risk curve is not well defined, especially at very high and low HDL-C levels. Current proportional hazards prediction models assume inverse linearity of effect, which may not accurately represent risk at these levels. SOURCES OF MATERIAL/UNASSIGNED:Clinical inattention to risk associated with low HDL-C may derive from randomized controlled trials (RCTs) aimed at raising HDL-C, though most failed to reduce ASCVD events when combined with statin-based therapy. However, these prior trials enrolled patients with HDL-C levels largely in the 35-45 mg/dL range. ABSTRACT OF FINDINGS/UNASSIGNED:Mounting post hoc evidence from RCTsß as well as new genetic and observational data suggests that very low HDL-C (less than 30 or 35 mg/dL) may signal a further increase in incident cardiovascular events. Moreover, when HDL-C exceeds 90 mg/dL, monotonic reduction of ASCVD risk appears to reverse. Because a pervasively agnostic view of the importance of both very low and high levels of HDL-C now exists, consideration should be given to incorporating nonlinear effects of HDL-C into future risk prediction models such that very low HDL-C and/or very high HDL-C levels could be considered as new risk-enhancing factors to promote more optimal risk stratification. CONCLUSION/CONCLUSIONS:When revision of the U.S. Cholesterol Guideline recommences, consideration should be directed to whether HDL-associated risk matches the assumptions of current statistical models. Thus, it may be both timely and opportune to revisit the "HDL Hypothesis" based on evolving scientific evidence.