Arquivos brasileiros de cardiologia最新文献

Background: D-limonene (D-L) is the major monocyclic monoterpene in citrus plants with anti-inflammatory properties. Pulmonary hypertension (PH) can cause right heart dysfunction and increases the risk of death, partially due to inflammatory response in the heart.

Objective: To evaluate the possible protective effect of D-L on cardiac function in a rat model of monocrotaline-induced PH (MCT-PH).

Methods: Electrocardiogram was monitored in vivo. Masson Trichrome technique was deployed to verify fibrosis in the heart. Contractility function of isolated atrial tissue was studied using organ bath chamber. Real-time quantitative PCR was applied to quantify inflammation in the right ventricle.

Results: The MCT-PH group showed electrical and structural heart remodeling, with the presence of fibrosis in the cardiac tissue and in vivo electrocardiographic changes. Treatment with D-L partially prevented the development of tissue fibrosis and the increase in P wave duration in the MCT-PH group. The contraction and relaxation velocity of isolated right and left atrium were accelerated in CTR and MCT-PH animals treated with D-L. Finally, D-L was able to prevent the abnormal expression of the key inflammatory cytokines (interleukin 1-β, interleukin 6 and tumor necrosis factor-α) in the right ventricle of MCT-PH animals. D-L was able to enhance the production of the anti-inflammatory cytokine Interleukin-10.

Conclusion: Our results showed that in vivo administration of D-L partially prevented the molecular, structural and functional remodeling of the heart in the MCT-PH model with attenuation of the inflammatory response in the heart.

Background: Increased oxygen tension and decreased prostaglandin levels cause ductal closure. The diagnostic role of systemic inflammatory indices in hemodynamically significant ductus arteriosus (hsPDA) in premature infants is unknown.

Objectives: We aimed to evaluate the role of systemic inflammatory indices in the predictivity of hsPDA.

Methods: Premature infants with gestational weeks (GW) of <32 weeks were evaluated retrospectively. Systemic inflammatory indices neutrophil-lymphocyte ratio (NLR), monocyte-lymphocyte ratio (MLR), platelet-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), pan-immune- inflammation value (PIV), and systemic inflammation response index (SIRI) were calculated. Systemic inflammatory indices were compared between hsPDA and non-hsPDA groups. A p <0.05 was considered as statistically significant.

Results: A total of 1228 patients were included in the study, including 447 patients in the hsPDA group and 781 patients in the non-hsPDA group. The PIV value [median (Q1 - Q3): 5.18 (2.38-10.42)] in the hsPDA group was statistically significantly higher than the PIV value [median (Q1 - Q3): 3.52 (1.41-6.45)] in the non-hsPDA group (p<0.001). According to the ROC analysis, the AUC value of PIV for the predictivity of hsPDA was 0.618, and the cutoff level was >8.66. After even multiple logistic regression analyses, PIV was shown to be a significant parameter for the diagnosis of hsPDA (OR 1.972, 95% CI 1.114-3.011. p=0.001).

Conclusions: A high PIV value may be a quickly used indicator with low-cost, simple, and easily accessible for the early diagnosis of hsPDA.

Background: Current guidelines advise exercise for most congenital heart disease patients (CHD). However, physical activity remains low in CHD individuals, with limited research on exercise's effects in adults.

Objectives: The aim of this study is to evaluate the safety and efficacy of exercise training on exercise capacity and quality of life in adult congenital heart disease (ACHD) patients.

Methods: We searched PubMed/Medline, Cochrane Library, Web of Science, and Scopus through December 2022 for randomized controlled trials assessing aerobic and resistance training effects on exercise capacity and quality of life in ACHD. Out of 3,517 citations, ten eligible articles were included.

Results: Meta-analysis of the included randomized controlled trials (286 participants) found no significant change in peak oxygen consumption or quality of life in ACHD with exercise training (pooled mean difference = 0.33 ml/kg/min [95% CI, -0.88 to 1.54 ml/kg/min]; p = 0.60; I2= 3%). However, the increase in maximum workload was significant (pooled mean difference = 8.86 watts [95% CI, 0.78 to 16.93], p = 0.03, I2 = 0%).

Conclusions: Our review confirms that exercise training increases the maximum workload in ACHD patients. However, the lack of a standardized protocol among exercise interventions in this population may have contributed to the absence of a significant change in peak VO2 and quality of life observed in the conducted studies. The heterogeneity of exercise programs could be a contributing factor to the inconsistency of the results. In this context, the implementation of standardized exercise protocols in future research, particularly with larger sample sizes, is crucial to enhance the comparability of outcomes. Well-designed randomized controlled trials studying structured exercise training in ACHD patients will provide clearer insights.

Background: Myocardial fibrosis (MF) occurs throughout the onset and progression of cardiovascular disease, and early diagnosis of MF is beneficial for improving cardiac function, but there is a lack of research on early biomarkers of MF.

Objectives: Utilizing bioinformatics techniques, we identified potential biomarkers for MF.

Methods: Datasets related to MF were sourced from the GEO database. After processing the data, differentially expressed genes were screened. Differentially expressed genes were enriched, and subsequently, protein-protein interaction (PPI) was performed to analyze the differential genes. The associated miRNAs and transcription factors were predicted for these core genes. Finally, ROC validation was performed on the core genes to determine their specificity and sensitivity as potential biomarkers. The level of significance adopted was 5% (p < 0.05).

Results: A total of 91 differentially expressed genes were identified, and PPI analysis yielded 31 central genes. Enrichment analysis showed that apoptosis, collagen, extracellular matrix, cell adhesion, and inflammation were involved in MF. One hundred and forty-two potential miRNAs were identified. the transcription factors JUN, NF-κB1, SP1, RELA, serum response factor (SRF), and STAT3 were enriched in most of the core targets. Ultimately, IL11, GADD45B, GDF5, NOX4, IGFBP3, ACTC1, MYOZ2, and ITGB8 had higher diagnostic accuracy and sensitivity in predicting MF based on ROC curve analysis.

Conclusion: Eight genes, IL11, GADD45B, GDF5, NOX4, IGFBP3, ACTC1, MYOZ2, and ITGB8, can serve as candidate biomarkers for MF. Processes such as cellular apoptosis, collagen protein synthesis, extracellular matrix formation, cellular adhesion, and inflammation are implicated in the development of MF.

Background: International cohort studies have consistently demonstrated an unfavorable prognosis in female patients after the first acute myocardial infarction (AMI) over the past decades. However, national data on this topic are limited.

Objectives: This study aims to compare national cohorts of men and women hospitalized due to the first acute myocardial infarction, examining long-term outcomes.

Methods: A retrospective, observational study using real-world data extracted from the global TriNetX platform, including patients of both sexes with a confirmed diagnosis of AMI according to the International Classification of Diseases (ICD), version 11, code I21. The level of statistical significance adopted in the analysis was 5% (0.05). The primary outcome assessed was a composite of death, new hospitalization for AMI, myocardial revascularization procedures, or heart failure after the hospital phase with a 5-year follow-up.

Results: Data from 29,041 patients were evaluated, of which 11,284 (38.4%) were women. The mean age of the female and male populations was 64.4 and 59.8 years, respectively. The group of women showed a higher occurrence of the composite outcome of death, new hospitalization for AMI, myocardial revascularization procedures, or heart failure after the hospital phase with a 5-year follow-up (OR 1.058; CI 1.005 - 1.113; p = 0.03).

Conclusions: In this large Brazilian cohort, the female sex was associated with a higher occurrence of cardiovascular events within 5 years after hospital discharge.

Background: Real-world study comparing female and male cohorts in the TriNetX network.

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Endomyocardial biopsy (EB) is the preferred procedure for post-heart transplant rejection diagnosis. The rigid bioptome technique has been used due to its greater simplicity and has been criticized for the potential risk of tricuspid regurgitation (TR). We aimed to review all the EBs performed by this technique in a tertiary center and estimate the rate of complications and/or aggravation of TR. Cross-sectional, retrospective, anterograde study. Data were collected from 729 EBs performed in 55 post-heart transplant patients with a rigid Scholten Novatome™ bioptome between September 2012 to March 2022. All EBs were performed via the right jugular vein under local anesthesia and through micro-puncture and ultrasound guidance. A total of 729 procedures had an echocardiography performed before and after the procedures. The estimate of TR was categorized as absent, minimal, mild, moderate, and severe. McNemar's chi-square test was used to analyze the degree of pre- and post-EB TR. There was a worsening enough to become moderate or severe post-biopsy TR in two (0.27%) procedures, and there was a slight change in TR from minimal to mild TR in 25 (3.42%) procedures. In 729 percutaneous EBs performed with a rigid bioptome, there was no myocardial perforation, cardiac tamponade or pneumothorax. One death occurred within 24 hours after the procedure for an unknown reason. EB using a rigid bioptome is safe and has not been associated with worsening TR in a follow-up of 729 EBs performed after cardiac transplantation. The overall complication rate, including moderate to severe TR, was 0.81%. The mortality rate was 0.14%.

Background: As the predominant leisure-time sedentary behavior, television viewing was documented to increase cardiovascular diseases in observational studies, yet the causal relationship and potential mechanisms remain to be determined.

Objectives: To systematically investigate the causal relationship between television viewing time, cardiovascular diseases, and potential mechanisms.

Methods: We conducted a two-sample Mendelian randomization (MR) analysis to estimate causal associations with cardiovascular diseases and biomarkers of cardiometabolic risk. The random inverse-variance weighted method was used as the primary estimate. To account for multiple comparisons, a Bonferroni correction p value for cardiovascular diseases and biomarkers of cardiometabolic risk was 0.0045 and 0.0024, respectively.

Results: Genetically instrumented television viewing time was associated with higher risks of type 2 diabetes (odd ratio [OR]=2.51; 95% confidence interval [CI]: 1.89-3.33; p<0.00001), hypertension (OR=2.11; 95% CI: 1.67-2.66; p<0.00001), coronary heart disease (OR=1.53; 95% CI: 1.23-1.91; p=0.00015), and heart failure (OR=1.42; 95% CI: 1.18-1.70; p=0.00017). Suggestive evidence of harmful associations was also observed for peripheral artery disease (OR=1.58; 95% CI: 1.07-2.34; p=0.02253) and ischemic stroke (OR=1.34; 95% CI: 1.10-1.63; p=0.00328). Biomarkers of cardiometabolic risk, including interleukin 10, leptin, visceral adipose, abdominal subcutaneous adipose, liver fat, body mass index, waist circumference, triglycerides, and C-reactive protein, were increased. Systolic blood pressure, heart rate, low-density lipoprotein, and total cholesterol were potentially increased while high-density lipoprotein was decreased. However, television viewing time had no effect on venous thromboembolism or pulmonary embolism.

Conclusion: Television viewing time was causally associated with increased risks of cardiovascular diseases, which may be explained by metabolic and inflammatory mechanisms.

Background: An overview of the effect of television viewing time on cardiovascular diseases and biomarkers of cardiometabolic risk.

Background: The optimal transfusion strategy in acute myocardial infarction (AMI)-associated anemia remains uncertain.

Objectives: To compare all-cause mortality between liberal versus restrictive transfusion strategies in patients with AMI-associated anemia, using a meta-analytic approach.

Methods: Pubmed, Embase, and ClinicalTrials.gov were systematically searched for randomized controlled trials (RCTs) comparing liberal and restrictive transfusion strategies in AMI-associated anemia. Random-effects meta-analysis and trial sequential analysis (TSA) were conducted to compare blood use, efficacy, and safety endpoints. The p-values were 2-sided with an α of 0.05.

Results: In a pooled analysis involving 4,217 participants from three RCTs followed-up for 30 days, no statistically significant differences emerged between restrictive and liberal strategies in all-cause mortality (RR 1.03; 95% CI 0.67-1.57; p=0.90) and other efficacy endpoints (recurrent AMI, unscheduled revascularization, acute heart failure, stroke, and acute kidney injury), as well as in safety endpoints including allergic reactions, infection, and acute lung injury. TSA did not reach futility boundaries. In patients assigned to restrictive strategy, substantial differences in transfusion use were observed across RCTs, correlating with mortality rates, and likely accounting for between-study heterogeneity in treatment effects.

Conclusions: In patients with AMI-associated anemia, there is no clear superiority between liberal and restrictive transfusion strategies in all-cause mortality or other major outcomes in 30 days. However, the heterogeneity observed in blood use between the restrictive groups likely explains variable findings across RCTs.