Endoscopic submucosal dissection (ESD) is a minimally invasive treatment for early gastric cancer that enables the en bloc resection of large lesions. However, it is associated with a significant risk of delayed bleeding, particularly in patients receiving antithrombotic therapy. Delayed bleeding after ESD causes anemia and serious systemic complications, including cardiovascular events. Here, we report a rare case of Takotsubo syndrome triggered by delayed bleeding after gastric ESD that culminated in cardiac arrest. A man in his 70s who underwent gastric ESD experienced delayed bleeding six days after the treatment, requiring emergency endoscopic hemostasis. The following day, the patient developed sudden ventricular fibrillation without prior chest symptoms. After resuscitation with electrical defibrillation, left ventriculography revealed apical ballooning consistent with Takotsubo syndrome. With intensive care, cardiac function recovered, and the patient was discharged ambulatory. Takotsubo syndrome is typically induced by stress, and often triggers psychological and physical stimuli. Although most patients present with chest pain or discomfort, our patient showed no preceding symptoms and developed sudden arrhythmia and cardiac arrest. This case highlights the need for aggressive bleeding prevention and enhanced post-ESD cardiac surveillance to mitigate rare but potentially fatal complications.
Abstract Background This study aimed to evaluate the safety and effectiveness of the Kanshas drug-coated balloon (DCB) with paclitaxel for the treatment of atherosclerotic lesions in the superficial femoral artery (SFA) and/or proximal popliteal artery (PA) over a 3-year period. Results A prospective, multicenter, single-arm trial enrolled 121 patients with symptomatic lower extremity artery disease (LEAD). At 3 years, the primary patency rate was 63.4%, and freedom from clinically driven target lesion revascularization (CD-TLR) was 83.2%. Sustained improvements were observed in Rutherford classification, ankle brachial index (ABI), and walking impairment questionnaire (WIQ) scores. No device- or procedure-related deaths or major amputations occurred. Conclusions The Kanshas DCB showed favorable safety and effectiveness for treating atherosclerotic lesions in the SFA and/or proximal PA over 3 years. Trail registration Registration ID: UMIN000034122. Registration Date: September 13, 2018. Registration site URL: https://center6.umin.ac.jp/cgi-openbin/ctr/ctr.cgi?function=brows&action=brows&recptno=R000038612&type=summary&language=J . Graphical Abstract
In the Phase III TASUKI-52 trial, nivolumab with carboplatin, paclitaxel (CP), plus bevacizumab significantly prolonged progression-free survival (PFS), and resulted in longer overall survival (OS) in patients with advanced nonsquamous non-small cell lung cancer (NSCLC). This final analysis evaluated 4-year treatment outcomes in terms of OS, PFS and duration of response (DOR) by investigator assessment and safety, as well as the background characteristics and treatment courses associated with 4-year survivors. Patients were randomized 1:1 to receive nivolumab (n = 275) or placebo (n = 275) in addition to CP plus bevacizumab. With a minimum follow-up of 53.1 months, nivolumab with CP plus bevacizumab continued to show improvement in OS (hazard ratio [HR], 0.71; 95% confidence interval [CI], 0.58-0.88) and PFS (HR: 0.61; 95% CI: 0.50-0.74) compared to placebo with CP plus bevacizumab. The 4-year OS rate was 34.7% in the nivolumab arm versus 22.1% in the placebo arm, and the 4-year PFS rate was 13.7% in the nivolumab arm versus 3.3% in the placebo arm. Among 4-year survivors, the median DOR was numerically longer in the nivolumab arm than in the placebo arm (34.7 vs. 13.5 months). No new safety signals were observed. Four-year survival in the nivolumab arm was associated with the absence of bone metastases and age < 65, but not with PD-L1 status and tumor size. In conclusion, treatment with nivolumab demonstrated long-term survival benefit and durable response, which supports nivolumab with CP plus bevacizumab as a first-line treatment option for advanced nonsquamous NSCLC. Trial Registration: ClinicalTrials.gov identifier: NCT03117049.
Background: No studies have compared aspirin to P2Y12 inhibitor monotherapy following short dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) in patients with diabetes. Methods and Results: We conducted a prespecified diabetes subgroup analysis of the 1-year STOPDAPT-3 trial; patients were randomized at the time of index PCI, and outcomes from 30 days to 1 year were assessed using a 30-day landmark analysis comparing 1-month DAPT followed by aspirin monotherapy (aspirin group) to 1-month prasugrel monotherapy followed by clopidogrel monotherapy (clopidogrel group). The effect of aspirin relative to clopidogrel was not significant for the coprimary cardiovascular endpoint (composite of cardiovascular death, myocardial infarction, definite stent thrombosis, or stroke) regardless of diabetes (aspirin/clopidogrel 5.3/5.6 vs. 3.9/3.7 per 100 person-years for diabetes vs. non-diabetes, respectively; hazard ratios [HRs] 0.96 [95% confidence interval {CI} 0.67-1.37] and 1.06 [95% CI 0.72-1.55], respectively; Pinteraction=0.71), but there was a significant interaction between diabetes and the effect of aspirin relative to clopidogrel for the coprimary bleeding endpoint (Bleeding Academic Research Consortium 3 or 5; aspirin/clopidogrel 2.8/1.8 vs. 1.3/2.0 per 100 person-years diabetes vs. non-diabetes, respectively; HR 1.54 [95% CI 0.88-2.71] vs. 0.65 [95% CI 0.36-1.17], respectively; Pinteraction=0.04). Conclusions: From 30 days to 1 year after PCI, cardiovascular outcomes were similar between aspirin and clopidogrel regardless of diabetes. A nominal bleeding interaction was observed; given the exploratory and underpowered subgroup analyses, this finding should be interpreted cautiously.
LBA8518 Background: Among common EGFR-mutant NSCLC, L858R mutation is suggested to be less sensitive to EGFR-TKIs and associated with poorer prognosis than ex 19 del. REVOL858R is the first randomized phase III trial conducted exclusively in patients with advanced/recurrent EGFR L858R–mutant NSCLC, comparing a treatment strategy of erlotinib plus ramucirumab (E+RAM) followed by osimertinib (OSI) upon detection of acquired T790M with first-line OSI monotherapy. Methods: Eligible patients were treatment-naive adults (≥20 years) with advanced/recurrent EGFR L858R–positive NSCLC and ECOG PS 0–1. Patients were randomized 1:1, stratified by clinical stage (IIIB/IIIC/IV vs postoperative recurrence), sex, and baseline brain metastasis (BM). Patients received OSI 80 mg once daily (Arm A) or E+RAM (E 150 mg once daily plus RAM 10 mg/kg every 2 weeks; Arm B). In Arm B, tumor rebiopsy or liquid biopsy at termination of E+RAM was mandated; patients with detected T790M subsequently received OSI, whereas those without T790M discontinued protocol treatment. The primary endpoint, time to failure of strategy (TFS), was defined as time from randomization to disease progression or death during OSI, or during the primary treatment when OSI was not administered (in Arm B). Results: Overall, 232 patients were randomized (Arm A n=116; Arm B n=116). Baseline characteristics were generally well balanced between the two arms. In the full analysis set, median TFS was 14.8 months in Arm A and 16.6 months in Arm B (HR 1.03; 95% CI 0.78–1.38; log-rank p=0.49). Key secondary endpoints and selected prespecified subgroup analyses of TFS are summarized in Table. The most common AEs (any grade) were diarrhea (41% vs 54%) and acneiform rash (30% vs 71%) in Arm A vs Arm B. Hypertension and proteinuria were observed in 39% and 18% of patients in Arm B, respectively. Interstitial lung disease occurred in 12 patients (10%) in Arm A, and 2 patients (2%) in Arm B. AEs leading to discontinuation of protocol treatment occurred in 21% vs 36% of patients (Arm A vs Arm B). Conclusions: A planned E+RAM-to-OSI strategy did not improve TFS compared with upfront OSI in EGFR L858R–mutated NSCLC. Safety findings were consistent with known profiles, with higher discontinuation for tolerability in the strategy arm. Trial information: jRCTs051200142. Clinical trial information: 051200142. Key secondary endpoints. Key secondary endpoint, median (months) Arm A (OSI) Arm B (E+RAM) HR (95% CI) OS 44.0 (31.1-NR) 38.4 (33.3-NR) 0.98 (0.66-1.45) 3-y OS (%) 56.1% 57.2% – ORR (%) 73.2% 66.3% – PFS1 14.8 14.9 1.08 (0.81-1.44) PFS2 23.8 25.1 0.96 (0.70-1.33) Time to treatment failure 12.6 11.2 1.34 (1.02-1.77) Key prespecified TFS subgroups <65 years / ≥65 years 18.4 / 14.8 21.2 / 16.0 0.90 (0.40-1.99) / 1.06 (0.78-1.45) With / Without baseline BM 11.8 / 19.2 14.7 / 17.8 0.81 (0.49-1.34) / 1.11 (0.79-1.57)
