Myocardial Infarction Group Research Articles

18F-NaF PET uptake characteristics of coronary artery culprit lesions in a cohort of patients of acute coronary syndrome with ST-elevation myocardial infarction and chronic stable angina: A hybrid fluoride PET/CTCA study

Background18F-NaF PET/CT identifies high-risk plaques due to active calcification in coronary arteries with potential to characterize plaques in ST-elevation myocardial infarction (MI) and chronic stable angina (CSA) patients. MethodsTwenty-four MI and 17 CSA patients were evaluated with 18F-NaF PET/CTCA for SUVmax and TBR values of culprit and non-culprit plaques in both groups (inter-group and intra-group comparison), and pre- and post-interventional MI plaques sub-analysis. ResultsCulprit plaques in MI patients had significantly higher SUVmax (1.6; IQR 0.6 vs 1.3; IQR 0.3, P = 0.03) and TBR (1.4; IQR 0.6 vs 1.1; IQR 0.4, P = 0.006) than culprit plaques of CSA. Pre-interventional culprit plaques of MI group (n = 11) revealed higher SUVmax (P = 0.007) and TBR (P = 0.008) values than culprit CSA plaques. Culprit plaques showed significantly higher SUVmax (P = 0.006) and TBR (P = 0.0003) than non-culprit plaques in MI group, but without significant difference between culprit and non-culprit plaques in CSA group. With median TBR cutoff value of 1.4 in MI culprit plaques, 6/7 plaques (85.7%) among the event prone non-culprit lesions had TBR values > 1.4 in CSA group. ConclusionThe study shows higher SUVmax and TBR values in MI culprit plaques and comparable TBR values for event prone plaques of CSA group in identifying high-risk plaques.

LuQi Formula Ameliorates Myocardial Fibrosis by Suppressing TLR4/MyD88/NF-κB Pathway and NLRP3 Inflammasome Activation in Mice with Myocardial Infarction.

Background Myocardial fibrosis caused by myocardial infarction (MI) is the key factor leading to cardiac remodeling; nod-like receptor family pyrin domain-containing 3 (NLRP3) plays an important role in regulation of myocardial injury; however, its relationship with TLR4/MyD88/NF-κB signaling pathway is largely unreported. In recent years, traditional Chinese medicine (TCM) prevention and treatment of cardiovascular diseases has shown its unique advantages and broad application prospects. LuQi Formula (LQF) has been used for more than 20 years in Shuguang Hospital (Shanghai, China), and it was confirmed that it can improve the clinical symptoms of patients after MI. Here, we investigated the mechanism of LQF by suppressing NLRP3 inflammasome activation and TLR4/MyD88/NF-κB pathway in mice with MI. Purpose The purpose of this study was to verify the positive effects of the LQF in ameliorating myocardial fibrosis and inflammasome infiltration in the MI mice in vivo. Methods Forty mice were randomized into four groups: the sham group, the MI group, the LQF group, and the perindopril group (n = 10 per group). Left anterior descending (LAD) coronary artery ligation was performed in all groups except the sham group. The mice were treated with LQF after MI. After 4 weeks, LDH, cTnI, IL-1β, and IL-18 were measured by enzyme-linked immunosorbent assay (ELISA) kit, and cardiac function was evaluated by echocardiography. Hematoxylin and eosin (H&E) and Masson staining were used to evaluate the myocardial injury and fibrosis. Western blot was used to evaluate the expression of collagen I, α-SMA, NLRP3 inflammasome, and TLR4/MyD88/NF-κB signaling pathway. Immunohistochemical analysis was used to further detect the expression of Fibronectin, α-SMA, collagen I, collagen III, NLRP3, and NF-κB in myocardial tissue. Results Compared with the MI group, the ejection fraction (EF) and fractional shortening (FS) in the LQF group were significantly improved, while the left ventricular end diastolic diameter (LVEDd) and left ventricular internal dimension systole (LVIDs) were significantly decreased. The representative staining of H&E and Masson showed that treatment with LQF could effectively reduce myocardial injury and fibrosis. ELISA results showed that serum LDH, cTnI, TNF-α, IL-18, and IL-1β in LQF group were significantly lower than those in MI group. The western blot results showed that the expressions of collagen I and α-SMA were decreased significantly in the LQF group. Moreover, the expressions of NLRP3 inflammasome and TLR4/MyD88/NF-κB signaling pathway were downregulated in the LQF treatment group. Conclusion Our results suggested that LQF could significantly improve cardiac function and ameliorate myocardial fibrosis. In addition, we found that LQF could downregulate the TLR4/MyD88/NF-κB signaling pathway and then inhibit the activation of NLRP3 inflammasome, suggesting that LQF alleviated cardiac fibrosis by decreasing the TLR4/MyD88/NF-κB signaling pathway and then inhibited NLRP3 inflammasome activation in MI mice, which indicates potential therapeutic effect of LQF on patients with MI.

Predictive value of left ventricular ejection fraction for the occurrence of postoperative myocardial infarction after coronary endarterectomy in patients with diffuse coronary artery disease

Objective: To investigate the predictive value of ejection fraction for the postoperative myocardial infarction after coronary endarterectomy (CE) in patients with diffuse coronary artery disease (DCAD). Methods: Patients who underwent cardiac artery bypass graft (CABG) surgery and CE in Beijing Anzhen Hospital affiliated to Capital Medical University from May 2018 to December 2020 were enrolled in this prospective observational study. Baseline features including age, sex and echocardiography parameters were obtained. Left ventricular ejection fraction(EF) was measured by echocardiography. The patients were divided into postoperative myocardial infarction (PMI) group and non-PMI group according to PMI occurrence. Linear regression analysis, logistic regression model, and receiver operating characteristic(ROC) curve were used to analyze the correlation between left ventricular ejection fraction and PMI and the influencing factors. Results: A total of 120 patients were enrolled in the study. There were 32 patients (27%) in the PMI group (male 27(84%), age (62±8)), inferior myocardial infarction occurred in 24 (75%) patients. There were 88 patients (73%) in the non-PMI group (male 70(80%), age (62±8)). EF (55% (49%, 64%) vs. 62% (55%, 67%), P=0.01) was significantly lower in the PMI group than in the non-PMI group. Perioperative TNI, IABP use and length of hospitalization were significantly higher in the PMI group than in the non-PMI group. Multivariate logistic regression showed that lower EF was an independent risk factor of PMI (OR=0.93, 95%CI: 0.89-0.98, P=0.01) after adjusting age, sex and body mass index. ROC curve analysis showed that EF<60% could sufficiently predict the occurrence of PMI (AUC= 0.67, sensitivity 64%, specificity 69%, P=0.01). Linear regression analysis showed that left ventricular end-diastolic diameter (OR=-0.52, 95%CI:-1.13-0.60, P<0.001), graft flow in left anterior descending (OR=-0.20, 95%CI:-0.15-0.01, P=0.02) and history of diabetes (OR=-0.28, 95%CI:-8.25-1.85, P=0.002) were negatively correlated with preoperative EF value. Conclusion: Lower preoperative EF is an independent risk factor for PMI after CABG and CE in DCAD patients, closely related to the left ventricular end-diastolic diameter, graft flow in left anterior descending artery and diabetes mellitus.

Long-term outcomes in patients with acute myocardial infarction and no ischemic changes on electrocardiogram

BackgroundAcute myocardial infarction (MI) is commonly associated with ischemic abnormalities on electrocardiography (ECG). However, a significant proportion of patients present with no ischemic changes (NIC), and their baseline characteristics and management differ considerably from those with other ECG patterns. In the era of rapid troponin assays, the exact prognostic effects of normal ECGs remain unclear. ObjectivesThis study aimed to compare the outcomes of patients with MI without ischemic changes and those with other ECG patterns. MethodsBetween 2012 and 2018, 155,073 patients with MI were enrolled in the prospective nationwide Polish Registry of Acute Coronary Syndromes (PL-ACS). The patients were assigned to one of the following groups: NIC, ST-segment elevation (STE), ST-segment depression (STD), T-wave inversion (TWI), and other ST-T abnormalities (STT). ResultsThe NIC group accounted for 9.56% of all patients. The in-hospital risk of death was lower in the TWI group than in the NIC group. In the STE, STD, and STT groups, the short-term results were substantially worse. During the 12-month observation period, TWI had the best prognosis. The worst long-term prognoses were associated with STT and STD. The outcomes of the STE and NIC groups were similar (12-month death rate 9.0% vs. 8.7%, respectively; P=0.534), despite the fact STE was an independent predictor of 12-month prognosis. ConclusionsThe prognosis of patients with MI and NIC is not as favorable as previously thought. Their long-term outcomes were equal to those of the TWI and STE MI groups.

Effect of Mitral Regurgitation on Left Ventricular Deformation in Myocardial Infarction Patients: Evaluation by Cardiac Magnetic Resonance Imaging.

Mitral regurgitation (MR) is a comorbidity of myocardial infarction (MI), which may promote the incidence of adverse cardiovascular clinical events. However, it is not yet completely understood how MR in MI patients is associated with impaired myocardial deformation. To determine the damaging myocardium effects of MR in MI patients in terms of the global peak strain (PS) and left ventricular (LV) function, and evaluate the independent risk factors impacting LV deformation after MI. Retrospective. One hundred eighty-six MI patients (17.7% female) and 84 normal control subjects (27.4% female). 3.0T; late gadolinium enhancement sequence, balanced steady-state free precession. LV function and LV global PS (global radial peak strain [GRPS]; global circumferential peak strain [GCPS]; and global longitudinal peak strain [GLPS]) were compared among normal controls, MI without MR (MR-) and MI with MR (MR+, mild, moderate, severe) patients. One-way analysis of variance (ANOVA) test, Mann-Whitney U test, Kruskal-Wallis test, and multiple linear regressions were used. A P value <0.05 indicated statistically significant difference (two-tailed). The MI (MR+) patients showed significantly lower LV global PS than both MI (MR-) and control groups in three directions (GRPS 16.66 ± 7.43%; GCPS -11.27 ± 4.27%; GLPS -7.75 ± 3.44%), and significantly higher LV end-systolic (128.85 [87.91, 188.01] mL) and end-diastolic volumes (210.29 [164.07, 264.00] mL) and significantly lower LV ejection fraction (38.23 ± 13.02%). Multiple regression analysis demonstrated that MR was independently associated with LV GCPS (β = -0.268) and GLPS (β = -0.320). LV infarct size was an independent indicator of LV GRPS (β = -0.215) and GCPS (β = -0.222). LV end-diastolic volume was an independent indicator of LV GRPS (β = -0.518), GCPS (β = -0.503), and GLPS (β = -0.331). MR may further exacerbate the reduction of LV global peak strains and function. The MR, infarct size, and LV end-diastolic volume can be used as independent association indicators for LV global PS in MI (MR+) patients. 4 Technical Efficacy Stage: 2 TOC Category: Chest.

Association Between Serum Galectin-3 Levels and Coronary Stenosis Severity in Patients With Coronary Artery Disease.

BackgroundThe relationship between galectin-3 (Gal-3) and coronary artery disease (CAD) has not been fully elucidated.AimThis study aimed to determine the relationship between the presence and severity of CAD and serum Gal-3 levels.Patients and MethodsThree-hundred thirty-one consecutive CAD patients were enrolled as the study group. An additional 62 patients without CAD were enrolled as the control group. Serum Gal-3 levels were separately compared between the non-CAD and CAD groups, among the stable CAD and Acute coronary syndrome (ACS) groups, and between CAD patients with low and high SYNTAX scores (SSs). The 1-year cumulative rate of major adverse cardiac events (MACEs) was also compared among ACS patients by Gal-3 levels.ResultsSerum Gal-3 was significantly higher in the CAD group than in the non-CAD group 3.89 (0.16–63.67) vs. 2.07 (0.23–9.38) ng/ml, P < 0.001. Furthermore, serum Gal-3 was significantly higher in the non-ST-segment elevation ACS (NSTE-ACS) group than that in the stable CAD group, 4.72 (1.0–16.14) vs. 2.23 (0.65–23.8) ng/ml, P = 0.04 and higher in the ST-segment elevation myocardial infarction (STEMI) group than that in the stable CAD group 7.87 (0.59–63.67) vs. 2.23 (0.65–23.8) ng/ml, P < 0.001. Serum Gal-3 level was an independent predictor of ACS compared with stable CAD group (OR = 1.131, 95% CI: 1.051–1.217, P = 0.001) as well as high SS (OR = 1.030, 95% CI: 1.021–1.047, P = 0.038) after adjust other confounding risk factors. Acute coronary syndrome patients with Gal-3 levels above the median (gal-3 = 4.78 ng/ml) showed a higher cumulative MACE rate than those with Gal-3 levels below the median. After adjusting other confounding risk factors, Gal-3 remained an independent risk factor for the cumulative rate of MACEs in ACS patients (6% higher rate of MACEs incidence per 1 ng/ml increment of Gal-3).ConclusionGalectin-3 correlated with the presence of CAD as well as coronary stability and complexity. Galectin-3 may be valuable in predicting mid-term prognosis in ACS patients.

Segmental speckle tracking strain and strain rate in stable coronary artery disease

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Northern Norway Regional Health Authority Background It is known that patients with coronary artery disease (CAD) display reduced global and regional strain and strain rate (SR). However, knowledge about segmental strain and SR in stable CAD patients is still limited. Purpose The purpose of this study was to explore whether segmental strain and SR analyses are different between patients with normal and stenotic coronary arteries among individuals with chest-pain. Methods A total of 510 patients with chest pain, referred to coronary computed tomography angiography (CCTA) and additional 102 patients with myocardial infarction (MI) were prospectively included. All patients underwent transthoracic echocardiography (TTE) with strain-rate analysis. All patients with CCTA-suspected CAD subsequently underwent invasive CAG, as well as in all MI patients. Global longitudinal strain (GLS) and average for segmental peak longitudinal strain during systole (PLS), peak systolic strain rate (PLSR S), peak early diastolic strain rate (PLSR E), post systolic shortening (PSS) measurements were analysed. Further, different cut-off values for reduced strain and SR were used to define the percentage of functionally reduced segments between patients with normal CAD (no CAD), MI, and stable CAD patients who were further treated by percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG). Results As shown in the table 1, all average segmental strain and SR parameters differed significantly between no CAD and MI groups. However, only PLSR E showed significant differences between no CAD and PCI groups . PLSR E, PLS and GLS showed significant differences between no CAD and CABG groups. The percentage of reduced segmental strain and SR showed similar results. Regarding the percentage of pathological segments at different cut-off values, PLSR E showed the most significant difference between these four groups at a cut-off value 1.5 (p &amp;lt; 0.001) (Figure 1). Conclusion Patients with MI or CABG display clearly reduced segmental strain and SR values. However, in patients with chest-pain, segmental PLSR E seemed to be the only indicator revealing subtle differences between patients with no CAD or those assigned to PCI. The diagnostic value of PLSR E needs to be investigated in further studies. Abstract Table 1 Abstract Figure 1

Serum Levels of Adropin and Some Biochemical Parameters in Acute Myocardial Infarcyion

Acute myocardial infarction (MI) occurs when flow of blood to the heart is suddenly cut off, that lead to damage of the tissue. This is causing by a blockage in one or more of the coronary arteries. A blockage can expand due to a buildup of plaque, a substance mostly made of fat, cholesterol, and cellular waste products. Atherosclerosis may be a chronic inflammation disease and it is an active process, it is having mainly role in the MI pathogenesis, the inflammatory responsible for to accelerate atherosclerosis, decrease anti inflammation associated with MI, novel marker Adropin has anti inflammation and cardiovascular protective role. The objective of this study was evaluate Adropin levels in acute Myocardial Infarction and find the correlation between Adropin, and cardiac biomarker (hs-TI, hs-CRP and CKMB). The patients in this study were 50 patients and 50 control, when measurement of Adropin in studies groups of MI found that decrease in concentration of serum Adropin in patents groups of compare with control. The conclusion was that Adropin can be used to diagnose acute myocardial infarction, along with the use of a Cardiac biomarker such: (hs-TI), (hs-CRP) and Creatine kinase (CK-MB).

The effect of eight weeks of interval training and quercetin nanoliposome supplementation on NF-κB and FGF-2 gene expression in the heart tissue of myocardial infarction rats

Background and aims: The activation of inflammatory reactions is essential immediately after the onset of myocardial infarction (MI). On the other hand, the path of inflammatory activators should be controlled to prevent the recurrence of MI. In this vein, the aim of this study was to examine the effect of eight weeks of interval training and quercetin nanoliposome consumption on nuclear factor kappa B (NF-κB) and fibroblast growth factor 2 (FGF-2) gene expression in the heart tissue of MI rats. Methods: In this experimental study, 30 male rats, aged approximately 6-8 weeks, were randomly divided into five groups including MI + training, MI + supplement, MI + training + supplement, healthy control, and MI. The MI was induced by the subcutaneous injection of isoprenaline hydrochloride at a dose of 80 mg/kg. Quercetin was daily administered at a dose of 0.25 mg for 8 weeks, and interval training was performed 5 days a week. NF-κB and FGF-2 gene expressions were measured by the real-time polymerase chain reaction. Finally, data were analyzed using the one-way analysis of variance (ANOVA) and Tukey’s post hoc tests (P&lt;0.05). Results: Training significantly increased NF-κB gene expression in the MI+ training, MI + supplement, and MI + training + supplement groups (P=0.001) while significantly decreasing FGF-2 gene expression in the MI group (P=0.04). Conclusion: Interval training may prevent the negative effects of MI by reducing pro-inflammatory gene expression in the heart tissue, leading to improved cardiovascular function and the prevention of this disease.

Decreased Iron Ion Concentrations in the Peripheral Blood Correlate with Coronary Atherosclerosis.

(1) Background: Obesity and diabetes continue to reach epidemic levels in the population with major health impacts that include a significantly increased risk of coronary atherosclerosis. The imbalance of trace elements in the body caused by nutritional factors can lead to the progression of coronary atherosclerosis. (2) Methods: We measured the concentrations of sodium (Na), potassium (K), magnesium (Mg), calcium (Ca), Zinc (Zn), and iron (Fe) in peripheral blood samples from 4243 patients and performed baseline analysis and propensity matching of the patient datasets. The patients were grouped into acute myocardial infarction (AMI, 702 patients) and stable coronary heart disease (SCAD1, 253 patients) groups. Both of these groups were included in the AS that had a total of 1955 patients. The control group consisted of 2288 patients. The plasma concentrations of calcium, magnesium, and iron were measured using a colorimetric method. For comparison, 15 external quality assessment (EQA) samples were selected from the Clinical Laboratory Center of the Ministry of Health of China. SPSS software was used for statistical analysis. The average values and deviations of all of the indicators in each group were calculated, and a p-value threshold of <0.05 was used to indicate statistical significance. (3) Results: The iron ion concentrations of the acute myocardial infarction (AMI) group were significantly lower than the control group (p < 0.05, AUC = 0.724, AUC = 0.702), irrespective of tendency matching. Compared to the data from the stable coronary artery disease (SCAD) group, the concentration of iron ions in the acute myocardial infarction group was significantly lower (p < 0.05, AUC = 0.710, AUC = 0.682). Furthermore, the iron ion concentrations in the (AMI + SCAD) group were significantly lower (p < 0.05) than in the control group. (4) Conclusions: The data presented in this study strongly indicate that the concentration of iron ions in the peripheral blood is related to coronary atherosclerosis. Decreases in the levels of iron ions in the peripheral blood can be used as a predictive biomarker of coronary atherosclerosis.

MicroRNA-489 Promotes the Apoptosis of Cardiac Muscle Cells in Myocardial Ischemia-Reperfusion Based on Smart Healthcare.

With the development of information technology, the concept of smart healthcare has gradually come to the fore. Smart healthcare uses a new generation of information technologies, such as the Internet of Things (loT), big data, cloud computing, and artificial intelligence, to transform the traditional medical system in an all-around way, making healthcare more efficient, more convenient, and more personalized. miRNAs can regulate the proliferation, differentiation, and apoptosis of human cells. Relevant studies have also shown that miRNAs may play a key role in the occurrence and development of myocardial ischemia-reperfusion injury (MIRI). This study aims to explore the effects of miR-489 in MIRI. In this study, miR-489 expression in a myocardial ischemia-reperfusion animal model and H9C2 cells induced by H/R was detected by qRT-PCR. The release of lactate dehydrogenase (LDH) and the activity of creatine kinase (CK) was detected after miR-489 knockdown in H9C2 cells induced by H/R. The apoptosis of H9C2 cells and animal models were determined by ELISA. The relationship between miR-489 and SPIN1 was verified by a double fluorescence reporter enzyme assay. The expression of the PI3K/AKT pathway-related proteins was detected by Western blot. Experimental results showed that miR-489 was highly expressed in cardiac muscle cells of the animal model and in H9C2 cells induced by H/R of the myocardial infarction group, which was positively associated with the apoptosis of cardiac muscle cells with ischemia-reperfusion. miR-489 knockdown can reduce the apoptosis of cardiac muscle cells caused by ischemia-reperfusion. In downstream targeting studies, it was found that miR-489 promotes the apoptosis of cardiac muscle cells after ischemia-reperfusion by targeting the inhibition of the SPIN1-mediated PI3K/AKT pathway. In conclusion, high expression of miR-489 is associated with increased apoptosis of cardiac muscle cells after ischemia-reperfusion, which can promote the apoptosis after ischemia-reperfusion by targeting the inhibition of the SPIN1-mediated PI3K/AKT pathway. Therefore, miR-489 can be one of the potential therapeutic targets for reducing the apoptosis of cardiac muscle cells after ischemia-reperfusion.

Natural cardiac regeneration conserves native biaxial left ventricular biomechanics after myocardial infarction in neonatal rats

After myocardial infarction (MI), adult mammals exhibit scar formation, adverse left ventricular (LV) remodeling, LV stiffening, and impaired contractility, ultimately resulting in heart failure. Neonatal mammals, however, are capable of natural heart regeneration after MI. We hypothesized that neonatal cardiac regeneration conserves native biaxial LV mechanics after MI. Wistar rat neonates (1 day old, n = 46) and adults (8–10 weeks old, n = 20) underwent sham surgery or permanent left anterior descending coronary artery ligation. At 6 weeks after neonatal MI, Masson's trichrome staining revealed negligible fibrosis. Echocardiography for the neonatal MI (n = 15) and sham rats (n = 14) revealed no differences in LV wall thickness or chamber diameter, and both groups had normal ejection fraction (72.7% vs 77.5%, respectively, p = 0.1946). Biaxial tensile testing revealed similar stress-strain curves along both the circumferential and longitudinal axes across a full range of physiologic stresses and strains. The circumferential modulus (267.9 kPa vs 274.2 kPa, p = 0.7847), longitudinal modulus (269.3 kPa vs 277.1 kPa, p = 0.7435), and maximum shear stress (3.30 kPa vs 3.95 kPa, p = 0.5418) did not differ significantly between the neonatal MI and sham groups, respectively. In contrast, transmural scars were observed at 4 weeks after adult MI. Adult MI hearts (n = 7) exhibited profound LV wall thinning (p < 0.0001), chamber dilation (p = 0.0246), and LV dysfunction (ejection fraction 45.4% vs 79.7%, p < 0.0001) compared to adult sham hearts (n = 7). Adult MI hearts were significantly stiffer than adult sham hearts in both the circumferential (321.5 kPa vs 180.0 kPa, p = 0.0111) and longitudinal axes (315.4 kPa vs 172.3 kPa, p = 0.0173), and also exhibited greater maximum shear stress (14.87 kPa vs 3.23 kPa, p = 0.0162). Our study is the first to show that native biaxial LV mechanics are conserved after neonatal heart regeneration following MI, thus adding biomechanical support for the therapeutic potential of cardiac regeneration in the treatment of ischemic heart disease.

Spinal Cord Stimulation Attenuates Neural Remodeling, Inflammation, and Fibrosis After Myocardial Infarction

ObjectivesSpinal cord stimulation (SCS) is an established neuromodulation method that regulates the cardiac autonomic system. However, the biological mechanisms of the therapeutic effects of SCS after myocardial infarction (MI) remain unclear. Materials and MethodsTwenty-five rabbits were divided into five groups: SCS-MI (voltage: 0.5 v; pulse width: 0.2 ms; 50 Hz; ten minutes on and 30 minutes off; two weeks; n = 5), MI (n = 5), sham SCS-MI (voltage: 0 v; two weeks; n = 5), sham MI (n = 5), and blank control (n = 5) groups. MI was induced by permanent left anterior descending artery ligation. SCS-MI and sham SCS-MI rabbits received the corresponding interventions 24 hours after MI. Autonomic remodeling was evaluated using enzyme-linked immunosorbent assay and immunohistochemistry. Inflammation and myocardial fibrosis were assessed using immunohistochemistry, quantitative polymerase chain reaction, hematoxylin and eosin staining, Masson staining, and Western blot. ResultsSCS improved the abnormal systemic autonomic activity. Cardiac norepinephrine decreased after MI (p < 0.01) and did not improve with SCS. Cardiac acetylcholine increased with SCS compared with the MI group (p < 0.05). However, no difference was observed between the MI and blank control groups. Growth-associated protein 43 (p < 0.001) and tyrosine hydroxylase (p < 0.001) increased whereas choline acetyltransferase (p < 0.05) decreased in the MI group compared with the blank control group. These changes were attenuated with SCS. SCS inhibited inflammation, decreased the ratio of phosphorylated-Erk to Erk (p < 0.001), and increased the ratio of phosphorylated-STAT3 to STAT3 (p < 0.001) compared with the MI group. Myocardial fibrosis was also attenuated by SCS. ConclusionsSCS improved abnormal autonomic activity after MI, leading to reduced inflammation, reactivation of STAT3, and inhibition of Erk. Additionally, SCS attenuated myocardial fibrosis. Our results warrant future studies of biological mechanisms of the therapeutic effects of SCS after MI.

Augmented early aged neutrophil infiltration contributes to late remodeling post myocardial infarction.

Neutrophils oscillate in number and phenotype after being released from bone marrow. Myocardial infarction (MI) outcome is associated with the time-of-day of ischemia onset. However, the underlying contributive factors of neutrophils to cardiac remodeling post MI remain unknown. We examined neutrophil infiltration into the heart and cardiac function and remodeling in C57BL/6J MI model created by permanent coronary ligation at different zeitgeber times (ZT). We found that cell surface markers (CD62L, CXCR2, CXCR4) of neutrophils in peripheral blood lost diurnal oscillation 24h post MI. Meanwhile, circadian gene Bmal1, Nr1d1, and Clock mRNA expression displayed disrupted diurnal patterns. Flow cytometry showed augmented aged neutrophil (CD11b+Ly6G+CD62Llow) infiltration into the heart along with increased circulating aged neutrophils in MI groups with more infiltration at ZT5 (p<0.05), but no difference for aged neutrophil infiltration at different ZT points in late stage. Infiltrated neutrophils had significantly higher CXCL2 and CXCR2 but lower CXCR4 gene expression (p<0.05). Mice that underwent ligation at ZT5 had high mortality rate and large infarct size. Echocardiography showed that those mice had significantly larger end diastolic and systolic volume and lower ejection fraction (p<0.05). Immunohistology revealed that those mice displayed more fibrosis, cardiomyocyte hypertrophy, and less angiogenesis compared to ZT13 or ZT21 group (p<0.05). However, treatment with anti-CXCL2 antibody significantly reduced LV dilatation, fibrosis, hypertrophy and improved cardiac function. These results indicate greater aged neutrophil infiltration into the heart contributes to cardiac hypertrophy, fibrosis, and dysfunction which suggests that blocking neutrophil aging may be a therapeutic alternative following acute myocardial infarction.

Akut Myokard Enfarktüsü için Potansiyel Yeni Bir Biyobelirteç Olarak Dolaşan Uzun İntergenik Kodlamayan RNA LINC01538: Prospektif Kohort Çalışma

Objective: Non-coding RNAs are the RNAs with no protein coding function, long non-coding RNAs (LncRNAs) are the non-coding RNAs with more than 200 nucleotides. During the journey of discovering novel biomarkers for diagnosis of myocardial infarction (MI), the principle of studying the LncRNA as a potential would be always attractive, as it needs easy sample collection, has high detection sensitivity and high myocardial tissue specificity. Our main objective was to investigate the potential of LINC01538 as a novel diagnostic biomarker for MI. Material and Methods: Quantitative real-time polymerase chain reaction (RT-qPCR) was used to assess the expression of the serum LINC01538 in 50 ST Elevation MI (STEMI) patients and 48 controls. Results: The study showed a significant increase in serum level expression of LINC01538 in MI patients compared to controls [12 (6.6- 21.8) vs. 0.07 (0.01-0.2), p<0.001]. LINC01538 expression level in MI group was positively correlated with creatine kinase MB and high sensitive cardiac troponin I (hs-cTnI) (r=0.39, p=0.006 and r=0.22, p=0.007, respectively). Hs-cTnI found to have diagnostic value for MI with an area under curve (AUC) 0.917 [95% confidence interval (CI): 0.855- 0.979, p<0.001] at an optimal cutoff point of 1.45 ng/L, 90% sensitivity and 91% specificity. However, LINC01538 showed the highest diagnostic value with an AUC 0.980 (95% CI: 0.942- 1, p<0.001) at an optimal cut-off point of 1.76, 100% sensitivity and 98% specificity. Conclusion: Our findings have, for the first time, demonstrated that circulating LINC01538 are highly expressed in patients with MI, functioning as potential novel biomarker for diagnosis.

Creatine Kinase-MB and Beta-Hydroxybutyrate Dehydrogenase with Antioxidant Agent in Heart Disease Patients

The research Measures the activity of CK-MB &amp; BHBDH enzymes with some biochemical parameters and TAO for the heart Patients group (147), also to the control group (94). The results showed an increase in activity for both enzyme CKMB (33.29±4.96 U/L) and BHBDH (224.12± 0.82 U/L) in serum for the heart Patients group compared to the control (8.67±0.41 U/L, 136.73±0.95 U/L) respectively. The results also showed a significant difference in the activity of CK-MB and BHBDH in serum for the angina pectoris group with the myocardial infarction group. The results indicated that there was a significant increase activity of peroxidase in serum for the heart Patients group (92.33 ± 4.68 U/L) compared to the control group (47.66± 0.60 U/L), while there was a significant decrease in the activity of Catalase and TAO concentration in serum for heart patients group (25.53 ±0.47 U/L, 0.89 ±0.01 µmol/ml) compared to the activity of Catalase and TAO concentration in serum for the control group (53.11±0.50 U/L, 1.261 ± 0.02 µmol/ml) respectively. Potassium, iron, and copper concentrations in the serum of the heart patients group were significantly higher than those in the serum of the control group (4.07 0.06 mmol/l, 122.45 0.95 g/dl, and 103.95 1.46 g/dl, respectively). Zinc concentration was also significantly lower in the serum of the heart patients group (73.48 2.08 g/dl) than in the control group. Although there was no discernible difference in the serum calcium concentration between the cardiac patient's group (8.53 0.08 mg/dl) and the control group (8.545 0.06 m/dl). Finally, the findings in the group of individuals with heart disease demonstrated a substantial negative correlation between the activity of serum CK-MB and serum calcium levels. It was also found that there was a substantial negative correlation between the serum CK-MB activity and the serum peroxidase and TAO concentrations, and a significant positive correlation between the serum catalase and iron concentrations

Effects of Foxc1 and Oct4 genes regulating BMSCs transplantation on cardiomyocyte apoptosis after acute myocardial infarction in rats

To investigate the effect of Foxc1 and Oct4 genes regulated by bone marrow mesenchymal stem cells (BMSCs) transplantation on cardiomyocyte apoptosis after acute myocardial infarction in rats. 180 healthy SD male rats were divided into 3 groups by random number table method, namely control group, acute myocardial infarction (AMI) group and BMSCs group. The rats were sacrificed 4 weeks after transplantation. The TUNEL method was used to detect the cardiomyocyte apoptosis index. The control group basically had no cardiomyocyte apoptosis, while the apoptosis indexes of AMI group (0.67 ± 0.14) was higher than that (0.31 ± 0.12) of BMSCs group (P < 0.05). The OD value of Foxc1 and Oct4 protein in BMSCs group was higher than those in AMI group (all P < 0.05). BMSCs transplantation can reduce cardiomyocyte apoptosis after AMI in rats. The mechanism may be related to the up-regulation of Oct4 and Foxc1 protein expression.

Different methods of femoropopliteal bypass grafting with autologous vein: propensity score matching analysis

To analyze immediate and long-term results of various methods of femoropopliteal bypass grafting with autologous vein using propensity score matching. A retrospective single-center open study included 464 patients who underwent femoropopliteal bypass grafting with an autologous vein between January 10, 2016 and December 25, 2019 at the Research Institute - Ochapovsky Regional Clinical Hospital No. 1. The following types of autovenous conduits were used: n=266 - reversed autologous vein (group 1); n=59 - in situ autologous vein (group 2); n=73 - upper limb autologous vein (group 3); n=66 - ex situ autologous vein (group 4). The long-term period was 16.6±10.3 months. We used propensity score matching analysis because patients were not comparable for some indicators. Groups 2-4 included small samples of patients, and their number was reduced to less than 10. This did not allow us to draw reliable conclusions about treatment outcomes. In this situation, we decided to allocate two groups: group 1 - ex situ femoropopliteal bypass grafting; group 2 - other variants of femoropopliteal bypass grafting with autologous vein. Propensity score matching allocated 299 people in group 1 and 46 patients in group 2. There were significant differences in early postoperative incidence of autologous vein thrombosis (group 1: n=3 (6.5%), group 2: n=79 (26.4%), p=0.003; OR= 0.19; 95% CI 0.05-0.64) and postoperative wound suppuration (group 1: n=2 (4.3%), group 2: n=52 (17.4%); p=0.02; OR=0.21; 95% CI 0.05-0.91). In long-term postoperative period, significant differences were obtained in the incidence of limb amputation (group 1: n=6 (13%), group 2: n=85 (28.4%); p=0.02; OR=0.37; 95% CI 0.15-0.92) and myocardial infarction (group 1: n=1 (2.2%), group 2: n=43 (14.4%); p=0.02; OR 0.13; 95% CI 0.01-0.98). Femoropopliteal bypass grafting ex situ is characterized by lower incidence of graft thrombosis, amputations of the limb, mild decrease in the incidence of infectious complications and all adverse cardiovascular events in early and late postoperative period compared to conventional surgery (reversed autologous vein, in situ autologous vein, upper limb autologous vein).

The Neutrophil/Lymphocyte Ratio is Associated with Different Stages of Development of Coronary Artery Disease

Introduction: Inflammation plays a role in coronary artery disease (CAD). The neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio (MLR) and platelet/lymphocyte ratio (PLR) are blood parameters associated with inflammation. We aimed to perform a systematic comparison and study the predictive values of these inflammatory parameters with respect to CAD stage. Method: A total of 513 patients who had undergone coronary angiography (CAG) were retrospectively analyzed. Clinical status, lipid profiles, CAG scans and hematological parameters were collected. NLR, MLR and PLR were calculated. All patients were classified into a normal coronary group (n=133), coronary atherosclerosis (CA) group (n=149), chronic coronary syndrome (CCS) group (n=175) or acute myocardial infarction (AMI) group (n=56). NLR, MLR and PLR were compared among groups. Results: NLR and MLR were higher in the CCS and AMI groups. PLR was higher in the AMI group. The AMI group had higher NLR, PLR and MLR than the CCS group. Logistic regression analysis revealed that NLR (OR:1.227, 95% CI: 1.016–1.482. P&lt;0.05) had a strong significant correlation with CAD. Area under the ROC curve of NLR was 0.580 (95% CI=0.516–0.644) in predicting CCS and 0.727 (95% CI=0.642–0.811) in predicting AMI. Conclusion: NLR may be associated with the occurrence and progression of CAD, and may serve as a marker of inflammation.

Comparison of the monocyte-to-HDL cholesterol ratio between patients with STEMI and NSTEMI: A retrospective observational study

Introduction This study sought to compare patients with ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction in terms of the monocyte-to-HDL cholesterol ratio. Materials and Methods A total of 79 patients with non-ST-segment elevation myocardial infarction and 30 patients with 30 ST-segment elevation myocardial infarction were included in the study. Demographics, comorbidities, smoking status, medical history, and initial laboratory findings were retrospectively noted from the hospital computer-based patient data system. Results Significant differences were detected between the ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction groups in relation to the neutrophil count [7.27 (6.05-9.05) versus 5.41 (4.26-7.21), p<0.001] and mean platelet volume [9.4 (8.8-10) versus 8.6 (7.3-9.5), p=0.002]. There was no statistically significant difference between the two groups in the term of the monocyte-to-HDL cholesterol ratio [0.016 (0.012-0.021) versus 0.016 (0.011-0.024), p=0.757, Bonferroni-corrected p value: 0.0033)]. Conclusion Based on the results of our study, the monocyte-to-HDL cholesterol ratio did not significantly differ between the patients with ST-segment elevation myocardial infarction and those with non-ST-segment elevation myocardial infarction.