Frontiers in Cardiovascular Medicine最新文献

Background: Cardiac amyloidosis (CA) is a challenging diagnosis, particularly when the classic signs, such as increased wall thickness in a non-dilated left ventricle (LV), are absent. This makes the diagnosis more difficult in patients with normal LV wall thickness. We present a case of CA without increased wall thickness and without the characteristic granular sparkling echotexture in a non-dilated LV.

Case summary: A 50-year-old female patient presented with worsening breathlessness on exertion, paroxysmal nocturnal dyspnea, oliguria, and lower-extremity edema. Electrocardiography showed low voltage in the limb leads and a pseudoinfarction pattern in the anterior leads. The echocardiographic evaluation revealed a non-dilated LV with normal wall thickness, no granular sparkling echotexture of the myocardium, a mildly dilated left atrium, restrictive filling (grade 3 diastolic dysfunction), and pericardial effusion. A follow-up quantitative echocardiographic study 2 weeks later showed a slight increase in LV wall thickness (still within the normal range), decreased global longitudinal strain, and a relative "apical sparing" pattern of longitudinal strain in the apex of the LV. After 1 month, LV wall thickness increased beyond the normal range, and the granular sparkling echotexture became evident. Cardiac amyloidosis was subsequently confirmed by delayed gadolinium enhancement on cardiac magnetic resonance imaging, abnormal serum-free light chain levels, positive serum immunofixation, and an extracardiac biopsy positive for amyloid.

Discussion: Patients presenting with normal wall thickness in a non-dilated LV might only be in an early stage of CA. Thus, the diagnosis can be easily overlooked. For smaller individuals, relative wall thickness (RWT) may be a more sensitive indicator for further investigation. In patients presenting with increased RWT, restrictive filling, and pericardial effusion in the absence of other plausible causes, CA should be considered, even in the absence of the classic echocardiographic signs of amyloid deposition. Furthermore, two-dimensional speckle-tracking echocardiography can enhance clinical suspicion of CA and should be recommended as part of the diagnostic workup.

Background: Dyslipidemia is a common condition in type two diabetic patients, and it is thought to have a significant role in moderating the cardiovascular risk associated with diabetes. Data on serum lipid profiles in type 2 diabetes patients from Bahir Dar, Ethiopia is limited. This study aimed to evaluate the prevalence of dyslipidemia among adult type 2 diabetes patients and to explore potential contributing factors.

Method and materials: A facility-based cross-sectional study was conducted with 354 type 2 diabetes mellitus patients from April 3 to June 4, 2023. Data were collected through the use of structured questionnaires and checklists. The data were entered into EpiData version 4.6 and analyzed using SPSS version 26. Logistic regression was employed to identify variables significantly associated with the outcomes, with a p-value ≤ 0.05 and a 95% confidence interval.

Results: A total of 369 individuals with diabetes were approached in this study, resulting in a response rate of 96%. The overall prevalence of dyslipidemia was 61.3% (95% CI: 56.2-66.7). Of those with dyslipidemia, 11% had a single serum lipid abnormality, while 50.3% had a combined serum lipid abnormality. Significant factors associated with dyslipidemia included being over 60 years old (AOR: 2.4, 95% CI: 1.2-5.0), poor fasting blood glucose control (AOR: 2.5, 95% CI: 1.2-5.1), being overweight (AOR: 5.8, 95% CI: 3.2-11), physical inactivity (AOR: 3.4, 95% CI: 1.7-7.0), and being a past alcohol drinker (AOR: 3.1, 95% CI: 1.3-7.4).

Conclusion: In the study area, a high prevalence of dyslipidemia was found among diabetic patients. Independent factors associated with dyslipidemia included older age, poor fasting blood glucose control, physical inactivity, a history of alcohol consumption, and being overweight. To address this issue, it is essential to implement preventive measures such as early detection, patient education, dietary monitoring, regular clinical visits, physical exercise, and weight management. These strategies represent the most effective approach to combating dyslipidemia.

Cholesterol aggregation in dendritic cells (DCs) triggers an inflammatory response and accelerates the development of atherosclerosis (AS). Resveratrol (RES), a natural compound with anti-inflammatory and cholesterol metabolism regulatory properties, has been shown to influence the maturation and inflammatory functions of DCs. However, its relationship with cholesterol metabolism remains unclear. This study aimed to explore the roles of RES in cholesterol metabolism and inflammatory behaviors of DCs in the context of AS. We analyzed the effect of RES on cholesterol efflux from ApoE^-/- bone marrow-derived dendritic cells (BMDCs) using qRT-PCR, Western blot, and cholesterol efflux assays; identified the inflammatory status of RES-treated BMDCs and co-cultured T cells using flow cytometry and ELISA; confirmed the effect of RES on blood lipids, atherosclerotic lesions, cholesterol metabolism, and inflammatory response in high-fat diet and lipopolysaccharide-treated ApoE^-/- mice; and explored the potential targets of RES in regulating inflammatory behavior via molecular docking. The results revealed that RES promotes cholesterol efflux, increases the expression of efflux transporter ABCA1, and decreases liver X receptor alpha (LXRα) expression in response to a decrease in intracellular cholesterol in ApoE^-/- BMDCs. RES also reduced MHC-II⁺ cells and downregulated costimulatory molecule CD80 in BMDCs with decreased IL-6 and increased IL-2 production, and suppressed T-cell activation and modulates IL-22 and IL-10 secretion via BMDCs. Furthermore, we confirmed that RES relieves arterial lesions and regulates blood lipids in ApoE^-/- mice. RES demonstrated ABCA1 upregulation and LXRα downregulation effects in the aorta and regulated costimulation molecules and Th17/Treg cytokines in the spleen. Furthermore, RES showed multiple hydrogen bonding and low binding energy with ABCA1, suggesting that ABCA1 is a potential target of RES to modulate the inflammatory properties of BMDCs. Our study demonstrated that RES regulates cholesterol efflux and inflammatory behavior in BMDCs, contributing to the control of AS progression and offering new insights for managing inflammatory diseases.

Introduction: Cardiac arrest during pregnancy is receiving increasing attention. However, there are few reports on cardiac arrest in nonpregnant women caused by abnormal uterine bleeding (AUB). We report a case in which extracorporeal cardiopulmonary resuscitation (ECPR) was used in a patient with cardiac arrest caused by AUB and coronary vasospasm.

Patient presentation: A 52-year-old female patient presented to the emergency department because of sudden chest pain, with a history of hypertension, coronary heart disease and AUB for more than half a month. At the initial stage of admission, cardiac arrest occurred after the ECG demonstrated ST-segment elevation in leads II, III and a VF. ECPR was started after traditional cardiopulmonary resuscitation, and coronary angiography was performed with the support of extracorporeal membrane oxygenation (ECMO). The left and right coronary arteries were slender and narrow, which was relieved after the injection of 100 µg nitroglycerine through the left coronary artery. After performing a coronary angiogram, the patient was given long-acting nitrates and calcium channel blockers orally, and her chest pain did not reoccur. The patient was weaned from ECMO support after 4 days.

Conclusion: This clinical case highlights the challenges that clinicians face in accurately diagnosing and possibly treating AUB and coronary vasospasm-induced acute myocardial infarction because of its rare occurrence and serious adverse events. ECPR can effectively improve the success rate of cardiopulmonary resuscitation.

Background: Acute type A aortic dissection (ATAAD) poses significant challenges in cardiovascular management due to its high morbidity and mortality rates. Postcardiotomy cardiogenic shock (PCS) is a severe complication following ATAAD repair that complicates postoperative recovery. Extracorporeal membrane oxygenation (ECMO) has emerged as a potential life-saving intervention in this context, yet the specific outcomes related to ECMO in ATAAD patients remain insufficiently studied.

Methods: This retrospective single-center study reviewed the medical records of 479 patients who underwent ATAAD surgery from September 2017 to June 2021. Patients were stratified into those requiring postoperative ECMO support and those who did not. Data collected included demographics, operative details, and postoperative outcomes.

Results: Of the cohort, 19 patients (4.0%) required ECMO support. The ECMO group exhibited significantly higher mortality rates (57.9% vs. 5.4%, p < 0.001) and increased complications, including a higher rate of continuous renal replacement therapy (84.2% vs. 24.3%, p < 0.001) and prolonged ICU stays (14.5 days vs. 7.6 days, p = 0.009). Survival analysis demonstrated a stark contrast in 3-year survival rates, with 36.8% for the ECMO group vs. 92.8% for non-ECMO patients (p < 0.001).

Conclusions: ECMO can be a crucial intervention for ATAAD patients suffering from PCS; however, it is associated with significantly higher mortality and complications. Despite lower long-term survival rates compared to non-ECMO patients, ECMO may offer a survival benefit as a salvage therapy. Interpretation is limited by the retrospective single-center design, small ECMO cohort size, and lack of post-discharge quality-of-life data.

Background: The association between obstructive sleep apnea (OSA) and plasma lipid concentrations is not consistent. This study aimed to investigate the association of plasma lipid concentrations with the prevalence of OSA among US adults, with an additional examination of the mediating effect of body mass index (BMI).

Methods: This cross-sectional study included 8,086 individuals who participated in the National Health and Nutrition Examination Survey (NHANES), conducted from 2005 to 2008 and 2015-2018. Multivariable logistic regression analysis was conducted to compute the odds ratios (ORs) and 95% confidence intervals (CIs) for the association between plasma lipid concentrations and the prevalence of OSA. Additionally, subgroup analysis was used to explore the potential interactions. Generalized additive models (GAM) were constructed to evaluate the nonlinear relationships between lipid concentrations and OSA. Furthermore, mediation analysis was performed to assess the potential mediating role of BMI.

Results: In the fully adjusted model, when comparing the lowest quartile, the ORs for the prevalence of OSA among participants in the highest quartile were 1.367 (95% CI, 1.107-1.688) for triglyceride and 1.212 (95% CI, 1.004-1.462) for low-density lipoprotein cholesterol (LDL-C). However, total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) were not associated with OSA. Notably, the relationship between triglyceride and OSA differed in the subgroups of gender, race, and body mass index (BMI) (P for interaction <0.05). Furthermore, we discovered an inverted U-shaped association between triglyceride and OSA (inflection point: 0.813 mmol/L). Causal mediation analysis revealed that BMI significantly mediated the relationship between triglyceride and the prevalence of OSA.

Conclusions: This study revealed that an elevated level of triglyceride increased the prevalence of OSA, and this effect was potentially mediated through BMI. Lowering triglyceride concentration may help to reduce the prevalence of OSA.

Atrial fibrillation (AF), the most prevalent cardiac arrhythmia, is closely linked to metabolic dysfunctions, including obesity, diabetes, and dyslipidemia. These lead to pathological changes in myocardial metabolism and mitochondrial energy metabolism, thereby aggravating AF's incidence and severity. This review introduces the role of metabolic dysfunctions in exacerbating AF, assesses the therapeutic potential of physical exercise and investigates it as a non-pharmacological intervention to alleviate these metabolic disturbances. Evidence suggests that regular physical activity not only enhances metabolic profiles but also reduces the frequency of AF episodes and improves overall cardiovascular health. At the same time, the review emphasizes the need for individualized exercise regimens, individualized to the metabolic and cardiac conditions of each patient to optimize benefits and minimize risks. Additionally, it calls for more basic studies and large-scale clinical trials to establish and refine evidence-based exercise guidelines specific to AF management.

Background: Inflammation significantly impacts chronic kidney disease (CKD) and acute myocardial infarction (AMI). This study investigates the prognostic value of inflammatory markers in predicting outcomes for CKD patients with AMI.

Methods: We enrolled patients diagnosed with CKD concomitant with AMI, choosing five inflammatory markers related to both diseases. Patients were categorized into elevated inflammatory markers group and control group based on inflammatory markers cut-off values for predicting in-hospital major adverse cardiac and cerebrovascular events (MACCE). Using univariate and multivariate logistic regression, we identified inflammation-related risk factors for MACCE. We adjusted covariates stepwise to explore the relationship between independent risk factors and adverse outcomes. We also evaluated the predictive value of these markers for MACCE by receiver operating characteristic (ROC) curves.

Results: In the multivariate logistic regression analysis, higher levels of neutrophil-to-lymphocyte ratio (NLR), and platelet to lymphocyte ratio (PLR) significantly increased risk of MACCE (all P < 0.05). After adjusting above two indicators, NLR was independently associated with in-hospital MACCE in CKD patients with AMI (OR = 10.764, 95% CI: 1.887-61.406, P = 0.007). Furthermore, compared to other inflammatory markers, NLR had the highest predictive value for MACCE in patients with AMI and CKD [Area Under the Curve (AUC): 0.748, 95% Confidence Interval (CI): 0.634-0.861, P < 0.001].

Conclusion: In CKD patients combined with AMI, elevated levels of inflammation markers could increase the risk of MACCE. NLR may provide superior predictive value compared to other markers.

Background: Acute myocardial infarction (AMI), particularly ST-segment elevation myocardial infarction (STEMI), significantly impacts global health, exacerbated by risk factors such as diabetes mellitus (DM). While the Gensini score effectively quantifies coronary artery lesions, its correlation with fasting blood glucose (FBG) levels, particularly in a non-linear fashion, has not been thoroughly explored in STEMI patients.

Methods: This study analyzed data from 464 STEMI patients treated with percutaneous coronary intervention at the First People's Hospital of Taizhou City, Zhejiang Province, China, from January 2010 to October 2014. We stratified patients into three FBG tertiles and utilized multiple statistical analyses, including least absolute shrinkage and selection operator (LASSO) regression and curve fitting, to examine the potential U-shaped relationship between FBG levels and Gensini scores.

Results: Our analysis revealed significant differences in Gensini scores across FBG tertiles, with both hypoglycemic and hyperglycemic extremes showing higher scores compared to the normoglycemic range. The curve fitting analysis confirmed a U-shaped relationship, suggesting a significant, non-linear association between FBG levels and coronary artery lesion severity, regardless of diabetes status.

Conclusions: Our findings underscore the complexity of glycemic control in STEMI management and suggest that both hypo- and hyperglycemia are significant risk factors for severe coronary lesions as quantified by the Gensini score. This study highlights the importance of comprehensive FBG monitoring and management to improve outcomes for STEMI patients.

Extracellular vesicles (EVs) are nanosized particles secreted by cells that play crucial roles in intercellular communication, especially in the context of cardiovascular diseases (CVDs). These vesicles carry complex cargo, including proteins, lipids, and nucleic acids, that reflects the physiological or pathological state of their cells of origin. Multiomics analysis of cell-derived EVs has provided valuable insights into the molecular mechanisms underlying CVDs by identifying specific proteins and EV-bound targets involved in disease progression. Recent studies have demonstrated that engineered EVs, which are designed to carry specific therapeutic molecules or modified to enhance their targeting capabilities, hold promise for treating CVDs. Analysis of the EV proteome has been instrumental in identifying key proteins that can be targeted or modulated within these engineered vesicles. For example, proteins involved in inflammation, thrombosis, and cardiac remodeling have been identified as potential therapeutic targets. Furthermore, the engineering of EVs to increase their delivery to specific tissues, such as the myocardium, or to modulate their immunogenicity and therapeutic efficacy is an emerging area of research. By leveraging the insights gained from multiomics analyses, researchers are developing EV-based therapies that can selectively target pathological processes in CVDs, offering a novel and potentially more effective treatment strategy. This review integrates the core findings from EV multiomics analysis in the context of CVDs and highlights the potential of engineered EVs in therapeutic applications.