Journal of Cardiovascular and Thoracic Research最新文献

Cyclophosphamide-induced cardiotoxicity, associated with its toxic metabolite acrolein, is a significant concern and unresolved issue, especially when cyclophosphamide is administrated in high doses. However, cardiotoxicity following low-dose cyclophosphamide has been also documented, especially in post-hematopoietic stem cell transplantation (post-HSCT) settings. Despite the involvement of multiple signaling pathways in cyclophosphamide-induced cardiomyopathy, the exact underlying mechanisms remain to be fully elucidated. This review outlines the current challenges of cyclophosphamide therapy in HSCT recipients. In addition, the promising therapeutic approaches by targeting acrolein's anti-angiogenic effect were thoroughly discussed to better manage post-HSCT cyclophosphamide-induced cardiotoxicity.

Introduction: Acute pulmonary thromboembolism (PTE) is one of the leading causes of death and severe disability. Considering the impact of inflammation and lipid profile on prevalence and prognosis of deep vein thrombosis and PTE, this study was conducted to assess the predictive value of lipid-to-neutrophil count ratios for the short-term survival of PTE patients.

Methods: This study is an analytical cross-sectional study. Data regarding the demographics, past medical history, vital signs, laboratory variables, and the outcomes of hospitalization were gathered from the Tabriz PTE registry. The receiver operating characteristics (ROC) curve and area under curve (AUC) were utilized for assessing the prognostic values. SPSS 26 was used for all of the statistical analysis.

Results: The population of this analytical cross-sectional study consists of 547 PTE patients of which 41 patients (7.5%) died during hospitalization. There was a significant difference between death and survived groups regarding cholesterol (146.00[60.50] vs. 165.50[59.75]; p-value<0.01), LDL (80.00[48.00] vs. 102.00[52.00]; p-value<0.01), HDL (31.00[19.00] vs. 35.00[14.00]; p-value=0.04). Cholesterol/neutrophil*1000 with a cut-off value of 22.014 (sensitivity: 56.7%; specificity: 61.3%), LDL/neutrophil*1000 with a cut-off value of 10.909 (sensitivity: 69.3%; specificity: 51.9%) and HDL/neutrophile *1000 with a cut-off value of 4.150 (sensitivity: 61.9%; specificity: 58.1%) can predict short-term survival in patients with acute PTE.

Conclusion: Based on our findings, patients with higher cholesterol/neutrophil, LDL/neutrophil, and HDL/neutrophil ratios have a better in-hospital prognosis and measurement of lipid-to-neutrophil ratio in the first 24 hours of hospitalization may be a valuable marker for determining the early prognosis of PTE. However, additional clinical studies are suggested for a more definitive conclusion.

Introduction: This study aims to determine the effects of fenugreek seed dry extract (FDE) on the glycemic indices, lipid profile, and prooxidant-antioxidant balance (PAB) in patients with type 2 diabetes (T2D).

Methods: A double-blind randomized clinical trial was carried out on 54 individuals with T2D. Participants were randomly assigned to a FDE group (received 3 tablets containing 335 mg of FDE daily for 8 weeks) or a placebo group (received tablets containing microcrystalline cellulose). Anthropometric indices, physical activity, diet, fasting blood sugar (FBS), serum insulin, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein (HDL-C), and PAB were assessed.

Results: An eight-week intake of 3 tablets containing 335 mg of FDE decreased serum insulin (P=0.016, P<0.001), HOMA-IR (P=0.009, P<0.001), TG (P<0.001, P=0.001), and PAB (P<0.001, P<0.001) compared to the baseline, in both placebo and intervention groups respectively. TC decreased significantly compared to the baseline in the placebo group (P=0.028), while HDL-C increased in the FDE group compared to the baseline (P<0.001) and placebo group (P=0.014).

Conclusion: In the present study even though changes of parameters were more in intervention group compared to the control group, we did not observe any significant differences between studied groups except for HDL-C. However, the effects might become apparent with a higher dosage, longer study duration, or a larger sample size compared to the placebo group. Further clinical trials are needed in this regard.

Introduction: FTO gene belongs to the non-heme Fe (II) and 2 oxoglutarate-dependent dioxygenase superfamily. Polymorphisms within the first intron of the FTO gene have been examined across various populations, yielding disparate findings.The present study aimed to determine the impact of two intronic polymorphisms FTO 30685T/G (rs17817449) and -23525T/A (rs9939609) on the risk of obesity in Punjab, India.

Methods: Genotypic and biochemical analysis were done for 671 unrelated participants (obese=333 and non-obese=338) (age≥18 years). Genotyping of the polymorphisms was done by PCR-RFLP method. However, 50% of the samples were sequenced by Sanger sequencing.

Results: Both the FTO variants 30685 (TT vs GG: odds ratio (OR), 2.30; 95% confidence interval (CI), 1.39-3.79) and -23525 (TT vs AA: odds ratio (OR), 2.78; 95% confidence interval (CI), 1.37-5.64) showed substantial risk towards obesity by conferring it 2 times and 3 times, respectively. The analysis by logistic regression showed a significant association for both the variants 30685T/G (rs17817449) and -23525T/A (rs9939609) (OR=2.29; 95%CI: 1.47-3.57) and (OR=5.25; 95% CI: 2.68-10.28) under the recessive genetic model, respectively. The haplotype combination TA (30685; -23525) develops a 4 times risk for obesity (P=0.0001). Among obese, the G allele of 30685T/G and A- allele of -23525T/A showed variance in Body mass index (BMI), waist circumference (WC), waist-to-height ratio(WHtR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and triglyceride(TG).

Conclusion: The present investigation indicated that both the FTO 30685T/G (rs17817449) and -23525T/A (rs9939609) polymorphisms have a key impact on an individual's vulnerability to obesity in this population.

Introduction: Plasma proteins play essential roles in myocardial infarction (MI) and atrial fibrillation (AF); however, it remains unknown whether the two disorders share causal plasma proteins.

Methods: The present study utilizes cis-protein quantitative trait loci (cis-pQTLs) for 4,719 plasma proteins to assess their causality on MI and AF.

Results: Two-sample Mendelian randomization (MR) identifies 21 and 9 plasma proteins for MI and AF, respectively (FDR P<0.05), with plasminogen (PLG) being a commonly protective factor against both diseases. Multi-trait MR suggests that PLG is also protective against coronary atherosclerosis. PheWAS analysis identifies associations of six cis-pQTLs with both MI and AF, i.e., rs11751347 (PLG), rs11591147 (PCSK9), rs77347777 (ITIH4), rs936228 (ULK3), rs2261033 (AIF1V), and rs2711897 (BDH2). Furthermore, interactions exist among the causal plasma proteins, with PLG directly interacting with multiple others. Drug-gene databases suggest that PLG activators, such as Urokinase, Reteplase, Streptokinase, Alteplase, Anistreplase, Tenecteplase, Desmoteplase, and Defibrotide sodium may serve as common therapeutic drugs for MI and AF.

Conclusion: Our study provides a causal inference of human plasma proteins in MI and AF. Several of the identified proteins and single nucleotide polymorphisms (sNPs) exert pleiotropic effects on other cardiometabolic phenotypes, indicating their crucial roles in the pathology of cardiovascular disease (CVD). Our study provides new insights into the shared causality and drugs for MI and AF.

Introduction: Aim of this study was to evaluate the predictive performance of systolic blood pressure (SBP) to left ventricular end-diastolic pressure (LVEDP) ratio for the prediction of in-hospital and short-term mortality in a contemporary cohort of patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) at a tertiary care cardiac center.

Methods: This study included a consecutive series of patients diagnosed with STEMI who underwent primary PCI. The SBP/LVEDP ratio and TIMI (Thrombolysis in Myocardial Infarction) score were calculated, and their ability to predict in-hospital and short-term mortality was evaluated by analyzing the area under the curve (AUC) on the receiver operating characteristics (ROC) curve.

Results: This study involved 977 patients, with 780 (79.8%) being male and a mean age of 55.6±11.5 years. Among them, 191 (19.5%) had an SBP/LVEDP≤5.4. The in-hospital mortality rate was 4.3% (42), and the short-term all-cause mortality rate after a mean follow-up of 5.9±2.4 months was 15% (140). Patients with SBP/LVEDP≤5.4 had higher in-hospital mortality rates (14.1% vs. 1.9%; P<0.001) and short-term mortality rates (35.1% vs. 9.8%; P<0.001) compared to those with SBP/LVEDP>5.4. The AUCs of SBP/LVEDP and TIMI for predicting in-hospital mortality were 0.766 [0.681-0.851] and 0.787 [0.713-0.861], respectively. For short-term mortality, the AUCs of SBP/LVEDP and TIMI were 0.731 [0.682-0.780] and 0.736 [0.690-0.782], respectively.

Conclusion: In conclusion, SBP/LVEDP showed sufficiently high predictive power comparable to the TIMI risk score. SBP/LVEDP is a readily available ratio that can rapidly provide valuable prognostic information during primary PCI.

Introduction: Prediabetes, characterized by mildly elevated blood sugar levels, significantly increases the risk of developing type 2 diabetes and cardiovascular disease. The condition is linked to higher levels of IL-18, TNF-α, and IL-6, indicating inflammation that may drive type 2 Diabetes Mellitus (T2DM). Despite the known role of inflammation in glucose homeostasis, the involvement of the Nuclear Factor of Activated T Cells 4 (NFATC4) gene in prediabetes remains underexplored. This case-control study aims to investigate the association between physiological, demographic, anthropometric, lifestyle factors, inflammatory markers and NFATC4 gene expression, in the context of prediabetes.

Methods: The study involved 300 participants aged 20 to 50, with 150 diagnosed with prediabetes and 150 healthy controls. After obtaining informed consent fasting venous blood samples were collected for comprehensive assessments, including biochemical, endocrinological and immunological analyses. Specifically, NFATC4 gene expression and inflammatory markers were measured.

Results: The findings revealed significantly elevated levels of IL-18, TNF-α, IL-6, and NFATC4 expression in prediabetic individuals compared to controls. Notably, strong positive correlations were observed between NFATC4 expression and the inflammatory markers. Receiver operating characteristic (ROC) curve analysis identified IL-18 and NFATC4 as the most promising biomarkers for predicting prediabetes, followed by TNF-α and IL-6. Multivariate regression analysis further identified socioeconomic status (SES), IL-18, NFATC4, TSH, triglycerides, and HDL as independent predictors of prediabetes.

Conclusion: These results highlight the key role of inflammation and NFATC4 in prediabetes, stressing the need for strategies to prevent progression to type 2 diabetes and cardiovascular issues.

Introduction: Limited real-world data exist regarding cardiovascular outcomes in post-COVID-19 individuals following discharge, particularly within the Asian Indian population. This study aims to explore the association between prior COVID-19 history and in-hospital outcomes in acute myocardial infarction patients.

Methods: Hospital database was searched for the patients who were diagnosed with Acute myocardial infarction (AMI) and were grouped according to absence (Group-A) or presence (Group-B) of history of severe COVID-19 hospitalization at least 3 months prior to the index event of AMI. Study primary endpoint was defined as major adverse cardiovascular events (MACE) comprising of Re-AMI, stroke, death (3P) and acute decompensated heart failure (4P), which were analyzed between these 2 study groups.

Results: Of 10,581 consecutive patients of AMI, 5.33% (n=564/10,581) patients had prior history of severe SARS-CoV-2 hospitalization beyond 3 months of index AMI. Past severe Covid-19 patients presenting with AMI were more likely to be younger (59.12+11.23 years vs. 52.01+10.05 years) and younger than 40 years of age. Patients in Group B demonstrated a notably higher prevalence of diabetes, hypertension, higher Killip class, and lower presenting LVEF compared to Group A. In-hospital cardiac arrest, stroke, heart failure and all-cause death were significantly higher in Group B patients. Higher unadjusted odds ratio for in hospital death OR=5.78 (2.56-10.23), 3-P MACE OR=2.33 (1.23-8.65) and 4-P MACE OR=2.58 (1.36-5.43) were found in patients with prior history of COVID-19. After adjusting for comorbidities, the ratio for in-hospital MACE was found to be non-significant.

Conclusion: Conventional risk factors and presence of comorbidities in individuals with prior history of COVID-19 hospitalization increased the risk of both 3P and 4P MACE during AMI.

Introduction: Acute kidney injury (AKI) is a common clinical occurrence causing high mortality and morbidity. In acute renocardiac syndrome, AKI leads to acute cardiac injury or/and dysfunction. This study aimed to investigate the antioxidative effects of Edaravone on cardiac tissues following the induction of renal ischemia-reperfusion injury (IRI) in rats.

Methods: Twenty-four male Wistar rats were randomly divided into four groups: IR+Edaravone, Edaravone, IR, and Sham groups (six rats per group). Non-traumatic clamps were used to stop the artery and vein blood flow of the left kidney in rats of the IR groups for 45 minutes. Thirty minutes before ischemia induction, Edaravone (3 mg/kg) was injected intraperitoneally in the IR+Edaravone group. Cardiac samples were subjected to biochemical analyses.

Results: The Results showed a significant increase in the enzymatic activity of glutathione peroxidase (P=0.01), catalase (P=0.03), and superoxide dismutase (P=0.02), and the levels of glutathione (P=0.012), and total antioxidant capacity (P<0.001) in the IR+Edaravone group in comparison to the IR group. Moreover, the total antioxidant capacity of the heart was increased in the Edaravone group compared to the control and IR groups (P<0.001), indicating the safety of the drug.

Conclusion: The results can reveal important insights into the protective effects of Edaravone against acute renocardiac syndrome.

Introduction: Mortality benefit of digoxin prescription in patients suffering from heart failure has been questioned many time. We evaluated these effects among admitted symptomatic heart failure patients.

Methods: We retrospectively divided our patients into two groups: group A (n=205) were digoxin prescribed, and group B (n=96) were digoxin naïve patients. Both groups' medical records were gathered for one year, and the study endpoints were compared between the two groups.

Results: The mean age was 62.3±12.1 years and 54.8 % were male. All-cause mortality and readmission occurred in 26.7% and 31.7% of individuals, respectively, without significant differences between the two groups. However, in subgroup analysis, there was a significant relationship between in-hospital mortality and the presence of cardiovascular risk factors.

Conclusion: Digoxin might increase in-hospital mortality in patients with underlying cardiovascular risk factors.