Cardiology Research and Practice最新文献

Introduction: Nondilated left ventricular cardiomyopathy (NDLVC) is a newly defined category of cardiomyopathy. We sought to evaluate and compare the phenotype of NDLVC with DCM using cardiac magnetic resonance (CMR) imaging and to investigate the prognostic significance of these conditions. Methods: One hundred and fifty patients suspected of having cardiomyopathy referred for CMR were recruited. We considered 3 groups; Group 1: NDLVC-reduced EF, (NDLVC-REF), LVEF ≤ 40%, Group 2: NDLVC-mildly reduced EF(NDLVC-MREF), 40 < LVEF < 50, Group 3: Dilated cardiomyopathy (DCM). All selected patients were followed up for a median of 24 months to determine the composite cardiac endpoint consisting of mortality and/or hospitalization for cardiovascular reasons (composite cardiac event (CCE)) as the primary endpoint. Results: The mean age (SD) was 42.6 (13.7) years (range: 18-77 years). There was no association between the presence of myocardial LGE and the development of atrial and/or ventricular arrhythmias. Atrial fibrillation was most common in the NDLVC groups during the follow-up period. Myocardial late gadolinium enhancement (LGE) was also more pronounced in the DCM group. Most patients in the NDLVC groups had no LGE. LGE in the midwall was the most common LGE pattern in all three groups and the septal wall was the most commonly affected area of the LV. There was no significant difference between the CMR findings of patients with and without CCE in each subgroup. However, the presence of myocardial replacement fibrosis was higher in patients with a CCE in total study population, (n = 144, 68% versus 32%, p=0.03), but the difference was not significant in subgroup analyzes. Conclusion: NDLVC has a relatively good prognosis in recent times. The consideration of NDLVC in a spectrum with DCM can be reasonable. However, the prognostic risk factors need to be investigated in more detail.

Aim: This study aimed to investigate the impact of the NOD1/Rip2 signaling pathway on macrophage inflammatory activation and polarity switching in ox-LDL-induced THP-1-derived macrophages. Methods: THP-1-derived macrophages were stimulated with various concentrations (10, 25, or 50 mg/L) of ox-LDL for different durations (8, 16, or 24 h). Quantitative real-time PCR was used to measure the mRNA expression of NOD1, Rip2, IL-10, IL-12, iNOS, and Arg-1. Western blotting was used to determine the protein levels of NOD1 and Rip2. The secretion of TNF-α and MCP-1 in the cell culture supernatants was measured via ELISA. Rip2 siRNA was used to inhibit the NOD1/Rip2 signaling pathway. Oil Red O staining was employed to visualize foam cell formation. CD86, CD80, and CD163 membrane molecules were analyzed via FACS. Results: After exposure to ox-LDL, the expression levels of NOD1 and Rip2 mRNAs and proteins in THP-1-derived macrophages increased in a dose- and time-dependent manner. This upregulation was accompanied by increased concentrations of TNF-α and MCP-1 in the cell culture supernatants. The effects of NOD1 and Rip2 expression upregulation were mitigated by Rip2 siRNA, as evidenced by decreased concentrations of TNF-α and MCP-1. Furthermore, ox-LDL downregulated the expression of M2 macrophage markers CD163, IL-12, and Arg-1 and upregulated the expression of M1 macrophage markers CD86, CD80, IL-10, and iNOS. The inhibition of Rip2 by siRNA reversed these effects and prevented the formation of foam cells. Conclusion: Our data show that the NOD1/RIP2 signaling pathway regulates the inflammatory activation of macrophages induced by ox-LDL and controls the macrophage polarity switch.

Purpose: This study aimed to investigate the impacts of tanshinone IIA (Tan IIA) on ischemia/reperfusion (I/R)-induced cardiomyocyte injury in coronary heart disease (CHD), and to determine whether Tan IIA regulates myocardial cell injury induced by I/R through the Hyaluronan Synthase 2/fibroblast growth factor 9 (HAS2/FGF9) axis.

Methods: Weighted gene co-expression network analysis (WGCNA) of the GSE23561 microarray dataset determined gene modules linked to CHD. The key genes were further explored through differential expression and protein-protein interaction (PPI) network analyses. Human AC16 cardiomyocytes were treated with Tan IIA, HAS2 knockdown, and FGF9 overexpression and they were exposed to normoxic, hypoxic, and I/R environments. Cell viability, apoptosis, gene/protein expression, and markers of oxidative stress were evaluated in vitro.

Results: The turquoise module was significantly correlated with CHD and HAS2 was identified as a hub gene. Under hypoxic conditions, Tan IIA exhibited a dose-dependent cardioprotective effect. Tan IIA ameliorated I/R-induced cellular injury, as evidenced by increased cell viability, decreased apoptosis, and regulation of key proteins (PCNA, Bax). After I/R conditions, knockdown of HAS2 increased cell viability and reduced apoptosis, whereas overexpression of FGF9 reversed these effects. Notably, HAS2 knockdown also ameliorated I/R-induced increases in inflammatory cytokines and oxidative stress, and synergistic protection was provided by combined treatment with FGF9 and Tan IIA.

Conclusion: Taken together, our findings confirm that Tan IIA protects cardiomyocytes from I/R-induced injury by controlling the HAS2/FGF9 axis. These findings reveal the potential therapeutic significance of Tan IIA in alleviating CHD-related myocardial dysfunction.

Background: Utilizing the two available prediction models, i.e., the dual antiplatelet therapy (DAPT) score and predicting bleeding complication in patients undergoing stent implantation and subsequent dual antiplatelet therapy (PRECISE-DAPT) score, we aimed to determine the appropriateness of the DAPT in patients with acute myocardial infarction (AMI) in patients undergoing percutaneous coronary intervention (PCI). Methods: We retrospectively enrolled 235 patients of AMI and for all the patients and thorough information regarding history, risk factors, and medications were collected. Both DAPT and PRECISE-DAPT scores were calculated. The patients were divided by their recommended cutoffs and the appropriateness of the duration of the recommended DAPT was measured based on the observed scores. Bleeding academic research consortium (BARC) classification was used to define the bleeding events. In the patients with DAPT score ≥ 2 and PRESICE-DAPT < 25, the prolonged use of DAPT was recommended. Results: Overall, 235 patients, predominantly male (78.7%), with baseline characteristics exhibiting high rate of smoking (31.1%), diabetes (35.3%), and hypertension (32.8%) were found. The widely prescribed DAPT combination was aspirin with clopidogrel (72.3% at discharge and 46% on current use). Among all the enrolled patients, 163 patients were on DAPT while 71 were on single antiplatelet therapy (SAPT). A significant association between DAPT and PRECISE-DAPT scores was noted in terms of SAPT and DAPT. The appropriateness of DAPT was checked based on the scores, where 81% of the patients with DAPT ≥ 2 and 77.24% with PRECISE-DAPT score < 25 were appropriately prescribed with DAPT. The primary reason for drug interruptions was self-advised. The incidence of bleeding events was observed to be 7.23%, among which 5.1% had Type 1 bleeding according to BARC. Conclusion: Both DAPT and PRECISE-DAPT scores could be used to determine the appropriateness of the recommendations of DAPT in patients with AMI or undergoing PCI.

Background: Atrial fibrillation (AF) is a common morbid arrhythmia that can cause thromboembolic events such as stroke. Despite advancements in diagnostic technologies, a significant number of AF patients may remain undetected and undiagnosed, and these asymptomatic patients possess sufficient risk of cardioembolic stroke. Identifying such patients through appropriate screening techniques and timely initiation of systemic anticoagulation therapy is essential to prevent such life-threatening complications. Objectives: The objectives of this study encompass screening of AF among residents of the Dhulikhel Municipality and identifying its prevalence, along with evaluation of stroke risk and use of antithrombotic therapy in patients confirmed with AF. Methods: All residents of four wards of Dhulikhel Municipality, aged 50 years and above (n = 2048), underwent one-time electrocardiogram (ECG) screening using a portable 12-lead ECG machine. The cardiologist checked the cardiogram, and suspected AF cases were referred to the hospital for further evaluation and appropriate management. They were followed up to find out information on disease confirmation and management. Results: Out of 2048 participants, AF was detected in 16 participants, resulting in an overall prevalence of 0.78% (CI 0.4%-1.3%). The prevalence of AF was highest (2.98%) in population aged 80 years and above. Among individuals with AF, the median age was 71.5 (66.3-79.5) years, 50.0% were male and 75.0% had high stroke risk as indicated by a CHA₂DS₂-VASc score ≥ 2. Among these patients, only 41.66% were treated with oral anticoagulants (OACs), while 58.34% were treated either with single or dual antiplatelet therapy (DAPT). Conclusion: This study provided important insight into the prevalence of AF at the community level. Many AF patients were at high risk of stroke, but the OAC use was less than 50%. Screening of AF needs to be carried out on a larger scale in Nepal for early detection and timely management of the disease.

In the elderly population, coronary heart disease (CHD) often coexists with hypertension. However, excessive blood pressure reduction can paradoxically increase the incidence of adverse events. Understanding the molecular mechanisms underlying hypertension and CHD in aged populations is crucial for developing targeted therapies and improving clinical outcomes. In this study, we constructed myocardial infarction (MI) and transverse aortic constriction (TAC) modelsY in aged mice to simulate the disease states of CHD and hypertension, respectively. Using integrated proteomic and phosphoproteomic analyses, we investigated the molecular signatures associated with MI and TAC in these models. Our aim was to identify key molecules involved in these conditions and to understand their unique and shared characteristics. Through our comprehensive proteomic and phosphoproteomic analysis, we identified a total of 1583 proteins and 232 phosphorylated proteins. We observed significant upregulation of heart disease markers such as Myh7, Xirp2, and Acta1, indicating the successful establishment of the MI and TAC models. The overlapped differentially expressed proteins (DEPs) and differentially phosphorylated proteins (DPPs) in MI and TAC were involved in heart failure-related processes including cardiac muscle contraction and hypertrophic cardiomyopathy, further supporting the validity of the models. Among the DEPs, Ppme1 was upregulated in the TAC model but downregulated in the MI model, while Sec31a and Gm56451 displayed the opposite expression patterns. Among the DPPs, Ablim1 and Atp2a2 were found to be significantly upregulated in the TAC model, whereas their expression was markedly reduced in the MI model. In addition, five other DPPs, including REV_Q3TAY5, Cbx3, PITPNB, Eif4b, and A0A1Y7VP73, were elevated in the MI model but decreased in the TAC model. In conclusion, these findings suggest that MI and TAC not only share certain molecular features but also retain their unique characteristics, providing potential biomarkers and therapeutic targets.

Background: The geriatric nutritional risk index (GNRI) is a valuable tool that may predict the prognosis of elderly patients with heart failure (HF). Malnutrition and low GNRI scores have been associated with a higher risk of hospitalization and mortality. This study aimed to investigate the association between GNRI and 6-month readmission for HF in elderly Chinese patients. Materials and Methods: The study utilized data from hospitalized HF patients by combining electronic medical records from the PhysioNet restricted health data database with external outcome data. In our study, we used the GNRI as the independent variable and assessed its association with the risk of readmission within 6 months. The main analytical methods were multivariable Cox regression, stratified analysis with interaction, threshold effect analysis, and Kaplan-Meier survival curves. Results: This study involved 767 elderly HF patients, 61.3% of whom had malnutrition. In the threshold analysis, HF patients' 6-month readmission risk was significantly reduced with increasing GNRI, with a hazard ratio (HR) and 95% confidence interval (CI) of 0.99 (0.97.1). Malnutrition group was associated with a higher risk of readmission within 6 months for HF patients in analyses that were controlled for confounding factors, with HRs and their 95% CI of 1.17 (0.99, 1.38), 1.18 (1, 1.4), and 1.44 (1.08,1.93), respectively. Subgroup analysis showed that GNRI levels had a consistent impact on outcome events, unaffected by covariates. Conclusions: GNRI was negatively correlated with the outcome event of readmission within 6 months in elderly HF patients. Malnutrition group showed a higher risk of readmission within 6 months.

Background: Data comparing the outcomes of loose versus rigorous validation strategies for pulmonary vein isolation (PVI) in patients with paroxysmal atrial fibrillation (PAF) are limited. We aimed to prospectively assess the effectiveness of loose versus rigorous validation for PVI in patients with PAF with a maintained sinus rhythm. Methods: Patients (n = 117) with PAF were randomized to receive either loose validation (n = 59) or rigorous validation (n = 58) after PVI. The presence of dormant conduction in loose validation was assessed only by adenosine administration followed by isoproterenol infusion. The complete absence of pulmonary vein (PV) potentials in rigorous validation was confirmed by the combination of the Lasso catheter with isoproterenol plus adenosine. Dormant conduction, revealed by validation after PVI, was ablated until all reconnections were eliminated. Results: The procedure time in the rigorous validation group was greater than that in the loose validation group (161.3 ± 52.7 min vs. 142.5 ± 37.6 min, p=0.03, respectively). After successful PVI, the detection of dormant PV reconnections in the rigorous validation group was significantly greater than that in the loose validation group (69.0% vs. 37.3%, p=0.001). However, after reisolation of the sites of dormant PV conduction, the postablation recurrence rates in 1.3 years were similar between the groups (79.2% vs. 83.6%, p=0.67). Conclusion: Rigorous validation can reveal dormant conduction in more than two-thirds of patients with PAF undergoing PVI. However, rigorous validation and additional ablation of the resulting connections do not improve long-term outcomes when a protocol that includes electrophysiological confirmation and pharmacological validation is used.

While percutaneous closure of patent foramen ovale (PFO) and atrial septal defect (ASD) are generally well-tolerated procedures, the development of postprocedure fever has been observed at a higher frequency than reported in the initial device trials. We performed a retrospective analysis of 62 patients who underwent PFO or ASD closure from January 1, 2020, to December 31, 2022, at Mayo Clinic, Arizona. Eight patients out of 62 (12.9%) developed fever following PFO or ASD closure. In each of the fever cases, the Gore Cardioform devices (W.L. Gore and Associates, Flagstaff, AZ) were used. No association was found between clinical characteristics or procedural details and the development of fever. The reactions occurred 24 to 48 hours following device implantation and resolved spontaneously. No evidence of infection was found upon diagnostic evaluation. There was a higher incidence of self-limited atrial fibrillation (AF) in the fever patients (37.5% vs. 18.5%) which was not statistically significant. All patients who developed fever had successful closure with no other subsequent clinical events. We have found a high incidence of fever following PFO or ASD closure using the Gore family of devices that has not been observed in prior years. A unifying etiology or risk factor, such as infection or medication, for the fever could not be identified. Long-term device success was achieved in all fever patients. This small retrospective study suggests that the observed fever is benign and self-limiting but further investigation is warranted to determine its true incidence, mechanism, and prognosis.