World Journal of Cardiology最新文献

As a non-communicable disease, cardiovascular disorders have become the leading cause of death for men and women. Of additional concern is that cardiovascular disease is linked to chronic comorbidity disorders that include nonalcoholic fatty liver disease (NAFLD). NAFLD, also termed metabolic-dysfunction-associated steatotic liver disease, is the greatest cause of liver disease throughout the world, increasing in prevalence concurrently with diabetes mellitus (DM), and can progress to nonalcoholic steatohepatitis that leads to cirrhosis and liver fibrosis. Individuals with metabolic disorders, such as DM, are more than two times likely to experience cardiac disease, stroke, and liver disease that includes NAFLD when compared individuals without metabolic disorders. Interestingly, cardiovascular disorders and NAFLD share a common underlying cellular mechanism for disease pathology, namely the silent mating type information regulation 2 homolog 1 (SIRT1; Saccharomyces cerevisiae). SIRT1, a histone deacetylase, is linked to metabolic pathways through nicotinamide adenine dinucleotide and can offer cellular protection though multiple avenues, including trophic factors such as erythropoietin, stem cells, and AMP-activated protein kinase. Translating SIRT1 pathways into clinical care for cardiovascular and hepatic disease can offer significant hope for patients, but further insights into the complexity of SIRT1 pathways are necessary for effective treatment regimens.

Heart failure (HF) is a major global health challenge, particularly among individuals with type 2 diabetes mellitus (T2DM), who are at significantly higher risk of developing HF. Diabetic cardiomyopathy, a unique form of heart disease, often progresses silently until advanced stages. Recent research has focused on sodium-dependent glucose transporter 2 inhibitors (SGLT2i), originally developed for hyperglycemia, which have shown potential in reducing cardiovascular risks, including HF hospitalizations, irrespective of diabetic status. In this editorial we comment on the article by Grubić Rotkvić et al published in the recent issue of the World Journal of Cardiology. The investigators examined the effects of SGLT2i on myocardial function in T2DM patients with asymptomatic HF, finding significant improvements in stroke volume index and reductions in systemic vascular resistance, suggesting enhanced cardiac output. Additionally, SGLT2i demonstrated anti-inflammatory and antioxidant effects, as well as blood pressure reduction, though the study's limitations-such as small sample size and observational design-necessitate larger randomized trials to confirm these findings. The study underscores the potential of early intervention with SGLT2i in preventing HF progression in T2DM patients.

Background: The combination of polycythemia vera (PV) with pathological cardiac hypertrophy is uncommon. In this study, we describe a case of PV accompanied by pathological cardiac hypertrophy. It is hypothesized that the pronounced cardiac hypertrophy in this patient has a strong connection with PV.

Case summary: In 2021, a 34-year-old Chinese man experienced chest constriction, shortness of breath, and palpitations during vigorous activity. Each episode lasted several minutes and resolved spontaneously following cessation of vigorous activity. He occasionally experienced syncope and vertigo without a headache. He underwent cardiac magnetic resonance imaging and was diagnosed with "hypertrophic cardiomyopathy (HCM)". He was discharged after receiving symptomatic treatment, which resulted in an improvement. He presented to our department with chest constriction, shortness of breath, and respiratory distress for one month while climbing to the second floor in 2023. His blood pressure was 180/100 mmHg at the time of admittance, and he was receiving antihypertensive treatment. He had a history of PV for 2 years without treatment. Symptomatic treatment was implemented concurrently with the administration of hydroxyurea upon admission. Good blood pressure control was observed during the long-term follow-up, and echocardiography did not reveal any progression of myocardial hypertrophy.

Conclusion: Clinicians managing PV patients should remain highly vigilant regarding the risks of thrombosis and cardiovascular complications, particularly in those with refractory hypertension.

We comment on an article by Grubić Rotkvić et al published in the recent issue of the World Journal of Cardiology. We specifically focused on possible factors affecting the therapeutic effectiveness of sodium-dependent glucose transporter inhibitors (SGLT2i) in patients with type 2 diabetes mellitus (T2DM) and their impact on comorbidities. SGLT2i inhibits SGLT2 in the proximal tubules of the kidneys, lowering blood glucose levels by inhibiting glucose reabsorption by the kidneys and causing excess glucose to be excreted in the urine. Previous studies have demonstrated a role of SGLT2i in cardiovascular function in patients with diabetes who take metformin but still have poor glycemic control. In addition, SGLT2i has been shown to be effective in anti-apoptosis, weight loss, and cardiovascular protection. Accordingly, it is feasible to treat patients with T2DM with cardiovascular or renal diseases using SGLT2i.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD), particularly in the presence of liver fibrosis, increases the risk of cardiovascular morbidity and mortality, but the nature of the cardio-hepatic interaction in the context type 2 diabetes mellitus (T2DM) is not fully understood.

Aim: To evaluate the changes in cardiac morphology and function in patients with T2DM and MASLD-associated liver fibrosis.

Methods: T2DM patients with MASLD underwent a medical evaluation that included an assessment of lifestyle, anthropometric measurements, vital signs, an extensive laboratory panel, and a standard echocardiography. Liver fibrosis was evaluated using two scores [Fibrosis-4 (FIB4) and Non-alcoholic fatty liver disease-Fibrosis Score (NFS)], and subjects were classified as having advanced fibrosis, no fibrosis, or an indeterminate risk. The correlations between structural and functional cardiac parameters and markers of liver fibrosis were evaluated through bivariate and multiple regression analyses. Statistical significance was set at P < 0.05.

Results: Data from 267 T2DM-MASLD subjects with complete assessment was analyzed. Patients with scores indicating advanced fibrosis exhibited higher interventricular septum and left ventricular (LV) posterior wall thickness, atrial diameters, LV end-systolic volume, LV mass index (LVMi), and epicardial adipose tissue thickness (EATT). Their mean ejection fraction (EF) was significantly lower (49.19% ± 5.62% vs 50.87% ± 5.14% vs 52.00% ± 3.25%; P = 0.003), and a smaller proportion had an EF ≥ 50% (49.40% vs 68.90% vs 84.21%; P = 0.0017). Their total and mid LV wall motion score indexes were higher (P < 0.05). Additionally, they had markers of diastolic dysfunction, with a higher E/e' ratio [9.64 ± 4.10 vs 8.44 (2.43-26.33) vs 7.35 ± 2.62; P = 0.026], and over 70% had lateral e' values < 10 cm/second, though without significant differences between groups. In multiple regression analyses, FIB4 correlated with left atrium diameter (LAD; β = 0.044; P < 0.05), and NFS with both LAD (β = 0.039; P < 0.05) and right atrium diameter (β = 0.041; P < 0.01), Moreover, LVMi correlated positively with age and EATT (β = 1.997; P = 0.0008), and negatively with serum sex-hormone binding protein (SHBP) concentrations (β = -0.280; P = 0.004). SHBP also correlated negatively with LAD (β = -0.036; P < 0.05).

Conclusion: T2DM patients with markers of MASLD-related liver fibrosis exhibit lower EF and present indicators of diastolic dysfunction and cardiac hypertrophy. Additionally, LVMi and LAD correlated negatively with serum SHBP concentrations.

Heart failure (HF) is a chronic disease associated with high morbidity and mortality rates. Renin-angiotensin-aldosterone system blockers (including angiotensin receptor/neprilysin inhibitors), beta-blockers, and mineralocorticoid receptor blockers remain the mainstay of pharmacotherapy for HF with reduced ejection fraction (HFrEF). However, despite the use of guideline-directed medical therapy, the mortality from HFrEF remains high. HF with preserved ejection fraction (HFpEF) comprises approximately half of the total incident HF cases; however, unlike HFrEF, there are no proven therapies for this condition. Sodium glucose cotransporter-2 inhibitors (SGLT-2is) represent a new class of pharmacological agents approved for diabetes mellitus (DM) that inhibit SGLT-2 receptors in the kidney. A serendipitous finding from seminal trials of SGLT-2is in DM was the significant improvement in renal and cardiovascular (CV) outcomes. More importantly, the improvement in HF hospitalization (HHF) in the CV outcomes trials of SGLT-2is was striking. Multiple mechanisms have been proposed for the pleiotropic effects of SGLT-2is beyond their glycemic control. However, as patients with HF were not included in any of these trials, it can be considered as a primary intervention. Subsequently, two landmark studies of SGLT-2is in patients with HFrEF, namely, an empagliflozin outcome trial in patients with chronic HF and a reduced ejection fraction (EMPEROR-Reduced) and dapagliflozin and prevention of adverse outcomes in HF (DAPA-HF), demonstrated significant improvement in HHF and CV mortality regardless of the presence of DM. These impressive results pitchforked these drugs as class I indications in patients with HFrEF across major guidelines. Thereafter, empagliflozin outcome trial in patients with chronic HF with preserved ejection fraction (EMPEROR-Preserved) and dapagliflozin evaluation to improve the lives of patients with preserved ejection fraction HF (DELIVER) trials successively confirmed that SGLT-2is also benefit patients with HFpEF with or without DM. These results represent a watershed as they constitute the first clinically meaningful therapy for HFpEF in the past three decades of evolution of HF management. Emerging positive data for the use of SGLT-2is in acute HF and post-myocardial infarction scenarios have strengthened the pivotal role of these agents in the realm of HF. In a short span of time, these classes of drugs have captivated the entire scenario of HF.

Background: Arterial cannulation sites for the surgical repair of type A aortic dissection (AAD) have evolved from right axillary artery (AA) cannulation to bilateral carotid artery (CA) based of femoral artery (FA) cannulation. Postoperative descending aorta remodeling is closely linked to the false lumen area ratio (FLAR), defined as false lumen area/aortic area, as well as to the incidence of renal replacement therapy (RRT).

Aim: To investigate the effect of the updated arterial cannulation strategy on descending aortic remodeling.

Methods: A total of 443 AAD patients who received FA combined cannulation between March 2015 and March 2023 were included in the study. Of these, 209 received right AA cannulation and 234 received bilateral CA cannulation. The primary outcome was the change in FLAR, as calculated from computed tomography angiography in three segments of the descending aorta: Thoracic (S1), upper abdominal (S2), and lower abdominal (S3). Secondary outcomes were the incidence of RRT and the serum inflammation response, as observed by the levels of high sensitivity C reaction protein (hs-CRP) and Interleukin-6 (IL-6).

Results: The postoperative/preoperative ratio of FLAR in S2 and S3 was higher in the AA group compared to the CA group (S2: 0.80 ± 0.08 vs 0.75 ± 0.07, P < 0.001; S3: 0.57 ± 0.12 vs 0.50 ± 0.12, P < 0.001, respectively). The AA group also had a significantly higher incidence of RRT (19.1% vs 8.5%, P = 0.001; odds ratio: 2.533, 95%CI: 1.427-4.493) and higher levels of inflammation cytokines 24 h after the procedure [hr-CRP: 117 ± 17 vs 104 ± 15 mg/L; IL-6: 129 (103, 166) vs 83 (69, 101) pg/mL; both P < 0.001] compared to the CA group.

Conclusion: The CA cannulation strategy was associated with better abdominal aorta remodeling after AAD repair compared to AA cannulation, as observed by a greater change in FLAR and lower incidence of RRT.

In heart failure with preserved ejection fraction, significant left ventricular diastolic abnormalities are present, despite a normal systolic ejection fraction. This article will consider whether this is consistent with the law of conservation of energy, also know as the first law of thermodynamics.

Background: Unroofed coronary sinus (UCS) is a rare subtype of atrial septal defect. It is frequently associated with a persistent left superior vena cava and is often part of a more intricate cardiac malformation.

Case summary: This report describes a rare case of an adolescent patient with UCS featuring atrial situs solitus, absence of the right superior vena cava and a persistent left superior vena cava draining into the left atrium consistent with total unroofing of the coronary sinus. This was associated with concurrent severe mitral insufficiency secondary to redundant and prolapsing leaflets, and a substantial left-to-right shunt across the coronary sinus orifice. A comprehensive examination of the existing literature is included, shedding light on the diagnostic challenges of UCS and describing the available surgical options within the context of mitral valve surgery.

Conclusion: UCS is a complex condition requiring careful consideration of associated anomalies and a tailored surgical approach.

In this letter, we comment on a recent case report by Sun et al in the World Journal of Cardiology. The report describes the successful management of a rare complication: The unloading or detachment of a bioresorbable stent (BRS) during percutaneous coronary intervention (PCI) in a male patient. The unloading of BRS was detected via angiography and intravascular ultrasound (IVUS) imaging of the left coronary artery and left anterior descending artery. Although this case is interesting, the authors' report lacked crucial details. Specifically, insufficient information about the type of BRS used, potential causes of BRS unloading, or whether optical coherence tomography (OCT) imaging for coronary arteries was performed before, during, or after PCI. The OCT imaging of coronary arteries before PCI can potentially prevent BRS unloading due to its higher resolution compared to IVUS. In addition, despite detecting myocardial bridging during the PCI, the authors did not provide any details regarding this variation. Here we discuss the various types of BRS, the importance of OCT in PCI, and the clinical relevance of myocardial bridging.