Current Cardiology Reviews - Volume 21, Issue 3, 2025

Dyspnea and exertional intolerance are the most common clinical manifestations of Heart Failure (HF). One of the possible mechanisms of both symptoms in HF patients is weakness of the inspiratory muscles.

Because the diaphragm is the main inspiratory muscle, this review aimed to investigate the contribution of diaphragmatic function to the genesis of dyspnea or exercise intolerance in HF patients.

Original articles, clinical trials, and cohort or case-control studies published between January 2003 and March 2023 were included. The population, variables, and outcome strategy were the basis of this review, including studies that assessed HF patients, diaphragmatic function, and dyspnea or exercise tolerance. The PubMed/MEDLINE, Embase, and BVS/LILACS databases were searched.

A total of 353 articles were identified from electronic databases. After removing duplicate articles and screening based on titles, abstracts, and full texts, nine articles were included in the qualitative synthesis of this review. These studies were quite heterogeneous in their methodologies; however, most, except two, demonstrated an association among diaphragmatic dysfunction, dyspnea, and exertional intolerance in HF patients.

Although few studies have assessed the contribution of diaphragmatic function to dyspnea and exertional intolerance in HF individuals, the vast majority of articles included in this review found such an association, especially when diaphragmatic function was assessed using ultrasound.

Chronic ischemic heart failure is a major global health issue despite advancements in therapy. Stem cell (SC) therapy has emerged as a potential treatment, but its effectiveness remains uncertain. This study aimed to systematically review and meta-analyze the current evidence on SC therapy's efficacy.

We conducted a comprehensive literature search in PubMed, Embase, and Cochrane databases up to April 2024. We included randomized controlled trials (RCTs) with blinded designs, focusing on patients with heart failure with reduced ejection fraction (HFrEF) treated with mesenchymal stem cells compared to placebo or sham interventions via percutaneous endomyocardial catheter systems. Data extraction, performed independently by two authors, focused on safety and efficacy variables. The meta-analysis used a random-effects model, with sensitivity analyses to address study heterogeneity.

Twenty studies were included in the meta-analysis. Significant improvements were observed in the stem cell group for left ventricular end-systolic volume (LVESV) (pooled effect size -7.59, 95% CI [-12.28 to -2.89], P=0.002) and stress SPECT outcomes (pooled effect size -5.33, 95% CI [-6.73 to -3.93], P<0.00001). Sensitivity analysis reduced heterogeneity in left ventricular end-diastolic function (LVEDF) (P=0.01, I²=54%) and revealed a significant benefit for stem cell therapy (pooled effect size -3.87, 95% CI [-6.77 to -0.97], P=0.009). No significant effects were observed for left ventricular ejection fraction (LVEF) or myocardial oxygen consumption (MVO2). Functional improvements in New York Heart Association (NYHA) classification were noted (OR=4.22, 95% CI (1.14-15.68), P=0.03), though no significant differences were found in safety outcomes, including major cardiovascular events, mortality, or rehospitalization rates.

Transendocardial SC therapy shows promise in improving certain cardiac parameters, though its impact on LVEF and MVO2 remains inconclusive, indicating the need for further research.

Atherosclerosis is a chronic disease caused by the accumulation of lipids, inflammatory cells, and fibrous elements in arterial walls, leading to plaque formation and cardiovascular conditions like coronary artery disease, stroke, and peripheral arterial disease. Factors like hyperlipidemia, hypertension, smoking, and diabetes contribute to its development. Diagnosis relies on imaging and biomarkers, while management includes lifestyle modifications, pharmacotherapy, and surgical interventions. Computational biology is transforming biological knowledge into clinical practice by identifying biomarkers that can predict clinical outcomes. This involves omics data, predictive modeling, and data integration. Statistical analysis-based methods are also being developed to develop and integrate methods for screening, diagnosing, and prognosing atherosclerosis.

The present work aimed to uncover critical genes and pathways to enhance the understanding of the mechanism of atherosclerosis. GSE23746 was analyzed to find differentially expressed genes (DEGs) using 19 control samples and 76 atherosclerotic samples.

A total of 76 DEGs were identified. Analysed DEGs using Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) to generate enrichment datasets. A Protein-protein Interaction (PPI) network of DEGs was created utilizing the Search Tool for the Retrieval of Interacting Genes (STRING).

Ten hub genes, namely EGR1, PTGS2, TNF, NFKBIA, CXCL8, TNFAIP3, CCL3, IL1B, PTPRC, and CD83, were found to be significantly linked to atherosclerosis. Furthermore, the metabolic pathway analysis through KEGG and STRING provides potential targets for therapeutic interventions through HUB genes to diagnose the illness at an early stage, which aids in the reduction of cardiovascular risk. From risk factor profiling to the discovery of novel biomarkers, several components such as phospholipids, ANGPTL3, LCAT, and the protein-encoded OCT-1 gene, play a vital role in crucial processes. These compounds are potential therapeutic targets for early diagnosis of atherosclerotic lesions and future novel biomarkers.

Long-term heart failure hospitalization (HFH) after radiofrequency catheter ablation (RFCA) in atrial fibrillation (AF) patients with heart failure and preserved ejection fraction (HFpEF) and its risk factors remain to be investigated.

AF patients with HFpEF who underwent RFCA from January, 2014 to December, 2018 from three centers were retrospectively included. Patients were assigned to the training and testing cohorts, respectively. In the training cohort, logistic regression analyses were performed to discriminate those with and without HFH. A scoring system was developed accordingly and validated.

A total of 417 AF patients with HFpEF receiving RFCA were enrolled. About 35 patients (8.4%) had HFH for 6 years. In the training cohort, the use of diuretics, atrial tachycardia (AT)/AF recurrence, prior HFH, and female sex were independent predictors of HFH in the multivariable analysis. A DAPF score (ranging from 0 to 9.0) was developed. The area under the receiver operating characteristic curve (AUC) of the DAPF score was 0.880 (95% CI, 0.830-0.929). A DAPF score ≥3.5 could predict HFH with a sensitivity of 81.8% and a specificity of 74.6%. The performance in the testing cohort remained robust (AUC, 0.858; 95% CI, 0.749-0.967).

HFH in patients with AF and HFpEF after RFCA is not rare. The DAPF score could predict the risk of HFH in AF patients with HFpEF after RFCA and guide our treatment strategy.

Peripheral arterial disease (PAD) is a marker of significant atherosclerotic cardiovascular disease and is associated with greater healthcare burden and worse prognosis in individuals with chronic inflammatory disease (CID). We aimed to investigate temporal trends and disparities of PAD-related mortality in populations with CID from 1999-2020 across six common CIDs (i.e., chronic viral hepatitis, human immunodeficiency virus, inflammatory bowel disease, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus).

United States (US) PAD and CID-related mortality and demographic data from 1999-2020 were extracted from the CDC database through the multiple-cause-of-death files. Age-adjusted mortality rates (AAMR) per 1,000,000 and 95% confidence intervals were standardized to the 2000 US population. The mortality trends were analyzed using Joinpoint Regression.

A total of 22,175 PAD-related deaths were recorded in the population with CID between 1999 and 2020. Mortality remained stable during the 22-year period (AAPC -0.04%, p=0.95) with a cumulative AAMR of 4.64. Mortality was highest in rural counties (AAMR 5.27), and among non-Hispanic Black populations (AAMR 7.06). Among the CID subtypes, PAD mortality was highest in populations with RA (AAMR 2.48) and lowest in populations with psoriasis (AAMR 0.11).

Our findings highlight the disparities of PAD mortality in patients with CID, with the Black population and rural communities disproportionately affected. Further investigation with individual-level data is warranted to identify the contributing factors for the observed disparities.

Managing hypertriglyceridemia-induced acute pancreatitis (HTG-AP) can be challenging, particularly due to the need for rapid triglyceride reduction to below 500mg/dL (5.645 mmol/L).

This is a case describing a 39-year-old female patient who presented to the Emergency Department with acute abdominal pain resulting from severe HTG-AP. However, under conventional therapy with oral lipid-lowering drugs, the triglyceride levels remained uncontrolled. Oral moderate-intensity statins could not only reduce low-density lipoprotein cholesterol (LDLc) by 25%-50%. However, increasing the dose could not further reduce blood lipids while increasing the risk of liver damage. After the administration of proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i), the triglyceride levels were well controlled with no additional side effects, and the symptoms of the patients were completely relieved.

In cases of unsatisfactory lipid control under conventional therapy, PCSK9i may offer a viable option for managing HTG-AP.