World Journal of Cardiology最新文献

Comments were made on some thought-provoking articles, which included articles that dealt with cardiac arrest (CA). Two articles on CA elaborate on the role of automated compression devices to provide chest compressions during cardiopulmonary resuscitation (CPR) in "hostile" environments and on a predictive model in cases of out-of-hospital CA (OHCA). CPR after CA has been practiced for centuries, and the evolution until current modern-day practices are discussed. The delay in adopting efficient techniques of resuscitation by the medical community for decades is also touched upon. Both in-hospital and OHCA are discussed along with guidelines and strategies to improve outcomes. Areas of possible research in the future are mentioned.

Clinical outcomes of catheter ablation remain suboptimal in patients with atrial fibrillation (AF), particularly in those with persistent AF, despite decades of research, clinical trials, and technological advancements. Recently, pulsed-field ablation (PFA), a promising non-thermal technology, has been introduced to improve procedural outcomes. Its unique feature of myocardial selectivity offers safety advantages by avoiding potential harm to vulnerable adjacent structures during AF ablation. However, despite the global enthusiasm within the electrophysiology community, recent data indicate that PFA is still far from being a "magic wand" for addressing such a complex and challenging arrhythmia as AF. More progress is needed in mapping processes rather than in ablation technology. This editorial reviews relevant available data and explores future research directions for PFA.

Background: Timely and accurate evaluation of the patient's pulmonary arterial pressure (PAP) is of great significance for the treatment of congenital heart disease. Currently, there is no non-invasive gold standard method for evaluating PAP.

Aim: To assess the prognostic value of lipocalin-2 (LCN2) in relation to PAP in patients with congenital heart disease associated with pulmonary artery hypertension.

Methods: We conducted a retrospective analysis of 69 pediatric patients diagnosed with ventricular septal defects. The patients' clinical and laboratory data were collected. The serum LCN2 concentrations were compared between the pulmonary arterial hypertension (PAH) group and the nonPAH group. The correlation of LCN2 concentration with PAH classification was evaluated using binary logistic regression analysis. The receiver operating characteristic (ROC) curve was used to evaluate the diagnostic potential of LCN2 for PAH.

Results: Serum LCN2 concentration significantly correlated with patients' mean PAP (r = 0.544, P < 0.001), but not correlated with creatinine (P = 0.446) or blood urea nitrogen (P = 0.747). LCN2 levels were significantly correlated with PAH in both univariate [odds ratio (OR) 1.107, 95%CI: 1.033-1.185, P = 0.004)] and multivariate regression analysis (OR 1.150, 95%CI: 1.027-1.288, P = 0.015). ROC curve analysis revealed an area under the curve of 0.783 for LCN2. At the cutoff value of 19.42 ng/mL, the sensitivity and specificity of LCN2 for diagnosing PAH is 90.19% and 55.56%, respectively. LCN2 concentration also significantly correlated with the post-repair mean PAP in patients with congenital heart disease (r = 0.532, P = 0.009).

Conclusion: LCN2 is emerging as a candidate biomarker for assessing PAP in patients with congenital heart disease. Its high sensitivity in diagnosing PAH makes it a valuable tool in patient management.

The maintenance of intracellular and extracellular adenosine triphosphate (ATP) levels plays a pivotal role in cardiac function. In recent years, burgeoning attention has been directed towards ATP-induced cell death (AICD), revealing it as a distinct cellular demise pathway triggered by heightened extracellular ATP concentrations, distinguishing it from other forms of cell death such as apoptosis and necrosis. AICD is increasingly acknowledged as a critical mechanism mediating the pathogenesis and progression of various cardiovascular maladies, encompassing myocardial ischemia-reperfusion injury, sepsis-induced cardiomyopathy, hypertrophic cardiomyopathy, arrhythmia, and diabetic cardiomyopathy. Consequently, a comprehensive understanding of the molecular and metabolic underpinnings of AICD in cardiac tissue holds promise for the prevention and amelioration of cardiovascular diseases. This review first elucidates the vital physiological roles of ATP in the cardiovascular system, subsequently delving into the intricate molecular mechanisms and metabolic signatures governing AICD. Furthermore, it addresses the potential therapeutic targets implicated in mitigating AICD for treating cardiovascular diseases, while also delineating the current constraints and future avenues for these innovative therapeutic targets, thereby furnishing novel insights and strategies for the prevention and management of cardiovascular disorders.

Background: Ventricular arrhythmia is a common type of arrhythmia observed in clinical practice. It is primarily characterized by premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Abnormal formation or transmission of cardiac electrical impulses in patients affects cardiac ejection function. It may present with symptoms such as palpitations, dyspnea, chest discomfort, and reduced exercise tolerance. In severe cases, ventricular arrhythmia can even lead to death. Therefore, prompt treatment is very much essential upon diagnosis. The symptoms did not improve after previous conventional drugs and electrical defibrillation treatment, but the ventricular arrhythmia was prevented after the addition of nicorandil.

Case summary: A 75-year-old female patient was admitted to the hospital because of intermittent chest tightness, shortness of breath for 10 days, and fainting once for 7 days. Combined with laboratory tests and auxiliary examination, the patient was tentatively diagnosed with coronary heart disease or arrhythmia-atrial fibrillation. After admission, the patient had intermittent ventricular arrhythmia, which was uncontrolled with lidocaine, defibrillation, and amiodarone. However, when she was treated with nicorandil, the ventricular arrhythmia stopped. Nicorandil mitigates the action potential duration by facilitating the opening of potassium ion channels, thereby regulating the likelihood of premature and delayed depolarization in two distinct phases and subsequently averting the onset of malignant ventricular arrhythmia. Nicorandil may inhibit ventricular arrhythmia by dilating coronary arteries, improving coronary microcirculation and reducing myocardial fibrosis.

Conclusion: Nicorandil is a drug with dual effects. It could be used as a new therapeutic option for inhibiting ventricular arrhythmias.

Heart failure (HF) is a major global public health concern, and one of the less commonly known risk factors for HF development is metabolic dysfunction-associated steatotic liver disease (MASLD), as they share a similar pathophysiological background. In this article, we evaluated a recently published review article by Arriola-Montenegro et al. This article briefly summarizes the common pathophysiology of HF and MASLD development and evaluates the available therapeutic options to treat both conditions. Clinical practice guidelines highlight the importance of initiating and titrating guideline-directed medication therapy (GDMT) for patients with HF with reduced ejection fraction. GDMT is comprised of the four pillars currently proposed in most clinical practice guidelines, namely angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitors, beta-blockers, mineralocorticoid receptor antagonists, and sodium-glucose co-transporter 2 inhibitors (SGLT-2i). Given the similarity of pathophysiology and risk factors, recent studies for GDMT regarding ACEIs, ARBs, mineralocorticoid receptor antagonists, and SGLT-2i have shown beneficial effects on MASLD. Nonetheless, other medications for both conditions and novel therapies require more robust data and well-designed clinical studies to demonstrate their efficacies in both conditions.

Background: Permanent pacemaker implantation has the potential to impact left ventricular (LV) function and hence quality of life (QoL) in the long term.

Aim: To assess the effect of single- and dual-chamber pacing on LV function and QoL.

Methods: This study included 56 patients who underwent permanent pacing: Dual pacing, dual sensing, dual responsive and rate responsive (DDDR) for the initial 3 months and ventricular pacing, ventricular sensing, inhibited response and rate responsive (VVIR) for the next 3 months, and DDDR mode for the last 3 months. Throughout the study period, various echocardiographic parameters, functional status, and QoL were measured to assess the impact of pacing on LV function compared with baseline and at every 3 months interval.

Results: A significant change appeared in cardiac function after VVIR pacing which included diastolic properties of LV as shown by increase in isovolumic relaxation time from (85.28 ± 9.54 ms) to (89.53 ± 9.65 ms). At the 3-, 6-, and 9-month follow-up, reduction in LV ejection fraction was observed to be 62.71 ± 4.66%, 61.07 ± 4.41%, and 58.48 ± 3.89%, respectively. An increase in the QoL scores was noted at every follow-up visit.

Conclusion: An apparent depressant effect on LV function due to right ventricular pacing, with a higher incidence of adverse outcomes in the VVIR mode. In addition, an upsurge in QoL scores for the study population was noted, which indicates improvement in the QoL of patients post-pacing, irrespective of the mode. Generally, the DDDR mode is a highly preferable pacing mode.

In this editorial we comment on the article by Safwan M et al. We especially focused on the cardiac function restoration by the use of mesenchymal stem cells (MSCs) therapy for heart failure (HF), which has emerged as a new treatment approach as "Living Biodrugs". HF remains a significant clinical challenge due to the heart's inability to pump blood effectively, despite advancements in medical and device-based therapies. MSCs have emerged as a promising therapeutic approach, offering benefits beyond traditional treatments through their ability to modulate inflammation, reduce fibrosis, and promote endogenous tissue regeneration. MSCs can be derived from various tissues, including bone marrow and umbilical cord. Umbilical cord-derived MSCs exhibit superior expansion capabilities, making them an attractive option for HF therapy. Conversely, bone marrow-derived MSCs have been extensively studied for their potential to improve cardiac function but face challenges related to cell retention and delivery. Future research is focusing on optimizing MSC sources, enhancing differentiation and immune modulation, and improving delivery methods to overcome current limitations.

Sodium-dependent glucose transporter 2 inhibitors (SGLT2i) have been increasingly used with proven efficacy in patients with heart failure (HF), regardless of diabetes status. Grubić Rotkvić et al recently published an observational study on SGLT2i therapy in patients with type 2 diabetes mellitus and asymptomatic HF. They found that the use of SGLT2i led to reduced cardiac load and improved cardiovascular performance, reinforcing the evolving paradigm that SGLT2i are not merely glucose-lowering agents but are integral to the broader management of cardiovascular risk in patients with type 2 diabetes mellitus. The study by Grubić Rotkvić et al contributes to the growing body of literature supporting the early use of SGLT2i in patients with diabetic cardiomyopathy, offering a potential strategy to mitigate the progression of HF. Future larger studies should be conducted to confirm these findings, and explore the long-term cardiovascular benefits of SGLT2i, particularly in asymptomatic patients at risk of developing HF.

The deleterious effects of long term right ventricular pacing are increasingly being recognized today. Current clinical practice favors the implantation of dual-chamber permanent pacemaker which maintains atrioventricular synchrony and is associated with better quality of life. However, despite the popular belief and common sense surrounding the superiority of dual-chamber pacing over single chamber pacing, the same has never been conclusively verified in clinical trials. Some observational evidence however, does exists which supports the improved cardiac hemodynamics, lower the rate of atrial fibrillation, heart failure and stroke in dual-chamber pacing compared to single-chamber pacing. In the index study by Haque et al, right ventricular pacing, particularly in ventricular paced, ventricular sensed, inhibited response and rate responsive pacemaker adversely impacted the left ventricular functions over 9-months compared to dual pacing, dual sensing, dual responsive and rate responsive pacemaker. Although there are key limitations of this study, these findings does support a growing body of evidence reinstating the superiority of dual chamber pacing compared to single chamber pacing.