Elevated levels of arterial lactate on admission were related to worse in-hospital mortality in patients with ADHF either with or without ACS, suggesting that the presence of high lactate in patients who enter the ICU with ADHF could help stratify the initial risk of early mortality.

BACKGROUND Atrial fibrillation (AF) has a genetic basis, and environmental factors can modify its actual pathogenesis.OBJECTIVE The purpose of this study was to construct a combined risk assessment method including both genetic and clinical factors in the Japanese population.METHODS We screened a cohort of 540 AF patients and 520 non-AF controls for single nucleotide polymorphisms (SNPs) previously associated with AF by genome-wide association studies. The most strongly associated SNPs after propensity score analysis were then used to calculate a weighted genetic risk score (WGRS). We also enrolled 1018 non-AF Japanese subjects as a validation cohort and monitored AF emergence over several years. Finally, we constructed a logistic model for AF prediction combining WGRS and clinical risk factors. RESULTSWe identified 5 SNPs (in PRRX1, ZFHX3, PITX2, HAND2, and NEURL1) associated with AF after Bonferroni correction. There was a 4.92-fold difference in AF risk between the highest and lowest WGRS calculated using these 5 SNPs (P 5 2.32 ! 10 210 ). Receiver operating characteristic analysis of WGRS yielded an area under the curve (AUC) of 0.73 for the screening cohort and 0.72 for the validation cohort. The predictive logistic model constructed using a combination of WGRS and AF clinical risk factors (age, body mass index, sex, and hypertension) demonstrated better discrimination of AF than WGRS alone (AUC 5 0.84; sensitivity 75.4%; specificity 80.2%).CONCLUSION This novel predictive model of combined AF-associated SNPs and known clinical risk factors can accurately stratify AF risk in the Japanese population.

Background Atrial fibrillation (AF) recurrence after radiofrequency catheter ablation (RFCA) still remains a serious issue. Ca 2+ handling has a considerable effect on AF recurrence. The histidine-rich calcium-binding protein ( HRC ) genetic single nucleotide polymorphism (SNP), rs3745297 (T>G, Ser96Ala), is known to cause a sarcoplasmic reticulum Ca 2+ leak. We investigated the association between HRC Ser96Ala and AF recurrence after RFCA in paroxysmal AF (PAF) patients. Methods and results We enrolled PAF patients who underwent RFCA ( N = 334 for screening and N = 245 for replication) and were genotyped for HRC SNP (rs3745297). The patient age was younger and rate of diabetes and hypertension lower in the PAF patients with Ser96Ala than in those without (TT/TG/GG, 179/120/35; 64±10/60±12/59±13 y, P = 0.001; 18.5/ 9.2/8.6%, P = 0.04 and 66.1/50.0/37.1%, P = 0.001, respectively). During a mean 19 month follow-up, 57 (17.1%) patients suffered from AF recurrences. The rate of an Ser96Ala was significantly higher in patients with AF recurrence than in those without in the screening set (allele frequency model: odds ratio [OR], 1.80; P = 0.006). We also confirmed this significant association in the replication set (OR 1.74; P = 0.03) and combination ( P = 0.0008). A multivariate analysis revealed that the AF duration, sinus node dysfunction, and HRC Ser96Ala were independent predictors of an AF recurrence (hazard ratio [HR], 1.04, P = 0.037; HR 2.42, P = 0.018; and HR 2.66, P = 0.007, respectively). Conclusion HRC SNP Ser96Ala is important as a new genetic marker of AF recurrence after RFCA.

Objective Very late stent thrombosis (VLST) remains an unresolved problem, and recent reports have indicated that VLST onset can occur in patients treated with both drug-eluting stents (DES) and bare metal stents (BMS). We evaluated the causes of VLST using optical coherence tomography (OCT). Methods OCT was performed in 22 patients (12 DES-treated patients, 10 BMS-treated patients). Because two instances of VLST occurred simultaneously in one case in the DES group, the DES group comprised 13 lesions, while the BMS group comprised 10 lesions. All struts were counted in each frame, and the proportion of uncovered or malapposed struts was calculated based on the overall number of struts in the stent. Results The interval from stent implantation to VLST onset was significantly longer in the BMS group. The proportion of uncovered struts and the ratio of malapposed struts were significantly higher in the DES group than in the BMS group. The OCT analysis demonstrated intimal hyperplasia or intimal disruption in all patients in the BMS group. However, in the DES group, severe hyperplasia and/or neoatherosclerosis was observed in only eight lesions (61.5%), while uncovered and malapposed struts were involved in the other lesions. Conclusion In most BMS-treated lesions, it appeared that VLST was caused by the occurrence of neoatherosclerosis after stent implantation. The causes of VLST in DES-treated lesions are more various and complicated than those observed for BMS-treated lesions.

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