Acute Phase Of Myocardial Infarction Research Articles

Supplemental Oxygen and Acute Myocardial Infarction - A Systematic Review and Meta-Analysis.

Background: In Japan, oxygen is commonly administered during the acute phase of myocardial infarction (MI) to patients without oxygen saturation monitoring. In this study we assessed the effects of supplemental oxygen therapy, compared with ambient air, on mortality and cardiac events by synthesizing evidence from randomized controlled trials (RCTs) of patients with suspected or confirmed acute MI.Methods and Results: PubMed was systematically searched for full-text RCTs published in English before June 21, 2020. Two reviewers independently screened the search results and appraised the risk of bias. The estimates for each outcome were pooled using a random-effects model. In all, 2,086 studies retrieved from PubMed were screened. Finally, 7,322 patients from 9 studies derived from 4 RCTs were analyzed. In-hospital mortality in the oxygen and ambient air groups was 1.8% and 1.6%, respectively (risk ratio [RR] 0.90; 95% confidence interval [CI] 0.38–2.10]); 0.8% and 0.5% of patients, respectively, experienced recurrent MI (RR 0.44; 95% CI 0.12–1.54), 1.5% and 1.6% of patients, respectively, experienced cardiac shock (RR 1.10; 95% CI 0.77–1.59]), and 2.4% and 2.0% of patients, respectively, experienced cardiac arrest (RR 0.91; 95% CI 0.43–1.94).Conclusions: Routine supplemental oxygen administration may not be beneficial or harmful, and high-flow oxygen may be unnecessary in normoxic patients in the acute phase of MI.

Accurate prediction of drug-induced heterogeneous response of red cell in vivo using a gravity-driven flow cytometry based on a microfluidic chip

The drug-induced diverse response among patients is a severe problem for improving hemorheological character. However, there is no validated method for personalized therapy to the best of our knowledge. Here, we apply a gravity-driven deformability cytometry platform (GD-DCP) to profile the drug response of the red cell deformability (RCD) at the single-cell level using pentoxifylline (PTX) as a model drug, the effect of different concentrations of PTX (0, 2, 20, 200 μg mL−1, the clinical dosage of PTX is 20 μg mL−1) on RCD in patients with cardiovascular disease was explored. Based on the GD-DCP, about 38 and 56% of the acute phase of acute myocardial infarction (AMI) patients in the acute phase and coronary heart disease (CHD) patients respond positively to PTX, respectively, indicating that PTX has a strong patient dependency on RCD. Moreover, RCD is observed to be significantly inversely correlated with the activation of membrane protein kinase C (PKC) as well as the concentration of Ca2+ (both P < 0.001). The results of animal experiments show that the protective effects of PTX on myocardial ischemia rats have substantial individual variation, too. It is noted that the effect of PTX is highly consistent between RCD in vitro and in vivo outcomes (blood viscosity, myocardial injury, and electrocardiogram (ECG)) in the same rat. All these new findings suggest that the GD-DCP is a promising method that uses deformability in vitro as one of the important criteria in personalized medicine, and our study provides unique insight into the individual-dependent mechanisms of PTX for improving RCD.

Plasma Exosome miRNAs Profile in Patients With ST-Segment Elevation Myocardial Infarction.

BackgroundCirculating microRNAs (miRNAs) have been found to have different expressions in different phases of acute myocardial infarction. The profiles of plasma exosome miRNAs in patients with ST-segment elevation myocardial infarction (STEMI) at 3–6 months postinfarction are unknown.ObjectiveThe aim of this study was to assess the profiles of plasma exosome miRNAs in patients with STEMI in comparison with healthy volunteers and to select specific exosome miRNAs related to pathophysiological changes post-STEMI.MethodsPlasma and echocardiography parameters were collected from 30 patients 3–6 months after STEMI and 30 healthy volunteers. Plasma exosome miRNAs were assessed by using high-throughput sequence (Illumina HiSeq 2500) and profile of the plasma exosome miRNAs was established in 10 patients and 6 healthy volunteers. The specific exosome miRNAs related to heart diseases were selected according to the TargetScan database. The specificity of the selected exosome miRNAs was evaluated in additional 20 post-STEMI patients and 24 healthy volunteers by using quantitative PCR (qPCR). Left ventricular remodeling (LVR) was defined using the European Association of Cardiovascular Imaging criteria according to echocardiography examination. Correlations between expression of the specific miRNAs and echocardiography parameters of LVR were assessed using the Spearman correlation analysis.ResultsTwenty eight upregulated miRNAs and 49 downregulated miRNAs were found in patients 3–6 months after STEMI (p < 0.01) in comparison with the healthy volunteers. The two least expressed and heart-related exosome miRNAs were hsa-miR-181a-3p (0.64-fold, p < 0.01) and hsa-miR-874-3p (0.50-fold, p < 0.01), which were further confirmed by using qPCR and demonstrated significant specificity in another 20 patients with post-STEMI comparing to 24 healthy volunteers [area under the curve (AUC) = 0.68, p < 0.05; AUC = 0.74, p < 0.05]. The expression of hsa-miR-181a-3p was downregulated in patients with LV adverse remodeling in comparison with patients without LV adverse remodeling and healthy volunteers.ConclusionCirculating exosome miR-874-3p and miR-181a-3p were downregulated in patients with STEMI postinfarction. Exosome hsa-miR-181a-3p might play a potential role in the development of LVR in patients with post-STEMI.

Clinical Value and Detection Rate Analysis of Electrocardiogram in the Diagnosis of Hyperacute Phase of Acute Myocardial Infarction

Clinical Value and Detection Rate Analysis of Electrocardiogram in the Diagnosis of Hyperacute Phase of Acute Myocardial Infarction

Predictive inflammatory biomarkers for left ventricular thrombus in acute myocardial infarction

Left ventricular thrombus (LVT) is a complication caused by acute myocardial infarction (MI). In addition to anterior localization and low left ventricular ejection fraction (LVEF), some studies suggest an association between LVT and the level of inflammatory biomarkers. The aim of our study was to assess the relationship between inflammatory biomarkers at the acute phase of MI and the presence of LVT assessed by cardiac magnetic resonance (CMR) in acute ST-elevation MI patients. In total, 187 patients with acute STEMI were included in the prospective HIBISCUS cohort. Blood samples were collected at 5 time-points: upon admission, 4, 24, 48 hours after admission (H4, H24, H48) and at 1 month (M1). Three groups of inflammatory biomarkers serum levels were assessed using ELISA assays at each time-point. Cellular biomarkers were assessed using fluorescence-activated cell sorting. All patients had a complete CMR study at one month. STEMI patients had a median age of 56 years [50–63], and 50% ( n = 101) had an anterior MI. Twenty-eight patients (15.0%) had an LVT. Patients with LVT presented a higher peak of interleukin-6 (IL-6) compared to patients without LVT (9.4 pg/mL [5.3–17.8] versus 4.2 pg/mL [1.9–9.9], respectively; P = 0.02). They also presented significantly higher peaks of suppressor tumor 2 (ST2) (34.9 ng/mL [21.0–59.9] versus 22.1 ng/mL [13.0–33.9], P = 0.0005), vascular cell adhesion molecule 1 (VCAM-1) (413 ng/L [363–535] versus 333 ng/L [282–434], P < 0.005), and C-reactive protein (47.4 mg/L [16.3–99.8] versus 12.0 mg/L [6.7–42.7], P = 0.004). Patients with LVT had higher numbers of monocytes (1.2 G/L [1.0–1.4] versus 0.9 G/L [0.7–1.1], P = 0.0001) and neutrophils (9.8 G/L [8.1–10.9] versus 7.2 G/L [5.5–9.1], P = 0.0002) compared to patients without. In the multivariate analysis adjusting on LVEF and infarct size (IS), only peak levels of monocytes, neutrophils and VCAM-1 remained significantly associated with LVT. High levels of circulating ST2, IL-6, VCAM-1, CRP, neutrophils and monocytes were associated with an increased risk of LV thrombus after STEMI.

P185 META–ANALYSIS OF PLACEBO–CONTROLLED TRIALS OF LEVOSIMENDAN IN ACUTE MYOCARDIAL INFARCTION

Abstract Introduction Despite the potential beneficial effects in the acute phase of myocardial infarction, the use of Levosimendan in recent guidelines is currently limited to patients with heart failure and a severe reduction in cardiac output not responding to standard therapy. In spite of everything, the haemodynamic effects of the drug that reduces afterload, the beneficial pleiotropic effects on myocardial stunning and the improvement of microcirculatory indices make Levosimendan still an interesting therapeutic prospect in AMI. Purpose of the Study The study aimed to analyse the available data of the use of Levosimendan in the acute setting of myocardial infarction Materials and Methods This review was registered in the International Prospective Register of Systematic Reviews (PROSPERO) and was conducted and presented according to best practice recommendations, including the Preferred Reporting Items for Systematic Reviews and Meta–Analyses (PRISMA) reporting guidelines. Seven selected studies were included in the meta–analysis. Meta–Analysis Levosimendan treatment was associated with a reduction in one year mortality and adverse event rates, without inconsistency. A trend of the increase of cardiac index and reduction of wedge pressure was evident, with an inconsistent effect on blood pressure and heart rate. No evidence of small study effects was found upon the inspection of funnel plots or regression tests. Finally, possibly given the limited number of included studies, metaregression analysis did not identify any major effect modifier. Discussion A clearly significant mortality reduction in the acute phase and long–term mortality induced by Levosimendan in AMI is evident. In the acute ischemic field, the haemodynamic properties of Levosimendan may explain part of the benefits. Levosimendan, over an inotropic effect, has a positive effect on ventriculo–arterial coupling, peripheral vasodilation consequently increasing tissue perfusion, anti–stunning effects and anti–inflammatory effects. Conclusions Our data support the idea that Levosimendan may already have a role in the treatment of acute ischemic heart disease. Further studies, specifically designed to investigate the early role in the treatment of ischemic heart failure are needed.

Прогностические маркеры исхода острого периода инфаркта миокарда

Исход острого периода инфаркта миокарда прогнозировался на основании статистического метода с применением алгоритма Data Mining «дерево решений». В качестве входных данных использовались чувствительные и специфические векторкардиографические показатели. Установлены прогностически значимые маркеры исхода острого периода инфаркта миокарда. Если возраст больного был 57 лет и более, а скорость распространения возбуждения по миокарду высоких отделов передней стенки левого желудочка замедлялась до 6,33 мв/с, прогнозировался летальный исход с точностью 92,86 %. В случае регистрации у пациента увеличения площади предсердных петель более 0,188 мм2 (в ВА2) с угловым расхождением петель QRS-P более 15,5° (в ВА1), размыкания петли QRS менее 2,834 мм (в 3-й проекции) и скорости распространения возбуждения в конечной части петли Т менее 2,338 мв/с (в ВА1) при различных значениях углового расхождения вектора QRS-Т (в ВА5) прогнозировался благоприятный исход с точностью 97,67 %.

Early outcome of surgical treatment of 20 cases of postinfartion ventricular septal rupture by extended sandwich patch technique via right ventricle approach

Objective: Different techniques have been described to repair post myocardial infarction ventricular septal rupture (VSR), each method may result in residual shunting, bleeding, and post-operative mortality. The aim of this report is to describe early results of extended sandwich technique through right ventricle in 20 consecutive patients.&#x0D; Patients and Methods: A retrospective, cross-sectional and descriptive study on 20 patients underwent surgery for myocardial infarction VSR by extended sandwich technique through right ventricle from 12/2018 to 3/2021 in Hanoi Heart Hospital.&#x0D; Result: 20 consecutive patients (10 women and 10 men) with postinfarction ventricular septal rupture (mean age 72 years, range 48-84) underwent surgical repair for by extended sandwich technique performed through right ventricle from December 2018 to August 2021 in our institute. Reconstruction of the septum was performed by two patches according to the method described by Asai et al. The mean aortic clamp time was 101. The mean extracorporeal circulation time was 143 min. Postoperative intensive care unit (ICU) stay averaged 4 days (range, 1-10 days). There was 30% hospital mortality. 10% postoperative residual shunting was detected, and no patient needed reoperation for bleeding.&#x0D; Conclusion: This method of extended sandwich technique through right ventricle was safe, simple, and it could be performed in acute phase of myocardial infarction.

Endotoxemia and cardiometabolic biomarkers in patients with acute myocardial infarction. Data from the RICO survey

The complex interplay between endotoxemia, inflammation and cardiometabolic diseases including acute myocardial infarction (MI) is poorly understood. From the RICO survey, patients admitted for acute MI were prospectively included (2016 to 2018). Patients with prior coronary artery disease (CAD) or chronic kidney disease were excluded. Blood samples were taken on admission. Endotoxemia was assessed by the LCM-SMS measurement of circulating levels of LPS-derived 3-hydroxymyristate (3HM), a component of the lipid A moiety. Among the 245 patients included, mean age was 62 ± 13 y, most were male (72%), almost half were hypertensive (43%), or current smokers (44%), 38% had hypercholesterolemia, or family history of CAD (31%), median(IQR) BMI was 27(25-29) kg/m 2 and 14% had diabetes. Median LDL-cholesterol was at 132 mg/dL, HDL-cholesterol at 47 mg/dL, total cholesterol at 209 mg/dL and triglycerides (TG) at 116 mg/dL, 3HM levels at 106(83-131) pmol/L. TG levels were the most strongly correlated with LPS levels ( r = 0.201, P = 0.002), beyond HbA 1c ( r = 0.197, P = 0.002), BMI ( r = 0.192, P = 0.003), cholesterol ( r = 0.191, P = 0.003), blood glucose ( r = 0.174, P = 0.006) and age ( r = 0.173, P = 0.007). Inflammatory biomarkers and cytokines (CRP, IL6, IL8, TNFα) did not significantly relate to 3HM levels. When compared with patients without diabetes, patients with diabetes had ≈40% higher levels of 3HM (140 vs. 103 pmol/L, P < 0.001). TG (ß(95%CI) = 0.288(7.757-20.357)) remained an independent determinant of 3HM levels, beyond age (ß(95%CI) = 0.184(0.274-1.374)), and HbA 1c (ß(95%CI) = 0.157(1.764-15.390)). In patients with acute MI, endotoxemia levels related mainly to chronic metabolic disorders including diabetes and hypercholesterolemia. The underlying mechanisms for the LPS-associated TG elevations and its clinical significance at the acute phase of MI remains to be explored.

Mid-regional pro-adrenomedullin and lactate dehydrogenase as predictors of left ventricular remodeling in patients with myocardial infarction treated with percutaneous coronary intervention.

The main impact of myocardial infarction (MI) is shifting from acute mortality to adverse remodeling, chronic left ventricular (LV) dysfunction, and heart failure. The aim of this study was to assess relationships between levels of circulating biomarkers and the function of LV after MI. This was a prospective study of 80 patients with MI treated with percutaneous coronary intervention. Novel biomarkers including mid‑regional pro‑adrenomedullin (MR‑proADM), Notch‑1, syndecan‑4, myeloperoxidase, S‑100 protein, soluble ST‑2, as well as markers of inflammatory response and tissue injury: galectin‑3, C‑reactive protein (CRP), lactate dehydrogenase (LDH), and interleukin‑6 (IL‑6) were assessed in the acute phase of MI. Echocardiography was performed at baseline and 6 month Results: Adverse remodeling, defined as more than 20% increase in LV end‑diastolic volume, occurred in 26% of patients. Reverse remodeling (>10% reduction in LV end‑systolic volume) was observed in 52% of patients. In the univariable analysis, higher levels of MR‑proADM and LDH were predictors of adverse remodeling and higher levels of MR ‑proADM, LDH, CRP, and IL ‑6 were negative predictors of reverse remodeling. In the multivariable model, LDH remained an independent predictor of adverse remodeling (odds ratio [OR], 3.13; 95% CI, 1.42-8.18; P = 0.003) and a negative predictor of reverse remodeling (OR, 0.37; 95% CI, 0.17-0.8; P = 0.005). LDH and MR ‑proADM seem to be promising biomarkers of adverse remodeling. On the other hand, higher levels of these biomarkers were associated with reduced chance of occurrence of favorable reverse remodeling in MI patients. However, further studies on larger groups of patients are necessary to confirm these data.

Abstract 13267: The Shifted Balance of Arginine Metabolites in Patients With Acute Myocardial Infarction and Its Association With the Composition of the Infarct-Related Culprit Lesion

Introduction: We hypothesize that acute phase of myocardial infarction (MI) is associated with suppression of nitric oxide synthase (NOS) and enhanced arginase activity. Moreover, this altered metabolic balance might correlate with the composition of vulnerable culprit lesion in the infarct-related coronary artery (IRA). Methods: Arginine metabolites (μM) including ornithine, citrulline, proline, spermine, spermidine, agmatine, homoarginine, creatine, asymmetric dimethylarginine (ADMA) and monomethyl-L-arginine acetate were measured using liquid chromatography and tandem mass spectrometry in 85 consecutive MI patients upon admission and at 6-month follow-up and were compared with the composition of the IRA culprit lesion assessed with optical coherence tomography (OCT). Results: The concentration of ornithine in acute phase of MI was higher by 44% and homoarginine by 62% whereas level of arginine was lower by 39% and citrulline by 64% (P&lt;0.001 for all), when compared to 6-month stable conditions. Following ischemia, the ratios of citrulline/arginine (0.10 [0.08; 0.14] vs 0.22 [0.18; 0.28]) and citrulline/ornithine (0.09 [0.07; 0.12] vs 0.47 [0.36; 0.55]) were decreased while the indices of ornithine/arginine (1.48 [1.08, 2.39] vs 0.50 [0.41, 0.60]) and homoarginine/arginine (0.17 [0.12; 0.22] vs 0.04 [0.03; 0.05]) were higher as compared with 6-month results (P&lt;0.001 for all). Both, concentrations of arginine metabolites and their ratios were not associated with the mechanism of IRA occlusion, the amount of calcium or lipids and the presence of intramural hematoma. However, in patients with (n=67) versus without (n=18) thin-cap fibroatheroma (TCFA) in OCT the higher median concentrations of ornithine (10.24 [7.86; 12.52] vs 7.82 [4.38; 9.57]), ADMA (0.40 [0.29; 0.49] vs 0.29 [0.23; 0.42]), homoarginine (1.02 [0.81; 1.27] vs 0.74 [0.62; 1.00]) and a higher ornithine/arginine ratio (1.73 [1.29; 2.54] vs 1.18 [1.01; 2.07]) with a lower citrulline/ornithine ratio (0.07 [0.09; 0.11] vs 0.13 [0.09; 0.15]) were found (P&lt;0.05 for all). Conclusions: During acute phase of MI the altered balance of arginine metabolites indicates NOS suppression and enhanced arginase activation and is associated with the presence of TCFA in IRA culprit lesion.

Innate Lymphoid Cells and Myocardial Infarction.

Myocardial infarction results from obstruction of a coronary artery that causes insufficient blood supply to the myocardium and leads to ischemic necrosis. It is one of the most common diseases threatening human health and is characterized by high morbidity and mortality. Atherosclerosis is the pathological basis of myocardial infarction, and its pathogenesis has not been fully elucidated. Innate lymphoid cells (ILCs) are an important part of the human immune system and participate in many processes, including inflammation, metabolism and tissue remodeling, and play an important role in atherosclerosis. However, their specific roles in myocardial infarction are unclear. This review describes the current understanding of the relationship between innate lymphoid cells and myocardial infarction during the acute phase of myocardial infarction, myocardial ischemia-reperfusion injury, and heart repair and regeneration following myocardial infarction. We suggest that this review may provide new potential intervention targets and ideas for treatment and prevention of myocardial infarction.

NETs promote pathogenic cardiac fibrosis and participate in ventricular aneurysm formation after ischemia injury through the facilitation of perivascular fibrosis

Fibrosis has been widely investigated in acute phase of myocardial infarction (MI). However, the mechanism of sustained fibrosis after MI hasn't been elucidated, which eventually gives rise to ventricular aneurysm (VA) formation chronic while lethal. Neutrophil as vital cell facilitating the fibrotic repair after acute MI may not project its effect to chronic phase unless neutrophil extracellular traps (NETs) were secreted and accumulating. The aim of this study was to investigate whether NETs contribute to the sustained fibrosis and VA formation after MI. We identified NETs in ventricular aneurysm of patients. Accordingly, NETs increased in peripheral blood of VA patients. Moreover, in rat VA NETs were also identified. Stimulated by NETs, the migration of fibroblast was enhanced and the differentiation of cardiac myofibroblast was initiated. Smad, MAPK and RhoA signaling pathways were activated by NETs incubation. And additional deposition with DNase I to disrupt NETs and abrogated NETs induced fibrosis both in vivo and vitro. These results collectively demonstrate a novel profibrotic role for NETs in chronic cardiac fibrosis and VA formation.

Glycosylated apolipoprotein J in cardiac ischaemia: molecular processing and circulating levels in patients with acute ischaemic events.

Using proteomics, we previously found that serum levels of glycosylated (Glyc) forms of apolipoprotein J (ApoJ), a cytoprotective and anti-oxidant protein, decrease in the early phase of acute myocardial infarction (AMI). We aimed to investigate: (i) ApoJ-Glyc intracellular distribution and secretion during ischaemia; (ii) the early changes in circulating ApoJ-Glyc during AMI; and (iii) associations between ApoJ-Glyc and residual ischaemic risk post-AMI. Glycosylated apolipoprotein J was investigated in: (i) cells from different organ/tissue origin; (ii) a pig model of AMI; (iii) de novo AMI patients (n = 38) at admission within the first 6 h of chest pain onset and without troponin T elevation at presentation (early AMI); (iv) ST-elevation myocardial infarction patients (n = 212) who were followed up for 6 months; and (v) a control group without any overt cardiovascular disease (n = 144). Inducing simulated ischaemia in isolated cardiac cells resulted in an increased intracellular accumulation of non-glycosylated ApoJ forms. A significant decrease in ApoJ-Glyc circulating levels was seen 15 min after ischaemia onset in pigs. Glycosylated apolipoprotein J levels showed a 45% decrease in early AMI patients compared with non-ischaemic patients (P < 0.0001), discriminating the presence of the ischaemic event (area under the curve: 0.934; P < 0.0001). ST-elevation myocardial infarction patients with lower ApoJ-Glyc levels at admission showed a higher rate of recurrent ischaemic events and mortality after 6-month follow-up (P = 0.008). These results indicate that ischaemia induces an intracellular accumulation of non-glycosylated ApoJ and a reduction in ApoJ-Glyc secretion. Glycosylated apolipoprotein J circulating levels are reduced very early after ischaemia onset. Its continuous decrease indicates a worsening in the evolution of the cardiac event, likely identifying patients with sustained ischaemia after AMI.

Newly Diagnosed Atrial Fibrillation in Acute Myocardial Infarction.

BackgroundIt remains controversial whether long‐term clinical impact of newly diagnosed atrial fibrillation (AF) in the acute phase of acute myocardial infarction (AMI) is different from that of prior AF diagnosed before the onset of AMI.Methods and ResultsThe current study population from the CREDO‐Kyoto AMI (Coronary Revascularization Demonstrating Outcome Study in Kyoto Acute Myocardial Infarction) Registry Wave‐2 consisted of 6228 patients with AMI who underwent percutaneous coronary intervention. The baseline characteristics and long‐term clinical outcomes were compared according to AF status (newly diagnosed AF: N=489 [7.9%], prior AF: N=589 [9.5%], and no AF: N=5150 [82.7%]). Median follow‐up duration was 5.5 years. Patients with newly diagnosed AF and prior AF had similar baseline characteristics with higher risk profile than those with no AF including older age and more comorbidities. The cumulative 5‐year incidence of all‐cause death was higher in newly diagnosed AF and prior AF than no AF (38.8%, 40.7%, and 18.7%, P<0.001). The adjusted hazard ratios (HRs) for mortality of newly diagnosed AF and prior AF relative to no AF remained significant with similar magnitude (HR, 1.31; 95% CI, 1.12–1.54; P<0.001, and HR, 1.32; 95% CI, 1.14–1.52; P<0.001, respectively). The cumulative 5‐year incidence of stroke decreased in the order of newly diagnosed AF, prior AF and no AF (15.5%, 12.9%, and 6.3%, respectively, P<0.001). The higher adjusted HRs of both newly diagnosed AF and prior AF relative to no AF were significant for stroke, with a greater risk of newly diagnosed AF than that of prior AF (HR, 2.05; 95% CI, 1.56–2.69; P<0.001, and HR, 1.33; 95% CI, 1.00–1.78; P=0.048, respectively). The higher stroke risk of newly diagnosed AF compared with prior AF was largely driven by the greater risk within 30 days. The higher adjusted HRs of newly diagnosed AF and prior AF relative to no AF were significant for heart failure hospitalization (HR, 1.73; 95% CI, 1.35–2.22; P<0.001, and HR, 2.23; 95% CI, 1.82–2.74; P<0.001, respectively) and major bleeding (HR, 1.46; 95% CI, 1.23–1.73; P<0.001, and HR, 1.36; 95% CI, 1.15–1.60; P<0.001, respectively).ConclusionsNewly diagnosed AF in AMI had risks for mortality, heart failure hospitalization, and major bleeding higher than no AF, and comparable to prior AF. The risk of newly diagnosed AF for stroke might be higher than that of prior AF.

Outcomes for patients with anterior myocardial infarction and prior cardiac arrest in the home automated external defibrillator trial (HAT)

BackgroundPatients with sudden cardiac arrest occurring in the acute phase of myocardial infarction (MI-SCA) are believed to be at similar risk of death after revascularization compared with MI patients without SCA (MI-no SCA). Among patients with anterior MI, we examined whether those with MI-SCA were at greater risk of all-cause mortality or sudden cardiac death (SCD) than MI-no SCA patients. MethodsThe Home Automated External Defibrillator Trial enrolled patients with anterior MI who had not received or were candidates for an implantable cardioverter defibrillator (ICD). Our cohort included patients with a reported SCA event, in the acute phase of an MI, prior to HAT trial enrollment. Cox proportional hazards models examined the adjusted association between MI-SCA versus MI-no SCA patients and all-cause mortality and sudden cardiac death (SCD). We also determined whether the relationship between prior SCA and outcomes changed with subsequent events (syncope, revascularization, and recurrent MI) during follow-up. ResultsOf 6849 patients, 650 (9.5%) had MI-SCA before trial enrollment. Approximately 48% of patients had the MI-SCA event ≤1 year prior to enrollment; 71% of SCA events were in-hospital. MI-SCA patients were younger, more frequently white, and had higher rates of prior PCI versus MI-no SCA patients. There were no differences in adjusted all-cause mortality (hazard ratio [HR 0.95; 95% CI 0.65–1.38]) or SCD (HR 1.12; 95% CI 0.68–1.83) for MI-SCA vs. MI-no SCA. After ICD implantation, MI-SCA patients experienced higher all-cause mortality risk (HR 5.01, 95% CI 1.05–23.79) versus MI-no SCA patients; there was no mortality difference between MI-SCA and MI-no SCA patients without ICD implantation (HR 0.89, 95% CI 0.60–1.31), [interaction p = 0.035]. ConclusionsPatients with MI-SCA had similar adjusted risk of all-cause mortality and SCD compared with MI-no SCA. After ICD implantation, MI-SCA patients had higher mortality compared with MI-no SCA patients.

Biomarkers of Systemic Versus Local Inflammation During the Acute Phase of Myocardial Infarction, as Predictors of Post-infarction Heart Failure

Abstract Background: The aim of this study was to investigate the correlation between serum biomarkers of left ventricular dysfunction and systemic inflammation in the first days after the acute episode, and to investigate their role for early identification of patients at high risk for post-infarction heart failure. Materials and methods: In total, 123 subjects admitted to the Intensive Cardiovascular Care Unit of the Cardiology Clinic of the Târgu Mureș County Clinical Emergency Hospital, Romania, with acute myocardial infarction were retrospectively analyzed in this study. Based on the level of NT-proBNP, the study population was divided into 2 groups: Group 1 (n = 92), with NT-proBNP &lt;3,000 pg/mL, and Group 2 (n = 31), with NT-proBNP &gt;3,000 pg/mL. Results: Biomarkers reflecting systemic inflammation presented significantly higher values in patients with elevated NT-proBNP (hs-CRP – 12.3 ± 8.9 mg/L vs. 3.6 ± 6.7 mg/L, p &lt;0.0001, and interleukin 6 – 27.6 ± 30.7 pg/mL vs. 8.6 ± 6.2 pg/mL, p &lt;0.0001). However, cell adhesion molecules VCAM and ICAM were not significantly different between the groups. Patients in Group 2 presented significantly higher rates of major cardiovascular events and rehospitalizations in the first year after the acute coronary event, with 13.33% event rate for patients in Group 2 compared to 8.7% in Group 1 (p &lt;0.05). Conclusions: Serum biomarkers of ventricular dysfunction are strongly associated with systemic inflammation and ventricular impairment in the immediate phase after an acute myocardial infarction. Systemic inflammation has a higher impact on the clinical outcomes and progression to heart failure than the local coronary inflammation expressed by cell adhesion molecules.

Adjustment Mechanisms in the Acute Phase of Myocardial Infarction in Men.

Stress and Coping Model and Post-Traumatic Growth Theory indicate adjustment procedures concepts after a crisis. The objective of this study was to assess the relationships between causal attributions, coping strategies and post-traumatic growth in male patients with acute myocardial infarction and variable cardiac function severity. Seventy-eight male patients surviving a myocardial infarction, were divided into two sub-groups based on left ventricular ejection fraction measurements [Group A (left ventricular ejection fraction: <45%, n = 34), Group B (left ventricular ejection fraction: ≥45%, n = 44)] and were interviewed after the acute phase of myocardial infarction, on the last day of their coronary unit stay. Medical data was obtained from their medical records. Causal Attributions' List, Coping Orientation to Problems Experienced and Post-Traumatic Growth Inventory were used. Causal attributions were found to be related to active coping, emotional support, religious coping and self-blame in both groups. Planning, positive reinterpretation and active coping were the strategies associated positively with most of the post-traumatic inventory subscales in total data analyses. Diverse coping strategies were associated with posttraumatic growth factors. It is important to assess adjustment mechanisms in the acute phase of myocardial infarction. A tailored scheme therapy, considering patient's needs, has to be planned.

Role of β-Adrenergic Receptors and Estrogen in Cardiac Repair after Myocardial Infarction: An Overview.

Acute myocardial infarction (MI) is associated with an intense inflammatory response that is critical for cardiac repair but is also involved in the pathogenesis of adverse cardiac remodeling, i.e., the set of size, geometry, and structure changes that represent the structural substrate for the development of post-MI heart failure. Deciphering the pathophysiological mechanisms underlying cardiac repair after MI is, therefore, critical to favorably regulate cardiac wound repair and to prevent development of heart failure. Catecholamines and estrogen play an active role in regulating the inflammatory response in the infarcted area. For example, stress-induced catecholamines alter recruitment and trafficking of leukocytes to the heart. Additionally, estrogen affects rate of cardiac rupture during the acute phase of MI, as well as infarct size and survival in animal models of MI. In this review, we will summarize the role of β-adrenergic receptors and estrogen in cardiac repair after infarction in preclinical studies.

INFLUENCE OF FIBRINOLYTIC THERAPY ON THE APPEARANCE OF COMPLICATIONS IN ACUTE PHASE OF MYOCARDIAL INFARCTION IN PATIENTS WITH CONCOMITANT DIABETES MELLITUS TYPE 2

It was examined 15 patients with acute myocardial infarction and were divided on groups depending on the presence or absence of concomitant diabetes mellitus type 2 and selected tactics of treatment (fibrinolytic or standart antiplatelet therapy). It was estimated requency of the complications development in acute period of myocardial infarction. It was found that patients with concomitant diabetes mellitus the most frequently had complicated course of acute phase of myocardial infarction in comparison with patients without previous fibrinolytic therapy. Using of fibrinolytic therapy has leveled the negative influence of diabetes mellitus on short-term prognosis of these patients. It’s confirmed the necessity of its carrying out in patients with co morbid pathology.