Atherosclerosis (AS) is a chronic vascular disease primarily affecting large and medium-sized arteries, involving complex pathological mechanisms such as inflammatory responses, lipid metabolism disorders and vascular plaque formation. In recent years, several emerging research hotspots have appeared in the field of atherosclerosis, including gut microbiota, pyroptosis, ferroptosis, autophagy, cuproptosis, exosomes and non-coding RNA. Traditional lipid-lowering drugs play a crucial role in the treatment of AS but are not able to significantly reverse the pathological changes. This article aims to summarize the latest research progress in the pathogenesis of AS and the diagnosis and treatment of the disease by comprehensively analyzing relevant literature mainly from the past five years. Additionally, the mechanisms of action and research advances of statins, cholesterol absorption inhibitors, fibrates and novel lipid-lowering drugs are reviewed to provide new insights into the diagnosis and treatment of AS.
Pulmonary hypertension (PH) is a life-threatening condition characterized by right ventricular (RV) remodeling, which is a major determinant of patient survival. The progression of right ventricular remodeling is significantly influenced by mitochondrial dysfunction, providing profound insights into vascular health and cardiovascular risk. In this review, we discuss the molecular targets, pathophysiological characteristics, and potential mechanisms underlying mitochondrial dysfunction in PH, encompassing disturbances in mitochondrial dynamics, inflammation, and dysregulation of mitochondrial energy metabolism. Finally, we review the primary therapeutic targets currently utilized to address cardiac dysfunction resulting from mitochondrial damage. Hopefully, this might inspire novel approaches to the management of cardiovascular disorders.
Systemic inflammation and glucose metabolism are strongly associated with survival in ST-elevation myocardial infarction (STEMI) patients. Therefore, we aimed to assess whether the glucose-to-lymphocyte ratio (GLR) could be used to predict the prognosis of STEMI patients who received emergency percutaneous coronary intervention (PCI) treatment.
The GLR was calculated as follows: GLR = glucose (mg/dL) / lymphocyte count (K/μL). Patients were divided into two groups according to the median GLR, with the low-GLR group (GLR <81) employed as the reference group. We used Cox proportional hazard regression analyses to determine the predictive value of clinical indicators. Kaplan‒Meier curves were used to plot survival curves for both groups. The receiver operating characteristic (ROC) curves were used to assess the predictive value of the GLR for the risk of all-cause mortality and cardiovascular mortality in STEMI patients. Meanwhile, to evaluate the predictive effectiveness of the models, we plotted the ROC curves for each model.
We retrospectively analyzed 1086 newly admitted patients with STEMI who underwent emergency PCI at the First Affiliated Hospital of Kunming Medical University from June 2018 to January 2023 (mean follow-up time, M ± standard deviation (SD): 1100.66 ± 539.76 days). The results showed that high GLR was associated with increased risks of all-cause mortality (hazard ratio (HR) = 2.530, 95% CI = 1.611–3.974, p < 0.001) and cardiovascular mortality (HR = 3.859, 95% CI = 2.225–6.691, p < 0.001). The optimal GLR threshold for predicting all-cause and cardiovascular death was 79.61 (K/μL), with a ROC for all-cause death of 0.678 (95% CI: 0.625–0.732, p < 0.001), a sensitivity of 77.4%, a specificity of 51.9%, and a ROC for cardiovascular death of 0.716 (95% CI: 0.666–0.767, p < 0.001), with a sensitivity of 88.4% and a specificity of 52.1%.
The GLR may potentially predict all-cause mortality and cardiovascular mortality in STEMI patients who received emergency PCI treatment. A high GLR was associated with a greater risk of all-cause mortality and cardiovascular mortality in STEMI patients.
Renal dysfunction (RD) is common in patients with heart failure (HF), however its impact on clinical outcomes in patients with tricuspid regurgitation (TR) and HF is still debated; therefore, we aimed to assess the impact of RD on clinical outcomes in this population.
All patients with HF and a prevalent or incident diagnosis of TR presenting at two centers between January 2020 and July 2021 were enrolled, in both acute (in-hospitalized patients) and chronic settings (outpatient). Patients were stratified according to the degree of RD (Group 1 <30 mL/min (n = 70), Group 2 30–59 mL/min (n = 123) and Group 3 ≥60 mL/min (n = 56).
Out of 249 patients, those with severe RD had lower left ventricular ejection fraction (41.8 ± 13.1% vs. 45.7 ± 14.2% vs. 48.6 ± 13.1%, p = 0.020) and tricuspid annular plane systolic excursion (16.6 ± 3.7 mm vs. 17.6 ± 4.0 mm vs. 20.0 ± 4.4 mm, p < 0.001) while brain natriuretic peptides levels were higher (979 ± 1514 pg/mL vs. 490 ± 332 pg/mL vs. 458 ± 543 pg/mL, p = 0.049) than in the other subgroups. After a median follow-up of 279 (interquartile range, IQR 195–481) days, all-cause mortality was higher in patients with severe RD (37.7% vs. 23.3% vs. 13.7%, p = 0.012). HF hospitalizations (32.7% vs. 31.2% vs. 30.6%, p = 0.970) and the composite of all-cause mortality or HF hospitalization (54.1% vs. 47.9% vs. 42.0%, p = 0.444) did not differ between subgroups.
Severe RD is highly present in patients with HF and TR and is associated with increased incidence of all-cause mortality.
Sodium–glucose cotransporter 2 inhibitors (SGLT2i) have been found to have potential hematopoietic effects in patients with heart failure (HF). However, these benefits have not been studied in patients with cardiac amyloidosis (CA). CA patients present with HF symptoms and often suffer from iron deficiency, which has a negative impact on erythropoiesis and leads to lower hemoglobin and hematocrit levels. We sought to determine the potential effects of SGLT2i on hematological parameters and functional capacity (FC) in CA patients.
A prospective analysis was conducted to compare the effects of SGLT2i in patients who received the best medical therapy (BMT) along with SGLT2i (n = 20), versus patients receiving only BMT without SGLT2i (n = 20) (historical control group). All patients underwent blood testing and cardiopulmonary exercise testing (CPET) at baseline (BL) and after 6 months [interquartile range (IQR): 4.0 to 8.0].
The SGLT2i-based therapy resulted in a significant improvement and difference in hematological parameters at 6 months follow-up compared to the control group. In the SGLT2i group, the mean hemoglobin level increased (+1.2 mg/dL), whereas in the control group, it decreased (–0.8 g/dL) (p < 0.001 for overall group comparison). The hematocrit showed a significant increase in the SGLT2i group (+4.4%) compared to a decrease in the control group (–1.8%) (p < 0.001). Additionally, the serum iron level improved in the SGLT2i-treated group (+ 5.5 [–5.0 to 17.5] μg/dL vs. –6.0 [–15.0 to 4.0] μg/dL, p = 0.121). Although there was no significant change in the peak oxygen consumption (peak VO2, (mL/min)/kg) (p = 0.206), as well as in pulmonary ventilation (VE)/carbon dioxide production (VCO2) slope in both groups (p = 0.964), the SGLT2i group maintained a peak VO2 and VE/VCO2 slope throughout the study.
SGLT2i therapy improved hematological parameters and stabilized the FC of CA patients.
Research results on the association between alcohol consumption and abdominal aortic calcification (AAC) has yielded inconsistent results. There is a paucity of evidence on the association of smoking and alcohol consumption with AAC in the general middle-aged and elderly population, including age subgroups. This study utilizes nationwide survey data to explore these associations.
Data from middle-aged and elderly National Health and Nutrition Examination Survey (NHANES) 2013–2014 participants receiving dual X-ray absorptiometry were analyzed. AAC severity was assessed using a scoring system with a maximum value of 24. Presence of AAC was defined as an AAC score >0, and severe AAC as an AAC score ≥6. Binary logistic regression was employed for analyzing the association of smoking and alcohol consumption-related indices with the presence of AAC, while cumulative odds logistic regression explored their associations with severe AAC.
Data of 3135 participants were analyzed. Investigation in the entire population found that smoking history was linked to both AAC and severe AAC. In contrast, alcohol consumption history was not linked to AAC or severe AAC. After adjusting for confounders, the findings confirmed a significant association of smoking history with AAC and severe AAC. No significant associations were found for current alcohol consumption with either AAC or severe AAC. Compared with never smokers, former smokers and current smokers experienced increased AAC risk. Former smokers had a significantly lower AAC risk compared to current smokers. Compared with never alcohol consumers, neither former nor current alcohol consumers experienced a different AAC risk. No difference in AAC risk was found between former and current alcohol consumers. Individuals consuming more than 2 drinks of alcohol per day suffered from a significant increase in risk of AAC. Subgroup analyses found elderly ever and current smokers suffered from a significantly elevated AAC risk, as did middle-aged ever smokers. Elderly ever and current alcohol consumers also experienced increased risk of AAC.
Smoking history is significantly associated with both AAC and severe AAC. The cardiovascular benefits associated with smoking cessation primarily manifest as reduction in risk of AAC presence rather than severe AAC. Elderly smokers are exposed to a greater risk of AAC. In contrast, alcohol consumption shows no association with severe AAC. Alcohol consumption is not associated with AAC except in heavy drinking and elderly subpopulations.
Lipoprotein(a) [Lp(a)] is associated with the development of coronary artery calcification (CAC), yet its exact function is not fully understood. This study sought to assess the relationship between Lp(a) levels and the risk of CAC in elderly diabetic patients.
This cross-sectional study included 486 elderly diabetic patients. The exposure factor was Lp(a) levels, categorized into three groups (T1, T2, T3). The outcome was the presence of CAC. The relationship between Lp(a) levels and CAC was evaluated using several statistical methods, including univariate and multivariate logistic regression, multivariable stratified analysis, receiver operating characteristic (ROC) curve analysis, and restricted cubic spline (RCS) analysis.
The highest Lp(a) group (T3) showed significantly higher prevalence of CAC compared to the T1 and T2 groups. Univariate logistic regression indicated a significant link between Lp(a) and CAC. Furthermore, multivariate logistic regression supported the finding that elevated Lp(a) levels correlated with a heightened risk of CAC in all models. Specifically, each unit rise in Lp(a) was associated with a notable increase in CAC risk, and Log10Lp(a) and each 1 standard deviation increase in Lp(a) also significantly elevated CAC risk. Multivariable stratified analysis demonstrated significant differences in CAC risk across various subgroups, including age ≤70 years, males, females, smokers, hypertensive, non-hypertensive, hyperlipidemic, non-hyperlipidemic, non-stroke, and non-chronic kidney disease patients. ROC curve analysis showed that adding Lp(a) to the baseline model improved the area under the curve from 0.741 to 0.755. RCS analysis indicated a significant, approximately linear association between Log10Lp(a) and CAC risk (p nonlinear = 0.115).
In an elderly diabetic population, elevated levels of Lp(a) were strongly linked to a greater risk of CAC. Integrating Lp(a) measurements with conventional risk factors improves the predictive accuracy for CAC.
Cardiovascular disease is the leading cause of death in most of the world. Previous meta-analyses of generic drugs for the treatment of cardiovascular disease have not provided sufficient evidence to demonstrate the true efficacy and safety of the drugs. Subsequently, concern exists regarding whether the use of generic drugs can fully substitute brand-name drugs in clinical treatment. To enhance the evidence for generic drugs, this meta-analysis compares the actual effectiveness of generic drugs with brand-name drugs in preventing and treating cardiovascular diseases. This study aimed to resolve the controversy over whether generic drugs in cardiovascular disease can replace brand-name drugs, fully evaluating the best evidence on the clinical equivalence of generic drugs.
The PubMed, Embase, The Cochrane Library, and Clinicaltrials.gov databases were searched. The search period included articles published before December 2023. Studies on generic and branded cardiovascular drugs were collected, and two independent reviewers screened eligibility, extracted study data, and assessed the risk of bias. Safety outcomes included major adverse cardiovascular events and other adverse events. Efficacy outcomes included relevant vital signs (e.g., blood pressure, heart rate, urine volume) and laboratory measures (e.g., international normalized ratio, low-density lipoprotein cholesterol, platelet aggregation inhibition). A meta-analysis and subgroup analysis were conducted using the Rev Man software.
A total of 4238 studies were retrieved, and 87 studies (n = 2,303,818) were included in the qualitative analysis. There were 57 quantitatively assessed studies (n = 560,553), including angiotensin II receptor blockers, beta-blockers, calcium channel blockers, antithrombotic drugs (anticoagulants or antiplatelet agents), diuretics, statins, and other classes of cardiovascular medications. Regarding clinical safety, 19 studies assessed the occurrence of major adverse cardiovascular events (MACEs) (n = 384,640), and 35 reported secondary adverse events (n = 580,125). In addition to the MACEs for statins (risk ratio (RR) 1.13 [1.05, 1.21]) and adverse events (AEs) for calcium channel blockers (RR 0.90 [0.88, 0.91]), there were no significant differences in the overall risk of MACEs (RR = 1.02 [0.90, 1.15]) and minor adverse events (RR = 0.98 [0.91, 1.05]) between generic and brand-name cardiovascular drugs. In terms of effectiveness, there were no significant differences observed between the two groups in blood pressure (BP), platelet aggregation inhibition (PAI), international normalized ratio (INR), low-density lipoprotein (LDL), and urinary sodium levels. Subgroup analyses for the region, study design, duration of follow-up, and grant funding revealed no significant differences in the risk of MACEs. However, the risk of AE was significantly higher in the Asian region for brand-name cardiovascular drugs than for generics. There was no statistically significant difference in risk between generic and brand-name drugs in the remaining subgroup analyses.
Cardiovascular drugs encompass many types; a minority of generic and brand-name drugs have discrepancies. Given the overall development trend of multi-manufacturer generic drugs in the future, this study provides a strong basis for the global application of generic drugs. The feasibility of generic drugs in terms of efficacy and safety in cardiovascular diseases is clarified. However, some drugs still need to be improved to replace the original drugs used in clinical practice completely. Therefore, large-sample, multicenter, high-quality studies are still required to guide the clinical use of cardiovascular drugs.
CRD42023481597, https://www.crd.york.ac.uk/PROSPERO/view/CRD42023481597.
Cardiovascular diseases (CVDs) remain a global health concern, prompting ongoing research into novel contributors to their pathogenesis. Due to the proximity of the coronary arteries and the myocardium in epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT), these tissues have emerged as key areas of interest for their potential influence on cardiac function and vascular health. This review synthesizes current research on the physiological and biological characteristics of EAT and PAT, exploring their composition and clinical measurement approaches. The roles of EAT and PAT in coronary artery disease (CAD), atrial fibrillation, and heart failure are discussed, and the contributions of EAT and PAT to these cardiovascular conditions are highlighted alongside their potential as therapeutic targets.
Anti-diabetic drugs have been noted to have a cardioprotective effect in patients with diabetes and heart failure (HF). The purpose of this study was to perform a Bayesian network meta-analysis to evaluate the impact of various anti-diabetic drugs on the prognosis of HF patients with and without diabetes.
We searched PubMed, Embase, Cochrane, and Web of Science for randomized controlled trials (RCTs) published before November 2024 that investigated the use of anti-diabetic medications in patients with HF. Primary outcomes included re-admission due to HF, all-cause death, cardiovascular death, serum N-terminal pro-brain natriuretic peptide (NTpro-BNP) levels, and left ventricular ejection fraction (LVEF). A Bayesian network meta-analysis was used to compare the effectiveness of different anti-diabetic drugs.
A total of 33 RCTs involving 29,888 patients were included. Sotagliflozin was the most effective in reducing the risk of re-admission due to HF and all-cause death, with a cumulative probability of 0.84 and 0.83, respectively. Liraglutide reduced the risk of cardiovascular death in HF patients with a cumulative probability of 0.97 and had the best efficacy in reducing NTpro-BNP levels with a cumulative probability of 0.69. Empagliflozin was best in improving LVEF in HF patients, with a cumulative probability of 0.69.
This Bayesian network meta-analysis demonstrates that sotagliflozin may be the best option for HF patients with and without diabetes. However, due to the small number of articles in this study, our results must be treated cautiously. Subsequently, there is an urgent need for more high-quality studies to validate our findings.
It is important to establish a coronary heart disease (CHD) prediction model with high efficiency and precision for early diagnosis of CHD using clinical information. While existing deep learning-based CHD prediction models possess the limitations of large datasets and long training time, existing machine learning-based CHD prediction models have the limitations of low accuracy and robustness, which are unsuitable for clinical application. This study aimed to design a fast and high-precision intelligent model using clinical information to predict CHD.
Five public datasets, including 303, 293, 303, 200, and 123 patients with 55, 14, 14, 14, and 14 attributes, respectively, were used for model training and testing. After data preprocessing, the singular value decomposition method was utilized to extract features to build the CHD prediction model. Then, the CHD prediction model was established using the 5-fold cross-validation method with a multilayer perceptron approach.
Results show that the established model performs better on the total dataset than the other models we built in this study. This machine learning-based CHD prediction model achieved an improved area under the curve (AUC) of 99.10%, with 96.63% accuracy, 96.50% precision, 97.4% recall, and 97.0% F1-score on the total dataset.
This high precision and efficiency achieved by the proposed model on different datasets would be significant for the prediction of CHD for medical and clinical diagnosis purposes.
This study aimed to evaluate the effectiveness of left bundle branch-optimized cardiac resynchronization therapy (LOT-CRT) in patients diagnosed with heart failure and reduced ejection fraction due to ischemic cardiomyopathy.
A total of 78 patients with ischemic cardiomyopathy who underwent pacemaker implantation at a single center between March 2020 and March 2022 were randomly assigned to two groups based on different pacing methods: LOT-CRT group (n = 39) and biventricular pacing (BVP) group (n = 35). Pacing threshold, impedance, electrocardiogram QRS wave duration during pacing, ventricular pacing ratio during follow-up, and cardiac ultrasound-related indicators were compared immediately after surgery and at the six-month follow-up.
The two groups were similar regarding baseline characteristics, cardiac ultrasound and magnetic resonance imaging (MRI) parameters, and overall cardiac function. However, the BVP group demonstrated higher pacing thresholds and impedance levels immediately after surgery and at the six-month follow-up (p < 0.001). Moreover, the X-ray exposure time was significantly longer in the BVP group compared to the LOT-CRT group. While no significant differences in QRS duration were observed between the groups preoperatively, the QRS duration in the LOT-CRT group was significantly shorter both immediately after surgery and during follow-up (p < 0.001). No significant differences were found between the groups in terms of the New York Heart Association (NYHA) functional class, left ventricular ejection fraction (LVEF), or left ventricular end-diastolic diameter (LVEDD). Six months post-surgery, both groups showed modest improvements in NYHA class, LVEF, and LVEDD, with the LOT-CRT group demonstrating significant improvements (p < 0.001).
LOT-CRT may be an alternative treatment for patients with heart failure complicated by left bundle branch block due to ischemic cardiomyopathy in whom BVP is ineffective.
Anemia or blood urea nitrogen (BUN) are both associated with atherosclerotic cardiovascular disease (ASCVD) in hypertension (HTN). However, the relationship between anemia, BUN, and ASCVD remains unclear in HTN. This study aimed to investigate the relationship between BUN, anemia, and ASCVD in HTN patients, and further investigated the moderating effect of anemia on the relationship between BUN and ASCVD.
In total, 15,109 HTN patients were included based on the National Health and Nutritional Examination Survey (NHANES) from 1999 to 2018. The weighted univariate logistic regression model was utilized to select potential covariates. The relationship between BUN, anemia, and ASCVD was investigated using weighted univariate and multivariate logistic regression models. All results were expressed as odds ratios (ORs) and 95% confidence intervals (CIs).
A total of 15,109 HTN patients were included for final analysis. BUN level ≥4.69 mmol/L was related to higher odds of ASCVD in HTN patients (OR = 1.68, 95% CI: 1.51–1.88). Similarly, anemia was also associated with increased odds of ASCVD in HTN patients (OR = 1.45, 95% CI: 1.22–1.73). In patients with anemia, a BUN level ≥4.69 mmol/L was associated with increased odds of ASCVD when compared to patients who had a BUN level <4.69 mmol/L (OR = 2.95, 95% CI: 2.05–4.25). Anemia affected the association between BUN and ASCVD in HTN patients.
Anemia moderates the association between BUN and ASCVD in HTN patients, amplifying the adverse effects. The findings show the importance of comprehensive management strategies that included renal function monitoring and anemia treatment in HTN patients.
Systolic blood pressure time in target range (SBP TTR) is a novel metric for blood pressure control. Previous studies have demonstrated an inverse association between SBP TTR and risks of cardiovascular events, but sex differences have never been reported. This study aims to investigate the sex-specific differences in the relationship using data from the Systolic Blood Pressure Intervention Trial (SPRINT).
This post hoc analysis included 8822 SPRINT participants with at least three follow-up systolic blood pressure (SBP) measurements within the first three months. SBP TTR was calculated using the Rosendaal method of linear interpolation. The primary endpoint was major adverse cardiovascular and cerebrovascular events (MACCE). Cox proportional hazards models and restricted cubic splines (RCS) were used to assess the association between SBP TTR and cardiovascular events.
Women accounted for 35.3% with a mean age of 68.6 ± 9.5 years, having a higher body mass index (p = 0.007) and a lower SBP TTR compared to men (p < 0.001). In the overall population and in women, each standard deviation (SD) increase in SBP TTR was associated with a reduced risk of MACCE (adjusted hazard ratio (HR) 0.89; 95% confidence interval (CI) 0.82–0.97; p = 0.007, and adjusted HR 0.85; 95% CI 0.74–0.99; p = 0.039, respectively) and acute decompensated heart failure (adjusted HR 0.86; 95% CI 0.73–0.99; p = 0.047, and adjusted HR 0.68; 95% CI 0.51–0.92; p = 0.011, respectively), while this was not observed in men. RCS indicated a similar trend in men only when SBP TTR exceeded 39%. Additional adjustments for mean SBP and SBP variability yielded similar outcomes.
The study demonstrates that in women, a higher SBP TTR is associated with a reduced risk of MACCE and acute decompensated heart failure, while in men, a similar trend is observed only when SBP TTR is higher, underscoring the necessity of considering sex differences in personalized blood pressure management strategies.
NCT01206062, https://www.clinicaltrials.gov/expert-search?term=NCT01206062.
Atrial fibrosis may act as a substrate for atrial fibrillation (AF) and atrial functional mitral regurgitation (MR); thus, recognition is required to select the optimal therapeutic intervention.
We examined clinical data from 1045 consecutive patients in three centers who underwent catheter ablation for persistent AF between 2020 and 2022. 75 patients met the moderate and severe MR criteria and completed a 1-year follow-up. Voltage mapping during the ablation procedure was reviewed to classify the extent of atrial fibrosis.
Significant atrial fibrosis was found in 34 patients (45.3%), and these patients had a higher prevalence of congestive heart failure (New York Heart Association (NYHA) II–III: 76.5% vs. 36.6%, p < 0.001) and an increased incidence of biatrial enlargement at baseline than the mild fibrosis group. At the 1-year post-ablation period, the entire cohort exhibited a decrease in left atrial size (41.6 ± 6.5 mm vs. 45.5 ± 5.3 mm, p < 0.001), and a significant reduction in MR was achieved in 70.7% of patients. The significant fibrosis group had a higher recurrence rate of atrial arrhythmias (55.9% vs. 22.0%, log-rank p = 0.002) and no significant change in atria size compared with baseline diameters (left atrium, 44.4 ± 6.4 mm vs. 47.2 ± 5.6 mm, p = 0.068; right atrium, 44.7 ± 11.2 mm vs. 46.7 ± 6.2 mm, p = 0.427).
This study revealed a considerable proportion of significant fibrosis in patients with atrial functional MR and AF, leading to limited effectiveness in reducing atrial size following catheter ablation. Optimal intervention to reduce atrial size and recurrent arrhythmias in this population requires further investigation.
The role of cognitive abilities in the development of arteriosclerotic disease is still not fully understood. The purpose of the present study was to evaluate the mediating role of lifestyle, socioeconomic status (SES) and conventional cardiovascular disease (CVD) risk factors in the association between cognitive ability at age 19 and subclinical atherosclerosis at age 60 years.
An observational study design was employed. Data on the results from cognitive tests of conscripts tested at age 19 were collected for 1009 men. At the age of 60, they were included in the trial VIsualiZation of asymptomatic Atherosclerotic disease for optimum cardiovascular prevention, which was conducted as part of the Västerbotten Intervention Program (VIPVIZA). VIPVIZA is a randomised controlled trial, aimed at primary prevention of CVD in Västerbotten County, Sweden. Prior to any intervention, they underwent carotid ultrasonography and CVD risk factor assessment. Lifestyle habits and marital status were self-reported, and education and urban or rural residency were registered. Crude associations between cognitive ability at age 19 and the risk of CVD, assessed with the European Systematic Coronary Risk Evaluation 2 (SCORE2), as well as subclinical atherosclerosis, as demonstrated by the presence of carotid plaques (no plaque, plaque unilateral, or plaque bilateral), were evaluated. A path-analytic model tested mediating factors from cognitive ability in young adulthood to subclinical atherosclerosis at age 60.
Results from cognitive tests at age 19 were in separate unadjusted analyses inversely and linearly associated with SCORE2 and with subclinical atherosclerosis. The association with carotid plaque at age 60 was mainly indirect and mediated by adult SES, which in turn had its main effect through adherence to healthy lifestyle habits via CVD risk of carotid plaques.
Cognitive ability at age 19 is a factor that is upstream of adult SES and our study indicates that cognitive ability at a young age has long-term consequences via SES and lifestyle habits for CVD risk and atherosclerosis.
NCT01849575, https://clinicaltrials.gov/study/NCT01849575?term=NCT01849575&rank=1.
The 4S-AF scheme, which comprises four domains related to atrial fibrillation (AF), stroke risk (St), symptom severity (Sy), severity of AF burden (Sb), and substrate (Su), represents a novel approach for structurally characterizing AF. This study aimed to assess the clinical utility of the scheme in predicting AF recurrence following radiofrequency catheter ablation (RFCA).
We prospectively enrolled 345 consecutive patients with AF who underwent initial RFCA between January 2019 and December 2019. The 4S-AF scheme score was calculated and used to characterize AF. The primary outcome assessed was AF recurrence after RFCA, defined as any documented atrial tachyarrhythmia episode lasting at least 30 seconds.
In total, 345 patients (age 61 (interquartile range (IQR): 53–68) years, 34.2% female, 70.7% paroxysmal AF) were analyzed. The median duration of AF history was 12 (IQR: 3–36) months, and the median number of comorbidities was 2 (IQR: 1–3), and 157 (45.5%) patients had left atrial enlargement. During a median follow-up period of 28 (IQR: 13–37) months, AF recurrence occurred in 34.4% of patients. After eliminating the Sy and St domains, both the 4S-AF scheme (hazard ratio (HR) 1.38, 95% confidence interval (CI): 1.19–1.59, p < 0.001) and severity of burden and substrate of atrial fibrillation (2S-AF) scheme scores (HR 1.59, 95% CI: 1.33–1.89, p < 0.001) were independent predictors of AF recurrence following RFCA. For each domain, we found that the independent predictors were Sb (HR 1.84, 95% CI: 1.25–2.72, p = 0.002) and Su (HR 1.71, 95% CI: 1.36–2.14, p < 0.001). Furthermore, the 4S-AF (area under the curve (AUC) 65.2%, 95% CI: 59.3–71.1) and 2S-AF scheme score (AUC 66.2%, 95% CI: 60.2–72.1) had a modest ability to predict AF recurrence after RFCA.
The novel 4S-AF scheme is feasible for evaluating and characterizing AF patients who undergo RFCA. A higher 4S-AF scheme score is independently associated with AF recurrence after RFCA. However, the ability of the 4S-AF scheme to discriminate between patients at high risk of recurrence was limited.
Frailty is a physical condition characterized by increased vulnerability to external stressors. This study investigated the impact of premorbid frailty, as measured by the Clinical Frailty Scale (CFS), on neurological prognosis in patients with out-of-hospital cardiac arrest (OHCA).
This is a single-center retrospective study. Data from 2006 to 2020 were analyzed for 595 adult OHCA patients admitted to the intensive care unit of National Taiwan University Hospital following resuscitation. Variables included demographics, medical history, resuscitation details, post-resuscitation data, and frailty assessments based on CFS. The primary outcome was favorable neurological performance, defined as a cerebral performance category (CPC) score of 2 or less at discharge.
In total, 523 of the 595 patients were included in the analysis. Among these, 224 survived, and 173 exhibited favorable neurological outcomes. Patients with favorable outcomes had significantly lower CFS scores than those with poor outcomes (3.2 ± 1.5 vs. 4.5 ± 1.8, p < 0.0001). The proportion of favorable neurological outcomes declined as CFS scores increased. Multivariate logistic regression analysis identified several factors independently associated with worse neurological outcomes: CFS >4 (odds ratio (OR): 0.301, 95% confidence interval (CI): 0.163–0.540), age >70 years (OR: 0.969, 95% CI: 0.953–0.986), history of malignancy (OR: 0.421, 95% CI: 0.209–0.813), epinephrine >2 mg during resuscitation (OR: 0.776, 95% CI: 0.712–0.840), and arterial blood gas pH <7.1 (OR: 28.396, 95% CI: 6.487–129.350). The model demonstrated good performance, with an area under the curve (AUC) value of 0.853. No significant relationships were observed between CFS and other variables.
CFS values ≤4 were independently associated with favorable neurological outcomes following OHCA.
Cardiovascular diseases continue to be the primary cause of mortality in industrialised countries, and atherosclerosis plays a role in their development. A persistent inflammatory condition affecting big and medium-sized arteries is known as atherosclerosis. It is brought on by dyslipidemia and is facilitated by the immune system’s innate and adaptive components. At every stage of the progression of atherosclerosis, inflammation plays a crucial role. It has been demonstrated that soluble factors, or cytokines, activate cells involved in the pathophysiology of atherosclerosis and have a significant impact on disease progression. Anti-inflammatory cytokines (such as interleukin (IL)-5 and IL-13) mitigate atherosclerosis, whereas pro-inflammatory cytokines (such as IL-1, IL-6) quicken the disease’s course. Of interest is the fact that a number of cytokines can exhibit both atherogenic and atheroprotective properties, which is the topic of study and discussion in this review. This review provides a comparative analysis of the functions of the main cytokines involved in the pathogenesis of atherosclerosis. Their functional relationships with each other are also shown. In addition, potential therapeutic strategies targeting these cytokines for the treatment of atherosclerosis are proposed, with an emphasis on recent clinical research in this area.
Cardiovascular-kidney-metabolic (CKM) syndrome is characterized by the interactions among the metabolic risk factors, chronic kidney diseases (CKD) and cardiovascular diseases (CVD). Social determinants of health (SDOH) include society, economy, environment, community and psychological factors, which correspond with cardiovascular and kidney events of the CKM population. SDOH are integral components throughout the entire spectrum of CKM, acting as key contributors from initial preventative measures to ongoing management, as well as in the formulation of health policies and the conduct of research, serving as vital instruments in the pursuit of health equity and the improvement of health standards. This article summarizes the important role of SDOH in CKM syndrome and explores the prospects of comprehensive management based on SDOH. It is hoped that these insights will offer valuable contributions to improving CKM-related issues and enhancing health standards.
Waist circumference (WC), an abdominal obesity index in the current metabolic syndrome (MetS) criteria, may not adequately reflect visceral fat accumulation. This brief review aims to examine the clinical significance of utilizing a body shape index (ABSI), a novel abdominal obesity index, to modify the MetS criteria, considering the predictive ability for vascular dysfunction indicated by the cardio-ankle vascular index (CAVI), as well as kidney function decline. First, the relationship of CAVI with kidney function is presented. Next, whether modification of the MetS diagnostic criteria by replacing the current high waist circumference (WC-MetS) with high ABSI (ABSI-MetS) improves the predictive ability for vascular and kidney dysfunction is discussed. Although limited to Asian populations, several cross-sectional and longitudinal studies support the relationship of CAVI with kidney function. Increased CAVI is associated with kidney function decline, and the CAVI cutoff for kidney outcomes is considered to be 8–9. In urban residents who underwent health screening, an increase in ABSI, but not body mass index (BMI) or WC, was associated with increased CAVI, suggesting that ABSI reflects vasoinjurious body composition. In several cross-sectional studies, ABSI-MetS was superior to WC-MetS in identifying individuals with increased CAVI. Furthermore, the predictive ability of ABSI-MetS in assessing kidney function decline was enhanced only in individuals with MetS, as determined in a longitudinal analysis. Using WC as a major criterion for MetS diagnosis may not adequately identify individuals at risk of vascular dysfunction and kidney function decline. This review shows that this problem may be solved by replacing WC with ABSI. Future research should explore whether ABSI-MetS also predicts cardiovascular events, and whether therapeutic intervention that reduces ABSI improves clinical outcomes.
Acute myocardial infarction is myocardial necrosis caused by acute and persistent ischemia and hypoxia in the coronary artery and severely affects public health. Recently, stem cell research has presented transformational developments in treating myocardial infarction. The Notch signaling pathway plays a crucial role in the post-myocardial infarction repair process and cardiac regenerative medicine. Additionally, the Notch signaling pathway can be involved in regulating the inflammatory response, myocardial fibrosis, oxidative stress, cardiomyocyte apoptosis, and cardiomyocyte regeneration after myocardial infarction. Moreover, the Notch signaling pathway is applied in cardiac tissue engineering. This review mainly elaborates on the research on the Notch signaling pathway in repairing myocardial infarction and cardiac regenerative medicine, aiming to provide a reference for treating acute myocardial infarction.
Congestive heart failure (CHF) represents an important health issue characterised by considerable morbidity and mortality. This study sought to identify risk factors for CHF and to evaluate clinical outcomes between CHF patients and control subjects.
Data were obtained through interviews, physical examinations, and medical records. Risk variables encompassed hypertension, diabetes, dyslipidaemia, tobacco use, alcohol use, sedentary lifestyle, dietary practices, age, gender, and familial history of cardiovascular disease. The outcomes were all-cause mortality, cardiovascular mortality, hospitalisation, major adverse cardiovascular events (MACE), quality of life as measured by the Minnesota Living with Heart Failure Questionnaire (MLHFQ), and functional level according to the New York Heart Association (NYHA) classification. Statistical analyses including t-tests, Chi-square tests, logistic regression and Cox regression.
The findings indicated that hypertension (71.8% vs. 38.5%, p < 0.001), diabetes (47.9% vs. 28.2%, p = 0.002), dyslipidaemia (54.7% vs. 41.0%, p = 0.04), smoking (42.7% vs. 29.1%, p = 0.03), and physical inactivity (65.8% vs. 41.9%, p < 0.001) were more prevalent in cases. Cases exhibited increased hospitalisations (1.8 ± 1.2 vs. 0.7 ± 0.9, p < 0.001), prolonged stays (10.5 ± 5.4 vs. 6.2 ± 3.8 days, p < 0.001), elevated 30-day rehospitalisation rates (21.4% vs. 8.5%, p = 0.007), and a greater incidence of intensive care units (ICU) admissions (17.1% vs. 6.0%, p = 0.01). All-cause mortality (35.9% vs. 17.1%, p = 0.001), cardiovascular mortality (25.6% vs. 10.3%, p = 0.003), and MACE (51.3% vs. 25.6%, p < 0.001) were greater in cases. Quality of life (45.8 ± 12.4 vs. 25.6 ± 10.3, p < 0.001) and functional status (55.6% vs. 23.9%, p < 0.001) were inferior in cases.
CHF patients had greater rates of modifiable risk variables and worse clinical outcomes than controls, underscoring the necessity for comprehensive risk management.
The prevalence of heart failure with preserved ejection fraction (HFpEF) is increasing annually, particularly among patients with metabolic disorders such as hypertension and diabetes. However, there is currently no treatment capable of altering the natural course of HFpEF. Recently, the interplay between oxidative stress and ferroptosis in cardiovascular diseases has drawn extensive attention; however, minimal research has been published on the mechanisms of oxidative stress and ferroptosis in HFpEF. This paper reviews the relevant mechanisms through which oxidative stress is induced and promotes ferroptosis during the development of HFpEF. The review also explores more efficacious treatment approaches for HFpEF by inhibiting oxidative stress and ferroptosis, thereby offering a theoretical foundation for verifying the feasibility of these methods for further research. As tumor-targeted therapy progresses, the survival period of tumor patients is prolonged, and cardiovascular events have gradually emerged as one of the most crucial causes of death among tumor patients. Hence, inhibiting the vascular endothelial growth factor (VEGF) pathway has become a major target in tumor treatment, significantly enhancing patient survival. Nevertheless, secondary cardiovascular complications and events, such as myocardial injury and subsequent heart failure, have severely impacted patient survival and quality of life. Therefore we have also explored the potential mechanism through which novel targeted anti-cancer drugs induce HFpEF via ferroptosis. Additionally, we reviewed the specific modes of action for preventing and treating HFpEF without influencing their anti-cancer therapeutic effect.
Cardiovascular diseases remain one of the leading causes of death worldwide. Given the limited self-repair capacity of cardiac tissue, cardiac tissue engineering (CTE) aims to develop strategies and materials for repairing or replacing damaged cardiac tissue by combining biology, medicine, and engineering. Indeed, CTE has made significant strides since the discovery of induced pluripotent stem cells (iPSCs) in 2006, including creating cardiac patches, organoids, and chip models derived from iPSCs, thus offering new strategies for treating cardiac diseases.
A systematic search for relevant literature published between 2003 and 2024 was conducted in the PubMed and Web of Science databases using “Cardiac Tissue Engineering”, “3D Bioprinting”, “Scaffold in Tissue Engineering”, “Induced Pluripotent Stem Cells”, and “iPSCs” as keywords.
This systematic search using the abovementioned keywords identified relevant articles for inclusion in this review. The resulting literature indicated that CTE can offer innovative solutions for treating cardiac diseases when integrated with three-dimensional (3D) bioprinting and iPSC technology.
Despite notable advances in the field of CTE, multiple challenges remain relating to 3D-bioprinted cardiac tissues. These include maintaining long-term cell viability, achieving precise cell distribution, tissue vascularization, material selection, and cost-effectiveness. Therefore, further research is needed to optimize printing techniques, develop more advanced bio-inks, explore larger-scale tissue constructs, and ensure the biosafety and functional fidelity of engineered cardiac tissues. Subsequently, future research efforts should focus on these areas to facilitate the clinical translation of CTE. Moreover, additional long-term animal models and preclinical studies should be conducted to ensure the biosafety and functionality of engineered cardiac tissues, thereby creating novel possibilities for treating patients with heart diseases.
Aortic diseases, such as aortic dissection and aortic rupture, often lead to catastrophic complications, significantly increasing morbidity and mortality. Population-based screening for early detection in asymptomatic individuals is not feasible due to high costs and practical challenges. However, recent advancements in four dimensions (4D) Flow magnetic resonance imaging (MRI) offer a comprehensive tool for evaluating hemodynamic changes within the aortic lumen. This technology allows for the quantification and visualization of flow patterns and the calculation of advanced hemodynamic parameters, such as wall shear stress (WSS). WSS is crucial in the development, risk stratification, and surgical outcomes of aortic diseases and their complications, enabling noninvasive and quantitative screening of high-risk populations. This review explores the current status and limitations of 4D flow MRI-derived WSS imaging for aortic disease.
Clinical trials of direct oral anticoagulants (DOACs) often exclude patients with advanced chronic kidney disease (CKD), creating uncertainty regarding their safety and efficacy compared with warfarin. This study addresses this gap by providing key insights into anticoagulation in this high-risk population. This study evaluated the effectiveness and safety of DOACs compared to warfarin and no anticoagulation therapy in atrial fibrillation (AF) patients with CKD stage G5 or on dialysis. This scoping review followed a six-stage framework and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. An exhaustive search of four databases identified relevant papers published through August 2024. The data extraction process was conducted independently, with subsequent qualitative and quantitative analyses conducted. Among the 33 studies included in the final analysis, DOACs, particularly apixaban, were associated with a 20–30% decreased major bleeding risk compared to warfarin. Stroke incidence was comparable between DOACs and vitamin K antagonists (VKAs), with apixaban showing improved prevention in severe CKD. Observational studies reported slightly lower mortality rates with DOACs, particularly apixaban, including fewer cardiovascular-related deaths than with VKAs. DOACs, particularly apixaban and rivaroxaban, demonstrate a favorable safety profile compared to warfarin, but show inconsistent evidence in balancing thromboembolic prevention and bleeding risks in patients with AF and CKD stage G5 or on dialysis. Future studies should focus on optimizing dosing strategies and evaluating long-term safety and efficacy.
Over the last two decades, the management of aortic stenosis has undergone significant transformation due to developments in surgical techniques and the introduction of transcatheter aortic valve implantation (TAVI). These transformations have enabled improved patient selection and treatments to be tailored based on individual clinical and anatomical characteristics. Both surgical and transcatheter options have resulted in reduced mortality and enhanced quality of life for patients with aortic stenosis. Nonetheless, treating patients with small aortic annulus remains challenging despite advances in current technology. The insertion of a small prosthetic valve, leading to patient prosthetic mismatch, has been associated with heart failure hospitalization, early structural valve degeneration, and long-term mortality. Although aortic root enlargement was historically employed to address this issue, stentless and sutureless valves in the supra-annular position and, more recently, TAVI have emerged as alternative treatments for patients with small annulus and severe aortic stenosis. This review will provide an overview of the prevalence and anatomical characteristics of patients with aortic stenosis and small annulus. Additionally, we will discuss current treatment options, including surgery and TAVI, used to mitigate procedural and long-term adverse outcomes in this group.
Due to the continued aging of the global population, cardiovascular diseases (CVDs) remain the main cause of death worldwide, with millions of fatalities from diseases, including stroke and coronary artery disease, reported annually. Thus, novel therapeutic approaches and targets are urgently required for diagnosing and treating CVDs. Recent studies emphasize the vital part of gut microbiota in both CVD prevention and management. Among these, Faecalibacterium prausnitzii (F. prausnitzii) has emerged as a promising probiotic capable of improving intestinal health. Although preliminary investigations demonstrate that F. prausnitzii positively enhances cardiovascular health, research specifically connecting this strain to CVD outcomes remains limited. Based on current research and assessment of possible clinical applications, this paper aimed to investigate the positive effects on cardiovascular health using F. prausnitzii and its metabolites. Targeting gut flora is expected to become a mainstay in CVD treatment as research develops.
Mitochondrial dysfunction in myocardium cells has been implicated in arrhythmogenesis, including ventricular tachycardia (VT). A carriage of point mitochondrial DNA (mtDNA) polymorphisms may contribute to the risk of certain arrhythmias. Therefore, it is hypothesized that mtDNA genotype could predict the risk of sustained VT (SVT). We aimed to explore whether specific mtDNA polymorphisms of peripheral blood mononuclear cells (PBMC) can serve as biomarkers for predicting the risk of SVT in patients with indications for an implantable cardioverter-defibrillator (ICD).
A total of 122 patients with ICD implantation indications who underwent transthoracic echocardiography (TTE) were enrolled in the study. Total DNA from PBMC was isolated using the phenol-chloroform extraction method. Genotyping of mtDNA polymorphisms A2706G, G3010A and G9055A was performed using restriction fragment length polymorphism analysis. Correlations between clinical parameters and mtDNA polymorphisms with SVT registered prior to ICD implantation were evaluated. Based on our data, we developed a risk model for SVT.
Prior to ICD implantation, 70 (56.6%) patients had SVT (1st group) and 52 (43.4%) patients did not have SVT (2nd group). Patients with SVT were significantly older than patients without SVT (66.9 ± 9.9 year vs. 59.5 ± 10.6 year, p < 0.001), had a lower value estimated glomerular filtration rate (eGFR) (65.7 ± 19.7 mL/min/1.73 m2 vs. 77.9 ± 16.1 mL/min/1.73 m2, p < 0.001) and less frequently had A2706G mtDNA polymorphism (55.7% vs. 76.9%, p = 0.015). According to the multivariable logistic regression, age (odds ratio (OR) = 1.055, 95% confidence interval (CI) 1.009–1.103, p = 0.017), eGFR (OR = 0.974, 95% CI 0.949–0.999, p = 0.041) and absence of A2706G mtDNA polymorphism (OR = 0.335, 95% CI 0.141–0.797, p = 0.013) were independently associated with the SVT. We constructed a logistic equation with calculation of the cut-off value. The discriminative ability of the receiver operating characteristic curve (area under the curve) was 0.761 (95% confidence interval 0.675–0.833; sensitivity 65.71%; specificity 76.92%).
In patients with ICD implantation indications, a carriage of mtDNA polymorphism A2706G is associated with SVT. Our risk model including age, eGFR and absence of A2706G mtDNA substitution was able to distinguish patients with SVT. Further investigations of their predictive significance are warranted.
NCT03667989 (https://clinicaltrials.gov/study/NCT03667989).
Previous studies have presented conflicting results on the correlation between metabolic syndrome (MetS) and subclinical atherosclerosis. However, the binary MetS definition cannot reflect the severity of metabolic disorders continuously and dynamically. The present study calculated the MetS score and explored the association between MetS score and subclinical atherosclerosis.
A total of 840 participants were included in this observational, cross-sectional study; 66.55% of participants were men, and the median age was 61.00 years (53.00, 67.00). Brachial–ankle pulse wave velocity (baPWV) and brachial flow-mediated dilation (bFMD) values were measured from October 2016 to January 2020. Spearman’s correlation and multiple linear regression analyses were conducted to explore the correlation between the MetS score and baPWV and bFMD. Arterial stiffness was defined as baPWV ≥1400 cm/s, while endothelial dysfunction was described as bFMD >6%. Multiple logistic regression was performed to explore the effects of MetS and MetS score on arterial stiffness and endothelial dysfunction.
The MetS score was significantly associated with baPWV (β = 73.59, 95% CI (42.70, 104.48); p < 0.001) and bFMD (β = –0.43, 95% CI (–0.75, –0.10); p = 0.010) after adjusting for covariates. Compared with the binary definition of MetS, the MetS score was a more significant predictor for arterial stiffness (odds ratio, OR = 2.63, 95% CI (1.85, 3.74); p < 0.001) and endothelial dysfunction (OR = 1.33, 95% CI (1.01, 1.76); p = 0.040). Leukocyte count (r = 0.32; p < 0.001) and high-sensitivity C-reactive protein (hs-CRP) (r = 0.17; p < 0.001) values were related to the MetS score.
The MetS score is a clinically accessible assessment of metabolic status that can identify individuals at higher risk of subclinical atherosclerosis.
Although numerous studies have investigated the prevalence of chronic heart failure (CHF) and the factors influencing frailty in patients with CHF, the findings remain inconsistent. Therefore, this review aimed to systematically evaluate the prevalence and associated frailty factors in patients with CHF to establish an evidence-based foundation for risk assessment and treatment strategies.
A comprehensive search was conducted across multiple databases, including EMBASE, the Cochrane Library, PubMed, Web of Science, CINAHL, Chinese Biological Medicine (CBM), CNKI, and Wan Fang up to August 25, 2024. The objective was to identify observational studies that examined factors influencing frailty in CHF patients. The quality of the selected studies was evaluated using appropriate assessment tools, and a meta-analysis was performed to determine the relevant factors associated with frailty in this population.
A total of 23 articles containing 6287 patients were included. The prevalence of frailty in patients with CHF was 39% (95% confidence interval (CI): 0.33–0.45). Factors shown to be positively associated with frailty in CHF patients were older age, cerebrovascular accidents, longer hospital stay, larger left atrial diameter, higher number of comorbidities, poor New York Heart Association (NYHA) functional class, and poor sleep quality. Conversely, higher albumin, hemoglobin, and left ventricular ejection fraction (LVEF) levels were negatively associated with frailty.
The prevalence of frailty in patients with CHF is relatively high and varies according to different assessment tools applied. Thus, establishing specific frailty assessment tools for CHF patients and providing targeted interventions based on important factors are essential for reducing the burden of frailty and improving outcomes.
CRD42023448771, https://www.crd.york.ac.uk/PROSPERO/view/CRD42023448771.
Pulmonary hypertension (PH) is a rare, life-threatening condition that can be associated with connective tissue disease (CTD). The incidence and prevalence of PH in CTD varies by disease, whereby certain disease manifestations are particularly associated with PH; nonetheless, once present, PH is almost uniformly a major driver of adverse outcomes. In this paper, the authors review the published literature on major CTDs, including systemic sclerosis and systemic lupus erythematosus, and summarize the risk factors for developing PH in each disease and risk factors for adverse outcomes and mortality among patients with CTD-PH. This review highlights the need for early diagnosis of PH in CTD and the impact of PH overlap syndromes on patient outcomes, providing the practicing clinician with a practical summary of CTD-PH.
This study aimed to systematically review and synthesize evidence comparing direct oral anticoagulants (DOACs) with vitamin K antagonists (VKAs) for anticoagulation in patients with atrial fibrillation (AF) and cardiac amyloidosis (CA).
A comprehensive search of PubMed and EMBASE databases was conducted through January 2024 to identify studies comparing DOACs and VKAs in AF patients with CA. Eligible studies underwent rigorous screening and data extraction to evaluate safety and efficacy outcomes.
Four studies met the criteria. The first study reported similar embolic event rates between DOACs (3.9%) and VKAs (2.9%) per 100 patient years, while major bleeding rates were 5.21% and 3.74%, respectively. The second paper found stroke rates of 2% for DOACs and 4% for VKAs, with bleeding complications observed in 10% of DOAC patients compared to 20% in VKA patients. The third cohort demonstrated that DOACs were associated with significantly lower risks of stroke and major bleeding compared to VKAs. The last study reported embolic event rates of 1.6 and 2.0 per 100 patient years for DOACs and VKAs, respectively. In the pooled analysis, DOACs were associated with a reduced risk of thromboembolic events (odds ratio [OR] = 0.52; 95% confidence interval [CI]: 0.32–0.84), and no difference in major bleeding between the two groups (OR = 0.61, 95% CI: 0.25–1.51).
Existing studies support the use of DOACs as a non-inferior therapeutic option compared to VKAs for preventing thromboembolism in patients with AF and cardiac amyloidosis. DOACs may also offer practical advantages, including reduced bleeding risks and ease of management, but further high-quality randomized controlled trials are needed to confirm these findings and guide clinical practice.
Duchenne muscular dystrophy (DMD) is a genetic progressive neuromuscular disorder characterized by early-onset proximal muscle weakness and significant long-term pulmonary and cardiac involvement. Due to the early pharmacological treatments and the wider adoption of non-invasive ventilation, life expectancy has significantly increased in recent years, highlighting the relevance of DMD-related cardiomyopathy and fatal arrhythmias, especially in the late stage of the disease. Current guideline-derived evaluation of sudden cardiac death (SCD) in DMD lacks accuracy, leading to inadequate arrhythmic risk stratification and jeopardized SCD prevention strategies. This review aims to outline these critical issues, proposing an integrative approach encompassing manifold tools such as an imaging-derived systematic and comprehensive evaluation (speckle-tracking echocardiography and magnetic resonance imaging), the electrophysiological study, the 3-dimensional electroanatomic mapping, and a multidimensional clinical examination. This approach might lead to more personalized management along with an effective arrhythmia-prevention strategy aiming to balance clinical care goals, patient expectations, and ethical considerations.
Stroke is a common cerebrovascular disease characterized by a high incidence rate, significant disability, frequent recurrence, and elevated mortality. Exercise plays a crucial role in stroke rehabilitation, yet the relationship between traditional Chinese exercise and stroke recovery remains unclear. This study aims to evaluate the effectiveness of various conventional Chinese exercises through a systematic network meta-analysis and identify the most effective interventions for improving the rehabilitation outcomes of stroke patients.
A systematic search was conducted in PubMed, Cochrane Library, Embase, Web of Science, China National Knowledge Infrastructure, Wanfang Data, and the China Science and Technology Journal Database (up to July 2024) to identify randomized controlled trials (RCTs) evaluating traditional Chinese exercises for stroke patients. Trials were included if they utilized at least one form of traditional Chinese exercise. The methodological quality of the included studies was assessed using the Cochrane Risk of Bias tool (ROB 2.0). Data analysis was performed using Stata 17.0 and the Mvmeta package, employing a random-effects model.
A total of 43 studies involving 2083 stroke patients were included. These studies assessed outcomes including upper limb motor function, lower limb motor function, overall motor ability, walking ability, balance ability, self-care ability, cognitive function, depression, quality of life, and sleep quality. Baduanjin, originating in the Song Dynasty and consisting of eight movements based on traditional Chinese medicine theories,was the most effective in improving upper limb motor function, overall motor ability, walking ability, self-care ability, cognitive function, quality of life, and sleep quality. Taiji, a practice integrating Chinese philosophy, martial arts, and wellness concepts, was the most effective in enhancing lower limb motor function. Wuqinxi, inspired by the dynamic movements of animals such as the tiger, deer, bear, apes, and birds, showed the best results for balance improvement. Liuzijue, a traditional exercise combining specific sound production, breathing, and movement, was most effective in alleviating depressive symptoms.
These findings suggest that Baduanjin may be the most effective intervention for stroke rehabilitation. However, further high-quality RCTs are required to confirm these results.
CRD42024566780, https://www.crd.york.ac.uk/PROSPERO/view/CRD42024566780.
The global prevalence of atrial fibrillation (AF) is growing with a significant increase in AF burden. The pathophysiology of AF is complex and exhibits a strong relationship with modifiable lifestyle AF risk factors, such as physical inactivity, smoking, obesity, and alcohol consumption, as well as co-morbidities, such as hypertension, diabetes mellitus, and cardiovascular disease. Current evidence suggests that cardiac rehabilitation and lifestyle risk factor modification can potentially lower the overall AF burden. Additionally, AF ablation can be an effective treatment for a rhythm control strategy, but reducing AF recurrences post-catheter ablation is paramount. Thus, addressing these modifiable lifestyle risk factors and co-morbidities is critical, as the recent 2024 European Society of Cardiology AF guidance update highlights. A comprehensive approach to treating these risk factors is essential, especially given the rising prevalence of AF. This article provides a state-of-the-art update on the evidence of addressing AF-related risk factors and co-morbidities, particularly in patients undergoing AF ablation.
Interactions between the heart and other organs have been a focus in acute decompensated heart failure (ADHF). However, the association between ADHF and pancreatic exocrine insufficiency (PEI), which may lead to malnutrition, remains unclear. We investigated the relationship between exocrine pancreatic enzymes and ADHF.
We enrolled 155 and 46 patients with and without ADHF, respectively. Serum amylase and lipase levels were compared between the two groups. In the ADHF group, factors correlating with serum amylase or lipase levels were assessed using multiple regression analysis, and changes in their levels throughout the hospital course were determined.
Patients with ADHF exhibited significantly lower amylase and lipase levels. In the same group, the significant independent correlates of lower amylase levels included a lower blood urea–nitrogen level (partial correlation coefficient, 0.530; p < 0.001), lower albumin level (partial correlation coefficient, 0.252; p = 0.015), and higher uric acid level (partial correlation coefficient, –0.371; p < 0.001). The significant independent correlates of lower lipase levels included coexisting atrial fibrillation (coefficient, 0.287; p = 0.026), lower creatinine level (coefficient, 0.236; p = 0.042), and higher B-type natriuretic peptide level (coefficient, –0.257; p = 0.013). Both amylase and lipase levels significantly increased following the improvement in ADHF.
In patients with ADHF, decreased serum amylase and lipase levels were associated with the congestion severity, suggesting that PEI may occur in patients with ADHF, potentially due to ADHF-related congestion.
This review examines the mechanisms of left ventricular dysfunction, focusing on the interplay between ventricular remodeling, autophagy, and mitochondrial dysfunction following myocardial infarction. Left ventricular dysfunction directly affects the heart’s pumping efficiency and can lead to severe clinical outcomes, including heart failure. After myocardial infarction, the left ventricle may suffer from weakened contractility, diastolic dysfunction, and cardiac remodeling, progressing to heart failure. Thus, this article discusses the pathophysiological processes involved in ventricular remodeling, including the injury and repair of infarcted and non-infarcted myocardia, adaptive changes, and specific changes in left ventricular systolic and diastolic functions. Furthermore, the role of autophagy in maintaining cellular energy homeostasis, clearing dysfunctional mitochondria, and the key role of mitochondrial dysfunction in heart failure is addressed. Finally, this article discusses therapeutic strategies targeting mitochondrial dysfunction and enhancing mitophagy, providing clinicians and researchers with the latest insights and future research directions.
The Coronary Artery Tree Description and Lesion Evaluation (CatLet©) angiographic scoring system is a newly developed tool to predict the long-term clinical outcomes for patients with acute myocardial infarction (AMI). This study aimed to evaluate the predictive value of this novel angiographic scoring system for cardiac mortality in AMI patients within 30 days of primary percutaneous coronary intervention (pPCI) in AMI patients.
Patients with AMI undergoing pPCI were consecutively enrolled between January 2012 and July 2013. The CatLet© score was calculated for all the lesions in the non-occlusive status and were tertile partitioned into three groups: CatLet-low ≤14 (N = 124), CatLet-mid 14–22 (N = 82), and CatLet-top ≥22 (N = 102). The primary endpoint was cardiac mortality at 30 days after the procedure. Survival curves were generated using the Kaplan-Meier method, and survival rates among the CatLet© score tertiles were compared using the Log-rank test. Furthermore, Cox regression analysis was performed to identify the associations between the predictors and clinical outcomes.
A total of 308 patients were included in the final analysis. The included patients were followed up for 30 days, with 19 (6.17%) cardiac death. Kaplan-Meier curves indicated that the CatLet-top tertile exhibited a significant increase in the risk of cardiac mortality when compared with the low and mid tertiles (p for trend <0.01); the CatLet© score remained an independent predictor of 30-day cardiac mortality in AMI patients after adjusting for clinical variables (HR (95% CI): 6.13 (1.29–29.17); p < 0.01). The multivariable analysis demonstrated that a per 1 unit increase in CatLet© score was associated with a 1.04 (1.01–1.06)-fold increased risk of cardiac death. The area under the receiver operating characteristic (ROC) curve (AUC) statistic for the CatLet© score was 0.80 (95% CI, 0.69–0.91), with a good calibration (χ2 = 12.92; p = 0.12).
The CatLet© score can be used to predict the short-term cardiac death in AMI patients. A CatLet© score ≥22 or ≥11 myocardial segments involved relative to the total 17 segments (the score divided by 2), including culprit or non-culprit vessels, accounting for 65% (11/17) of left ventricle mass involved, is significantly associated with poor prognosis. The current study has extended the application of the CatLet© score in clinical practice.
ChiCTR-POC-17013536. Registered 25 November, 2017, https://www.chictr.org.cn/showproj.html?proj=22814.