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Hypocapnia and its relationship with in-hospital mortality in acute heart failure patients: Insights from the Indonesian multicenter ICCU registry Prasetya, Indra; Afifah, Yuri; Anjarwani, Setyasih; Juzar, Dafsah A.; Bagaswoto, Hendry P.; Muzakkir, Akhtar F.; Habib, Faisal; Astiawati, Tri; Wirawan, Hendy; Ilhami, Yose R.; Djafar, Dewi U.; Sungkar, Safir; Danny, Siska S.; Rohman, Mohammad S.
Narra J Vol. 5 No. 1 (2025): April 2025
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v5i1.1638

Abstract

Acute heart failure (AHF) presents serious risks for hospitalized patients. The aim of this study was to explore the relationship between arterial partial pressure of carbon dioxide (PaCO2) levels and outcomes in AHF patients admitted to the intensive cardiovascular care unit (ICCU), utilizing data from the IndONEsia ICCU Registry (One ICCU Registry). A multicenter retrospective observational study was performed covering data between August 2021-2023. Participants were categorized by PaCO2 levels: hypocapnia (<35 mmHg), normocapnia (35–45 mmHg), and hypercapnia (>45 mmHg). The primary outcomes included ICCU mortality, in-hospital mortality, and 30-day mortality, whereas the length of the stays in the ICCU or hospital and ventilation requirement were set as the secondary outcomes. Mortality risks were assessed using Cox proportional hazards models. Of the 1,870 patients, 1,102 (58.96%) had hypocapnia, 645 (34.5%) had normocapnia, and 123 (6.5%) had hypercapnia. Hypocapnia patients had significantly higher ICCU, in-hospital, and at 30-day mortality rates compared to normocapnic patients (all p<0.001), along with longer lengths of stay in ICCU and in hospital (p<0.001). Hypocapnia significantly increased noninvasive and mechanical ventilation requirement compared to normocapnia patients. Multivariate analysis identified factors impacting patients’ survival, including age, treatment with angiotensin-converting enzyme inhibitors (ACEi)/angiotensin II receptor blockers (ARBs) drugs, and severity scores such as the quick sequential organ failure assessment (qSOFA) and simplified acute physiology score II (SAPS II). In conclusion, hypocapnia in AHF patients could increase in-hospital, ICU and 30-days mortality rates and length of hospital stays, as well as noninvasive and mechanical ventilation requirements.
Outcomes of first-generation versus second-generation drug-eluting stents in calcified coronary lesions: A meta-analysis Rohman, Mohammad S.; Fajar, Jonny K.; Widyaningsih, Melly C.; Aziizah, Yusnia N.; Khasanah, Uswatun A.; Nendro, Farid EB.; Beting, Euphrasiane G.; Tanaem, Vini S.; Jannati, Desi; Putri, Wanda M.; Tamara, Fredo
Narra J Vol. 5 No. 2 (2025): August 2025
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v5i2.2100

Abstract

The choice between first-generation drug-eluting stents (DES) and second-generation DES in managing calcified coronary lesions remains a topic of debate. The aim of this study was to compare outcomes between first-generation DES and second-generation DES in patients with calcified coronary lesions. This meta-analysis study was conducted from October to November 2024. The databases used were Embase, Scopus, and PubMed. Relevant articles were collated, and data regarding outcomes in patients with calcified coronary lesions treated with first-generation and second-generation DES were included to calculate the pooled effect size. The statistical analysis was performed using the Mantel-Haenszel method. Six articles were included in the study. The results indicated that calcified coronary lesions treated with first-generation DES were associated with increased risks of all-cause mortality (Odd ratios (OR): 1.23; 95% confidence interval (95%CI): 1.05–1.45; p-Egger= 0.9346; p-Heterogeneity: 0.9720; p=0.0120), myocardial infarction (OR: 1.48; 95%CI: 1.22–1.80; p-Egger: 0.6472; p-Heterogeneity: 0.5890; p<0.0001); and target lesion revascularization (TLR) (OR: 1.47; 95%CI: 1.24–1.74; p-Egger: 0.9982; p-Heterogeneity: 0.5950; p<0.0001), in comparison with second-generation DES. In contrast, when comparing first- and second-generation DES in terms of cardiac death and major adverse cardiovascular events, a similar risk was depicted. This study compared the outcomes of first-generation and second-generation DES in the management of patients with calcified coronary lesions, which may serve as a reference for selecting DES in the patient population.
Colchicine attenuates chemical hypoxia-induced pyroptosis through downregulation of nuclear factor kappa B and caspase-1 in cardiomyocytes Satrijo, Budi; Rohman, Mohammad S.; Aulanni'am, Aulanni'am; Sujuti, Hidayat; Lestari, Bayu
Narra J Vol. 5 No. 2 (2025): August 2025
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v5i2.2245

Abstract

Myocardial infarction (MI) is the leading cause of mortality worldwide. During MI, cardiomyocyte necrosis and inflammation are crucial in the post-MI cardiac remodeling process, including pyroptosis. Although colchicine is a well-known anti-inflammatory drug that has been clinically studied in the context of MI, its role in cardiac pyroptosis remains unclear. The aim of this study was to investigate the role of colchicine in pyroptosis in vitro, using CoCl2-induced H9c2 cells. Prior to the primary experiment, the hypoxic model in H9c2 cells was optimized by evaluating hypoxia-inducible factor-1 alpha (HIF-1α) expression and viability in cells exposed to various concentrations of CoCl2 at different time intervals. Subsequently, an in vitro hypoxia model was established by treating H9c2 cells with CoCl2 (600 µM), with or without colchicine (1 µM), for 3 hours. Flow cytometry was used to measure the expression of nuclear factor-kappa beta (NF-κB), interleukin 18 (IL-18), caspase-1, and HIF-1α in pyroptotic cells. Immunofluorescence was used to assess caspase-1 localization and its colocalization with propidium iodide during late-stage pyroptosis. Our data indicated that CoCl2-induced hypoxia significantly upregulated NF-κB, caspase-1, and IL-18 expression, and increased pyroptotic cell death in H9c2 cells. Colchicine treatment attenuated these effects, leading to a marked reduction in NF-κB, caspase-1, and IL-18 expression in hypoxic cells. Colchicine treatment significantly decreased the number of late pyroptotic cells. The protective effect of colchicine was more pronounced in late hypoxia (24-hour) setting compared to early hypoxia (3-hour). These findings suggest that colchicine attenuates cardiac pyroptosis in hypoxic H9c2 cells, as evidenced by the significant downregulation of key proteins involved in this pathway, including NF-κB, caspase-1, and IL-18. This protective effect appeared to be more effective in late hypoxia.