Diabetic cardiomyopathy (DCM) is a specific type of cardiomyopathy that is independent of hypertension and coronary artery disease, and is closely associated with the high incidence and mortality of heart failure in people with diabetes. DCM causes microvascular disease, myocardial metabolic disorder, and myocardial fibrosis, thereby leading to left ventricular remodeling, diastolic and/or systolic dysfunction, and eventually progressing to congestive heart failure. Recent studies have highlighted the crucial roles of mitochondrial dysfunction in the pathogenesis of DCM, including aspects such as glucose-lipid metabolic disorder, oxidative stress damage, calcium regulation disorder, respiratory chain uncoupling, kinetic imbalance, and mitochondrial DNA damage. Increasing numbers of targets and drugs are being identified to ameliorate mitochondrial dysfunction and consequently slow DCM progression. This article reviews the newly identified targets and drugs in the past decade, to provide new insights for DCM prevention and treatment.

Background: With distal transradial access (dTRA), the postoperative compression time remains significantly longer than the recommended range via in practice. This study investigated whether intravenous protamine sulfate might shorten the postoperative compression time and increase safety after coronary angiography via dTRA. Methods: In this retrospective study, patients who underwent coronary angiography were enrolled and divided into two groups. The study group received a slow intravenous injection of 15–20 mg protamine sulfate before sheath retraction. The primary endpoint was the puncture compression time after coronary angiography. Results: A total of 97 patients in the protamine group and 293 in the control group were enrolled. Intraoperative heparin use, contrast dose, angiography duration, and radiation dose did not differ significantly between groups. The mean compression time in the control group was 2.9 ± 0.5 hours, whereas that in the protamine group was 1.6 ± 0.9 hours (P < 0.001). No significant difference was observed in postoperative minor or major hemorrhage or hematoma between groups. Ultrasound 24 hours after angiography indicated an incidence of radial artery thrombosis of 1.1% in the control group and 4.3% in the protamine treatment group, with no statistically significant difference between groups (P = 0.209), and no radial artery occlusion in either group. Logistic regression suggested that radial artery thrombosis was associated with intraoperative heparin dose and a history of chronic kidney disease. Conclusion: Intravenous application of protamine after coronary angiography via dTRA can significantly shorten the time of postoperative compression hemostasis and has good performance in terms of safety.

Background: Mounting evidence indicates that opioid-sparing anesthesia (OSA) decreases opioid-related adverse events. Our goal was to determine whether OSA might improve initial recovery after cardiac surgery. Methods: Data from patients who underwent elective heart surgery between July 2023 and July 2024 were analyzed. Eligible patients were divided into an OSA group or a control group. Patients in the OSA group received 0.5 to 1 μg·kg−1 sufentanil and ultrasound-guided nerve block after anesthetic induction, whereas patients in the control group received traditional high-dose opioid management. Patients in both groups were managed with the same sedatives, muscle relaxants, and other drugs. The main outcome was the overall 15-item Quality of Recovery (QoR-15) survey score 24 hours after surgery. Results: A total of 1916 patients were scanned, and 1218 patients were included in the analysis: 392 in the OSA group and 826 in the control group. The QoR-15 global score measured 24 hours after surgery was 119.29 ± 3.25 in the OSA group and 113.87 ± 3.44 in the control group (P < 0.001). The OSA group had lower numeric rating scale scores 24 hours and 72 hours after surgery (P < 0.001) than the control group. The median (interquartile range) postoperative mechanical ventilation time was 1.0 (0–5) hours in the OSA group and 8.0 (6–14) hours in the control group (P < 0.001), and the duration of hospitalization was 11.5 (9–14) days and 12 (10–14) days, respectively (P = 0.012). Conclusion: OSA based on ultrasound-guided nerve blocks significantly improved QoR-15 scores after cardiac surgery and is expected to be a reasonable analgesic protocol to improve the prognosis of cardiac patients.

The heart is the central organ of the human circulatory system. Both congenital and acquired structural changes in the heart can lead to hemodynamic alterations affecting the function of various organs, including the brain. Recent advancements in magnetic resonance imaging (MRI) have provided further evidence of the heart’s influence on the brain. Investigating this connection is crucial for understanding the pathological mechanisms through which cardiac abnormalities contribute to brain-related diseases, and providing additional support for the heart-brain axis theory. Herein, the correlation between heart disease and brain structural changes and complications, determined through brain MRI, is discussed, and the key genes involved in these processes are summarized, to explore the pathophysiological mechanisms underlying heart-brain diseases. These insights may provide a basis for screening and intervening in patients with neurological complications arising from cardiac conditions.

Cardiovascular disease remains a leading cause of death and disability worldwide. Heart failure (HF) is the end stage of various cardiovascular diseases. Despite recent advancements in understanding of HF pathogenesis and treatment, the prognosis of patients with HF remains poor. Inflammation is a key player in the development of HF, and its role in the pathogenesis of HF has been extensively studied. Inflammation is associated with elevated HF risk and adverse prognosis. Targeting cardiac inflammation has been suggested as a promising treatment strategy for HF. However, almost all clinical trials on the anti-inflammatory treatment of HF have not indicated improved clinical outcomes, and some have reported deterioration of the condition, possibly because of limited understanding of the specific role of inflammation in HF. The summary of inflammatory mechanisms contributing to the pathogenesis of different HF types, current anti-inflammation therapies for HF, and the results of clinical trials could provide new perspectives for understanding and targeting the role of inflammation in HF through the development of effective clinical therapeutic strategies.

Cardiac rehabilitation (CR) remains an integral part of heart failure (HF) management, yet certain groups of patients with HF, particularly those with implantable devices, and those who are older and/or frail, are often precluded from CR. We performed a narrative review discussing the benefits of CR in these groups of patients, highlighting evidence from the existing literature. We further discuss special considerations for this patient group, including CR implementation for their long-term management. Hesitancy in referring vulnerable groups of patients with HF, specifically those with advanced HF, has led to poor outcomes in this patient cohort. However, we discuss the growing evidence supporting the use of CR, thus demonstrating the importance of HF services working closely with multi-disciplinary teams to better integrate CR into existing HF programs.

Aortic dissection is a life-threatening condition with complex immunological underpinnings. This study was aimed at exploring the causal relationships among immune cells, inflammatory proteins, and aortic dissection, through Mendelian randomization analysis. We used a two-step Mendelian randomization approach to assess potential mediators, focusing on the roles of blood immune cells and inflammatory proteins. We analyzed GWAS data for 731 immune cell traits, 91 inflammatory proteins, and aortic dissection. Single-nucleotide polymorphisms were used as instrumental variables, and analyses were conducted with inverse variance weighting and sensitivity tests to ensure robustness. Our results identified 11 immune cells, including myeloid dendritic cells and monocytes, with significant protective or risk-enhancing effects on aortic dissection. Specifically, CD62L-CD86+ myeloid dendritic cells and CD86+ myeloid dendritic cells demonstrated protective effects, whereas CD14+ CD16+ monocytes were identified as risk factors. Furthermore, the inflammatory protein TRAIL mediated the relationships between specific immune cell types and aortic dissection. Monocyte cell count was identified as a key mediator between myeloid dendritic cells and aortic dissection, thus revealing an immune-mediated pathway that might potentially be targeted for therapeutic intervention. These findings provide new insights into the immunological mechanisms contributing to aortic dissection.

Patients with chronic kidney disease (CKD) often encounter cardiovascular complications, most commonly coronary heart disease. Although coronary artery bypass grafting is an effective treatment for this condition, many patients experience cognitive dysfunction after cardiac surgery. The complex interactions among functional status, general anesthesia, cardiopulmonary bypass, and surgical trauma in patients with CKD elevate the risk of neurological issues and increase the mortality rates after surgery. Consequently, both quality of life and overall prognosis are significantly affected. By reviewing recent research on postoperative cognitive dysfunction in patients with CKD, we sought to clarify the underlying mechanisms affecting this population and gain theoretical insights to help decrease perioperative CKD occurrence.