Tachycardia-induced cardiomyopathy is poorly recognized pre-ablation. It remains unclear of better patient selection and timing for catheter ablation in persistent atrial fibrillation (PerAF) with heart failure (HF).Consecutive patients with PerAF and left ventricular ejection fraction (LVEF) <50% referred for AF ablation were retrospectively included. The impact of LV size, heart rate (HR), and LVEF pre-ablation were analyzed for assessing LV systolic function recovery, defined as LVEF increase of ≥20% or to a value ≥55% after ablation.A total of 120 patients (2017-2020) were included. After 19 ±14 months post ablation, LVEF improvement was similar in patients with normal or dilated LV (18.3 ± 9.4% vs. 16.1 ± 10.8%, P = .25), rapid or controlled HR (19.5 ± 10% vs. 16.1 ± 10%, P = .09), but higher in HFrEF (HF with reduced EF) than HFmrEF (HF with midrange EF) (21.6 ± 10.3% vs. 14.9 ± 9.3%, P < .01). There was more LV systolic function recovery in those with normal to moderate LV dilation (80%, odds ratio [OR] 15.22, P < .01), HR ≥80 bpm (79%, OR 5.38, P < .01) and HFmrEF (80%, OR 4.03, P < .01). The overall AF freedom was similar between normal and dilated LV (59% vs. 62%, P = .95), rapid and controlled HR (67% vs. 56%, P = .18), and HFmrEF and HFrEF (65% vs. 50%, P = .19).Catheter ablation is effective independent of LV dilation, rate control or HFrEF. Patients with normal to moderate LV dilation, resting HR ≥80 bpm and HFmrEF may be candidates for early PerAF ablation to achieve LVEF normalization.
Rate-distortion optimized rate control is one of the superior features of JPEG2000. The calculation of delta-distortion for each pass is the key to implementing rate control. The paper presents a simplified model of delta-distortion calculation. Compared with the one in the verification mode (VM) of the JPEG2000 standard, this model has the following merits: code-block memory access free; lower memory requirement; lower computational complexity; less negative impact on image quality.
Collagen I is the main component of extracellular matrix in cardiac fibrosis. Our previous studies have reported inhibition of farnesylpyrophosphate synthase prevents angiotensin II-induced cardiac fibrosis, while the exact molecular mechanism was still unclear. This paper was designed to investigate the effect of alendronate, a farnesylpyrophosphate synthase inhibitor, on regulating angiotensin II-induced collagen I expression in cultured cardiac fibroblasts and to explore the underlying mechanism. By measuring the mRNA and protein levels of collagen I, we found that alendronate prevented angiotensin II-induced collagen I production in a dose-dependent manner. The inhibitory effect on collagen I expression was reversed by geranylgeraniol, and mimicked by inhibitors of RhoA/Rho kinase pathway including C3 exoenzyme and GGTI-286. Thus we suggested geranylgeranylation-dependent RhoA/Rho kinase activation was involved in alendronate-mediated anti-collagen I synthetic effect. Furthermore, we accessed the activation status of RhoA in alendronate-, geranylgeraniol- and GGTI-286-treated cardiac fibroblasts and gave an indirect evidence for RhoA activation via geranylgeranylation. Then we came to the conclusion that in cardiac fibroblasts, alendronate could protect against angiotensin II-induced collagen I synthesis through inhibition of geranylgeranylation and inactivation of RhoA/Rho kinase signaling. Targeting geranylgeranylation and RhoA/Rho kinase signaling will hopefully serve as therapeutic strategies to reduce fibrosis in heart remodeling.
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