Scandinavian Cardiovascular Journal最新文献

Background: Patients with atrial fibrillation (AF) are often treated with antiarrhythmic drugs (AADs) to maintain sinus rhythm and with heart rate-lowering drugs to achieve the optimal rate control. In this study, we investigated trends in the use of AADs and rate control drugs in Finnish patients with AF.

Methods and results: The Finnish AntiCoagulation in Atrial Fibrillation (FinACAF) study is a nationwide study including all patients with AF in Finland from 2007 to 2018. The number of AAD purchases and the proportions of all prevalent AF patients in a certain year of interest were calculated. In total, 391030 AF patients were identified between 2007 and 2018, and 39,816 (10.2%) of them had purchased either class I or III AADs. The proportion of patients using classes I and III AADs decreased from 8.6% to 6.3%. Flecainide and amiodarone were the most often used AADs. The use of flecainide and amiodarone decreased from 4.9% to 3.9% and 1.9% to 1.5%, respectively. The proportion of patients on beta-blockers remained stable at 75%. Dronedarone became available in 2011 when it also was the most used (0.8% of patients), but the use decreased thereafter. The use of sotalol and digoxin decreased from 1.5% to 0.6% and 24.6% to 11.0% over the study period.

Conclusion: The number of AAD purchases increased alongside with the increasing prevalence of AF, whereas the proportion of AF patients on classes I and III AADs and digoxin decreased between 2007 and 2018. Flecainide remained the most used AAD followed by amiodarone.

Objectives. This study investigated the role and underlying regulatory mechanisms of circular RNA fibronectin type III domain containing 3B (circFNDC3B) in abdominal aortic aneurysm (AAA). Methods. The expression of circFNDC3B in AAA and normal tissues was assessed by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). To evaluate the biological functions of circFNDC3B, assays were employed including 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry, and Caspase-3 activity assays. Additionally, RNA immunoprecipitation (RIP), dual-luciferase reporter assay, Western blotting, and rescue experiments were utilized to elucidate the molecular mechanism of circFNDC3B. Results. Our findings revealed a significant upregulation of circFNDC3B expression in AAA clinical specimens compared to normal tissues. Functionally, overexpression of circFNDC3B inhibited vascular smooth muscle cells (VSMCs) proliferation and induced apoptosis, contributing to AAA formation in the Ang II-induced AAA model. Mechanistically, circFNDC3B acted as a molecular sponge for miR-1270, leading to the upregulation of programmed cell death 10 (PDCD10). Decreased expression of PDCD10 abrogated the -promoting effects of circFNDC3B overexpression on AAA development. Conclusions. This study demonstrates that circFNDC3B promotes the progression of AAA by targeting the miR-1270/PDCD10 pathway. Our findings suggest that circFNDC3B as well as miR-1270/PDCD10 pathway may serve as a potential therapeutic target for AAA treatment.

Background. Colchicine is an anti-inflammatory drug with promising efficacy for preventing cardiovascular events. We aimed to assess the pooled effect of colchicine on ischemic stroke among patients with established atherosclerotic cardiovascular diseases. Methods. PubMed, Scopus, Web of Science, and the Cochrane Library were systematically searched from the inception to August 5, 2024. A random-effects (DerSimonian-Laird) model was used to conduct this meta-analysis. The inclusion criteria were as follows: (I) being a randomized controlled trial; and (II) measuring the efficacy of colchicine compared to placebo for preventing ischemic stroke among those with established atherosclerotic cardiovascular diseases. Results. We identified 13 eligible clinical trials with 24900 participants. Colchicine significantly decreased the risk of ischemic stroke (relative risk (RR) 0.85, 95% confidence interval (CI) (0.72, 0.99), I²=2.92%) among those with established atherosclerotic cardiovascular diseases. Colchicine was more effective when used at 0.5 mg/day (RR 0.86, 95% CI (0.75, 0.99)), prescribed for more than 30 days (RR 0.86, 95% CI (0.75, 1.00)) or for more than 90 days (RR 0.65, 95% CI (0.46, 0.92)), or administered for patients with acute coronary syndrome (RR 0.46, 95% CI (0.23, 0.92)). In addition, colchicine was more effective in studies with a sample size of more than 500 patients, consistent with sensitivity analysis, which indicated that the results relied on large-sized clinical trials. Conclusion. Colchicine may decrease the risk of ischemic stroke among patients with established atherosclerotic cardiovascular diseases, particularly after long-term use; however, future studies are needed due to inconsistencies between existing trials.

Aims: Coronavirus disease (COVID-19) can affect cardiovascular function in health and disease. The present study assessed the effect of prior COVID-19 infection on cardiovascular phenotype at rest and in response to exercise in middle age and older individuals.

Methods: This case-control, single-centre study recruited 124 participants: 84 with a history of COVID-19 (59.9 ± 7.41 years, 54.8% female) and 40 participants without history of COVID-19 infection (62.8 ± 7.14 years, 62.5% female). All participants underwent non-invasive assessment of arterial function using pulse wave velocity (PWV), augmentation index (Alx) and hemodynamic function (i.e., cardiac index (CI), stroke volume index (SVI), heart rate (HR), mean arterial blood pressure (MAP)) at rest. Cardiopulmonary exercise stress testing with simultaneous gas exchange and hemodynamic (bioreactance) measurements was also performed.

Results: There were no differences between COVID-19 and non-COVID-19 groups in PWV (COVID-19: 7.52 ± 1.66 m/s, non-COVID-19: 7.32 ± 1.79 m/s, p = 0.440); Alx (COVID-19: 29.2 ± 9.12%, non-COVID-19: 29.2 ± 8.44%, p = 0.980); CI (COVID-19: 2.85 ± 0.39 L/min/m², non-COVID-19: 2.79 ± 0.37 L/min/m², p = 0.407); SVI (COVID-19: 46.5 ± 7.54 mL/m², non-COVID-19: 47.0 ± 7.59 mL/m², p = 0.776), HR (COVID-19: 62.3 ± 10.6 beats/min, Non-COVID-19: 60.2 ± 8.52 beats/min, p = 0.263), or MAP (COVID-19: 98.1 ± 11.2 mmHg, non-COVID-19: 96.6 ± 9.46 mmHg, p = 0.464). COVID-19 participants however demonstrated lower O₂ consumption at anaerobic threshold (15.5 ± 4.25 vs 16.8 ± 4.51 mL/kg/m², p = 0.034), peak cardiac index (10.4 ± 2.3 vs 11.3 ± 2.5 L/min/m², p = 0.040) and peak stroke volume index (82.1 ± 25.3 vs 98.6 ± 37.6 mL/m², p = 0.028).

Conclusion: Healthy middle-age and older individuals with history COVID-19 infection demonstrate reduced exercise tolerance and cardiac function response to exercise.

Objectives. Current guidelines recommend that surveillance imaging should be performed at least every third year for patients with ascending thoracic aortic aneurysm (ATAA) even though such aneurysms' growth rate is mostly minimal. The purpose of this study was to clarify the pattern of the growth of ATAAs in a real-life patient population to adjust the optimal timing of aortic surveillance for each patient. Methods. This study includes patients (n = 209) who had been followed due to ATAA in the central hospital of North Karelia in Eastern Finland between years 2007 and 2023. Aortic imaging was performed using either computed tomography (CT) or transthoracic echocardiography (TTE). In the CT images, the aortic dimensions were measured according to guidelines in four levels of the ascending aorta. TTE measurements were collected from medical records. Measurements were used to explore the pattern of the ATAA growth. Results. During the mean surveillance time 5.0 ± 3.5 years, the median growth rate of ATAAs was 0.37 mm/year. One fifth (21.5%) of the aneurysms showed no expansion during the follow-up. Despite the minimal growth rate during surveillance, some patients ended up exceeding the cut-off for preventive surgery. Among the patients, who showed expansion during the follow-up, the linear model seemed to best describe the growth of ATAA. Conclusions. The majority of the patients had a very low ATAA growth rate. Based on this study, the growth of ATAAs could be described using a linear model, which could, in turn, be used to predict the growth of an aneurysm.

Objectives. The aim of this study was to investigate the expression of long non-coding RNA (lncRNA) brain and reproductive organ-expressed protein (BRE) antisense RNA 1 (BRE-AS1) in patients with acute myocardial infarction (AMI) and its effect on ischemia/reperfusion (I/R)-induced oxidative stress and apoptosis of cardiomyocytes. Methods. Serum BRE-AS1 levels in patients with AMI was detected using quantitative real-time polymerase chain reaction (qRT-PCR). The diagnostic and prognostic values of BRE-AS1 were evaluated. H9c2 cells were treated with hypoxia/reoxygenation to establish an in vitro myocardial infarction cell model. The levels of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 were detected by enzyme-linked immunosorbent assay (ELISA). Levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were determined by commercial kits. Cell counting kit-8 (CCK-8) and flow cytometry were used to evaluate the cell viability and cell apoptosis. Results. The expression of BRE-AS1 in serum of patients with AMI is upregulated, which shows the clinical diagnostic value for AMI. In the I/R injury cell model, the knockout of BRE-AS1 can significantly alleviate the increase in TNF-α, IL-1β, and IL-6 levels, inhibit the production of LDH and MDA, increase the activities of SOD and GSH-Px, promote the cell viability and suppress cell apoptosis. Conclusions. Abnormally elevated BRE-AS1 has a high diagnostic value for AMI as well as a prognostic value for major adverse cardiovascular events (MACEs). The elevation of BRE-AS1 promoted oxidative stress injury and cell apoptosis in vitro.

Objectives: This study aims to identify the risk factors contributing to in-hospital mortality in patients with acute ST-elevation myocardial infarction (STEMI) who develop acute heart failure (AHF) post-percutaneous coronary intervention (PCI). Based on these factors, we constructed a nomogram to effectively identify high-risk patients.

Methods: In the study, a collective of 280 individuals experiencing an acute STEMI who then developed AHF following PCI were evaluated. These subjects were split into groups for training and validation purposes. Utilizing lasso regression in conjunction with logistic regression analysis, researchers sought to pinpoint factors predictive of mortality and to create a corresponding nomogram for forecasting purposes. To evaluate the model's accuracy and usefulness in clinical settings, metrics such as the concordance index (C-index), calibration curves, and decision curve analysis (DCA) were employed.

Results: Key risk factors identified included blood lactate, D-dimer levels, gender, left ventricular ejection fraction (LVEF), and Killip class IV. The nomogram demonstrated high accuracy (C-index: training set 0.838, validation set 0.853) and good fit (Hosmer-Lemeshow test: χ² = 0.545, p = 0.762), confirming its clinical utility.

Conclusion: The developed clinical prediction model is effective in accurately forecasting mortality among patients with acute STEMI who develop AHF after PCI.

Objectives: Minimally invasive cardiac surgery techniques are increasingly used but have longer cardiopulmonary bypass time, which may increase inflammatory response and negatively affect coagulation. Our aim was to compare biomarkers of inflammation and coagulation as well as transfusion rates after minimally invasive mitral valve repair and mitral valve surgery using conventional sternotomy.

Design: A prospective non-randomized study was performed enrolling 71 patients undergoing mitral valve surgery (35 right mini-thoracotomy and 36 conventional sternotomy procedures). Blood samples were collected pre- and postoperatively to assess inflammatory response. Thromboelastometry (ROTEM) was performed to assess coagulation, and transfusion rates were monitored.

Results: The minimally invasive group had longer cardiopulmonary bypass times compared to the sternotomy group: 127 min ([115-146] vs 79 min [65-112], p < 0.001) and were cooled to a lower temperature during cardiopulmonary bypass, 34 °C vs 36 °C (p = 0.04). IL-6 was lower in the minimally invasive group compared to the conventional sternotomy group when measured at the end of the surgical procedure, (38 [23-69] vs 61[41-139], p = 0.008), but no differences were found at postoperative day 1 or postoperative day 3. The transfusion rate was lower in the minimally invasive group (14%) compared to full sternotomy (35%, p = 0.04) and the chest tube output was reduced, (395 ml [190-705] vs 570 ml [400-1040], p = 0.04).

Conclusions: Our data showed that despite the longer use of extra corporal circulation during surgery, minimally invasive mitral valve repair is associated with reduced inflammatory response, lower rates of transfusion, and reduced chest tube output.