Clinical Benefits of Oral Anticoagulants for Elderly Patients With Cardioembolic Stroke at High Bleeding Risk.

BACKGROUND/AIM: The relationship between the severity of cardioembolic stroke (CES) and oral anticoagulant (OAC) treatment before stroke onset in very elderly (≥80 years) patients with nonvalvular atrial fibrillation (NVAF) at high bleeding risk remains unknown. PATIENTS AND METHODS: A total of 364 consecutive patients (≥80 years) with CES and NVAF within 48 h following stroke onset were investigated. High bleeding risk was defined as follows: Bleeding history, renal dysfunction (creatinine clearance <30 ml/min), low body weight (≤45 kg), and antiplatelet or nonsteroidal anti-inflammatory drug use. Patients were divided into two groups: High bleeding risk (n=214) and non-high bleeding risk (n=150). We assessed stroke severity and functional outcome between the two groups, and evaluated the effect of therapy with direct OAC (DOAC) on stroke severity in the high-risk group. RESULTS: The high-risk group had a worse modified Rankin Scale (mRS) at discharge than the non-high-risk group [median: 4 (range=2-5) vs. 3 (range=1-4); p=0.02]. Patients in the high-risk group were categorized according to OAC treatment before stroke onset: No OAC (n=148), warfarin (n=46), and DOAC (n=20). The numbers of patients with National Institutes of Health Stroke Scale score (NIHSS) ≥8 on admission in these groups were 104 (70%), 30 (65%), and 8 (40%) (p=0.03), respectively. Multivariate analysis confirmed that DOAC therapy had a lower odds ratio (OR) for severe stroke (NIHSS ≥8) on admission (OR relative to no OAC=0.22, 95% confidence interval=0.08-0.62; p=0.005) and poor functional outcome (mRS ≥4) at discharge (OR=0.31, 95% confidence interval=0.11-0.90; p=0.03). CONCLUSION: Very elderly patients with CES at high bleeding risk have unfavorable functional outcomes. DOAC administration may be associated with reduced stroke severity.

Serial longitudinal changes of coronary calcified plaques with clear outer borders under intensive lipid management: insights from optical coherence tomography.

Percutaneous coronary intervention (PCI) for calcified lesions is one of the most challenging procedures related to worse clinical outcomes. To stabilize vulnerable plaques, intensive lipid management is recommended; however, the serial changes of calcified plaques under intensive lipid management are unknown. A total of 31 patients (mean age, 63 ± 10 years; men, 29 patients) who underwent PCI with intensive lipid management were retrospectively studied. We evaluated the serial longitudinal changes of calcified plaques with clear outer borders using optical coherence tomography (OCT) at two time points: at the time of PCI (baseline) and the chronic phase. The median interval from PCI to chronic phase was 287 (233-429) days. Twenty-eight patients (90.3%) had increased calcium volume at the chronic phase compared with those at baseline (2.6 [1.3-5.1] vs. 1.8 [0.7-4.3] mm2, p < 0.05), and the median increase rate of calcium volume was 27.4% at the chronic phase. According to the median increase rate of calcium volume (27.4%), patients were divided into the following two groups: rapid progression (≥ 27.4%, RP group) and non-rapid progression (< 27.4%, non-RP group). The RP group had more patients with diabetes, and diabetes was independently associated with rapid progression by multivariate analysis. Furthermore, patients with diabetes had significantly higher changes in calcium index and volume from the baseline to the chronic phase than those without diabetes. Coronary calcification progression during relatively short intervals was observed using OCT even under intensive lipid management. Diabetes was an independent predictor for rapid coronary calcification progression.

A clinical study of patients with pericentromeric deletion and duplication within 16p12.2-p11.2.

The short arm of chromosome 16 is rich in segmental duplications that result in chromosomal rearrangements through non-allelic homologous recombination. Several syndromes resulting from microdeletions or microduplications in this region have been reported. The chromosome 16p12.2-p11.2 deletion syndrome, 7.1- to 8.7-Mb [OMIM#613604] is characterized by minor facial anomalies, feeding difficulties, a significant delay in speech development, and recurrent ear infections. Reciprocal duplications of 16p12.2-p11.2 have been reported in some patients with autism. We identified a patient with a 16p12.2-p11.2 deletion and a patient with a 16p12.2-p11.2 duplication using oligonucleotide SNP array. The patient with the deletion showed severe developmental delay without autism. The patient with the deletion shared clinical features with previously reported patients. The patient with the duplication showed mild developmental delay and autism. She had dysmorphic features including a round face, a large mouth, and relative macrocephaly. We reviewed the reports of the two syndromes and compared the clinical manifestations. The 16p12.2-p11.2 duplication syndrome is a new syndrome with autism spectral disorders and dysmorphic features.