International heart journal最新文献

This study probed into the mechanism of USP30 in mitophagy and pyroptosis during heart failure (HF).A cell model was constructed with oxygen-glucose deprivation (OGD), and an HF rat model was generated by permanently ligating the left anterior descending branch of the left coronary artery. Loss-of-function experiments were carried out with the use of si-USP30 and si-PINK1. Cell viability was assessed using MTT, and cell death was measured by LDH release. Mitophagy was analyzed using immunofluorescence double staining, mitochondrial membrane potential (MMP) changes were detected by JC-1, and ROS levels were measured using specific kits. WB was performed to detect autophagy markers LC3II/I and p62, pyroptosis-related proteins NLRP3, active-caspase-1, GSDMD-N, and PINK1/Parkin protein expression. The inflammatory cytokines IL-18 and IL-1β were measured by ELISA. Histological changes and fibrosis in heart tissue were observed by H&E and Masson staining.USP30 was expressed abundantly in OGD-induced H9C2 cells and HF rats. USP30 knockdown enhanced viability, mitophagy, MMP, and LC3II/I but reduced death, NLRP3, p62, active-caspase-1, and GSDMD-N protein expression, and ROS, IL-1β, and IL-18 levels in OGD-treated H9C2 cells. PINK1 knockdown or mitophagy inhibition abolished the effects of USP30 knockdown on mitophagy and pyroptosis in OGD-treated H9C2 cells. Additionally, USP30 knockdown improved cardiac function and mitophagy while repressing pyroptosis in HF rats.In summary, USP30 controls mitophagy and pyroptosis in HF by mediating the PINK1/Parkin pathway.

Acute coronary syndrome (ACS) is a rare complication of infective endocarditis (IE) and is associated with high mortality. Typically, coronary artery occlusion is a complication of bacterial autologous valve IE. We present the case of a 74-year-old woman with a history of aortic valve replacement for aortic stenosis who was receiving immunosuppressive therapy for rheumatoid arthritis. Upon admission, she was diagnosed with ST-elevation myocardial infarction (STEMI), and coronary angiography (CAG) revealed complete occlusion in the terminal branches of the left circumflex coronary artery (LCX #12 and #14). On day 3 of admission, three-dimensional transesophageal echocardiography (3D-TEE) was performed, and vegetation was detected, leading to IE diagnosis.The patient underwent prosthetic valve replacement on day 4. Subsequent blood cultures grew Candida albicans, and histopathological examination using Grocott staining confirmed the presence of Grocott-positive fungi within the vegetation, leading to a definitive diagnosis of prosthetic valve endocarditis (PVE) caused by Candida albicans; this management resulted in favorable outcomes. The present case suggests that fungal PVE can also complicate STEMI, and real-time 3D-TEE was instrumental in diagnosing and accurately assessing the vegetation in this condition.

In patients diagnosed with ST-segment elevation myocardial infarction (STEMI), despite exhibiting normal patency in the culprit arteries following percutaneous coronary intervention (PCI), coronary microvessels do not recover adequately, leading to microvascular dysfunction (MVD). Limited data are available regarding microcirculation assessed through invasive measures during the midterm period. This study aimed to investigate the assessment of MVD in STEMI patients using the index of microvascular resistance (IMR) during the midterm period.We prospectively evaluated 41 patients with STEMI who underwent PCI. IMR was measured by placing a coronary pressure wire with intravenous adenosine at 1 week as the acute phase and at 6 months after primary PCI as the midterm period. An improvement in IMR was observed from baseline to follow-up, with values changing from 30.00 (15.00-45.50) to 19.00 (10.50-30.50) (P = 0.020). The degree of MVD significantly decreased during follow-up (from 61.0% to 34.1%, McNemar's test: P = 0.016). Compared to patients with normal microcirculation, those with MVD (IMR > 25) at midterm follow-up exhibited significantly elevated levels of brain natriuretic peptide (180.25 [68.25-370.65] pg/mL versus 75.90 [18.70-169.70] pg/mL, P = 0.043) and prolonged symptom-onset-to-balloon time (727.00 [213.50-1170.00] minutes versus 186.00 [125.00-316.00] minutes, P = 0.002).These findings indicate that the extent of MVD 6 months post-PCI has significantly diminished compared to discharge levels and is associated with symptom-onset-to-balloon time. Therefore, MVD in patients with STEMI can potentially improve in the midterm under specific circumstances.

The psoas muscle area (PMA) and rectus femoris muscle area (RFMA) have been used to estimate whole-body muscle mass in elderly patients. However, it is unclear whether combining these measurements can improve the predictive ability of traditional risk factors for adverse clinical events in elderly patients with aortic valve stenosis (AVS). We analyzed data from 153 patients with AVS who underwent transcatheter aortic valve replacement (TAVR), and measured PMA and RFMA using computed tomography (CT) before the procedure. This study assessed a composite of adverse clinical events including all-cause death and heart failure (HF) requiring hospitalization for up to 3 years after TAVR. During the follow-up period, 31 patients experienced adverse clinical events (19 died, and 12 had HF). The multivariate Cox hazards analysis demonstrated that patients exhibiting lower PMA (males with < 3.36 cm²/m² and females with < 2.52 cm²) and lower RFMA (males with < 3.26 cm²/m² and females with < 3.15 cm²/m²) had a higher probability of experiencing adverse clinical events compared to those with higher PMA and RFMA values, whether in combination or alone (P < 0.05). Additionally, net reclassification improvement (NRI) and integrated discrimination improvement (IDI) analyses showed that the combination of lower PMA and RFMA had a greater incremental effect on the predictive value of clinical risk factors for adverse clinical events. Therefore, the combined measurement of skeletal muscles using CT scans may be a valuable tool for assessing the risk of AVS in elderly patients undergoing TAVR.

Heart failure is associated with poor quality of life and mortality, and the prevalence of heart failure is increasing together with aging of the population. Approximately 50% of patients with heart failure present as HFpEF, and the survival of HFpEF patients is as poor as that of HFrEF patients. Furthermore, therapies for HFpEF are limited and are not proven to improve prognosis, except for SGLT2 inhibitors. HFpEF is more prevalent in women and the risk of HFpEF increases more drastically with aging in women than men. HFpEF is a syndrome with multiple comorbidities, and modeling HFpEF in animal models has been attempted by reproducing major comorbidities highly associated with human HFpEF. In order to elucidate the female-specific mechanisms of HFpEF, we established a new mouse model by applying additional stressors on the basis of obesity and post-menopausal model. Ovariectomy or epinephrine injection was added to a high-fat diet-induced obesity model. Ovariectomy exacerbates obesity and serial epinephrine injections ameliorate obesity. Exercise tolerance in treadmill testing was inversely correlated with body weight, and was reduced more than expected based on body weight in mice that underwent ovariectomy and epinephrine injection (OVX + Epi group). In a pressure-volume analysis, the end-diastolic pressure at afterload increase was significantly high in OVX + Epi mice, which is considered to reflect left ventricular diastolic dysfunction. In conclusion, this study demonstrated that epinephrine and depletion of female sex hormone by ovariectomy reproduce the pathology of obesity-induced cardiac phenotype, which might represent an early phase of HFpEF conditions.

The prognosis of patients with aortic aneurysm (AA) and cardiovascular comorbidities remains suboptimal compared to that of the general population, highlighting the need for reliable mortality biomarkers. Apolipoprotein A2 (ApoA2) is a structural and functional component of high-density lipoprotein cholesterol (HDL-C), but its relevance to all-cause mortality remains unclear. Therefore, we investigated the prognostic value of ApoA2 in patients with AA after surgical repair. ApoA2 levels were measured in 203 consecutive patients with AA who were successfully treated with surgical repair. The primary focus was the predictive value of ApoA2 levels for mortality events. During a median follow-up of 3.5 years, mortality events were observed in 32 patients (15.8 %). Patients with mortality events had lower ApoA2 levels than the survivors [22.0 (19.0, 25.0) mg/dL versus 25.0 (22.0, 29.0) mg/dL, P < 0.001]. ApoA2 was inversely correlated with age, BNP, C-reactive protein (CRP), and fibrinogen levels and positively correlated with eGFR. Multivariate Cox analysis identified ApoA2 (HR 0.92, 95% CI 0.86-0.99), eGFR < 60 mL/minute/1.73 m² (HR 3.49, 95% CI 1.49-8.20), COPD (HR 2.63, 95% CI, 1.07-6.49), and thoracic AA (HR 2.54, 95% CI 1.25-5.18) as independent mortality predictors. Moreover, the addition of ApoA2 levels significantly improved the discriminative ability of the baseline risk factors in predicting mortality (AUC 0.79 versus 0.73, P = 0.04). Therefore, ApoA2 is a potential biomarker for predicting long-term mortality in patients with AA following surgical repair, and may contribute to improved risk stratification in this high-risk population.

This study aimed to investigate the association between brain-derived neurotrophic factor (BDNF) levels and the no-reflow phenomenon in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI).This retrospective study included 100 patients with STEMI from January 2023 to December 2023. Patients were classified into an observation group (slow flow or no-reflow) and a control group (normal flow) based on the post-PCI Thrombolysis in Myocardial Infarction (TIMI) flow grades.The observation group exhibited significantly higher BDNF and creatine kinase-MB (CK-MB) levels and significantly lower left ventricular ejection fraction (LVEF) than the control group (P < 0.05). Logistic regression analysis identified diabetes, higher Killip class, lower eGFR, reduced LVEF, multivessel disease, high thrombus burden, elevated B-type natriuretic peptide (BNP), and increased BDNF levels as independent predictors of the no-reflow phenomenon (P < 0.05). Correlation analysis showed that BDNF levels were negatively correlated with TIMI flow grade (r = -0.303, P < 0.01) and LVEF (r = -0.717, P < 0.01) and positively correlated with left ventricular internal dimension in systole (LVIDs; r = 0.509, P < 0.01), STEMI onset time (r = 0.685, P < 0.01), CK-MB (r = 0.689, P < 0.01), TnT (r = 0.708, P < 0.01), and TnI (r = 0.781, P < 0.01).Higher BDNF levels were significantly associated with impaired myocardial perfusion and reduced cardiac function, as indicated by a lower pre-PCI LVEF. These findings suggest that BDNF may serve as a potential biomarker for the no-reflow phenomenon in patients with STEMI. Further studies are needed to clarify the relationship between BDNF levels and post-PCI recovery of cardiac function.

Chronic heart failure (CHF) triggers a cascade of events involving parthanatos and pyroptosis, culminating in cellular malfunction, inflammation, and tissue degeneration. This study aims to inquire into the inherent mechanism of chrysophanol (CHR) in the treatment of CHF.In vitro, we cultured the rat embryonic cardiomyocyte cell line H9c2. Parthanatos was initiated through N-methyl-N'-nitro-N'-nitrosoguanidine (MNNG) induction, followed by treatment with varying concentrations of CHR. The evaluation of parthanatos and pyroptosis in cardiomyocytes was assessed by western blotting. In vivo, the transverse aortic constriction (TAC) model was used to simulate CHF. The hemodynamic indices were performed to evaluate cardiac function in rats. The degree of inflammatory cell infiltration and fibrosis within cardiac tissue was assessed using hematoxylin and eosin staining and Masson's trichrome staining, respectively. Cardiac tissues were obtained and subjected to immunohistochemical analysis to assess PARP-1 expression. Subsequently, dual immunofluorescence staining (caspase-1 and NLRP3) was conducted, aiming to comprehensively evaluate the status of parthanatos and pyroptosis in the cardiac tissues of rats.In contrast to the MNNG or TAC group, the groups administered with CHR exhibited an inhibitory effect on Reactive oxygen species (ROS) expression, as well as parthanatos and pyroptosis proved by cell and animal experiments (P < 0.05). The reduced expression of PAR, PARP-1, AIF, NLRP3, IL-1β, caspase-1, and cleaved-GSDMD compared with the MNNG or TAC group proved it (P < 0.05). Moreover, compared with the TAC group, CHR significantly improved the cardiac histology of TAC rats. These findings collectively suggested the potential of CHR in ameliorating CHF.CHR may mitigate CHF in rats by modulating ROS-mediated parthanatos and pyroptosis.

A 66-year-old elderly woman undergoing regular dialysis for chronic renal failure was admitted to our hospital with acute pancreatitis. Coronary angiography revealed stress cardiomyopathy and cardiogenic shock. The patient was successfully treated with early Continuous Renal Replacement Therapy (CRRT). After 3 weeks of hospitalization, her left ventricular ejection fraction improved significantly.