Severity Of Myocardial Infarction Research Articles

Myeloperoxidase induces monocyte migration and activation after acute myocardial infarction.

Myocardial infarction (MI) is a significant contributor to morbidity and mortality worldwide. Many individuals who survive the acute event continue to experience heart failure (HF), with inflammatory and healing processes post-MI playing a pivotal role. Polymorphonuclear neutrophils (PMN) and monocytes infiltrate the infarcted area, where PMN release high amounts of the heme enzyme myeloperoxidase (MPO). MPO has numerous inflammatory properties and MPO plasma levels are correlated with prognosis and severity of MI. While studies have focused on MPO inhibition and controlling PMN infiltration into the infarcted tissue, less is known on MPO's role in monocyte function. Here, we combined human data with mouse and cell studies to examine the role of MPO on monocyte activation and migration. We revealed a correlation between plasma MPO levels and monocyte activation in a patient study. Using a mouse model of MI, we demonstrated that MPO deficiency led to an increase in splenic monocytes and a decrease in cardiac monocytes compared to wildtype mice (WT). In vitro studies further showed that MPO induces monocyte migration, with upregulation of the chemokine receptor CCR2 and upregulation of inflammatory pathways identified as underlying mechanisms. Taken together, we identify MPO as a pro-inflammatory mediator of splenic monocyte recruitment and activation post-MI and provide mechanistic insight for novel therapeutic strategies after ischemic injury.

Oxidation-reduction imaging of myoglobin reveals two-phase oxidation in the reperfused myocardium.

Myocardial infarction (MI) is a serious acute cardiovascular syndrome that causes myocardial injury due to blood flow obstruction to a specific myocardial area. Under ischemic-reperfusion settings, a burst of reactive oxygen species is generated, leading to redox imbalance that could be attributed to several molecules, including myoglobin. Myoglobin is dynamic and exhibits various oxidation-reduction states that have been an early subject of attention in the food industry, specifically for meat consumers. However, rarely if ever have the myoglobin optical properties been used to measure the severity of MI. In the current study, we develop a novel imaging pipeline that integrates tissue clearing, confocal and light sheet fluorescence microscopy, combined with imaging analysis, and processing tools to investigate and characterize the oxidation-reduction states of myoglobin in the ischemic area of the cleared myocardium post-MI. Using spectral imaging, we have characterized the endogenous fluorescence of the myocardium and demonstrated that it is partly composed by fluorescence of myoglobin. Under ischemia-reperfusion experimental settings, we report that the infarcted myocardium spectral signature is similar to that of oxidized myoglobin signal that peaks 3h post-reperfusion and decreases with cardioprotection. The infarct size assessed by oxidation-reduction imaging at 3h post-reperfusion was correlated to the one estimated with late gadolinium enhancement MRI at 24h post-reperfusion. In conclusion, this original work suggests that the redox state of myoglobin can be used as a promising imaging biomarker for characterizing and estimating the size of the MI during early phases of reperfusion.

Temporary transvenous cardiac pacing in cathlab - myocardial infarction versus other causes - differences, complications, and prognosis. Data from a single-center retrospective analysis.

Transvenous temporary cardiac pacing (TTCP) is a lifesaving procedure, but the incidence of complications and prognosis depends on the underlying cause. The aim of this study was to compare the characteristics, complications, and prognosis in patients with myocardial infarction (MI) requiring TTCP vs. patients with TTCP due to other causes. The present analysis involved 244 cases in whom TTCP was performed between 2017 and 2021 in a high-volume cathlab. All the procedures were performed by an interventional cardiologist. MI constituted 46.3% of the patients (n = 113), including 63 ST-segment elevation MI patients (55.75%). Non-MI patients (control group) consisted of patients with any cause of bradycardia requiring TTCP. Myocardial infarction patients requiring TTCP are younger and have a higher prevalence of hypertension and heart failure. The pacing lead is more frequently inserted during asystole/resuscitation, and pacing was needed for a longer time. MI patients required cardiac implantable electronic device implantation less frequently than in other causes (22% vs. 82%, p < 0.01). The incidence of TTCP complications did not differ. The incidence of in-hospital death was 6.5-fold higher in TTCP patients with MI. Logistic regression showed MI to be a strong predictor of in-hospital death (odds ratio: 8.1; 95% confidence interval: 1.3-57.9). In-hospital mortality in MI patients requiring TTCP is 6.5-fold higher than in other patients with bradycardia. The complication rate of TTCP is similar in MI and non-MI patients. It is not TTCP but the severity of MI itself and the fact that a pacing lead is frequently implanted in asystole or during resuscitation that is responsible for the higher mortality rate.

Role of Heart Rate Variability in the Association between Myocardial Infarction Severity and Post-Myocardial Infarction Distress.

Myocardial infarction (MI) results in mental health consequences, including depression and post-traumatic stress disorder (PTSD). The risk and protective factors of such mental consequences are not fully understood. This study examined the relation between MI severity and future mental health consequences and the moderating role of vagal nerve activity. In a reanalysis of data from the Myocardial Infarction-Stress Prevention Intervention (MI-SPRINT) study, 154 post-MI patients participated. MI severity was measured by the Killip Scale and by troponin levels. Depression and PTSD symptoms were assessed with valid questionnaires, both at 3 and 12 months. Vagal nerve activity was indexed by the heart rate variability (HRV) parameter of the root-mean square of successive R-R differences (RMSSD). Following multivariate analyses, the association between MI severity and distress was examined in patients with low and high HRV (RMSSD = 30 ms). In the full sample, the Killip index predicted post-MI distress only at 3 months, while troponin predicted distress at 3- and 12-months post-MI. However, HRV moderated the effects of the Killip classification; Killip significantly predicted symptoms of depression and PTSD at 3- and 12-months post-MI, but only in patients with low HRV. Such moderation was absent for troponin. MI severity (Killip classification) predicted post-MI depression and PTSD symptoms, but only in patients with low HRV, suggesting that the vagal nerve is a partial protective (moderating) factor in the relation between Killip score and post-MI distress.

Inflammatory Bowel Disease Increases the Severity of Myocardial Infarction after Acute Ischemia-Reperfusion Injury in Mice.

(1) Background: Increased risk of myocardial infarction (MI) has been linked to several inflammatory conditions, including inflammatory bowel disease (IBD). However, the relationship between IBD and MI remains unclear. Here, we implemented an original mouse model combining IBD and MI to determine IBD's impact on MI severity and the link between the two diseases. (2) Methods: An IBD model was established by dextran sulfate sodium (DSS) administration in drinking water, alone or with oral C. albicans (Ca) gavage. IBD severity was assessed by clinical/histological scores and intestinal/systemic inflammatory biomarker measurement. Mice were subjected to myocardial ischemia-reperfusion (IR), and MI severity was assessed by quantifying infarct size (IS) and serum cardiac troponin I (cTnI) levels. (3) Results: IBD mice exhibited elevated fecal lipocalin 2 (Lcn2) and IL-6 levels. DSS mice exhibited almost two-fold increase in IS compared to controls, with serum cTnI levels strongly correlated with IS. Ca inoculation tended to worsen DSS-induced systemic inflammation and IR injury, an observation which is not statistically significant. (4) Conclusions: This is the first proof-of-concept study demonstrating the impact of IBD on MI severity and suggesting mechanistic aspects involved in the IBD-MI connection. Our findings could pave the way for MI therapeutic approaches based on identified IBD-induced inflammatory mediators.

ВАРИАБЕЛЬНОСТЬ ГЕНОВ НАТРИЙУРЕТИЧЕСКИХ ПЕПТИДОВ И АНТИОКСИДАНТНОЙ ЗАЩИТЫ У ПАЦИЕНТОВ С ИНФАРКТОМ МИОКАРДА

Introduction. Cardiovascular diseases (CVD) continue to be the subject of scientific research in relation to molecular genetic predictors of their development. It has been proven that diseases of the cardiovascular continuum have a multifactorial nature with a significant genetic component, including the hereditary risk of myocardial infarction (MI). CVDs are characterized by a complex genetic structure with diverse combinations of single nucleotide polymorphic variants (SNVs). A promising task is to study the relationship of SNV adaptogenesis genes: inflammatory response, myocardial and endothelial dysfunction with developed MI in the Siberian population. Purpose: to reveal the relationship between SNV genes of natriuretic peptides and the antioxidant defense system with the development of myocardial infarction. Materials and methods. The material for the study was genomic DNA isolated from the peripheral blood of patients (n=146, 38 women and 108 men) admitted for treatment at the Kuzbass Clinical Cardiological Dispensary, Kemerovo, with a diagnosis of MI. The control group is represented by a population sample of residents of the city of Kemerovo (n=300, 190 women and 110 men). 20 polymorphic variants of 7 natriuritic peptide genes (NPPA, NPPA-AS1, NPPB, NPPC, NPR1, NPR2, NPR3) and 5 genes of the antioxidant defense system (SOD2, NCF4, CBR1, CBR3, CAT) were selected for the study. Genotyping of selected polymorphic variants was performed by real-time PCR using TaqMan technology. Statistical data analysis was carried out using GraphPad Prism 8 and SNPstats software. Results. Protective associations of allelic variants of the CBR1 rs9024 genes (OR=0.21 (95% CI 0.13-0.34); p=0.0001) and CBR3 (OR=0.44 (95% CI 0.28-0) .69); p=0.001) regardless of gender according to the dominant model of inheritance. When separating patients by gender, it was found that in men, the rs9024 CBR1 allele A (OR=0.20 (95% CI 0.11-0.36); p&lt;0.0001) and the rs1056892 CBR3 allele A (OR=0, 51 (95% CI 0.28-0.91); p=0.022) have a protective effect in the development of MI according to the dominant model of inheritance. Allele T rs2236289 (OR=1.93 (95% CI 1.04-3.58); p=0.035) and allele A rs7034957 (OR=1.88 (95% CI 1.03-3.45); p =0.038) of the NPR2 gene are associated with a risk effect on the development of myocardial infarction in men according to the dominant model of inheritance. In women, rare alleles of the polymorphic loci rs13288085 (OR=0.25 (95% CI 0.08-0.73); p=0.0034) and rs7034957 (OR=0.30 (95% CI 0.11-0, 79); p=0.007) of the NPR2 gene, rs9024 (OR=0.21 (95% CI 0.09-0.47); p=0.00001) of CBR1, as well as rs1056892 (OR=0.31 (95% CI 0.15-0.64); p=0.0014) CBR3 are characterized by a protective effect on the development of MI according to the dominant model of inheritance. Conclusion. It has been shown that polymorphism of genes for natriuretic peptides and antioxidant protection may have a risky and protective effect in relation to predisposition to the development of MI. The obtained preliminary results indicate the need for further studies of the identified SNV genes of adaptogenesis in relation to the severity of MI and the risk of recurrent cardiovascular events in the long-term period after MI.

Abstract P1114: Preclinical Large Animal Assessment Of Safety And Engraftment Of Hicms Nanofiber Cardiac Patch Transplantation For Cardiac Repair

Background: Myocardial infarction (MI) is a leading cause of death in the United States. However, none of the therapies can regenerate the damaged heart muscle. Objective: The objective of this study was to assess the safety and engraftment of a nanofiber cardiac patch laden with human iPSC-derived cardiomyocytes (hiCMs) and transplanted in a preclinical porcine MI model. Methodology: MI was induced in pigs via advancing a balloon catheter from the femoral artery into the left anterior descending coronary artery (LAD) below the first diagonal branch (D1) and the balloon was inflated for 90-min to induce myocardial ischemia. Immunosuppressant drug Tacrolimus was given orally one-week before the cardiac patch transplantation and continued for up to 4-weeks post-cardiac patch transplantation. Epicardial transplantation of aligned nanofiber cardiac patch (2 layers) loaded with hiCMs was performed at one-week post MI. Magnetic resonance Imaging (MRI) was performed prior to the MI induction (Baseline), 1-week post-MI and at 4-weeks post cardiac patch transplantation to assess severity of MI and cardiac function. At 4-weeks post-MI, pigs were euthanized, and the heart tissues were processed for immunostaining to confirm the retention and engraftment (Human Nuclear Antibody staining) of the implanted cells in the host myocardium. Results: (a) A significant increase in ST-elevation following 90-min of MI, (b) Incidence of cardiac arrhythmias were not observed post cardiac patch transplantation, confirming the safety of cardiac patch, (c) No teratomas were observed at the transplanted site, indicating safety of terminally differentiated hiCMs and (d) Immunofluorescence staining of cardiac sections in the transplanted cardiac patch area confirmed engraftment of transplanted cells via anti-human nuclear antibody, which demonstrates the survival and engraftment of implanted cells. Conclusions: In summary, we have demonstrated for the first time that aligned nanofiber cardiac patch loaded with hiCMs is safe and can enhance retention of transplanted cells. Further studies are warranted to assess the long-term efficacy of cardiac patch transplantation in improving the cardiac function and to perform first-in-human clinical trials in the near future.

RANTES (CCL5) as a biomarker of clinical outcomes in STEMI patients

RANTES or CCL5 is a chemokine that mediates chemotaxis and activation of T cells, monocytes, granulocytes, mast cells and dendritic cells. It is involved in the pathogenesis of several diseases including atherosclerosis but its role at the acute phase of myocardial infarction (MI) is not clear. Our objective is to determine whether the serum level of RANTES is a marker of the severity of acute MI. The study included 260 consecutive STEMI patients who underwent PCI into a prospective cohort. For determination of circulating RANTES serum level, peripheral venous blood samples were taken at 5 time points: admission, 4, 24, 48 hours and 1 month after admission (H0, H4, H24, H48, M1). RANTES serum levels were assessed using enzyme-linked immunosorbent assay (ELISA). Patients underwent cardiac magnetic resonance imaging at one month. Major adverse cardiovascular events (MACE: death, hospitalization for heart failure, MI, stroke) were prospectively recorded over the 12-month follow-up. Mean age of the study population was 59 ± 12 years and 54.6% patients exhibited anterior MI. Serum RANTES level raised from 12.6 [7.6–20.8] ng/mL at H0 to 13.9 [7.6–20.8] ng/mL at H4 and decreased gradually until 1 month at 9.3 [4.9–13.6] ng/mL (Kruskal–Wallis test, P < 0.0001). RANTES area under curve (AUC) level was not correlated with IS (r = −0.03, P = 0.70) or LVEF assessed by MRI (r = 0.02, P = 0.80). Patients with a RANTES AUC serum level below the first tertile value of the population (411.0 ng.h.mL−1) were more likely to have a MACE during the first 12 months after STEMI [hazard ratio at 2.9 (1.3–6.6), P = 0.01]. In a multivariable Cox regression analysis with a model including age, gender, troponin peak, and TIMI flow grade after PCI, RANTES AUC serum level below the first tertile remained associated with an increased risk of experiencing MACE during the 12 months of follow-up [adjusted HR = 2.6 (1.2–5.8), P = 0.02]. A low level of circulating RANTES at the acute phase of STEMI was associated with an increased risk of experiencing MACE in our population. Serum RANTES might be a valuable prognostic marker in STEMI patients.

Роль генов систем натрийуретических пептидов и антиоксидантной защиты в формировании риска развития инфаркта миокарда (предварительные результаты пилотного исследования)

Aim: to reveal a relationship of single-nucleotide polymorphic variants of the genes of the natriuretic peptides, antioxidant defense systems and the endothelial function with the development of myocardial infarction. Patients and Methods: the study included 146 patients with myocardial infarction (MI) and maintained or moderately decreased left ventricular ejection fraction: 108 males and 38 females with a mean age of 57 (51; 64) years. The control group was composed of Kemerovo city residents without acute MI (n=300, 190 females and 110 males). To make the evaluation, genomic DNA was isolated from the peripheral blood by phenol- chloroform extraction according to the standard protocol. Real-time PCR method was used for genotyping. To conduct the study, 24 polymorphic variants of 14 genes (those of the natriuretic peptides, antioxidant defense systems and the endothelial function) were selected. Results: significant associations with the allelic variants of CBR1 and CBR3 genes (carbonyl reductase 1 and 3 genes) of the antioxidant defense system were found in the sample of studied patients with MI (not divided by gender or age). When the patients were divided by gender, the following associations were found: in males the single-nucleotide polymorphic variant (SNPV) genotypes CBR1 rs9024 and CBR3 rs1056892 had the protective effect against susceptibility to myocardial infarction (dominant inheritance pattern). It was demonstrated that allelic variants in the NPR2 gene (the gene of atrial natriuretic peptide receptor 2) comprised a risk factor for MI development. In females, a relationship between the assessed genetic factors and the MI development (dominant inheritance pattern) could be associated with SNPV genotypes NPR2 rs13288085 and rs7034957, CBR1 rs9024, and CBR3 rs1056892 which are characterized by the protective effect. Conclusion: some polymorphic variants of the genes of the natriuretic peptide and antioxidant defense systems are associated with the risk and the protective effect against MI susceptibility. The preliminary findings indicate that it is necessary to continue investigations of the identified single-nucleotide polymorphic variants and to assess their impact on the MI severity and the risk of recurrent cardiovascular events in the long-term perspective. KEYWORDS: myocardial infarction, gene, natriuretic peptides, antioxidant defense, polymorphic variants. FOR CITATION: Khutornaya M.V., Khryachkova O.N., Sinitskaya A.V. et al. Role of the genes of the natriuretic peptide and antioxidant defense systems in creating the risk of myocardial infarction development (the preliminary results of a pilot study). Russian Medical Inquiry. 2023;7(1):5–12 (in Russ.). DOI: 10.32364/2587-6821-2023-7-1-5-12.

Abstract 15021: Kinetics and Prognosis Value of Rantes (ccl5) at the Acute Phase of Stemi

Introduction: CCL5 or RANTES is a chemokine that mediates chemotaxis and activation of T cells, monocytes, granulocytes, mast cells and dendritic cells. It is involved in the pathogenesis of several diseases including atherosclerosis but little is known about its role at the acute phase of myocardial infarction (MI). Hypothesis: We questioned whether the serum level of RANTES might be a marker of the severity of acute MI. Methods: We prospectively enrolled 251 consecutive STEMI patients who underwent PCI into a prospective cohort. Blood samples were collected at 5 time points: admission, 4, 24, 48 hours and 1 month after admission (H4, H24, H48, M1). RANTES serum levels were assessed using an ELISA assay. Patients underwent cardiac magnetic resonance imaging at one month. Clinical outcomes were prospectively recorded over 12 months. Results: Mean age of the study population was 59±12 years and 54.6% patients exhibited anterior MI. Serum RANTES level raised from 12.6 [7.6-20.8] ng/mL at H0 to 13.9 [7.6-20.8] ng/mL at H4 and decreased gradually until 1 month at 9.3 [4.9-13.6] ng/mL (Kruskal-Wallis test, p&lt;0.0001). RANTES area under curve (AUC) level was not correlated with IS (r =-0.03, p=0.70) or LVEF assessed by MRI (r=0.02, p=0.80). Patient with a RANTES AUC serum level below the first tertile value of the population (411.0 ng.h.mL -1 ) were more likely to have a MACE during the first 12 months after STEMI (hazard ratio at 2.9 (1.3-6.6), p=0.01). In a multivariable Cox regression analyses with a model including age, gender, troponin peak, and TIMI flow grade after PCI, RANTES AUC serum level below the first tertile remained associated with an increased risk of experiencing MACE during the 12 months of follow-up (adjusted HR = 2.6 (1.2-5.8), p=0.02) Conclusion: A low level of circulating RANTES at the acute phase of STEMI was independently associated with an increased risk of experiencing MACE in our population. Serum RANTES might be a valuable prognostic marker in STEMI patients.

Role of bilirubin in the prognosis of coronary artery disease and its relationship with cardiovascular risk factors: a meta-analysis

BackgroundBilirubin is a heme catabolism product with antioxidant, anti-inflammatory, and anti-apoptotic properties and is implicated in the prognosis of several diseases. This study evaluates the prognostic role of bilirubin in coronary artery disease (CAD) patients.MethodsAfter identifying studies from the literature, meta-analyses were performed to achieve a) overall estimates of serum total bilirubin levels in patients with myocardial infarction (MI), non-MI CAD and healthy individuals; b) odds ratios (OR) of adverse outcomes between higher and lower total bilirubin levels; c) standardized mean difference (SMD) in total bilirubin levels in patients with high vs low CAD severity; and d) correlation between disease severity and total bilirubin. Metaregression analyses were performed to examine the relationship between cardiovascular risk factors and increasing quantiles of total bilirubin levels.ResultsForty-three studies were identified. Pooled serum total bilirubin levels were 0.72 mg/dl [95% confidence interval (CI): 0.60, 0.83] in MI patients; 0.65 mg/dl [95% CI: 0.60, 0.69] in non-MI CAD patients; and 0.66 mg/dl [95% CI: 0.56, 0.75] in healthy individuals. Higher total bilirubin levels were associated with greater odds of adverse outcomes in MI patients (OR: 1.08 [95% CI: 0.99, 1.18]) but lower odds in non-MI CAD patients (OR: 0.80 [95%CI: 0.73, 0.88]). Compared to non-severe cases, total bilirubin levels were higher in patients with severe MI (SMD 0.96 [95% CI: − 0.10, 2.01]; p = 0.074) but were lower in severe non-MI CAD patients (SMD − 0.30 [95%CI: − 0.56, − 0.03]; p = 0.02). Total bilirubin levels correlated positively with MI severity (r = 0.41 [95% CI: 0.24, 0.59]; p < 0.01) but correlated negatively with non-MI CAD severity (r = − 0.17 [95% CI: − 0.48, 0.14]; p = 0.28). Female sex was inversely associated with increasing quantiles of bilirubin (meta-regression coefficient: − 8.164 [− 14.531, − 1.769]; p = 0.016) in MI patients.ConclusionPrognostic role of bilirubin for CAD appears complicated, as different odds are observed for MI and non-MI CAD patients which weakens the case of causal involvement of bilirubin in CAD etiology or prognosis.

Assessing myocardial infarction severity from the urban environment perspective in Wuhan, China.

Health inequalities are globally widespread due to the regional socioeconomic inequalities. Myocardial infarction (MI) is a leading health problem causing deaths worldwide. Yet medical services for it are often inequitably distributed by region. Moreover, studies concerning MI's potential spatial risk factors generally suffer from difficulties in focusing on too few factors, inappropriate models, and coarse spatial grain of data. To address these issues, this paper integrates registered 1098 MI cases and urban multi-source spatio-temporal big data, and spatially analyses the risk factors for MI severity by applying an advanced interpretable model, the random forest algorithm (RFA)-based SHapley Additive exPlanations (SHAP) model. In addition, a community-scale model between spatio-temporal risk factors and MI cases is constructed to predict the MI severity of all communities in Wuhan, China. The results suggest that those risk factors (i.e., age of patients, medical quality, temperature changes, air pollution and urban habitat) affect the MI severity at the community scale. We found that Wuhan residents in the downtown area are at risk for high MI severity, and the surrounding suburb areas show a donut-shape pattern of risk for medium-to-high MI severity. These patterns draw our attention to the impact of spatial environmental risk factors on MI severity. Thus, this paper provides three recommendations for urban planning to reduce the risk and mortality from severe MI in the aspect of policy implication.

Relationship of Midkine in Myocardial Infarction patients and some biochemical parameters

Objectives: This study aims to estimate the concentrations of MK, hs-CRP, TnI, AST, ALT and ALP in serum for MI in comparison to wholesome controls, in an effort to check the quantity of this impact at the pathological condition, in addition to understanding the position of MK in MI sufferers and its relationship to liver function tests and may be used as biochemical markers to decide the severity of MI in sufferers.&#x0D; Methods: The studying include the investigation of midkine (MK), High-sensitivity C-reactive protein (hs-CRP), Troponin I (TnI), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and alkaline phosphatase (ALP) levels in myocardial infarction (MI) patients. The study includes (84) samples: 34 of myocardial infarction patients (19 male and 15 female) and 50 sample of apparently healthy as control group (25 male and 25 female). Samples were collected during the period from Jan. 2021 to July 2021 from in-patients of Cardiac Surgery Center admitted at Ibn Sina Teaching Hospital and Mosul General Hospital, Mosul, Iraq with matching age ranged between 26-86 years. The clinical diagnosis in each case is made according to a cardiovascular specialist.&#x0D; Results: The results showed that there was a significant increase in MK, TnI, GOT, GPT and ALP for all studied groups (males and females) of MI patients compared with control groups, and there was no any a significant in hs-CRP. Beside of, showed significant positive correlation between MK with BMI, hs-CRP, TnI, AST, ALT and ALP in control and patients group. Whereas there were no any correlation between MK with age, in patients and control under study.&#x0D; Conclusion: The study indicated that the MK increased in patients with myocardial infarction, and it’s increased in males more than female patients, and that may act as a good markers for diagnosis of myocardial infarction disease.

Associations of serum high-sensitivity C-reactive protein and prealbumin with coronary vessels stenosis determined by coronary angiography and heart failure in patients with myocardial infarction.

To explore the associations of serum high-sensitivity C-reactive protein (hs-CRP) and prealbumin (PAB) with the number of diseased coronary vessels, degree of stenosis and heart failure in patients with myocardial infarction (MI). A total of 39 MI patients treated in the Cardiology were selected as the observation group, and another 41 patients with normal results of coronary angiography during the same period were selected as the control group. The general data of patients were recorded in detail, the content of serum hs-CRP and PAB in the peripheral blood was detected, and the number of diseased coronary vessels and the degree of stenosis were detected via coronary angiography. Compared with those in control group, the blood pressure and heart rate significantly rose, the content of indexes related to the severity of MI were significantly increased, the content of hs-CRP was significantly increased, and the content of PAB was significantly decreased in observation group. Hs-CRP was positively correlated with the number of diseased coronary vessels, degree of stenosis and heart failure in patients, but PAB was negatively correlated with the above factors. The survival rate of MI patients with high content of hs-CRP was obviously lower than that of patients with low content of hsCRP. Serum hs-CRP and PAB are closely associated with the number of diseased coronary vessels, degree of stenosis and heart failure in MI patients.

Angiotensin II inhibition increases diuresis during acute sympathetic activation in intact and denervated kidneys in rats with chronic myocardial infarction.

We examined urine excretion during primary acute sympathetic activation (PASA) in Wistar-Kyoto rats with myocardial infarction (MI). The rats underwent unilateral renal denervation (RDN) 7weeks after coronary artery ligation. 4-10days later, an acute experiment was performed under anesthetized conditions (n = 8 rats). Isolated carotid sinus pressure was changed stepwise from 60 to 180mmHg, and the relationship between the arterial pressure (AP) and the normalized urine flow (nUF, urine flow normalized by the body weight) was examined. After obtaining the control data, an angiotensin II type 1 receptor blocker telmisartan (2.5mg/kg) was intravenously administered. The effects of RDN, telmisartan, and heart weight (biventricular weight) on the relationship between AP and nUF were examined using multiple regression analyses. Regarding the slope of nUF versus AP (nUFslope), the constant term of the regression was positive (0.315 ± 0.069 μL·min-1·kg-1·mmHg-1), indicating that nUF increased with AP. The heart weight had a negative effect on nUFslope (P < 0.05), suggesting that the severity of MI was associated with the impairment of urine excretion. Telmisartan increased nUFslope by 0.358 ± 0.080 μL·min-1·kg-1·mmHg-1 (P < 0.001), whereas RDN had no significant effect on this parameter. The results indicate that unilateral RDN was unable to abolish the effect of the renin-angiotensin system on urine excretion during PASA. Circulating or locally produced angiotensin II, rather than ongoing renal sympathetic nerve activity, played a dominant role in the impairment of urine excretion during PASA in rats with chronic MI.

Cardiac biomarker release following myocardial infarction: role of exercise

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): ZonMw Background Regular exercise training is an important factor in the prevention of myocardial infarction (MI) and engagement in exercise training is associated with reduced mortality risks following MI. However, the relation between exercise engagement and the magnitude of cardiac biomarker release following MI have not been investigated yet. Purpose To explore the relation between exercise engagement and cardiac biomarker release following a MI. We hypothesized that exercise engagement is associated with lower peak concentrations of cardiac biomarker following MI compared to their non-exercising peers. Methods In this cohort study, we recruited hospitalised MI patients and retrospectively assessed the amount of exercise engagement in the seven days preceding MI onset. Exercise levels were evaluated using a validated questionnaire during a bedside interview. Patients were assigned to the exercise group if they performed any moderate-to-vigorous intensity exercise in the week prior MI and to the control group if they did not perform exercise. Maximum concentrations of cardiac troponin T (max-cTnT), in ng/mL, and creatine kinase (max-CK), in U/L, during hospital stay were extracted from digital health records. Both cardiac biomarker data were classified into 3 groups; 0-499 (small), 500-1499 (medium), and ≥1500 (large). The association of exercise engagement on post-MI cardiac biomarkers was analysed using the Mann-Witney U-test and the chi-square test. Results We included 200 MI patients (male: 64.5%, age 65.2 ± 10.4, 49% STEMI, 51% NSTEMI) of which 39 (19.5%) patients were allocated to the exercise group and 161 (80.5%) to the control group. No differences in time from symptom onset to coronary angiography (565 [136-2048] min versus 581 [135-2059] min, p=0.767) or incident hospital-based major adverse cardiac events (5.6% vs 5.1%, p=0.910) was found across groups. Albeit lower, those engaged in exercise do not significantly differ from controls in post-MI max-cTnT concentrations (788 [326-1344] ng/mL vs 1197 [340-3590] ng/mL, p=0.103) and max-CK concentrations (382 [211-744] U/L vs 564 [203-1374] U/L, p=0.147). The magnitude of max-cTnT was more often classified as ‘small’ in the exercise versus control group (x² (2) = 7.71, p=0.021), whilst a trend was found for max-CK levels (x² (2) = 4.97, p=0.083). Conclusion Engagement in exercise prior to MI may be associated with lower cardiac biomarker release. This could add novel insights into the potential protective effects of exercise engagement in the severity of MI.

Mild Cognitive impairment Occurs in Rats During the Early Remodeling Phase of Myocardial Infarction

Cognitive impairment is a common health problem among people with heart failure (HF). Increases in oxidative stress, brain inflammation, and microglial hyperactivity have been reported in preclinical models of myocardial infarction (MI)-induced HF. We tested the hypothesis that oxidative stress, brain inflammation, mitochondrial dysfunction, and cell death participate in cognitive impairment in the early remodeling phase of MI. Rats underwent either a sham or permanent left anterior descending coronary ligation to induce MI. 1-week post-operation, MI rats with % left ventricular ejection fraction (%LVEF) ≥50 were assigned as a HF with preserved ejection fraction (HFpEF) group and MI rats with %LVEF <50 were assigned as a HF with reduced ejection fraction (HFrEF) group. Cognitive function and biochemical markers were assessed at week 5. The mean value of %LVEF in HFpEF and HFrEF were 63.62 ± 8.33 and 42.83 ± 3.93 respectively, which were lower than in the sham group, suggesting that these rats developed MI with cardiac dysfunction. Hippocampal dependent cognitive impairment was observed in MI rats. Serum, brain, and mitochondrial oxidative stress were all increased in MI rats, along with apoptosis, resulting in dendritic spine loss. However, brain inflammation and AD proteins did not change. In conclusion, during the early remodeling phase of MI, a high level of oxidative stress appears to be a major contributor of cellular damage which is associated with mild cognitive impairment. However, the severity of MI, as evidenced by the %LVEF, was not associated with the degree of cognitive impairment.

Low Molecular Weight Apolipoprotein(a) Phenotype Rather Than Lipoprotein(a) Is Associated With Coronary Atherosclerosis and Myocardial Infarction.

Background and AimsCurrent evidence suggests that lipoprotein(a) [Lp(a)] level above 50 mg/dL is associated with increased cardiovascular risk. Our study aim was to determine the relationship of apolipoprotein(a) [apo(a)] phenotypes and Lp(a) concentration below and above 50 mg/dL with coronary atherosclerosis severity and myocardial infarction (MI).Material and MethodsThe study population consisted of 540 patients (mean age 54.0 ± 8.8 years, 82% men) who passed through coronary angiography. The number of diseased major coronary arteries assessed atherosclerosis severity. Lipids, glucose, Lp(a) levels and apo(a) phenotypes were determined in all patients. All patients were divided into four groups: with Lp(a) <50 mg/dL [ “normal” Lp(a)] or ≥50 mg/dL [hyperLp(a)], and with low-molecular (LMW) or high-molecular weight (HMW) apo(a) phenotypes.ResultsBaseline clinical and biochemical characteristics were similar between the groups. In groups with LMW apo(a) phenotypes, the odds ratio (OR; 95% confidence interval) of multivessel disease was higher [10.1; 3.1–33.5, p < 0.005 for hyperLp(a) and 2.2; 1.0–4.9, p = 0.056 for normal Lp(a)], but not in the group with HMW apo(a) and hyperLp(a) [1.1; 0.3–3.3, p = 0.92] compared with the reference group with HMW apo(a) and normal Lp(a). Similarly, MI was observed more often in patients with LMW apo(a) phenotype and hyperLp(a) and normal Lp(a) than in groups with HMW apo(a) phenotype.ConclusionThe LMW apo(a) phenotype is associated with the severity of coronary atherosclerosis and MI even when Lp(a) level is below 50 mg/dL. The combination of Lp(a) level above 50 mg/dL and LMW apo(a) phenotype increases the risk of severe coronary atherosclerosis, regardless of other risk factors.

The Impact of Resilience, Alexithymia and Subjectively Perceived Helplessness of Myocardial Infarction on the Risk of Posttraumatic Stress

The aim of this study was to investigate the impact of resilience, alexithymia and the subjectively perceived severity (fear of death, pain intensity, helplessness) of myocardial infarction (MI) on posttraumatic symptom severity (PTSS) after MI. Patients were assessed with the Posttraumatic Diagnostic Scale (PDS), Resilience Scale (RS-11) and Toronto Alexithymia Scale (TAS-20). Subjectively perceived severity of MI was measured with three items on a 10-point Likert scale. To test our hypothesis, we applied Pearson correlations as well as multiple hierarchical linear regression analyses. A higher resilience score was significantly associated with lower (r = − .39, p < .001) PTSS. Higher scores of alexithymia (r = .38, p < .01) and subjectively perceived helplessness (r = .42, p < .001) were associated with higher PTSS. Multiple hierarchical linear regression analyses revealed that resilience, the TAS-20 subscale difficulty identifying feelings (DIF) and especially subjectively perceived helplessness were independent significant predictors for the PTSS, adjusted R2 = .29, F(5, 102) = 9.57, p < .001. Our results suggest that resilience reduces the PTSS whereas alexithymia and subjectively perceived helplessness increase the risk. Especially the subjectively perceived helplessness explains a high degree of variance of PTSS and should be assessed to hindering further mental health burden.

Meta-Analysis of Nonrandomized Studies to Assess the Optimal Timing of Coronary Artery Bypass Grafting After Acute Myocardial Infarction

The optimal timing of coronary artery bypass grafting (CABG) in patients after an acute myocardial infarction (MI) is unknown. We performed a systematic review and meta-analysis of studies comparing mortality rates in patients who underwent CABG at different time intervals after acute MI. Bias assessments were completed for each study, and summary of proportions of all-cause mortality were calculated based on CABG at various time intervals after MI. A total of 22 retrospective studies, which included a total of 137,373 patients were identified. The average proportion of patients who died when CABG was performed within 6hours of MI was 12.7%, within 6 to 24hours of MI was 10.9%, within 1day of MI was 9.8%, any time after 1day of MI was 3.0%, within 7days of MI was 5.9%, and any time after 7days of MI was 2.7%. Interstudy heterogeneity, assessed using I2 values, showed significant heterogeneity in death rates within subgroups. Only 1 study accounted for immortal time bias, and there was a serious risk of selection bias in all other studies. Confounding was found to be a serious risk for bias in 55% of studies because of a lack of accounting for type of MI, MI severity, or other verified cardiac risk factors. The current publications comparing timing of CABG after MI is at serious risk of bias because of patient selection and confounding, with heterogeneity in both study populations and intervention time intervals.