Dear Editor,
We read with great interest the article by Sim et al. [1] published in the Journal of Internal Medicine. The authors conducted a retrospective study involving 198 patients to examine the impact of extracorporeal membrane oxygenation (ECMO) initiation timing during routine cardiopulmonary resuscitation (CPR) on patient survival prognosis. The study's findings underscore the crucial role of ECMO in routine CPR, particularly highlighting that an early initiation of ECMO significantly enhances patient survival outcomes. We commend the authors for optimizing the timing of ECMO initiation in clinical practice. However, several aspects warrant further discussion.
First, the article selectively analysed patients who received ECMO but did not provide detailed information regarding the exclusion and selection criteria. For instance, there is no clear explanation of how patients with severe comorbidities or a higher risk of death were managed. This omission could result in a non-representative sample, potentially affecting the generalizability of the study's conclusions.
Second, the article inadequately addresses the neurological prognosis of the patients, as it fails to include data on their long-term neurological outcomes post-discharge (after 3 or 6 months). Given that neurological recovery following cardiac arrest may take an extended period [2], this limitation hinders a comprehensive understanding of the patient's long-term prognosis.
Third, although the article focuses on the timing of ECMO initiation, it does not analyse other concurrent treatments (e.g., high-quality CPR, medications, and temperature management) compared to ECMO. This omission prevents a clear delineation of ECMO's unique contribution relative to other interventions throughout the treatment process [3].
In conclusion, we appreciate the authors for highlighting the significance of timely ECMO initiation during CPR to improve patient survival. This work will raise healthcare professionals’ awareness of the critical importance of early ECMO initiation and contribute to the rapid advancement of this field.
Zegang Ruan: Methodology; writing—original draft; investigation. Yuhao Gan: Methodology; writing—original draft; investigation. Chenyang Xu: Writing—review and editing; supervision.
The authors declare no conflicts of interest.
Hereditary transthyretin amyloidosis (ATTRv) is a hereditary disease that affects multiple bodily systems. Although sonography generally reveals enlargement of nerves in the limbs, the brachial plexus, and vagus nerve, the clinical significance of these findings remains unclear.
We performed sonographic measurements of the median nerve, cervical spinal nerves at the C5–C7 level, and the vagus nerve in patients with ATTRv and healthy controls. Clinical profiles and cardiac and gastrointestinal examination results were also collected for linear regression analysis.
We recruited 47 patients with ATTRv (males/females: 34/13, age: 65.6 ± 5.3 years). The sampled segments were all significantly larger than those of the controls. In the clinical profiles, the sum of the Z scores of the neck triangle nerves (cervical spinal nerves and vagus nerve) and of all nerves (cervical spinal nerves, vagus nerve, and median nerve at the wrist) significantly correlated with the familial amyloid polyneuropathy stage, onset of autonomic nervous system (ANS) symptoms, and autonomic symptom scores. On cardiac examinations, several ultrasonography and magnetic resonance imaging parameters (primarily those that reflect heart volume) were found to be significantly correlated with the sum of the Z scores of the cervical spinal nerves but not with the Z score of the vagus nerve. In gastrointestinal evaluation, the cross-sectional area of the vagus nerve was correlated with gastric emptying time parameters on scintigraphy.
Neck triangle nerve enlargement on sonography correlated with parameters related to ANS dysfunction, indicating that nerve enlargement observed on ultrasonography may serve as a potential surrogate biomarker of ATTRv.
To compare the efficacy of romosozumab (ROMO) and denosumab (DEN) in prevalent long-term glucocorticoid (GC) users.
Adult patients receiving oral prednisolone (≥5 mg/day) with high risk of fracture were randomized to receive subcutaneous ROMO (210 mg monthly) or DEN (60 mg 6-monthly) for 12 months, followed by DEN for two more doses. The primary end point was the change in spine bone mineral density (BMD) from Months 0 to 12. Secondary end points included changes in BMD of the spine/hip/femoral neck and bone turnover markers at various time points and adverse events.
Seventy patients (age 62.6 ± 9.1 years; 96% women; median prednisolone dose 5.0 mg/day; duration of therapy 10.7 ± 7.4 years) were enrolled, and 63 completed the study. At Month 12, the spine BMD increased significantly in both ROMO (+7.3% ± 4.5%; p < 0.001) and DEN (+2.3% ± 3.1%; p < 0.001) groups. The absolute spine BMD gain from Months 0 to 12 was significantly greater in ROMO-treated patients (p < 0.001). Although the total hip BMD at Month 12 also increased significantly in the ROMO (+1.6% ± 3.3%; p = 0.01) and DEN groups (+1.6% ± 2.6%; p = 0.003), the absolute BMD gain was not significantly different between the groups. At Month 24, the spine BMD continued to increase in both the ROMO (+9.7% ± 4.8%; p < 0.001) and DEN group (+3.0% ± 3.0%; p < 0.001) compared to baseline, and the absolute BMD gain remained significantly greater in ROMO-treated patients. The total hip BMD continued to increase in both groups (ROMO +2.9% ± 3.7%; p < 0.001; DEN +2.2% ± 3.4%; p = 0.001), but the changes from baseline were similar. Injection site reaction was more frequently reported in ROMO-treated patients.
ROMO was superior to DEN in raising the spine BMD at Month 12 in chronic GC users. After switching to DEN, ROMO-treated patients continued to gain spine BMD to a greater extent than DEN until Month 24.
Because angiotensin (Ang) II is an essential vasoconstrictive peptide, we analyzed the impact of its post-translational modification to pyruvamide–Ang II (Ang P) by pyridoxal-5′-phosphate (PLP) on blood pressure. PLP is a less expensive vitamin B6 derivative and, therefore, could be a cost-effective drug against hypertension.
Effect of Ang P on calcium ion entry into vascular smooth muscle cells (VSMCs) was analyzed. Binding affinity of Ang P to angiotensin II type 1 receptor (AT1R) was measured. Vasoconstrictive effect of Ang P was investigated using the bioassay of isolated perfused rat kidneys. Spontaneously hypertensive rats (SHR) were administered PLP. Additionally, Wistar Kyoto rats (WKY) received Ang II and PLP. Blood pressure was measured time-dependently.
Ang II, incubated with PLP, was post-translationally modified to Ang P. Calcium ion entry in VSMCs was significantly lower with Ang P compared to Ang II. Binding affinity of Ang P to AT1R was lower compared to Ang II. Perfusion pressure of isolated perfused rat kidneys increased less by Ang P than by Ang II. Blood pressure of SHR treated with PLP decreased significantly. Blood pressure of WKY rats treated with Ang II was increased to hypertensive values, whereas blood pressure of WKY rats cotreated with Ang II and PLP was not.
PLP induces a post-translational modification of Ang II decreasing blood pressure in rats. Assuming that increased PLP intake in the form of vitamin B6 might reduce blood pressure in hypertensive patients, PLP might be a cost-effective drug against hypertension.
Limited evidence exists on the role of depression in the risk of developing stroke and other cardiovascular outcomes in patients who have undergone percutaneous coronary interventions (PCI). We investigated this relationship with data from the Korean National Health Insurance Service database.
Our nationwide retrospective cohort study included 164,198 patients who had undergone PCI between 2010 and 2017. Depression was defined with the ICD-10 codes recorded prior to the PCI. The primary outcome was a new-onset stroke following the PCI. Secondary outcomes included PCI with myocardial infarction (MI), revascularization (PCI or coronary artery bypass grafting), and all-cause mortality. A multivariable Cox proportional hazards regression analysis was used to calculate adjusted hazard ratios (aHR) and 95% confidence intervals (CI), adjusting for potential confounders, including sociodemographic and lifestyle factors, comorbidities, and MI at the index PCI.
Over a median follow-up of 5.0 years, acute stroke occurred in 5.7% of patients with pre-existing depression (17.4% of the study population), compared to 3.5% of those without depression. Depression was associated with a 27% increased risk of acute stroke (aHR 1.27, 95% CI 1.20–1.35). Additionally, depression was linked with a 25% elevated risk of all-cause death (aHR 1.25, 95% CI, 1.21–1.29) and an 8% increased risk of revascularization (aHR 1.08, 95% CI 1.04–1.11). The associations with the risk of stroke and all-cause mortality were stronger in patients under 65 years.
Our findings suggest that pre-existing depression may increase the risk of stroke and all-cause mortality following PCI, particularly in patients under 65 years. Additionally, depression was significantly associated with an increased need for revascularization. This underscores the potential benefits of managing depression to reduce stroke risk and overall cardiovascular outcomes following PCI.
Frailty and delirium are two common geriatric syndromes sharing several clinical characteristics, risk factors, and negative outcomes. Understanding their interdependency is crucial to identify shared mechanisms and implement initiatives to reduce the associated burden. This literature review summarizes scientific evidence on the complex interplay between frailty and delirium; clinical, epidemiological, and pathophysiological commonalities; and current knowledge gaps. We conducted a PubMed systematic search in June 2023, which yielded 118 eligible articles out of 991. The synthesis of the results—carried out by content experts—highlights overlapping risk factors, clinical phenotypes, and outcomes and explores the influence of one syndrome on the onset of the other. Common pathophysiological mechanisms identified include inflammation, neurodegeneration, metabolic insufficiency, and vascular burden. The review suggests that frailty is a risk factor for delirium, with some support for delirium associated with accelerated frailty. The proposed unifying framework supports the integration and measurement of both constructs in research and clinical practice, identifying the geroscience approach as a potential avenue to develop strategies for both conditions. In conclusion, we suggest that frailty and delirium might be alternative—sometimes coexisting—manifestations of accelerated biological aging. Clinically, the concepts addressed in this review can help approach older adults with either frailty or delirium from a different perspective. From a research standpoint, longitudinal studies are needed to explore the hypothesis that specific pathways within the biology of aging may underlie the clinical manifestations of frailty and delirium. Such research will pave the way for future understanding of other geriatric syndromes as well.
Madariaga MLL, Guthmiller JJ, Schrantz S, Jansen MO, Christenson C, Kumar M, Prochaska M, Wool G, Durkin-Celauro A, Oh WH, Trockman L, Vigneswaran J, Keskey R, Shaw DG, Dugan H, Zheng N-Y, Cobb M, Utset H, Wang J, Stovicek O, Bethel C, Matushek S, Giurcanu M, Beavis KG, di Sabato D, Meltzer D, Ferguson MK, Kress JP, Shanmugarajah K, Matthews JB, Fung JF, Wilson PC, Alverdy JC, Donington JS (University of Chicago, Chicago, USA). Clinical predictors of donor antibody titre and correlation with recipient antibody response in a COVID-19 convalescent plasma clinical trial (Original). J Intern Med., 2021;289:559–573. https://doi.org/10.1111/joim.13185
In the author byline, one of the author names was incorrect and should have been corrected from Christensen C. to Christenson C.
The online version of the article has been updated.
We apologize for this error.
α1-Antitrypsin deficiency is characterized by elevated elastase activity and excessive elastin degradation, which may impact cancer development and progression. We tested the hypothesis that individuals with α1-antitrypsin deficiency have increased susceptibility to cancer in the Danish population.
In a nationwide nested study, we identified 2702 individuals with α1-antitrypsin deficiency and 26,750 control subjects without α1-antitrypsin deficiency matched on age, sex, and municipality. We recorded admissions due to cancer as outcomes during a median follow-up of 62 years.
Individuals with α1-antitrypsin deficiency versus control subjects had an increased hazard of skin cancer (2.18, 95%CI: 1.81–2.63), leukemia (1.76, 1.12–2.79), liver cancer (3.91, 2.23–6.85), and cancer overall (1.25, 1.13–1.38). Corresponding hazard ratios when the entire Danish population was used as control group were 3.02 (2.55–3.58), 1.83 (1.19–2.81), 4.46 (2.74–7.28), and 1.45 (1.31–1.59). When the analysis was stratified according to comorbidities, the hazard for skin cancer was higher in those with chronic obstructive pulmonary disease (COPD) (3.59, 2.60–4.95) and skin disease (2.93, 2.19–3.92) but remained elevated in those without any of these diseases. Hazards for skin cancer in individuals with α1-antitrypsin deficiency were similar when stratified by liver cirrhosis and ischemic heart disease (ps for interaction: ≥0.76). Hazards for liver cancer in individuals with α1-antitrypsin deficiency versus control subjects were similar when stratified according to liver cirrhosis, COPD, skin disease, and ischemic heart disease (ps for interaction: ≥0.13).
Individuals with α1-antitrypsin deficiency have increased risks of skin cancer, leukemia, and liver cancer in the Danish population.
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