Search Results (6)

Background: Ischemic heart disease (IHD) impacts the quality of life and is the most frequently reported cause of morbidity and mortality globally. Aims: To assess the changes in the exhaled volatile organic compounds (VOCs) in patients with vs. without ischemic heart disease (IHD) confirmed by stress computed tomography myocardial perfusion (CTP) imaging. Objectives: IHD early diagnosis and management remain underestimated due to the poor diagnostic and therapeutic strategies including the primary prevention methods. Materials and Methods: A single center observational study included 80 participants. The participants were aged ≥ 40 years and given an informed written consent to participate in the study and publish any associated figures. Both groups, G1 (n = 31) with and G2 (n = 49) without post stress-induced myocardial perfusion defect, passed cardiologist consultation, anthropometric measurements, blood pressure and pulse rate measurements, echocardiography, real time breathing at rest into PTR-TOF-MS-1000, cardio-ankle vascular index, bicycle ergometry, and immediately after performing bicycle ergometry repeating the breathing analysis into the PTR-TOF-MS-1000, and after three minutes from the end of the second breath, repeat the breath into the PTR-TOF-MS-1000, then performing CTP. LASSO regression with nested cross-validation was used to find the association between the exhaled VOCs and existence of myocardial perfusion defect. Statistical processing performed with R programming language v4.2 and Python v.3.10 [^R], STATISTICA program v.12, and IBM SPSS v.28. Results: The VOCs specificity 77.6% [95% confidence interval (CI); 0.666; 0.889], sensitivity 83.9% [95% CI; 0.692; 0.964], and diagnostic accuracy; area under the curve (AUC) 83.8% [95% CI; 0.73655857; 0.91493173]. Whereas the AUC of the bicycle ergometry 50.7% [95% CI; 0.388; 0.625], specificity 53.1% [95% CI; 0.392; 0.673], and sensitivity 48.4% [95% CI; 0.306; 0.657]. Conclusions: The VOCs analysis appear to discriminate individuals with vs. without IHD using machine learning models. Other: The exhaled breath analysis reflects the myocardiocytes metabolomic signature and related intercellular homeostasis changes and regulation perturbances. Exhaled breath analysis poses a promise result to improve the diagnostic accuracy of the physical stress tests using machine learning models. Full article

An 8-month-old intact male domestic shorthair cat was referred to the Emergency Service of the Veterinary Teaching Hospital (VTH) of the Department of Veterinary Science of the University of Parma (Italy) from the Parma municipal multi-cat shelter, during the winter season (January 2023), for lethargy, anorexia, hypothermia, and hypoglycemia. At the VTH, upon cardiologic examination, an increase in heart rate, under normal blood pressure conditions, was detected. Signalment, clinical history, basal metabolic panel (BMP), ultrasound investigations, and cytological findings were all consistent with a diagnosis of feline infectious peritonitis (FIP). FIP was confirmed in the effusive abdominal fluid by a molecular genetic test (real-time PCR for feline coronavirus RNA). The molecular genetic investigation also detected an FCoV S gene single-nucleotide mutation: biotype M1058L. At necropsy, an effusive collection was recorded in the abdomen, thoracic cavity, and pericardium sac. White parenchymal nodules, of about 1 mm diameter, were found on the surface and deep in the lungs, liver, kidneys, and heart. Histopathology revealed the typical FIP pyogranulomatous vasculitis and IHC confirmed the presence of the FIP virus (FIPV) antigen. The most relevant histopathological finding was the myocarditis/myocardial necrosis associated with the presence of the S gene-mutated FCoV (M1058L biotype). This is the first case of myocarditis in a cat positive for the FCoV/FIP M1058L biotype. Further studies are necessary to support the mutated FCoV M1058L biotype, as an uncommon, but possible, causative pathogen of myocarditis in FCoV/FIP-positive cats. Studies including several FCoV/FIP M1058L-positive cases could allow us to make a correlation with heart gross pathology, histopathology, and immunolocalization of the FCoV/FIP M1058L biotype in the myocardium. The investigation will potentially allow us to determine the effective tropism of the FCoV/FIP M1058L biotype for myocardiocytes or whether myocardiocyte lesions are evident in the presence of concomitant causes related to the patient, its poor condition, or external environmental distress such as cold season, and whether the aforementioned concomitant events are correlated. Full article

Myocardial fibrosis (MF) is a common pathological feature of many heart diseases and seriously threatens the normal activity of the heart. Jiaogulan (Gynostemma pentaphyllum) tea is a functional food that is commercially available worldwide. Gypensapogenin I (Gyp I), which is a novel dammarane-type saponin, was obtained from the hydrolysates of total gypenosides. It has been reported to exert a beneficial anti-inflammatory effect. In our study, we attempted to investigate the efficiency and possible molecular mechanism of Gyp I in cardiac injury treatment induced by ISO. In vitro, Gyp I was found to increase the survival rate of H9c2 cells and inhibit apoptosis. Combined with molecular docking and Western blot analysis, Gyp I was confirmed to regulate the TLR4/NF-κB/NLRP3 signaling pathway. In vivo, C57BL6 mice were subcutaneously injected with 10 mg/kg ISO to induce heart failure. Mice were given a gavage of Gyp I (10, 20, or 40 mg/kg/d for three weeks). Pathological alterations, fibrosis-, inflammation-, and apoptosis-related molecules were examined. By means of cardiac function detection, biochemical index analysis, QRT-PCR monitoring, histopathological staining, immunohistochemistry, and Western blot analysis, it was elucidated that Gyp I could improve cardiac dysfunction, alleviate collagen deposition, and reduce myocardial fibrosis (MF). In summary, we reported for the first time that Gyp I showed good myocardial protective activity in vitro and in vivo, and its mechanism was related to the TLR4/NF-κB/NLRP3 signaling pathway. Full article

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and catheter ablation, which can be used in symptomatic patients refractory to antiarrhythmic therapy. Pulmonary vein isolation (PVI) remains the cornerstone of any ablation procedure. A major limitation of current catheter ablation procedures is important to recognize because even when the PVI is performed in highly experienced centers, PVI reconnection was documented in about 20% of patients. Therefore, better technology is needed to improve ablation lesions. One of the novelties in recent years is pulsed filed ablation (PFA), a non-thermal energy that uses trains of high-voltage, very-short-duration pulses to kill the cells. The mechanism of action of this energy consists of creating pores in the myocardiocyte cell membrane in a highly selective and tissue-specific way; this leads to death of the target cells reducing the risk of damage to surrounding non-cardiac tissues. In particular during the animal studies, PVI and atrial lines were performed effectively without PV stenosis. Using PFA directly on coronary arteries, there was no luminal narrowing, there has been no evidence of incidental phrenic nerve injury, and finally, PFA has been shown not to injure esophageal tissue when directly applied to the esophagus or indirectly through ablation in the left atrium. The aim of this review is to report all published animal and clinical studies regarding this new technology to treat paroxysmal and persistent AF. Full article

In heart failure, iron deficiency is a common comorbid disease that negatively influences exercise tolerance, number of hospitalizations and mortality rate, and this is why iron iv supplementation is recommended. Little is known about the changes in iron-related proteins in the human HF myocardium. The purpose of this study was to assess iron-related proteins in non-failing (NFH) vs. failing (FH) human myocardium. The study group consisted of 58 explanted FHs; control consisted of 31 NFHs unsuitable for transplantation. Myocardial proteins expressions: divalent metal transporter (DMT-1); L-type calcium channel (L-CH); transferrin receptors (TfR-1/TfR-2); ferritins: heavy (FT-H) or light (FT-L) chain, mitochondrial (FT-MT); ferroportin (FPN), regulatory factors and oxidative stress marker: 4-hydroxynonenal (4-HNE). In FH, the expression in almost all proteins responsible for iron transport: DMT-1, TfR-1, L-CH, except TfR-2, and storage: FT-H/-L/-MT were reduced, with no changes in FPN. Moreover, 4-HNE expression (pg/mg; NFH 10.6 ± 8.4 vs. FH 55.7 ± 33.7; p < 0.0001) in FH was increased. HNE-4 significantly correlated with DMT-1 (r = −0.377, p = 0.036), L-CH (r = −0.571, p = 0.001), FT-H (r = −0.379, p = 0.036), also FPN (r = 0.422, p = 0.018). Reducing iron-gathering proteins and elevated oxidative stress in failing hearts is very unfavorable for myocardiocytes. It should be taken into consideration before treatment with drugs or supplements that elevate free oxygen radicals in the heart. Full article

T-LAK-cell-originated protein kinase (TOPK) is a PDZ-binding kinase (PBK) that was recently identified as a novel member of the mitogen-activated protein kinase (MAPK) family. It has been shown to play an important role in many cellular functions. However, its role in cardiac function remains unclear. Thus, we have herein explored the biological function of TOPK in myocardial ischemia/reperfusion (I/R) and oxidative stress injury in H9C2 cardiomyocytes. I/R and ischemic preconditioning (IPC) were induced in rats by 3-hour reperfusion after 30-min occlusion of the left anterior descending coronary artery and by 3 cycles of 5-min I/R. Hydrogen peroxide (H₂O₂) was used to induce oxidative stress in H9C2 cardiomyocytes. TOPK expression was analyzed by western blotting, RT-PCR, immunohistochemical staining, and immunofluorescence imaging studies. The effects of TOPK gene overexpression and its inhibition via its inhibitor HI-TOPK-032 on cell viability and Bcl-2, Bax, ERK1/2, and p-ERK1/2 protein expression were analyzed by MTS assay and western blotting, respectively. The results showed that IPC alleviated myocardial I/R injury and induced TOPK activation. Furthermore, H₂O₂ induced TOPK phosphorylation in a time-dependent manner. Interestingly, TOPK inhibition aggravated the H₂O₂-induced oxidative stress injury in myocardiocytes, whereas overexpression relieved it. In addition, the ERK pathway was positively regulated by TOPK signaling. In conclusion, our results indicate that TOPK might mediate a novel survival signal in myocardial I/R, and that its effect on anti-oxidative stress involves the ERK signaling pathway. Full article