Arquivos brasileiros de cardiologia最新文献

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Background: Chronic Chagas cardiomyopathy (CCC) is caused by an inflammatory process induced by Trypanosoma cruzi, which leads to myocarditis with reactive and reparative fibrosis. CCC progresses with myocardial perfusion abnormalities and histopathological events that affect cardiorespiratory fitness (CRF).

Objectives: We evaluated the effects of aerobic physical training (APT) on myocardial perfusion and on morphological and functional impairments related with inflammation and fibrosis in Syrian hamsters with CCC. As a secondary objective, we analyzed the cross-sectional areas of the skeletal muscle.

Methods: Hamsters with CCC and their respective controls were divided into four groups: CCC sedentary, CCC-APT, sedentary control and APT control. Seven months after infection, the animals underwent echocardiography, myocardial perfusion scintigraphy and cardiopulmonary exercise testing. Moderate-intensity APT was performed for fifty minutes, five times a week, for eight weeks. Subsequently, the animals were reassessed. Histopathological analysis was conducted after the above-mentioned procedures. The level of significance was set at 5% in all analyses (p<0.05).

Results: CCC sedentary animals presented worse myocardial perfusion defects (MPD) over time, reduced left ventricle ejection fraction (LVEF) and showed more inflammation and fibrosis when compared to other groups (mixed ANOVA analysis). Conversely, APT was able to mitigate the progression of MPD, ameliorate inflammation and fibrosis and improve CRF efficiency in CCC-APT animals.

Conclusions: Our study demonstrated that APT ameliorated cardiac dysfunction, MPD, and reduced inflammation and fibrosis in CCC hamster models. Additionally, CCC-SED animals presented skeletal muscle atrophy while CCC-APT animals showed preserved skeletal muscle CSA. Understanding APT's effects on CCC's pathophysiological dimensions is crucial for future research and therapeutic interventions.

Background: The association between the length of sleep and atherosclerosis has been reported in many observational studies. However, little is known about its significance as a risk factor for atherosclerosis or as a negative consequence of atherosclerosis.

Objective: This study aimed to assess the causal association between sleep duration and the risk of atherosclerosis using publicly available genome-wide association studies (GWAS) summary statistics.

Methods: We employed a two-sample Mendelian randomization (MR) method with 2 cohorts from MRC-IEU (n=460,099) and UK Biobank (n=361,194) to investigate the causal association between sleep duration and the risk of atherosclerosis. Three methods including the inverse-variance weighted (IVW) technique, Robust adjusted profile score (RAPS), and simple-and weighted-median approach were used to obtain reliable results, and an odds ratio with a 95% confidence interval (CI) was calculated. P<0.05 was considered as a statistical difference. In addition, MR-Egger regression, Radial MR, MR-PRESSO, and leave-one-out analyses were used to assess the possible pleiotropy effects.

Results: No causal association of sleep duration with atherosclerosis was found [OR (95%CI): 0.90 (0.98-1.00), p = 0.186]. Leave-one-out, MR-Egger, and MR-PRESSO analyses failed to detect horizontal pleiotropy.

Conclusions: This MR analysis indicated no causal association between genetically predicted sleep duration and atherosclerosis across European populations.

Background: The analysis of indicators such as hospital readmission rates is crucial for improving the quality of services and management of hospital processes.

Objectives: To identify the variables correlated with hospital readmission up to 30 days following coronary artery bypass grafting (CABG).

Methods: Cross-sectional cohort study by REPLICCAR II database (N=3,392) from June 2017 to June 2019. Retrospectively, 150 patients were analyzed to identify factors associated with hospital readmission within 30 days post-CABG using univariate and multivariate logistic regression. Analysis was conducted using software R, with a significance level of 0.05 and 95% confidence intervals.

Results: Out of 3,392 patients, 150 (4,42%0 were readmitted within 30 days post-discharge from CABG primarily due to infections (mediastinitis, surgical wounds, and sepsis) accounting for 52 cases (34.66%). Other causes included surgical complications (14/150, 9.33%) and pneumonia (13/150, 8.66%). The multivariate regression model identified an intercept (OR: 1.098, p<0.00001), sleep apnea (OR: 1.117, p=0.0165), cardiac arrhythmia (OR: 1.040, p=0.0712), and intra-aortic balloon pump use (OR: 1.068, p=0.0021) as predictors of the outcome, with an AUC of 0.70.

Conclusion: 4.42% of patients were readmitted post-CABG, mainly due to infections. Factors such as sleep apnea (OR: 1.117, p=0.0165), cardiac arrhythmia (OR: 1.040, p=0.0712), and intra-aortic balloon pump use (OR: 1.068, p=0.0021) were predictors of readmission, with moderate risk discrimination (AUC: 0.70).

Background: Pulmonary hypertension is a condition that involves the remodeling of the right ventricle. Ongoing remodeling is also associated with disease prognosis. During the restructuring process, complex changes such as hypertrophy and dilatation may also be reflected in electrocardiographic parameters.

Objectives: Our study aimed to investigate the relationship between prognosis and electrocardiographic parameters in patients with pulmonary arterial hypertension.

Methods: The study was designed retrospectively and included patients diagnosed with pulmonary arterial hypertension between 2010 and 2022. The patients were divided into two groups based on their survival outcome. Various parameters, including electrocardiographic, demographic, echocardiographic, catheter, and blood parameters, were compared between the two groups. A p-value of <0.05 was considered statistically significant.

Results: In the multivariate Cox analyses, the parameters that were found to be independently associated with survival were the 6-minute walk test, mean pulmonary artery pressure, presence of pericardial effusion, and time between the beginning of the QRS and the peak of the S wave (RS time) (p<0.05 for each). Of all the parameters, RS time demonstrated the best diagnostic performance (AUC:0.832). In the survival analysis, a significant correlation was found between RS time and survival when using a cut-off value of 59.5 ms (HR: 0.06 [0.02-0.17], p < 0.001).

Conclusions: According to the results of our study, a longer RS time is associated with poor prognosis in patients with pulmonary arterial hypertension. We can obtain information about the course of the disease with a simple, non-invasive parameter.

Cardiovascular disease is the predominant cause of mortality on a global scale. Research indicates that women exhibit a greater likelihood of presenting with non-obstructive coronary artery disease (CAD) when experiencing symptoms of myocardial ischemia in comparison to men. Additionally, women tend to experience a higher burden of symptoms relative to men, and despite the presence of ischemic heart disease, they are frequently reassured erroneously due to the absence of obstructive CAD. In cases of ischemic heart disease accompanied by symptoms of myocardial ischemia but lacking obstructive CAD, it is imperative to consider coronary microvascular dysfunction as a potential underlying cause. Coronary microvascular dysfunction, characterized by impaired coronary flow reserve resulting from functional and/or structural abnormalities in the microcirculation, is linked to adverse cardiovascular outcomes. Lifestyle modifications and the use of anti-atherosclerotic and anti-anginal medications may offer potential benefits, although further clinical trials are necessary to inform treatment strategies. This review aims to explore the prevalence, underlying mechanisms, diagnostic approaches, and therapeutic interventions for coronary microvascular dysfunction.

Background: PRKAG2 syndrome typically manifests in adolescence and early adulthood, progressing with left ventricular hypertrophy, arrhythmias, and risk of sudden death. Findings of echocardiographic markers before clinical manifestation in children of patients affected by the disease can facilitate prevention strategies and therapeutic planning for this patient group.

Objective: To identify the existence of echocardiographic findings that manifest early in children of parents affected by PRKAG2 syndrome, while they are still asymptomatic.

Methods: In this cross-sectional observational study, 7 participants who were children of parents with established diagnosis of PRKAG2 syndrome, between the ages of 9 months and 12 years, with proven genetic diagnosis, underwent conventional and advanced echocardiography. Their findings were compared to those of a control group composed of 7 age- and sex-matched volunteers who were healthy from a cardiovascular point of view. P values < 0.05 were considered significant.

Results: Conventional echocardiography showed statistically significantly higher values in the case group for left atrium, interventricular septum, left ventricular posterior wall, indexed ventricular mass, and relative wall thickness (p < 0.05). Global longitudinal systolic strain on 2-dimensional echocardiography did not show statistical significance between the case and control groups. None of the parameters on 3-dimensional echocardiography showed statistical significance between groups.

Conclusion: Children diagnosed with PRKAG2 showed echocardiographic findings indicative of a tendency toward cardiac hypertrophy. Echocardiography can be a useful tool in the evaluation and follow-up of this patient group before the onset of clinical manifestations.

In childhood and adolescence, cardiomyopathies have their own characteristics and are an important cause of heart failure, arrhythmias, sudden death, and indication for heart transplantation. Diagnosis is a challenge in daily practice due to its varied clinical presentation, heterogeneous etiologies, and limited knowledge of tools related to clinical and molecular genetics. However, it is essential to recognize the different phenotypes and prioritize the search for the etiology. Recent advances in precision medicine have made molecular diagnosis accessible, which makes it possible to individualize therapeutic approaches, stratify the prognosis, and identify individuals in the family who are at risk of developing the disease. The objective of this review is to emphasize the particularities of cardiomyopathies in pediatrics and how the individualized approach impacts the therapy and prognosis of the patient. Through a systematized approach, the five-stage protocol used in our service is presented. These stages bring together clinical evaluation for determining the morphofunctional phenotype, identification of etiology, classification, establishment of prognosis, and the search for personalized therapies.